Clinical Medicine and Surgery I · Exam 4 — Clin Med Pro Guide

Name of Condition

Primary (essential) hypertension (HTN); adult hypertension Slides 4, 10

Definition

Persistent blood pressure (BP) elevation with no single identifiable cause; ACC/AHA (American College of Cardiology/American Heart Association) categories: normal <120/<80; elevated 120–129/<80; stage 1 130–139 or 80–89; stage 2 ≥140 or ≥90; use the higher category when systolic and diastolic differ Slides 4, 10

Etiology (cause)

Polygenic susceptibility interacting with environmental exposures over time; a combination of mechanisms, not a single cause Slides 10, 11

Epidemiology (who)

About 90–95% of hypertension; adult prevalence 47.7% (≥130/80 or on medication), rising with age (23.4% at 18–39, 52.5% at 40–59, 71.6% at ≥60); 59.2% aware, 51.2% treated, 20.7% controlled; common in middle/older age but not restricted to it Slides 7, 8, 10

Risk Factors

Advancing age; family history; excess (central) adiposity; high dietary sodium; physical inactivity; excess alcohol; dyslipidemia; insulin resistance Slide 10

Pathology

Vascular narrowing raises resistance; sympathetic activation raises heart rate and output; RAAS (renin-angiotensin-aldosterone system): angiotensin II vasoconstricts and releases aldosterone (salt and water retention); impaired natriuresis (kidneys need higher pressure to excrete salt) Slide 11

Clinical Manifestation

Most patients have no reliable BP-related symptoms; headache is common but nonspecific and not a valid indicator of BP level or control; feeling well does not establish control Slide 37

Diagnosis

Averaged, properly measured readings (rest ≥5 minutes, back supported, arm at heart level, correct cuff, ≥2 readings) → confirm out of office (home BP twice daily for 7 days, averaged) → diagnose pattern; baseline: CMP (comprehensive metabolic panel), eGFR (estimated glomerular filtration rate), UACR (urine albumin-to-creatinine ratio), urinalysis, CBC (complete blood count), glucose or HbA1c (hemoglobin A1c), lipids, TSH (thyroid-stimulating hormone), 12-lead ECG (electrocardiogram), annual retinal exam Slides 38, 44, 45, 51

Treatment/Therapy

Lifestyle for all (DASH (Dietary Approaches to Stop Hypertension) diet, sodium <2,300 mg/day, aerobic plus resistance exercise, weight loss, limit alcohol, stop smoking); goal <130/80; stage 1: drug if CVD (cardiovascular disease), diabetes, CKD (chronic kidney disease), or PREVENT 10-year risk ≥7.5%, one agent; stage 2: two agents; first-line thiazide-type diuretic (chlorthalidone preferred), ACE (angiotensin-converting enzyme) inhibitor or ARB (angiotensin receptor blocker), dihydropyridine CCB (calcium channel blocker); never ACE inhibitor + ARB; Black adults: thiazide or CCB; pregnancy: labetalol, nifedipine, methyldopa (avoid ACE inhibitor/ARB) Slides 46, 53, 55, 61, 62, 65

Mortality ★

Not covered in the lecture

Name of Condition

Hypertensive emergency Slide 5

Definition

Severe BP (blood pressure) elevation with acute hypertension-mediated organ injury; no absolute numeric cutoff (often >180 systolic and/or >120 diastolic, but lower values with injury qualify); severe BP without acute organ injury is not an emergency Slides 5, 69

Etiology (cause)

Not covered in the lecture

Epidemiology (who)

Not covered in the lecture

Risk Factors

Not covered in the lecture

Pathology

Autoregulation is impaired at severely elevated BP, so overly rapid lowering causes hypoperfusion injury Slide 69

Clinical Manifestation

Acute organ injury: hypertensive encephalopathy, acute pulmonary edema, AKI (acute kidney injury), aortic dissection, ACS (acute coronary syndrome); red flags: confusion, seizures, altered consciousness, visual disturbance, focal deficit, abrupt severe headache, chest/back pain, dyspnea, oliguria; optic disc edema on fundoscopy Slides 5, 37, 40

Diagnosis

Organ injury, not the number, defines it; do not delay while awaiting repeat visits; ECG (electrocardiogram), troponin, BNP/NT-proBNP (B-type natriuretic peptide); creatinine, urinalysis, UACR (urine albumin-to-creatinine ratio); urgent CT (computed tomography) or MRI (magnetic resonance imaging) for neurologic signs; chest radiograph for pulmonary edema or widened mediastinum Slides 5, 42, 44, 49

Treatment/Therapy

Stabilize airway, breathing, circulation; IV (intravenous) access, continuous monitoring; titratable IV agent matched to organ syndrome; lower MAP (mean arterial pressure) ≤20–25% in hour 1, ~160/100–110 over 2–6 hours, normal over 24–48 hours (except aortic dissection, some strokes); too-rapid lowering risks stroke, myocardial injury, renal failure; pulmonary edema: IV nitroglycerin or nitroprusside, oxygen, CPAP (continuous positive airway pressure), or BiPAP (bilevel positive airway pressure), loop diuretic if overloaded Slides 69, 76

Mortality ★

Not covered in the lecture

Name of Condition

Hypertensive urgency (term no longer used) Slide 5

Definition

Severe BP (blood pressure) elevation (typically systolic ≥180 and/or diastolic ≥110–120 mm Hg) without signs of acute, life-threatening target-organ damage Slide 5

Etiology (cause)

Not covered in the lecture

Epidemiology (who)

Not covered in the lecture

Risk Factors

Not covered in the lecture

Pathology

Not covered in the lecture

Clinical Manifestation

No acute organ injury; the same BP (e.g., 226/128) in an asymptomatic outpatient is not an emergency Slides 5, 76

Diagnosis

Not covered in the lecture

Treatment/Therapy

Not covered in the lecture

Mortality ★

Not covered in the lecture

Name of Condition

Resistant hypertension (apparent vs true) Slides 6, 66

Definition

BP (blood pressure) above goal despite concurrent use of 3 antihypertensives of different, complementary classes at maximally tolerated doses Slides 6, 66

Etiology (cause)

Apparent resistance: measurement error (cuff size, technique), white coat effect, medication nonadherence (most common cause), high sodium or alcohol intake, interfering drugs (NSAIDs (nonsteroidal anti-inflammatory drugs), stimulants), undiagnosed OSA (obstructive sleep apnea) or secondary hypertension Slide 66

Epidemiology (who)

Not covered in the lecture

Risk Factors

Not covered in the lecture

Pathology

Not covered in the lecture

Clinical Manifestation

Persistently elevated BP on three drugs; resistant BP is a clue to secondary hypertension (e.g., with hypokalemia or snoring and witnessed apneas) Slides 12, 66, 73

Diagnosis

Before labeling: confirm adherence, cuff size, technique; out-of-office BP to exclude white coat effect; screen secondary causes (aldosterone-renin ratio after correcting hypokalemia; sleep study) Slides 66, 74

Treatment/Therapy

Optimize diuretic (switch HCTZ (hydrochlorothiazide) to chlorthalidone); maximize ACE (angiotensin-converting enzyme) inhibitor/ARB (angiotensin receptor blocker) + dihydropyridine CCB (calcium channel blocker); add spironolactone (best-evidence 4th agent; monitor potassium, creatinine); then beta blocker, alpha-1 blocker, central agent, or hydralazine/minoxidil; refer to hypertension specialist Slides 58, 67

Mortality ★

Not covered in the lecture

Name of Condition

Secondary hypertension Slide 12

Definition

Hypertension attributable to an identifiable underlying condition or exposure Slide 12

Etiology (cause)

Common: OSA (obstructive sleep apnea), CKD (chronic kidney disease), primary aldosteronism, drugs/alcohol, renovascular disease; uncommon: hypo-/hyperthyroidism, pheochromocytoma/paraganglioma, aortic coarctation, Cushing syndrome Slides 12, 24

Epidemiology (who)

About 5–25% estimate; varies by population and how aggressively it is sought Slide 12

Risk Factors

Not covered in the lecture

Pathology

Not covered in the lecture

Clinical Manifestation

Early, abrupt new-onset, or resistant BP (blood pressure) or sudden loss of prior control; unexplained hypokalemia; organ damage disproportionate to BP; abnormal renal function; snoring/apneas, paroxysmal headache/sweating, proximal weakness Slide 12

Diagnosis

Focused testing by suspected cause: aldosterone-renin ratio, plasma/urinary metanephrines, cortisol testing, renal duplex/CTA/MRA, sleep study, TSH (thyroid-stimulating hormone) Slide 50

Treatment/Therapy

Not covered in the lecture

Mortality ★

Not covered in the lecture

Name of Condition

Secondary hypertension due to CKD (chronic kidney disease); renal parenchymal disease Slides 13, 16

Definition

Hypertension from chronic kidney abnormality persisting ≥3 months; bidirectional: CKD raises BP (blood pressure) and uncontrolled BP accelerates kidney injury Slide 13

Etiology (cause)

Diabetic nephropathy; glomerular disease; polycystic kidney disease Slides 13, 16

Epidemiology (who)

Hypertension is present in >80% of patients with chronic renal failure; prevalence 14% in the secondary-cause table Slides 13, 24

Risk Factors

Screening indications: diabetes, obstruction, hematuria, urinary frequency/nocturia, incontinence, analgesic abuse, family history of polycystic kidney disease Slide 24

Pathology

Impaired sodium excretion → extracellular volume expansion; RAAS (renin-angiotensin-aldosterone system) and sympathetic activation raise vascular resistance; hypertension raises intraglomerular pressure → glomerular scarring (vicious cycle) Slides 13, 14

Clinical Manifestation

Elevated creatinine/reduced eGFR (estimated glomerular filtration rate); albuminuria; hematuria or casts (RBC (red blood cell) casts suggest glomerulonephritis); peripheral edema; structural renal disease on imaging Slide 13

Diagnosis

Kidney abnormality ≥3 months; assess both eGFR and UACR (urine albumin-to-creatinine ratio), since albuminuria shows damage before eGFR falls; urinalysis; renal ultrasound Slide 13

Treatment/Therapy

Control BP and reduce sodium retention to slow renal decline; ACE (angiotensin-converting enzyme) inhibitor or ARB (angiotensin receptor blocker) for CKD with albuminuria (renoprotective) Slides 13, 14, 56, 62

Mortality ★

Prognosis: uninterrupted, the cycle causes progressive kidney damage and rising BP Slide 14

Name of Condition

Renovascular hypertension due to RAS (renal artery stenosis): atherosclerotic RAS; FMD (fibromuscular dysplasia) Slide 15

Definition

Hypertension caused by renal artery stenosis Slide 15

Etiology (cause)

Atherosclerotic RAS; FMD (non-inflammatory, non-atherosclerotic vessel-wall disease with abnormal cell growth causing narrowing, bulges, 'string-of-beads' look) Slide 15

Epidemiology (who)

Atherosclerotic: older patients with established vascular disease; FMD: younger women; prevalence 0.1–5% in the secondary-cause table Slides 15, 24

Risk Factors

Generalized atherosclerotic disease (coronary or peripheral artery disease); early-onset hypertension in women (FMD) Slides 15, 24

Pathology

Atherosclerotic RAS is often bilateral with progressive renal decline; FMD narrows arteries Slide 15

Clinical Manifestation

Resistant or abrupt BP (blood pressure) elevation; abdominal bruit; asymmetric kidneys; recurrent flash pulmonary edema; marked acute creatinine rise after starting an ACE (angiotensin-converting enzyme) inhibitor or ARB (angiotensin receptor blocker) Slide 15

Diagnosis

Renal artery duplex ultrasound first-line screen; CTA (computed tomography angiography) or MRA (magnetic resonance angiography) for anatomic detail; catheter renal angiogram is the gold standard, reserved for selected cases and intervention planning Slide 16

Treatment/Therapy

Medical management for many atherosclerotic lesions; revascularization (FMD often percutaneous) helps most with flash pulmonary edema, progressive renal decline, or refractory BP, refer early; no ACE inhibitor/ARB in severe bilateral RAS or RAS of a solitary kidney Slides 15, 16

Mortality ★

Not covered in the lecture

Name of Condition

Primary aldosteronism (primary hyperaldosteronism) Slides 17, 18

Definition

Autonomous aldosterone production independent of the renin-angiotensin system Slide 17

Etiology (cause)

Aldosterone-producing adenomas; bilateral idiopathic hyperaldosteronism Slide 17

Epidemiology (who)

Prevalence 5–25% in the secondary-cause table Slide 24

Risk Factors

Screen if resistant BP (blood pressure), unexplained or diuretic-induced hypokalemia, adrenal incidentaloma, early-onset or familial hypertension (or early stroke), OSA (obstructive sleep apnea) Slides 17, 24

Pathology

Aldosterone excess → sodium retention, potassium loss, metabolic alkalosis Slide 17

Clinical Manifestation

Hypertension, often without obvious electrolyte abnormality; hypokalemia may cause weakness, cramps, polyuria, nocturia Slide 17

Diagnosis

Morning seated plasma aldosterone:plasma renin activity ratio; positive if >20:1 to 30:1 with aldosterone >15–20 ng/dL; correct hypokalemia first (falsely lowers ratio); endocrinology confirms with saline suppression test; adrenal CT (computed tomography) with contrast for adenoma Slides 17, 18, 74

Treatment/Therapy

Unilateral adrenalectomy is definitive for an adenoma; MRAs (mineralocorticoid receptor antagonists: spironolactone, eplerenone) are valuable Slides 18, 58

Mortality ★

Not covered in the lecture

Name of Condition

OSA (obstructive sleep apnea)-related hypertension Slide 19

Definition

Secondary hypertension driven by recurrent upper-airway obstruction in sleep, with blunted nocturnal dipping (BP (blood pressure) fails to fall normally during sleep) Slide 19

Etiology (cause)

Recurrent upper-airway obstruction causing intermittent hypoxemia and arousal Slide 19

Epidemiology (who)

Prevalence 25–50% in the secondary-cause table (listed first among common causes) Slide 24

Risk Factors

Obesity Slide 19

Pathology

Intermittent hypoxemia and arousal → sustained sympathetic activation → vasoconstriction, fluid retention, blunted nocturnal dipping Slide 19

Clinical Manifestation

Loud snoring, witnessed apneas, gasping; nonrestorative sleep, daytime sleepiness; obesity; resistant or nocturnal hypertension Slides 19, 24

Diagnosis

STOP-BANG screen (Snoring, Tiredness, Observed apnea, blood Pressure, BMI (body mass index), Age, Neck circumference, Gender; ≥5 = high risk); confirm with polysomnography or home sleep apnea testing Slides 19, 50

Treatment/Therapy

Treat OSA (CPAP (continuous positive airway pressure), continuous positive airway pressure) and continue indicated BP therapy; CPAP alone does not reliably normalize BP Slide 19

Mortality ★

Prognosis: blunted nocturnal dipping is closely linked to cardiovascular risk Slide 19

Name of Condition

Drug-induced and alcohol-related hypertension Slide 20

Definition

Hypertension caused or worsened by medications, substances, supplements, or alcohol Slide 20

Etiology (cause)

NSAIDs (nonsteroidal anti-inflammatory drugs), corticosteroids; stimulants, decongestants (pseudoephedrine), cocaine, SNRIs (serotonin-norepinephrine reuptake inhibitors); estrogen contraceptives, calcineurin inhibitors, erythropoietin, some cancer therapies; excess alcohol or withdrawal; licorice, herbal supplements; abrupt clonidine stop Slide 20

Epidemiology (who)

Prevalence 2–20% in the secondary-cause table Slide 24

Risk Factors

Not covered in the lecture

Pathology

NSAIDs and corticosteroids cause sodium and water retention and blunt antihypertensives; sympathomimetics raise adrenergic tone and vascular resistance Slide 20

Clinical Manifestation

Alcohol withdrawal or abrupt clonidine withdrawal can produce acute severe (rebound) hypertension Slides 20, 59

Diagnosis

Thorough medication and supplement review, including over-the-counter drugs, recreational substances, and adherence Slide 20

Treatment/Therapy

Not covered in the lecture

Mortality ★

Not covered in the lecture

Name of Condition

Thyroid disease (hyperthyroidism, hypothyroidism)-related hypertension Slide 21

Definition

Secondary hypertension from hyperthyroidism or hypothyroidism Slides 12, 21

Etiology (cause)

Not covered in the lecture

Epidemiology (who)

Each <1% in the secondary-cause table (uncommon causes) Slide 24

Risk Factors

Not covered in the lecture

Pathology

Hyperthyroidism: increased cardiac output; hypothyroidism: increased vascular resistance Slide 21

Clinical Manifestation

Hyper: tachycardia, mainly systolic BP (blood pressure) rise, warm moist skin, heat intolerance, tremulousness, palpitations, weight loss, eye signs, goiter; hypo: bradycardia, often diastolic rise, dry skin, cold intolerance, constipation, hoarseness, weight gain Slides 21, 24

Diagnosis

TSH (thyroid-stimulating hormone) first-line screen, then free T4 or T3 as indicated; TSH is also a baseline screen in all hypertension Slides 21, 50, 51

Treatment/Therapy

Not covered in the lecture

Mortality ★

Not covered in the lecture

Name of Condition

Cushing syndrome Slide 21

Definition

Glucocorticoid excess state causing secondary hypertension Slide 21

Etiology (cause)

Not covered in the lecture

Epidemiology (who)

<0.1% in the secondary-cause table Slide 24

Risk Factors

Not covered in the lecture

Pathology

Glucocorticoid excess promotes sodium retention and vasopressor sensitivity Slide 21

Clinical Manifestation

Proximal muscle weakness; easy bruising, thin skin; broad purple striae (>1 cm); central adiposity, facial rounding; rapid central weight gain, facial plethora, depression, hyperglycemia Slides 21, 24

Diagnosis

When phenotype supports: 24-hour urinary cortisol, late-night salivary cortisol, or low-dose DST (dexamethasone suppression test) Slides 21, 50

Treatment/Therapy

Not covered in the lecture

Mortality ★

Not covered in the lecture

Name of Condition

Pheochromocytoma (grouped with paraganglioma in the secondary-cause table) Slides 22, 24

Definition

Rare catecholamine-secreting tumor, usually in the adrenal medulla Slide 12

Etiology (cause)

Not covered in the lecture

Epidemiology (who)

<0.6% (pheochromocytoma/paraganglioma) in the secondary-cause table Slide 24

Risk Factors

Family history of pheochromocytoma/paraganglioma; MEN2 (multiple endocrine neoplasia type 2), von Hippel-Lindau, neurofibromatosis type 1; adrenal incidentaloma Slide 24

Pathology

Catecholamine excess → sustained or paroxysmal hypertension; catecholamine vasoconstriction causes volume contraction → orthostatic hypotension Slide 22

Clinical Manifestation

Episodic (sometimes continuous) hypertension; '5 Ps': pressure (headache), perspiration, palpitations, pallor, tremor; paroxysmal triad of severe headache, sweating, palpitations; orthostatic symptoms Slides 12, 22

Diagnosis

Plasma free metanephrines or 24-hour urinary fractionated metanephrines (high sensitivity) Slides 22, 50

Treatment/Therapy

Alpha blockade (phenoxybenzamine) BEFORE beta blockade (propranolol); isolated beta blockade can precipitate hypertensive crisis via unopposed alpha vasoconstriction; refer to endocrinology Slide 22

Mortality ★

Not covered in the lecture

Name of Condition

Coarctation of the aorta Slide 23

Definition

Not covered in the lecture

Etiology (cause)

Not covered in the lecture

Epidemiology (who)

0.1% in the secondary-cause table; young adult with hypertension (<30 years) Slide 24

Risk Factors

Not covered in the lecture

Pathology

Not covered in the lecture

Clinical Manifestation

Upper-extremity hypertension with weak or delayed femoral pulses (radial-femoral delay); leg systolic BP (blood pressure) lower than arm (normally higher); whooshing 'machine-like' systolic murmur posteriorly (left paravertebral interscapular area); left thoracotomy scar if repaired Slides 23, 24, 39, 40

Diagnosis

Compare arm and leg BPs; echocardiogram establishes the diagnosis; confirm with CT (computed tomography) or MRI (magnetic resonance imaging) Slides 23, 39

Treatment/Therapy

Refer to vascular surgeon or structural cardiologist; transcatheter intervention (balloon angioplasty vs stent) or surgical repair Slide 23

Mortality ★

Not covered in the lecture

Name of Condition

Hypertensive cardiovascular disease; LVH (left ventricular hypertrophy) Slide 26

Definition

Hypertension-mediated cardiac damage: thickened, stiff left ventricle with impaired diastolic relaxation Slide 26

Etiology (cause)

Chronic pressure overload from hypertension Slide 26

Epidemiology (who)

Not covered in the lecture

Risk Factors

Not covered in the lecture

Pathology

LVH → reduced compliance → HFpEF or HFrEF (heart failure with preserved or reduced ejection fraction) as myocardium decompensates; impaired coronary reserve and accelerated atherosclerosis → ischemia Slide 26

Clinical Manifestation

S4 gallop or sustained LV (left ventricular) impulse; heart failure; ischemia; atrial and ventricular arrhythmias including atrial fibrillation Slide 26

Diagnosis

ECG (electrocardiogram): LVH voltage criteria (specific, not sensitive), lateral ST depression/T-wave inversion = strain pattern; echocardiogram if suspected HF (heart failure), murmur, LVH on ECG, dyspnea; BNP/NT-proBNP (B-type natriuretic peptide) for HF; normal ECG or EF (ejection fraction) does not exclude disease Slides 41, 42, 43, 49

Treatment/Therapy

Effective BP (blood pressure) control can regress LVH and reduce HF risk; HFrEF: ACE (angiotensin-converting enzyme) inhibitor/ARB (or ARNI (angiotensin receptor-neprilysin inhibitor)), beta blocker, MRA (mineralocorticoid receptor antagonist), diuretic Slides 26, 62

Mortality ★

Prognosis: LVH independently increases cardiovascular risk beyond measured BP Slide 26

Name of Condition

Hypertensive cerebrovascular disease and cognitive impairment Slide 27

Definition

Hypertension-related stroke (ischemic and intracerebral hemorrhage) and chronic small-vessel brain injury Slide 27

Etiology (cause)

Sustained systolic burden (even with controlled diastolic BP (blood pressure)); chronic small-vessel injury Slide 27

Epidemiology (who)

Not covered in the lecture

Risk Factors

Not covered in the lecture

Pathology

Small-vessel injury → white matter changes, lacunar infarcts Slide 27

Clinical Manifestation

Ischemic stroke, intracerebral hemorrhage; progressive cognitive impairment even without clinically evident stroke Slide 27

Diagnosis

Thorough neurologic exam; urgent CT (computed tomography) or MRI (magnetic resonance imaging) for acute deficits, severe headache, or encephalopathy Slide 49

Treatment/Therapy

Long-term BP reduction is among the most effective stroke prevention; control early; acute stroke follows a distinct BP protocol; prior stroke/TIA (transient ischemic attack): ACE (angiotensin-converting enzyme) inhibitor/ARB and/or thiazide Slides 27, 62

Mortality ★

Not covered in the lecture

Name of Condition

Hypertensive kidney disease (nephrosclerosis) Slide 28

Definition

Chronic hypertension-induced injury to renal vessels, glomeruli, and interstitium Slide 28

Etiology (cause)

Chronic hypertension Slide 28

Epidemiology (who)

Not covered in the lecture

Risk Factors

Not covered in the lecture

Pathology

Nephrosclerosis, glomerulosclerosis, tubulointerstitial fibrosis; kidney injury amplifies hypertension via impaired sodium excretion and RAAS (renin-angiotensin-aldosterone system) activation Slide 28

Clinical Manifestation

Not covered in the lecture

Diagnosis

Rising albuminuria (UACR, urine albumin-to-creatinine ratio) and declining eGFR (estimated glomerular filtration rate) are earliest markers, trend over time; creatinine, urinalysis for casts/hematuria; rule out other causes (diabetes, glomerulonephritis, obstruction) Slides 28, 49

Treatment/Therapy

ACE (angiotensin-converting enzyme) inhibitor or ARB (angiotensin receptor blocker) in CKD (chronic kidney disease) with albuminuria (renoprotective) Slides 56, 62

Mortality ★

Prognosis: the bidirectional cycle accelerates if untreated Slide 28

Name of Condition

Aortic dissection (hypertensive complication) Slide 29

Definition

Intimal tear and dissection of the aortic wall; an acute hypertension-mediated organ injury Slides 5, 29

Etiology (cause)

Chronic hypertension increases hemodynamic stress on the aortic wall Slide 29

Epidemiology (who)

Not covered in the lecture

Risk Factors

Chronic hypertension Slide 29

Pathology

Not covered in the lecture

Clinical Manifestation

Abrupt, severe chest, back, or abdominal pain, tearing or ripping, maximal at onset; pulse deficits, asymmetric arm BPs (blood pressures), aortic regurgitation murmur, new neurologic deficit; no pulse deficit does not exclude Slide 29

Diagnosis

Immediate CT (computed tomography) angiography; chest radiograph may show widened mediastinum but a normal film does not exclude Slides 29, 42

Treatment/Therapy

Urgent cardiothoracic and vascular surgery involvement; excluded from the general emergency MAP (mean arterial pressure) targets Slides 29, 69

Mortality ★

Not covered in the lecture

Name of Condition

Atherosclerotic complications of hypertension Slide 30

Definition

Not covered in the lecture

Etiology (cause)

Not covered in the lecture

Epidemiology (who)

Not covered in the lecture

Risk Factors

Smoking, dyslipidemia, diabetes, and inactivity synergistically amplify risk Slide 30

Pathology

Elevated BP (blood pressure) → endothelial shear stress, intimal injury, LDL (low-density lipoprotein) oxidation, smooth muscle proliferation → accelerated plaque formation Slide 30

Clinical Manifestation

CAD (coronary artery disease) and acute MI (myocardial infarction); ischemic stroke and TIA (transient ischemic attack); PAD (peripheral arterial disease: reduced distal pulses) Slides 30, 40

Diagnosis

Pulse and vascular examination with targeted imaging for peripheral pathology Slides 40, 49

Treatment/Therapy

Treat total cardiovascular risk, not BP alone: antiplatelet and lipid-lowering therapy where indicated; CAD/angina: beta blocker, ACE (angiotensin-converting enzyme) inhibitor/ARB, CCB (calcium channel blocker) Slides 30, 62

Mortality ★

Not covered in the lecture

Name of Condition

Hypertensive retinopathy Slide 31

Definition

Progressive hypertension-related retinal microvascular changes; the most common HTN (hypertension)-related ocular disease Slide 31

Etiology (cause)

Hypertension: generalized narrowing and nicking reflect current and previous BP (blood pressure); focal narrowing, hemorrhages, exudates reflect current BP only Slide 31

Epidemiology (who)

Not covered in the lecture

Risk Factors

Not covered in the lecture

Pathology

Not covered in the lecture

Clinical Manifestation

Stage 1 generalized arteriolar narrowing; stage 2 focal narrowing, AV (arteriovenous) nicking, copper wiring (opacified arteriolar wall); stage 3 flame-shaped hemorrhages, cotton wool spots, hard exudates; stage 4 optic disc swelling (acute hypertensive injury) Slides 32, 33, 34, 35, 40

Diagnosis

Fundoscopy in every newly diagnosed HTN (only noninvasive view of vasculature); annual eye exam/retinal scans with ophthalmology or optometry referral Slides 31, 51

Treatment/Therapy

HTN control can lead to regression Slide 31

Mortality ★

Prognosis: predicts long-term stroke risk independent of BP; retinal arterial narrowing predicts future HTN Slide 31

Name of Condition

White coat hypertension Slide 48

Definition

Elevated office BP (blood pressure) with normal home BP Slide 48

Etiology (cause)

Not covered in the lecture

Epidemiology (who)

Not covered in the lecture

Risk Factors

Not covered in the lecture

Pathology

Not covered in the lecture

Clinical Manifestation

Not covered in the lecture

Diagnosis

Out-of-office (home or ambulatory) monitoring; must be excluded before labeling resistant hypertension Slides 45, 48, 66

Treatment/Therapy

Requires surveillance Slide 48

Mortality ★

Not covered in the lecture

Name of Condition

Masked hypertension; masked uncontrolled hypertension Slide 48

Definition

Normal office BP (blood pressure) with elevated home BP; masked uncontrolled: treated patient controlled in office but not at home Slide 48

Etiology (cause)

Not covered in the lecture

Epidemiology (who)

Not covered in the lecture

Risk Factors

Not covered in the lecture

Pathology

Not covered in the lecture

Clinical Manifestation

Not covered in the lecture

Diagnosis

Out-of-office confirmation is essential in high-risk patients Slide 48

Treatment/Therapy

Not covered in the lecture

Mortality ★

Prognosis: significant cardiovascular risk despite normal office readings Slide 48

Name of Condition

Hypotension Slide 8

Definition

A decrease in systemic blood pressure (BP) below normal level; BP norms are affected by age; consider comorbidities and relative hypotension; each reading is a "snapshot" in time. Slides 8, 20

Etiology (cause)

Toxic/overdose (acute: medication-mediated, toxic exposure); infection (long-lasting acute: bacteremia, sepsis, septic shock); cardiogenic (chronic: heart failure with reduced ejection fraction (HFrEF), cardiomyopathy). Slide 22

Epidemiology (who)

Not covered in the lecture

Risk Factors

Intro case: 74-year-old woman on antihypertensives (lisinopril, metoprolol) plus a sodium-glucose cotransporter-2 (SGLT-2) inhibitor and a glucagon-like peptide-1 (GLP-1) agonist, 40-pound weight loss, BP 102/66. Slides 3–4

Pathology

Syncope is the result of symptomatic hypotension → cerebral hypoperfusion, from low peripheral resistance or low cardiac output. Slides 9, 19

Clinical Manifestation

Syncope, near-syncope, orthostatic changes, dizziness, lightheadedness, malaise. Acute: sudden onset, usually symptomatic, usually specific triggers. Chronic: waxes and wanes, intermittently symptomatic, underlying cause may be unavoidable. Slides 5, 21

Diagnosis

Build a differential: what it is, what it could be confused with, what is deadly/can't miss; if all diagnoses share one etiology, add at least 1 from 2 other sources (infection, obstructive, structural); VINDICATES mnemonic (vascular, infectious, neoplastic, degenerative/drugs, idiopathic/iatrogenic, congenital, autoimmune, trauma, endocrine/metabolic). Slides 6, 26

Treatment/Therapy

Remove the offending agent or trigger (iatrogenic → reduce/remove medication; reflex → reduce/remove trigger; orthostasis → treat underlying condition); patient education (understanding is the key to compliance); midodrine (alpha-1 agonist), fludrocortisone (mineralocorticoid), droxidopa (metabolized into norepinephrine); epinephrine, norepinephrine, dopamine, phenylephrine, vasopressin in emergency department and intensive care unit only. Slide 23

Mortality ★

Not covered in the lecture

Name of Condition

Syncope; near-syncope (presyncope) Slide 8

Definition

Syncope: transient, self-limited loss of consciousness (LOC) with inability to maintain postural tone, then spontaneous recovery (from transient global cerebral hypoperfusion). Near-syncope: preceding symptoms such as dizziness, lightheadedness, tunnel vision. Slides 8, 17

Etiology (cause)

Most common: orthostatic (neurogenic, non-neurogenic), reflex (situational, vasovagal), cardiogenic (arrhythmia, structural, vascular). Non-hypotensive causes: hypoglycemia, seizure, toxic/overdose, electrolyte imbalance, hypoxia (chronic obstructive pulmonary disease, congestive heart failure), anxiety, anemia, postural orthostatic tachycardia syndrome (POTS); HEAD-HEART-VESSELS mnemonic. Slides 9, 17, 19

Epidemiology (who)

Not covered in the lecture

Risk Factors

Not covered in the lecture

Pathology

Symptomatic hypotension → cerebral hypoperfusion. Slides 9, 19

Clinical Manifestation

Dizziness, lightheadedness, tunnel vision before loss of consciousness; spontaneous recovery. Slide 8

Diagnosis

History; cases model the work-up: orthostatic vitals, electrocardiogram (ECG), blood glucose, complete blood count (CBC) and comprehensive metabolic panel (CMP); against seizure: no tonic-clonic activity, tongue biting, incontinence, or postictal confusion. Slides 13, 15, 27, 31, 35, 40

Treatment/Therapy

Treat the cause: remove the offending agent or trigger; iatrogenic → reduce/remove medication; reflex → reduce/remove trigger; orthostasis → treat underlying condition. Slide 23

Mortality ★

Not covered in the lecture

Name of Condition

Orthostatic syncope, neurogenic (neurogenic orthostatic hypotension) Slide 11

Definition

A sustained drop in blood pressure (BP) on standing or sitting upright, caused by damage or dysfunction in the autonomic nervous system. Slide 11

Etiology (cause)

Autonomic dysfunction. Slide 11

Epidemiology (who)

Diabetes, genetic disorder, autoimmune disorder; examples: diabetes, Parkinson disease, multiple system atrophy. Slides 11, 36

Risk Factors

Case 2: long-standing diabetes with peripheral neuropathy (diabetic autonomic neuropathy). Slide 31

Pathology

Inadequate norepinephrine release from sympathetic postganglionic neurons → inadequate vasoconstriction, heart rate rises less than expected. Slide 11

Clinical Manifestation

Orthostatic BP drop with minimal heart rate (HR) increase; volume depletion usually absent; autonomic symptoms often present. Case 2: lightheadedness, weakness, dimming vision then loss of consciousness after standing; reduced vibration and light-touch sensation in both feet. Slides 36, 28–29

Diagnosis

History is the most important part. Orthostatic vitals: systolic BP (SBP) fall >20 mmHg or diastolic BP fall >10 mmHg within 3 minutes of standing, or SBP fall >30 mmHg with elevated baseline BP/supine hypertension. Case 2: 142/82 HR 72 → 108/66 HR 76 (BP drop without compensatory HR rise). Slides 13, 30, 31

Treatment/Therapy

Slow positional changes; treat the underlying cause; midodrine (alpha-1 agonist) best for neurogenic syncope, avoid with supine hypertension, severe heart disease, chronic kidney disease; droxidopa: mild efficacy, better with supine hypertension, usually an adjunct to midodrine or fludrocortisone. Slides 13, 23

Mortality ★

Not covered in the lecture

Name of Condition

Orthostatic syncope, non-neurogenic (non-neurogenic orthostatic hypotension) Slide 12

Definition

A sustained drop in blood pressure (BP) on standing or sitting upright that is not a result of autonomic dysfunction. Slide 12

Etiology (cause)

Hypovolemia, medication, advanced age; examples: diarrhea, hemorrhage, diuretics. Slides 12, 36

Epidemiology (who)

Dehydration, blood loss, poor intake, medication use. Slide 12

Risk Factors

Case 3: diarrhea, decreased oral intake, recent hydrochlorothiazide (HCTZ) dose increase (with lisinopril). Slides 33, 35

Pathology

Reduced cardiac output and/or impaired vasoconstriction without a primary autonomic disorder → poor brain perfusion. Slide 12

Clinical Manifestation

Orthostatic BP drop with significant heart rate (HR) increase; volume depletion often present; autonomic symptoms usually absent. Case 3: dry oral mucous membranes; lightheadedness, weakness, dimming vision on standing quickly. Slides 36, 32–33

Diagnosis

Orthostatic vitals: systolic BP (SBP) fall >20 mmHg or diastolic BP fall >10 mmHg within 3 minutes of standing, or SBP fall >30 mmHg with elevated baseline BP/supine hypertension. Case 3: 138/78 HR 68 → 108/64 HR 92 (intact baroreceptor-mediated sympathetic response); electrocardiogram (ECG) normal sinus rhythm. Slides 13, 34, 35

Treatment/Therapy

Slow positional changes; treat the underlying cause (the real diagnosis); iatrogenic → reduce or remove the medication. Slides 13, 23

Mortality ★

Not covered in the lecture

Name of Condition

Vasovagal (reflex) syncope; "the common faint" Slide 14

Definition

Reflex syncope triggered by emotional stress, fear, pain, heat exposure, or prolonged standing; most common type. Slide 14

Etiology (cause)

Unclear; possible genetic predisposition. Slide 14

Epidemiology (who)

Most common in young women; 85% of syncopal episodes age <40; 50% in elderly. Slide 14

Risk Factors

Triggers: emotional stress, fear, pain, heat exposure, prolonged standing. Slide 14

Pathology

Transient increase in parasympathetic outflow + sympathetic inhibition → bradycardia, vasodilation, reduced cardiac output → systolic blood pressure falls → cerebral blood flow drops below autoregulation limits; subtypes: vasodepressor, mixed, cardioinhibitory. Slides 14, 19

Clinical Manifestation

Case 1 reflex-syncope prodrome: warmth, nausea, diaphoresis, lightheadedness, then rapid recovery. Slide 27

Diagnosis

History, history, history (the most important part); patient keeps a log of pattern and frequency. Slide 15

Treatment/Therapy

Trigger avoidance; safety precautions during unavoidable triggers. Slide 15

Mortality ★

Not covered in the lecture

Name of Condition

Situational (reflex) syncope; Case 1: micturition syncope Slides 14, 27

Definition

Reflex syncope triggered by certain bodily functions or physical actions (e.g., cough, sneeze, micturition). Slides 14, 17

Etiology (cause)

Nocturnal urination triggers an exaggerated autonomic reflex: increased vagal activity, decreased sympathetic vascular tone. Slides 27, 17

Epidemiology (who)

Not covered in the lecture

Risk Factors

Case 1: alcohol, relative dehydration, alpha-1 blocker (tamsulosin) with angiotensin-converting enzyme (ACE) inhibitor (lisinopril); night-time, abrupt standing from bed, voiding while standing. Slides 25, 27

Pathology

Bradycardia and/or peripheral vasodilation → transient hypotension and cerebral hypoperfusion. Slide 27

Clinical Manifestation

Brief prodrome of warmth, nausea, diaphoresis, lightheadedness ("swimmy" head), then rapid recovery; normal vitals and exam afterward. Slides 24, 25, 27

Diagnosis

History; rule out hypoglycemia (normal glucose), infection/metabolic cause (unremarkable complete blood count (CBC) and comprehensive metabolic panel (CMP)), stroke/transient ischemic attack (no deficit), dysrhythmia (normal electrocardiogram (ECG)). Slides 15, 27

Treatment/Therapy

Trigger avoidance; safety precautions during unavoidable triggers; reduce or remove the trigger. Slides 15, 23

Mortality ★

Not covered in the lecture

Name of Condition

Cardiogenic syncope (with or without hypotension) Slide 16

Definition

Syncope of cardiac etiology, with or without hypotension; three types: arrhythmia, structural, vascular. Slide 16

Etiology (cause)

Arrhythmia: atrial fibrillation, paroxysmal supraventricular tachycardia, premature ventricular contractions/ventricular tachycardia, QT syndromes, heart blocks. Structural: myocardial infarction (MI), cardiomyopathy, heart failure, valvular disease. Vascular: peripheral vascular disease, dissection, aneurysm, stroke, pulmonary embolism. Slide 16

Epidemiology (who)

Not covered in the lecture

Risk Factors

Case 4: hypertension, coronary artery disease after MI with percutaneous coronary intervention ×2, ischemic cardiomyopathy with heart failure with reduced ejection fraction (ejection fraction 30%). Slides 38, 40

Pathology

Low cardiac output (arrhythmia, structural cardiac, other causes). Slide 19

Clinical Manifestation

Case 4: abrupt witnessed collapse without warning, minimal prodrome, brief "racing" heart beforehand; anxious, pale, blood pressure 88/54, heart rate 148, rapid regular rhythm. Slides 37, 38, 40

Diagnosis

Arrhythmia: electrocardiogram (ECG), monitor, stress test, cardiology consult. Structural: echocardiogram, stress echo, cardiology consult. Vascular: emergent testing in the emergency department, cardiology consult. Case 4: ECG = nonsustained ventricular tachycardia; complete blood count and comprehensive metabolic panel to reduce suspicion of a metabolic/infectious process. Slides 16, 39, 40

Treatment/Therapy

Not covered in the lecture

Mortality ★

Not covered in the lecture

Name of Condition

Postural orthostatic tachycardia syndrome (POTS); the slide expands it as "positional", but the standard name is postural Slide 18

Definition

Heart rate increase of >30 beats per minute, or exceeding 120 beats per minute, within 10 minutes of standing; usually improves lying down; in adolescents the threshold is an increase of 40 beats per minute. Slide 18

Etiology (cause)

Not covered in the lecture

Epidemiology (who)

Age 15-50; usually female > male; associated with Ehlers-Danlos syndrome. Slide 18

Risk Factors

Ehlers-Danlos syndrome association. Slide 18

Pathology

Not covered in the lecture

Clinical Manifestation

Tachycardia ± lightheadedness, dizziness, fainting, palpitations on standing; listed among non-hypotensive causes of syncope. Slides 18, 17

Diagnosis

Tilt-table test (sensitivity 40%, specificity >80%). Slide 18

Treatment/Therapy

Increase water and salt intake; fludrocortisone (mineralocorticoid; best with POTS; causes salt and water retention, avoid in congestive heart failure). Slides 18, 23

Mortality ★

Not covered in the lecture

Name of Condition

Dyslipidemia (lipid disorders) Slides 12, 16

Definition

Disorder of lipoprotein metabolism: decreased HDL-C (high-density lipoprotein cholesterol) and/or elevated TC (total cholesterol), LDL-C (low-density lipoprotein cholesterol), non-HDL-C (all cholesterol except HDL) or TG (triglycerides). Slide 12

Etiology (cause)

Primary (genetic) or secondary: sedentary lifestyle with a diet high in carbohydrates and saturated/trans fat; diabetes mellitus; alcohol; CKD (chronic kidney disease); hypothyroidism; obstructive liver disease; medications. Slides 16, 42, 58

Epidemiology (who)

Primary (genetic) causes are the most common etiology in children; mixed dyslipidemia is the most common type seen in clinical practice. Slides 42, 54

Risk Factors

High-carbohydrate diet, obesity/insulin resistance/T2DM (type 2 diabetes mellitus), nephrotic syndrome and Cushing syndrome raise hepatic VLDL (very-low-density lipoprotein); saturated/trans fat, hypothyroidism and liver disorders down-regulate LDL receptors; alcohol ↑TG; CKD. Drugs: estrogen, glucocorticoids, beta blockers, isotretinoin, bexarotene (↑TG); anabolic steroids (↓HDL-C). Slides 58–62

Pathology

Genetic mechanisms: overproduction or defective clearance of TG or LDL; excessive clearance or underproduction of HDL. Atherosclerosis risk rises directly with serum cholesterol. Slides 15, 42

Clinical Manifestation

Usually no signs or symptoms; found on lab values. Eruptive xanthomas (clusters of small yellowish papules; very high chylomicrons or VLDL); tendinous xanthomas (nodules on the Achilles, patellar or hand tendons; high LDL); tuberous xanthomas (large smooth nodules over elbows and buttocks); xanthelasma (yellow plaques on the eyelids); corneal arcus before 40 (white-gray ring at the edge of the cornea); the last four usually signal a genetic cause. Premature CAD (coronary artery disease, ages 30–50); pancreatitis. Slides 31–37

Diagnosis

Lipid panel: TC <200 desirable, >240 high; LDL-C <100 optimal, >190 very high; HDL-C <40 low, >60 high; TG <150 normal, >500 very high. Screen by overall cardiovascular risk: TC + HDL-C need no fast (TC:HDL ratio best CHD (coronary heart disease) predictor); slide 66: TG and calculated LDL-C need a 9–12 hour fast; 2018 guideline: a non-fasting full panel is acceptable for screening, fasting if TG ≥400. First step: find which lipoproteins are up or down; rule out secondary, then primary causes before a statin. Slides 39, 40, 64, 66, 69, 92–94

Treatment/Therapy

Lifestyle changes, drug therapy and a clinician–patient risk discussion; LDL-C is the primary target. Lifestyle: saturated fat <7% of calories, soluble fiber, plant stanols/sterols, 5–10% weight loss, 30 min/day activity, stop smoking. Statins first (high intensity ≥50%, moderate 30–<50%, low <30% LDL-C reduction); add-ons: ezetimibe, bile acid sequestrants, niacin, fibrates, fish oil, PCSK9 (proprotein convertase subtilisin/kexin type 9) inhibitors, bempedoic acid, inclisiran, evinacumab. Monitor lipids, liver function, CK (creatine kinase); recheck lipids 4–12 weeks after starting or adjusting and judge response by percentage LDL-C reduction. Slides 69, 72, 74–75, 78–90, 103, 107

Mortality ★

Untreated abnormal cholesterol predicts higher cardiovascular morbidity and mortality; CHD is the leading cause of death in US men and women. Slides 13, 39

Name of Condition

Atherosclerosis; ASCVD (atherosclerotic cardiovascular disease); CHD (coronary heart disease) Slides 13–14

Definition

Not covered in the lecture

Etiology (cause)

LDL (low-density lipoprotein) carries the highest risk, VLDL (very-low-density lipoprotein) increased risk, HDL (high-density lipoprotein) decreased risk; risk rises directly with serum cholesterol; Lp(a) (lipoprotein(a)) is a causal factor. Slides 7, 14, 15

Epidemiology (who)

CHD is the leading cause of death in US men and women; over $200 billion a year spent, reflecting poor prevention and uncontrolled risk factors. Slide 13

Risk Factors

Smoking; HTN (hypertension; ≥140/90 or on medication); low HDL <40 (≥60 removes one risk factor); family history of premature CHD (male first-degree relative <55, female <65); age (men ≥45, women ≥55); obesity, diabetes, inactivity. CHD risk equivalents: MI (myocardial infarction), angina, PAD (peripheral artery disease), AAA (abdominal aortic aneurysm), symptomatic carotid disease, diabetes. 2018 risk enhancers: premature ASCVD in family, LDL-C (LDL cholesterol) ≥160, CKD (chronic kidney disease), metabolic syndrome, preeclampsia or early menopause, inflammatory disease, South Asian ancestry, TG (triglycerides) ≥175. Slides 20, 21, 29, 105

Pathology

Not covered in the lecture

Clinical Manifestation

Major ASCVD events: recent ACS (acute coronary syndrome), history of MI, ischemic stroke, symptomatic PAD (claudication with ABI (ankle-brachial index) <0.85, revascularization or amputation); premature CAD (coronary artery disease) in genetic dyslipidemia. Slides 27, 37

Diagnosis

Risk estimation: ACC/AHA (American College of Cardiology/American Heart Association) Pooled Cohort Equation, ages 40–79 without cardiovascular disease, finds statin candidates (10-year risk low <5%, borderline 5–<7.5%, intermediate ≥7.5–<20%, high ≥20%); older Framingham score; PREVENT calculator. Very high risk = multiple major ASCVD events, or one plus multiple high-risk conditions. CAC (coronary artery calcium) score if the statin decision is uncertain. Slides 22–27, 71, 96, 100, 106

Treatment/Therapy

2018 guideline: clinical ASCVD → high-intensity statin to cut LDL-C ≥50% (moderate if not tolerated); very high risk with LDL-C ≥70 on maximal statin → add ezetimibe, then a PCSK9 (proprotein convertase subtilisin/kexin type 9) inhibitor. Primary prevention: LDL-C ≥190 → high-intensity statin with no risk calculation; diabetes, age 40–75 → moderate-intensity statin; age 40–75, risk ≥7.5% → moderate-intensity statin (≥30% cut) after a risk discussion, ≥20% → ≥50% cut; risk enhancers favor treating. Slides 96–107

Mortality ★

Elevated cholesterol raises cardiovascular morbidity and mortality (Framingham); CHD is the leading US cause of death; fish oil is linked to fewer CHD deaths. Slides 13, 18, 87

Name of Condition

Severe hypertriglyceridemia Slide 43

Definition

TG (triglycerides) >500 mg/dL with elevated total cholesterol and reduced HDL-C (high-density lipoprotein cholesterol); LDL-C (low-density lipoprotein cholesterol) and apoB (apolipoprotein B) usually not elevated. Slide 43

Etiology (cause)

Impaired lipolysis of TG. Secondary: high-carbohydrate diet, obesity/insulin resistance/T2DM (type 2 diabetes mellitus), alcohol, CKD (chronic kidney disease), nephrotic syndrome, estrogen, glucocorticoids, beta blockers, isotretinoin, bexarotene. Slides 43, 59, 60, 62

Epidemiology (who)

Usually a polygenic tendency combined with secondary factors such as obesity or insulin resistance. Slide 43

Risk Factors

Obesity, insulin resistance, alcohol; with TG ≥500 rule out diabetes, CKD, alcoholism, pregnancy, hypothyroidism. Slides 43, 60, 92

Pathology

Impaired lipolysis of TG (no enzyme named). Slide 43

Clinical Manifestation

Risk of acute pancreatitis; eruptive xanthomas (clusters of small yellowish papules) with extremely high chylomicrons or VLDL (very-low-density lipoprotein). Slides 32, 43

Diagnosis

TG 150–199 borderline, 200–499 high, >500 very high. Non-HDL-C (total cholesterol minus HDL-C) assesses heart-disease risk better than LDL-C in hypertriglyceridemia. Slides 40, 115–116

Treatment/Therapy

Lower LDL-C first. 2018 guideline: TG 175–499 → lifestyle, secondary causes, statin intensity; TG ≥500 → very low-fat diet (<15% of calories), weight management, activity and a fibrate to prevent pancreatitis. (Carter taught the older ATP III rule: TG >200 after the LDL goal → fibrate or niacin.) Fibrates lower TG most. Slides 86, 116, 118

Mortality ★

Not covered in the lecture

Name of Condition

FCS (familial chylomicronemia syndrome); a cause of severe hypertriglyceridemia Slide 44

Definition

Fasting TG (triglycerides) >500 mg/dL, usually >1000 mg/dL. Slide 44

Etiology (cause)

A primary (genetic) cause of dyslipidemia; mechanism not given. Slides 41, 44

Epidemiology (who)

Can present in childhood or adulthood. Slide 44

Risk Factors

Not covered in the lecture

Pathology

Not covered in the lecture

Clinical Manifestation

Severe abdominal pain from acute pancreatitis; eruptive xanthomas (clusters of small yellowish-white papules on back, buttocks, extensor arms and legs); lipemia retinalis (opalescent, milky retinal blood vessels on fundoscopy); hepatosplenomegaly possible. Slide 44

Diagnosis

Fasting TG >500, usually >1000 mg/dL; fundoscopic exam. Slide 44

Treatment/Therapy

No FCS-specific treatment; general TG ≥500 management: very low-fat diet (<15% of calories), weight management, activity and a fibrate. Slide 118

Mortality ★

Not covered in the lecture

Name of Condition

Hypercholesterolemia Slide 45

Definition

Elevated LDL-C (low-density lipoprotein cholesterol). Slide 45

Etiology (cause)

Impaired hepatic LDL uptake from reduced LDL-receptor expression or activity (saturated/trans-fat diet, hypothyroidism, estrogen deficiency); also Cushing syndrome, liver disorders, nephrotic syndrome, glucocorticoids. Slides 45, 59–62

Epidemiology (who)

Not covered in the lecture

Risk Factors

Saturated/trans-fat diet, hypothyroidism, estrogen deficiency. Slide 45

Pathology

Reduced LDL-receptor expression or activity → impaired LDL uptake by the liver. Slide 45

Clinical Manifestation

Premature ASCVD (atherosclerotic cardiovascular disease); tendinous xanthomas (nodules on tendons) with high LDL. Slides 33, 45

Diagnosis

LDL-C <100 optimal, 100–129 near optimal, 130–159 borderline high, 160–189 high, >190 very high. Rule out hypothyroidism (check thyroid), nephrotic syndrome, primary biliary cirrhosis, anorexia nervosa. Slides 40, 61, 92

Treatment/Therapy

LDL-C is the primary target; statins first. LDL-C ≥190: high-intensity statin with no risk calculation; add ezetimibe if LDL-C stays ≥100; then consider a PCSK9 (proprotein convertase subtilisin/kexin type 9) inhibitor if multiple risk factors. Slides 69, 79, 101

Mortality ★

Not covered in the lecture

Name of Condition

HoFH (homozygous familial hypercholesterolemia) Slides 46–48

Definition

Codominant genetic disorder with two mutant alleles; LDL-C (low-density lipoprotein cholesterol) usually >190 with normal TG (triglycerides). Receptor-negative (<2% normal LDL-receptor activity) or receptor-defective (2–25%). Slides 46–48

Etiology (cause)

LDL-receptor gene mutation → reduced receptor function and slower LDL clearance (deck also says increased LDL production). Slides 46, 47

Epidemiology (who)

1 in 1 million people worldwide. Slide 48

Risk Factors

Strong family history of high lipids in parents and other first-degree relatives. Slide 50

Pathology

Reduced LDL-receptor function → reduced clearance of LDL from the circulation. Slides 46, 47

Clinical Manifestation

Childhood cutaneous xanthomas (hands, wrists, elbows, knees, heels, buttocks); symptomatic atherosclerosis before puberty; total cholesterol ~400 to >1000 mg/dL; tendon xanthomas (nodules on tendons); premature ASCVD (atherosclerotic cardiovascular disease). Slides 46, 49

Diagnosis

Confirmed by skin biopsy with measurement of LDL-receptor activity. Slide 50

Treatment/Therapy

LDL apheresis is the treatment of choice (dialysis-like removal of LDL particles). Most need several drugs: high-intensity statin, plus ezetimibe and niacin; refractory → PCSK9 (proprotein convertase subtilisin/kexin type 9) inhibitors; evinacumab (deck: "Envinacumab") as IV (intravenous) adjunct from age 12; liver transplant supplies LDL receptors. Familial hypercholesterolemia diagnosed at age 0–19 → statin. Slides 88, 89, 96, 109

Mortality ★

Untreated receptor-negative patients rarely live past the second decade; receptor-defective develop CVD (cardiovascular disease) by 30. Accelerated atherosclerosis can cause disability and sudden death in childhood. Slides 48, 49

Name of Condition

HeFH (heterozygous familial hypercholesterolemia) Slide 51

Definition

One mutant allele; LDL-C (low-density lipoprotein cholesterol) 200–400 mg/dL with normal TG (triglycerides). Slides 47, 51

Etiology (cause)

LDL-receptor gene mutation (codominant inheritance). Slides 46, 47

Epidemiology (who)

1 in 250 people worldwide; up to 5% of premature MIs (myocardial infarctions) in men <55 and women <65. Slide 51

Risk Factors

Not covered in the lecture

Pathology

Reduced LDL-receptor function → reduced LDL clearance. Slide 46

Clinical Manifestation

High cholesterol from birth, usually found on routine screening; corneal arcus (white-gray ring at the edge of the cornea) common; tendon xanthomas (nodules on the hand extensor, elbow, knee and mainly Achilles tendons) in ~75%; subperiosteal xanthomas (smooth swellings over bone, e.g., the knee). Slides 33, 51, 52

Diagnosis

No definitive diagnostic test. Slide 52

Treatment/Therapy

Aggressively reduce vascular risk factors (smoking, hypertension, diabetes); diet low in saturated fat and cholesterol; high-intensity statin, plus ezetimibe and niacin; refractory → PCSK9 (proprotein convertase subtilisin/kexin type 9) inhibitors; inclisiran if more LDL-C lowering is needed. Familial hypercholesterolemia diagnosed at age 0–19 → statin. Slides 90, 96, 110

Mortality ★

Not covered in the lecture

Name of Condition

FDB (familial defective apolipoprotein B-100) Slide 53

Definition

Elevated LDL-C (low-density lipoprotein cholesterol); a cause of hypercholesterolemia. Slide 53

Etiology (cause)

Defective apoB-100, the liver-made structural protein of VLDL (very-low-density lipoprotein), IDL (intermediate-density lipoprotein), LDL and Lp(a) (lipoprotein(a)); mechanism not given. Slides 9, 53

Epidemiology (who)

1 in 1500 people worldwide. Slide 53

Risk Factors

Not covered in the lecture

Pathology

Not covered in the lecture

Clinical Manifestation

Tendon xanthomas (nodules on tendons); premature ASCVD (atherosclerotic cardiovascular disease). Slide 53

Diagnosis

Elevated LDL-C alone. Slide 53

Treatment/Therapy

Not covered in the lecture

Mortality ★

Not covered in the lecture

Name of Condition

Mixed dyslipidemia Slide 54

Definition

TG (triglycerides) >150 mg/dL plus LDL-C (low-density lipoprotein cholesterol) >130 mg/dL or non-HDL-C (all cholesterol except high-density lipoprotein cholesterol) >160 mg/dL. Slide 54

Etiology (cause)

Genetic predisposition plus medical conditions and environmental factors. Slide 54

Epidemiology (who)

Most common type of dyslipidemia seen in clinical practice. Slide 54

Risk Factors

Not covered in the lecture

Pathology

Not covered in the lecture

Clinical Manifestation

Increased risk of ASCVD (atherosclerotic cardiovascular disease). Slide 54

Diagnosis

TG >150 with LDL-C >130 or non-HDL-C >160 mg/dL. Slide 54

Treatment/Therapy

Not covered in the lecture

Mortality ★

Not covered in the lecture

Name of Condition

FDBL (familial dysbetalipoproteinemia); a cause of mixed dyslipidemia Slide 55

Definition

TG (triglycerides) and total cholesterol both elevated (250–500 mg/dL) from accumulated chylomicron and VLDL (very-low-density lipoprotein) remnants. Slide 55

Etiology (cause)

Rare disorder from apoE (apolipoprotein E) mutation; linked to apoE2 homozygosity but needs environmental and/or other genetic factors. Slide 55

Epidemiology (who)

Rare. Slide 55

Risk Factors

Environmental and/or other genetic factors on top of apoE2 homozygosity. Slide 55

Pathology

Chylomicron and VLDL remnants accumulate (apoE is critical to TG clearance). Slides 11, 55

Clinical Manifestation

Distinctive cutaneous xanthomas: palmar xanthomas (on the palms) and tuberoeruptive xanthomas (nodules mixed with eruptive papules). Slide 56

Diagnosis

TG and total cholesterol both elevated, 250–500 mg/dL. Slide 55

Treatment/Therapy

Not covered in the lecture

Mortality ★

Prognosis: associated with accelerated atherosclerosis. Slide 56

Name of Condition

Low HDL-C (high-density lipoprotein cholesterol) Slide 111

Definition

HDL-C <40 mg/dL is low; ≥60 is a negative risk factor (removes one). Metabolic syndrome cutoff: men <40, women <50. Slides 21, 38, 40

Etiology (cause)

Genetic: excessive clearance or underproduction of HDL; anabolic steroids lower HDL. Slides 42, 62

Epidemiology (who)

Not covered in the lecture

Risk Factors

Rule out diabetes mellitus, cigarette smoking, obesity. Slide 92

Pathology

Less reverse cholesterol transport (HDL carries excess cholesterol from the periphery to the liver for excretion in bile, "clearing away plaque"). Slides 6, 14

Clinical Manifestation

Not covered in the lecture

Diagnosis

Lipid panel; HDL-C <40 is low. Slide 40

Treatment/Therapy

Best raised by lifestyle: stop smoking (up to +10%), weight loss (6 lb ≈ +1 mg/dL), aerobic exercise (~+5%; brisk 30 min/day, 5 days/week), healthier fats (olive, peanut, canola; saturated fat <7%), moderate alcohol. Drugs: niacin raises it most, then fibrates, statins, ezetimibe. Slides 79, 84–86, 112–113

Mortality ★

Not covered in the lecture

Name of Condition

Lp(a) (lipoprotein(a)) Slide 7

Definition

LDL-like (low-density lipoprotein-like) particle carrying apoB-100 (apolipoprotein B-100) plus a distinct protein, apo(a) (apolipoprotein(a)). Slides 7, 11

Etiology (cause)

Not covered in the lecture

Epidemiology (who)

Not covered in the lecture

Risk Factors

Independent, causal risk factor for ASCVD (atherosclerotic cardiovascular disease); Lp(a) >50 mg/dL (or >125 nmol/L) is a risk enhancer. Slides 7, 96, 105

Pathology

Cleared by the liver; uptake pathway unknown. Slide 7

Clinical Manifestation

Not covered in the lecture

Diagnosis

Measured in selected individuals. Slides 96, 105

Treatment/Therapy

If elevated, needs aggressive therapy to lower LDL. Slide 7

Mortality ★

Not covered in the lecture

Name of Condition

Metabolic syndrome Slide 38

Definition

Any 3 of: waist >40 in (men) or >35 in (women); TG (triglycerides) >150 mg/dL; HDL (high-density lipoprotein) <40 men, <50 women; BP (blood pressure) >130/>85; fasting glucose >110 mg/dL. Slide 38

Etiology (cause)

Not covered in the lecture

Epidemiology (who)

Not covered in the lecture

Risk Factors

Not covered in the lecture

Pathology

Not covered in the lecture

Clinical Manifestation

The five defining findings: abdominal obesity, high TG, low HDL, raised BP, raised fasting glucose. Slide 38

Diagnosis

Any 3 of the 5 criteria. Slide 38

Treatment/Therapy

Lifestyle therapy is the primary intervention in all age groups. Slide 98

Mortality ★

Not covered in the lecture

★ Severe = area under 1.0, mean gradient over 40, jet over 4 ("4, 40 and 1"); angina 5 / syncope 3 / heart failure 2 years; preload dependent

Name of Condition

Aortic stenosis (AS) Slide 11

Definition

Obstruction of left ventricular outflow across the aortic valve; the most common valvular disease Slide 11

Etiology (cause)

Degenerative (atherosclerosis: hyperlipidemia, diabetes, smoking): most common cause over age 70; congenital bicuspid aortic valve: most common cause under 70; acquired: rheumatic heart disease (autoimmune reaction to group A beta-hemolytic streptococci), endocarditis Slide 12

Epidemiology (who)

80% of symptomatic AS patients are men; present in 25% of patients over 65 and 35% over 70; 10–20% progress to significant AS within 10–15 years Slide 13

Risk Factors

Hypertension; hyperlipidemia; smoking Slide 13

Pathology

LV (left ventricular) outflow obstruction → LV pressure overload → myocyte remodeling → concentric LVH (left ventricular hypertrophy) → diastolic HF (heart failure) with preserved ejection fraction Slides 14, 15

Clinical Manifestation

Symptoms rare until orifice ~1 cm (normal 3–4 cm), age 60–80; insidious. Cardinal symptoms with survival: angina 5 y, syncope 3 y (both usually exertional), CHF (congestive heart failure)/exertional dyspnea 2 y (most common, worst prognosis). Harsh systolic ejection crescendo-decrescendo murmur at 2nd right ICS (intercostal space)/RUSB (right upper sternal border), radiates to carotids; decreased by Valsalva, standing, handgrip; increased by squatting, sitting forward. Forceful LV apex beat with delayed/weak carotid pulse suggests severe AS Slides 16, 17, 22

Diagnosis

ECG (electrocardiogram): LVH in severe AS (low sensitivity); TTE (transthoracic echocardiogram): thickened, calcified leaflets, reduced systolic opening, LVH; TEE (transesophageal echocardiogram) useful for congenital; left heart catheterization definitive. Severe: area <1.0 cm², mean gradient >40 mmHg, jet velocity >4.0 m/s; moderate area 1.0–1.5, gradient 25–40 mmHg, jet 3.0–4.0; mild area >1.5, gradient <25 mmHg, jet <3.0. Exertional chest pressure, shortness of breath or syncope → echo Slides 18, 19, 22

Treatment/Therapy

Medical therapy not effective (mild/moderate only); preload dependent: avoid strenuous activity/competitive sports, dehydration, hypovolemia; if hypertension avoid beta blockers and calcium channel blockers; if angina avoid nitrates. Surgery if severe AS AND symptomatic LV systolic dysfunction, or bicuspid valve: TAVR (transcatheter aortic valve replacement); mechanical valve (lifelong anticoagulation) vs biological (none); children/young adults: PABV (percutaneous aortic balloon valvuloplasty). Refer all AS on echo to cardiology Slides 20, 21, 22

Mortality ★

Symptomatic AS 3-year mortality 75%; prognosis severely worsens once symptomatic; survival after onset: angina 5 y, syncope 3 y, CHF 2 y; average age of death 63 (graph) Slides 16, 22

★ Corrigan pulse goes with aortic regurgitation; severe = regurgitant fraction 50% or more; the murmur is diastolic (slide 28 corrected in class)

Name of Condition

Aortic regurgitation / insufficiency (AR) Slide 23

Definition

Incomplete aortic valve closure causing blood to flow back into the LV (left ventricle) Slide 23

Etiology (cause)

Valve disease, aortic root disease or both. Valvular: congenital bicuspid, endocarditis, rheumatic fever, myxomatous (collagen), trauma, syphilis, ankylosing spondylitis. Root: aortic dissection, cystic medial degeneration, Marfan syndrome, nonsyndromic familial aneurysm, aortitis, hypertension. Acute AR: myocardial infarction, endocarditis, aortic dissection, trauma Slides 24, 26

Epidemiology (who)

Not covered in the lecture

Risk Factors

Not covered in the lecture

Pathology

Incomplete closure → diastolic backflow into LV → eccentric hypertrophy and dilation → LV dilation (systolic HF (heart failure)) → HF with reduced ejection fraction Slide 25

Clinical Manifestation

Acute: cardiogenic shock, pulmonary edema. Chronic: asymptomatic 10–15 years until decompensation; CHF (congestive heart failure) symptoms (exertional sinus tachycardia, exertional dyspnea, orthopnea, PND (paroxysmal nocturnal dyspnea), diaphoresis, anginal pain). High-pitched blowing DIASTOLIC murmur (slide 28's "Holosystolic" struck in class) at 3rd ICS (intercostal space)/LUSB (left upper sternal border), radiates to apex, severity proportional to duration, displaced PMI (point of maximal impulse); decreased by Valsalva, standing; increased by squatting, sitting forward, handgrip. de Musset sign (head bobbing); Corrigan pulse (water hammer or collapsing pulse: very rapid upstroke then rapid collapse); bounding pulses, wide pulse pressure, thrills Slides 26, 27, 28

Diagnosis

ECG (electrocardiogram): LVH (left ventricular hypertrophy) in chronic AR, non-specific; echo: determines the cause of AR (aortic root dilation, aortic dissection; slide 29's "MR" corrected to AR in class); diastolic fluttering of the anterior mitral leaflet where the jet strikes it (slide 29; his in-class change to "aortic leaflet" is not accurate); catheterization definitive but not necessary. Severity: severe = regurgitant fraction 50% or more (moderate 30–49%, mild <30%) Slides 29, 30

Treatment/Therapy

AR with HF with preserved ejection fraction or asymptomatic: afterload reduction (ACE inhibitor (angiotensin-converting enzyme inhibitor)/ARB (angiotensin receptor blocker), dihydropyridine calcium channel blockers, hydralazine). Acute severe AR: emergency valve replacement/repair (ideally <24 h); if delayed, ICU IV (intravenous) diuretics plus nitroprusside (the slide also lists dobutamine as a "vasodilator"; it is an inotrope). Chronic AR with mildly reduced or reduced ejection fraction (symptomatic or not): surgical candidate. Refer any audible murmur; dilated aortic root monitored by cardiology Slides 31, 32

Mortality ★

Untreated severe AR with mildly reduced or reduced ejection fraction: survival 2–3 years (clarified in the lecture) Slide 31

★ Left atrial enlargement → atrial fibrillation (most patients with an affected left atrium); rheumatic heart disease most common cause

Name of Condition

Mitral stenosis (MS) Slide 33

Definition

Obstruction of left atrial outflow across the mitral valve Slide 33

Etiology (cause)

Rheumatic heart disease: most common cause Slide 34

Epidemiology (who)

80% of MS due to rheumatic fever are women; usually diagnosed ~20 years after rheumatic fever; rare in developed countries (less rheumatic fever) Slide 34

Risk Factors

Rheumatic fever Slide 34

Pathology

Thickened, immobile leaflets narrow the orifice → raised LA (left atrial) size/pressure → AF (atrial fibrillation; thromboembolism risk) → pulmonary vasoconstriction, raised pulmonary artery pressure, RV (right ventricular) pressure overload → right HF (heart failure); HF with preserved ejection fraction Slides 35, 36

Clinical Manifestation

Symptoms rare until orifice ~1/3 normal; left-sided HF symptoms (dyspnea on exertion, cough, orthopnea, paroxysmal nocturnal dyspnea, fatigue); hemoptysis (high LA pressure ruptures bronchial vein anastomoses); hoarseness, Ortner syndrome (enlarged LA compressing the left recurrent laryngeal nerve); dysphagia (LA on esophagus). Low-pitched decrescendo-crescendo rumbling diastolic murmur at apex, starting with an opening snap (sound after S2 as the stiff valve opens); bell, left lateral decubitus; softer with Valsalva, like most murmurs (slide 38's "increased with Valsalva" is not accurate) Slides 37, 38

Diagnosis

ECG (electrocardiogram): LA abnormality, AF common in severe MS, RVH (right ventricular hypertrophy) with pulmonary hypertension; TTE (transthoracic echocardiogram): large LA, stenotic mitral valve; catheterization not necessary. Severe: area <1.0 cm², mean gradient >10 mmHg, peak velocity >3.0 m/s, proximal flow always present (the slide's mild and moderate bands overlap at 1.5 and are not keyed). Dyspnea on exertion or orthopnea → echo Slides 39, 40, 43

Treatment/Therapy

Asymptomatic in sinus rhythm: no therapy; dyspnea/orthopnea: loop diuretics (furosemide, bumetanide). Surgery if severe MS AND symptomatic dyspnea or pulmonary hypertension: percutaneous balloon valvotomy; valve replacement (moderate symptoms or pulmonary hypertension). Refer everyone with MS on echo Slides 41, 42, 43

Mortality ★

Not covered in the lecture

Name of Condition

Mitral regurgitation / insufficiency (MR) Slide 44

Definition

Incomplete mitral valve closure causing blood to flow back into the LA (left atrium) during systole (slide 44 mislabels this line "Mitral Stenosis") Slide 44

Etiology (cause)

Acute: MI (myocardial infarction) with papillary muscle rupture, infective endocarditis, rheumatic fever, chordae tendineae rupture, acute LV dilation (myocarditis/ischemia), prosthetic mitral valve failure. Chronic: MVP (mitral valve prolapse), infective endocarditis, rheumatic fever, HOCM (hypertrophic obstructive cardiomyopathy), dilated cardiomyopathy Slide 45

Epidemiology (who)

Not covered in the lecture

Risk Factors

Not covered in the lecture

Pathology

Systolic backflow into LA → LA dilation with pressure/volume overload → LV dilation with eccentric hypertrophy (systolic HF (heart failure)). Acute MR: reduced LA/LV pressures avoid right HF; chronic → right HF → HF with reduced ejection fraction → combined right and left HF Slides 46, 47

Clinical Manifestation

Mild–moderate isolated MR usually asymptomatic; palpitations; acute: left-HF symptoms (dyspnea, fatigue, orthopnea, paroxysmal nocturnal dyspnea, rales, elevated JVP (jugular venous pressure), leg edema); chronic → left HF → pulmonary hypertension → combined HF. Holosystolic blowing murmur at apex, best in left lateral decubitus, radiates to axilla, ± S3, ± thrill; increased by squatting, handgrip; decreased by standing, Valsalva Slides 47, 48

Diagnosis

ECG (electrocardiogram): LA enlargement, LVH (left ventricular hypertrophy) in severe MR (low sensitivity); TTE (transthoracic echocardiogram): regurgitant flow, LVH, LA enlargement; left heart catheterization not required. Severity: severe = regurgitant fraction 50% or more (moderate 30–49%, mild <30%) Slides 49, 50

Treatment/Therapy

Medical: increase forward cardiac output while reducing regurgitant volume; treat comorbid AF (atrial fibrillation) and pulmonary hypertension. Surgery for severe MR, symptomatic LV systolic dysfunction, ejection fraction <60%, LV end-systolic dimension >40 mm: mitral valve clip, TMVR (transcatheter mitral valve replacement), mechanical valve (lifelong anticoagulation) vs biological (none) Slides 51, 52

Mortality ★

Not covered in the lecture

Name of Condition

Mitral valve prolapse (MVP) Slide 54

Definition

Flaring of the mitral valve leaflets into the left atrium during systole Slide 54

Etiology (cause)

Myxomatous degeneration of the mitral valve Slide 54

Epidemiology (who)

Usually healthy women 15–30 years old Slide 54

Risk Factors

Not covered in the lecture

Pathology

Congenital condition (slide 54; endorsed in the lecture: "because you were born that way") Slide 54

Clinical Manifestation

Usually benign and asymptomatic; mid-systolic click at the apex; may develop MR (mitral regurgitation) symptoms and signs Slide 54

Diagnosis

Echocardiogram: thickened, redundant mitral leaflets (>5 mm) Slide 54

Treatment/Therapy

Usually none; if it progresses to MR: clip, TMVR (transcatheter mitral valve replacement), biological or mechanical replacement Slide 54

Mortality ★

Not covered in the lecture

Name of Condition

Pulmonic stenosis (PS) Slide 55

Definition

Right ventricular outflow obstruction of blood to the lungs Slide 55

Etiology (cause)

Almost always congenital; carcinoid disease; commonly part of tetralogy of Fallot Slide 55

Epidemiology (who)

Not covered in the lecture

Risk Factors

Not covered in the lecture

Pathology

Increased RV (right ventricular) pressure → RV pressure overload → RVH (right ventricular hypertrophy; diastolic failure); RV volume overload → dilated right HF (heart failure; systolic failure) Slide 56

Clinical Manifestation

Mild–moderate usually asymptomatic; severe: right-HF symptoms (exertional dyspnea, fatigue, angina, syncope). Harsh high-pitched crescendo-decrescendo mid-systolic ejection murmur at left 2nd–4th ICS (intercostal space)/LUSB (left upper sternal border), increases with inspiration; split S2. Late: right HF, hepatomegaly, ascites, edema Slide 57

Diagnosis

ECG (electrocardiogram): right axis deviation, RVH (right ventricular hypertrophy); echo: abnormal valve motion, increased peak jet on Doppler (the grading table is not tested: "not the lesser valves") Slide 58

Treatment/Therapy

Mild–moderate: none. Severe with symptoms: diuretics for right-HF symptoms, pulmonic balloon valvuloplasty; severe congenital may need replacement. Refer to cardiology if seen on echo Slide 59

Mortality ★

Mild–moderate: 94% 20-year survival Slide 59

★ Iatrogenic is the most common cause (said three times); true for significant regurgitation

Name of Condition

Pulmonic regurgitation / insufficiency (PR) Slide 60

Definition

Incomplete pulmonic valve closure causing blood to flow back into the RV (right ventricle) Slide 60

Etiology (cause)

High-pressure cause: pulmonary hypertension. Low-pressure causes: congenital (bicuspid); carcinoid disease; iatrogenic (after surgical valvotomy/valvectomy/valvuloplasty for RV (right ventricular) outflow obstruction) = MOST COMMON cause of significant regurgitation (slide 61, confirmed in the lecture); overall, mild regurgitation from pulmonary hypertension is commoner Slide 61

Epidemiology (who)

Not covered in the lecture

Risk Factors

Not covered in the lecture

Pathology

Retrograde flow from the pulmonary artery → RV overload Slide 62

Clinical Manifestation

Right-sided HF (heart failure): fatigue, peripheral edema, JVD (jugular venous distension), ascites. Brief high-pitched decrescendo early diastolic murmur at 2nd left ICS (intercostal space), radiating to mid right sternal border with full inspiration (Graham Steell murmur); louder with more venous return (inspiration, squatting, supine), softer with less (expiration, standing) Slides 62, 63

Diagnosis

Usually an incidental finding on echocardiogram or physical exam Slide 64

Treatment/Therapy

Treat the underlying condition; refer when seen on echo or with right-HF symptoms/signs (slide 64's "almost always congenital, no treatment required" conflicts with slide 61 and is not keyed) Slide 64

Mortality ★

Not covered in the lecture

Name of Condition

Tricuspid stenosis (TS) Slide 65

Definition

Obstruction of inflow from the RA (right atrium) to the RV (right ventricle) across a narrowed tricuspid valve (slide 66; slide 65's "from the LA" is a deck error) Slides 65, 66

Etiology (cause)

Most commonly rheumatic fever (usually with rheumatic mitral disease); carcinoid disease. Slide 65's "in the US almost always congenital" is not accurate Slide 65

Epidemiology (who)

Most common in women Slide 65

Risk Factors

Not covered in the lecture

Pathology

Narrowed tricuspid valve → obstructed RA-to-RV inflow → RA dilation and hypertrophy, low cardiac output, portal congestion → right HF (heart failure) without RV dysfunction Slide 66

Clinical Manifestation

Mild–moderate usually asymptomatic; severe: fluttering discomfort in the neck, cold skin (low cardiac output), RUQ (right upper quadrant) pain (enlarged liver). Soft opening snap and mid-diastolic rumble at left lower sternal border near the xiphoid, increases with inspiration; JVD (jugular venous distension); suffusion sign (dusky face with dilated scalp veins when supine; not tested, per the lecture) Slide 67

Diagnosis

ECG (electrocardiogram): RA enlargement out of proportion to RVH (right ventricular hypertrophy); echo: abnormal valve motion, increased peak jet (the grading table is not tested: "not the lesser valves") Slide 68

Treatment/Therapy

Severe with symptoms: low salt, diuretics, aldosterone antagonist; bioprosthetic valve replacement preferred; balloon valvotomy and repair reserved for hepatic congestion that may lead to cirrhosis or severe systemic venous congestion. Refer if seen on echo or HF symptoms Slide 69

Mortality ★

Not covered in the lecture

★ Tricuspid endocarditis is usually intravenous drug use; Carvallo sign separates it from mitral regurgitation

Name of Condition

Tricuspid regurgitation / insufficiency (TR) Slide 70

Definition

Incomplete closure causing blood to flow from the RV (right ventricle) back into the RA (right atrium) Slide 70

Etiology (cause)

Most commonly tricuspid annulus dilation from RV dilation in pulmonary hypertension; primary: infective endocarditis in IV (intravenous) drug users Slide 70

Epidemiology (who)

IV drug users (primary TR from endocarditis) Slide 70

Risk Factors

Pulmonary hypertension; IV drug use Slide 70

Pathology

Not covered in the lecture

Clinical Manifestation

Mild–moderate usually asymptomatic; severe: pedal edema, ascites. Holosystolic murmur at left mid/lower sternal border near the epigastrium; increases with inspiration (Carvallo sign: inspiratory increase in a right-sided murmur), which distinguishes it from MR (mitral regurgitation); elevated JVP (jugular venous pressure) with neck pulsations; venous thrill on the right jugular vein Slides 71, 9

Diagnosis

Echocardiogram Doppler: regurgitation; prolapsed, scarred or displaced leaflets Slide 72

Treatment/Therapy

Treat the underlying condition; annuloplasty if due to annular dilation; valve repair or replacement if primary cause. Refer when identified on echo or with right heart failure symptoms Slide 72

Mortality ★

Not covered in the lecture

★ Mechanical valve: vitamin K antagonist (warfarin) only; stick with the higher target when both valves are mechanical; bridge with heparin

Name of Condition

Valve replacement / prosthetic heart valves (a management topic, not a disease) Slides 74, 75

Definition

Mechanical (titanium and carbon) vs biological (pig or cow tissue) valves Slides 21, 52

Etiology (cause)

Not covered in the lecture

Epidemiology (who)

Valve type by age: mechanical for a younger patient, bioprosthetic or transcatheter for an older one (slide 74's TAVR/TMVR "<55" and mechanical "<70" are reversed; not keyed); bioprosthetic preferred if life expectancy is shorter than the valve's expected longevity or anticoagulation is contraindicated Slide 74

Risk Factors

Not covered in the lecture

Pathology

Not covered in the lecture

Clinical Manifestation

Not covered in the lecture

Diagnosis

Not covered in the lecture

Treatment/Therapy

Mechanical: lifelong anticoagulation; VKA (vitamin K antagonist) recommended over no VKA and over antiplatelet agents; target INR (international normalized ratio) 2.5 (2.0–3.0) mechanical aortic, 3.0 (2.5–3.5) mechanical mitral, 3.0 (2.5–3.5) both positions; warfarin is the most common VKA; if surgery requires switching to heparin, bridge until INR is therapeutic. Bioprosthetic: no anticoagulation beyond the immediate postoperative period Slides 21, 52, 74, 75

Mortality ★

Not covered in the lecture

Name of Condition

Acute rheumatic fever (named on the deck's objectives slide only; no section) Slide 2

Definition

Not covered in the lecture

Etiology (cause)

Rheumatic heart disease: autoimmune reaction to group A beta-hemolytic streptococci Slide 12

Epidemiology (who)

Rare in developed countries (decreased incidence); 80% of mitral stenosis from rheumatic fever is in women, usually diagnosed ~20 years after rheumatic fever Slide 34

Risk Factors

Not covered in the lecture

Pathology

Not covered in the lecture

Clinical Manifestation

Not covered in the lecture

Diagnosis

Not covered in the lecture

Treatment/Therapy

Not covered in the lecture

Mortality ★

Not covered in the lecture

★ The right coronary artery supplies the atrioventricular node (complete heart block); the anterior interventricular artery is the LAD, the most common culprit

Name of Condition

Ischemic heart disease; coronary artery disease (CAD) / ischemia; ischemic myocardium Slides 1, 4, 5

Definition

Mismatch between myocardial oxygen demand and oxygen supply Slide 5

Etiology (cause)

↓ oxygen supply: atherosclerosis, thrombus/embolus, anemia, spasm, dissection, carboxyhemoglobin, hypoxia; ↑ oxygen demand: exercise, emotional stress, LVH (left ventricular hypertrophy)/cardiomyopathy, hyperthyroidism, hyperthermia, cocaine Slide 6

Epidemiology (who)

Culprit vessel in acute MI (myocardial infarction): ★ AIV (anterior interventricular artery) = LAD (left anterior descending) 40–50%, the most common; RCA (right coronary artery) 30–40%; left circumflex 15–20%. ★ RCA supplies the AV (atrioventricular) node (complete heart block); SA (sinoatrial) node from the RCA in 60%, circumflex in 40% Slides 11, 14

Risk Factors

Nonmodifiable: age ≥45 men / ≥55 women; male > premenopausal female (gap narrows by ~80); sudden death/MI in male first-degree relative <55 or female <65. Modifiable: obesity, dyslipidemia, diabetes, smoking (strong predictor, especially women <45), hypertension, excessive alcohol, sedentary lifestyle, poor stress management Slides 21–23

Pathology

Heart is 0.3% of body weight but uses 7% of oxygen; irreversible injury in 40–60 min; anaerobic shift ↑ lactic acid; injury from free radicals, lactic acid, ↑ extracellular calcium; wall hypokinesia/akinesia/dyskinesia. Atherosclerosis (fat, smooth muscle, fibroblasts, matrix): thick-cap atheroma vs thin-cap fibroatheroma; plaque rupture → platelet activation + tissue factor → clotting cascade → fibrin Slides 7–9, 17–20

Clinical Manifestation

Typical pain: substernal pressure, worse with exertion, radiates to neck/shoulder, shortness of breath, diaphoresis, relieved by nitroglycerin; ischemia may be silent Slides 25, 29–30

Diagnosis

All chest pain: chest X-ray + STAT ECG (electrocardiogram); CBC (complete blood count), metabolic panel, PT/PTT (prothrombin/partial thromboplastin time), troponin, lipids; maybe drug screen, D-dimer, lipase, pro-BNP (pro-B-type natriuretic peptide). Risk scores: GRACE, TIMI (Thrombolysis in Myocardial Infarction), PURSUIT, HEART. ★ Cardiac CT (computed tomography) calcium score = risk stratification, not ACS (acute coronary syndrome); treadmill ECG; nuclear stress (abnormal → cardiac catheterization; the slide's sensitivity/specificity figures are not tested); echo (regional wall motion); coronary CT angiography Slides 32–35

Treatment/Therapy

Per syndrome (see cards below); risk-factor control: blood pressure, lipids, glucose, weight loss, alcohol restriction, exercise, smoking cessation, stress Slide 79

Mortality ★

LV (left ventricular) involvement carries higher mortality; sudden cardiac death is the first manifestation of CAD in >20% Slides 12, 85

★ Silent ischemia in diabetes, neuropathy and a transplanted heart presents as dyspnea, nausea or fatigue; angina is not positional

Name of Condition

Angina pectoris Slides 24, 27

Definition

Transient myocardial ischemia not long or severe enough to cause MI (myocardial infarction); symptoms recur Slide 27

Etiology (cause)

Oxygen supply/demand mismatch Slides 5–6

Epidemiology (who)

Not covered in the lecture

Risk Factors

Coronary artery disease risk factors Slides 22–23

Pathology

Intermittent ischemia short of infarction Slide 27

Clinical Manifestation

Substernal pressure/squeezing/tightness/burning/band-like, worse with exertion, radiates to neck/shoulder, shortness of breath, diaphoresis, relieved by nitroglycerin, not positional; Levine sign (clenched fist held over the sternum). ★ Silent ischemia (diabetes, neuropathy, transplanted heart) → dyspnea, cough, nausea/vomiting, abdominal pain, diaphoresis, dizziness, fatigue. Referred: jaw, tooth, arm, back, scapula, epigastric/left upper quadrant Slides 25–31

Diagnosis

Chest-pain workup; stress testing; echo; coronary CT (computed tomography) angiography Slides 32, 35

Treatment/Therapy

See stable angina: sublingual nitroglycerin is the cornerstone Slides 39–41

Mortality ★

Not covered in the lecture

★ Call EMS if pain is unimproved 5 minutes after one nitroglycerin dose or after 3 doses; coronary angiography is the gold standard

Name of Condition

Stable angina; SIHD (stable ischemic heart disease) Slides 36–37

Definition

Angina usually brought on by activity and relieved by rest and nitroglycerin (unstable angina occurs at rest) Slides 37, 86

Etiology (cause)

Exertion raises myocardial oxygen demand Slides 6, 37

Epidemiology (who)

Most common form of angina pectoris Slide 37

Risk Factors

Coronary artery disease risk factors Slides 22–23

Pathology

Not covered in the lecture

Clinical Manifestation

Pain with exertion; improves with nitroglycerin; resolves with rest Slides 37, 86

Diagnosis

Stress-test ECG (electrocardiogram) changes, usually T-wave inversion: exercise treadmill, nuclear stress, cardiac CT (computed tomography); ★ coronary angiography is the gold standard for CAD (coronary artery disease) Slide 38

Treatment/Therapy

Sublingual nitroglycerin (venodilator: ↓ preload → ↓ wall stress → ↓ oxygen demand; also dilates arteries); call EMS (emergency medical services) if no relief 5 min after a dose or after 3 doses; lifestyle modification; beta-blocker (calcium channel blocker if contraindicated); statin; aspirin; prevention: aspirin + clopidogrel, more effective together Slides 39–41

Mortality ★

Not covered in the lecture

★ Troponin I numbers "for testing" (slide 72a, shown in class): standard >0.04 ng/mL, high-sensitivity 12 ng/L women / 20 ng/L men; rule-out tool, repeat it; TIMI 3 or higher → early invasive approach

Name of Condition

ACS (acute coronary syndromes) Slides 4, 42–43

Definition

Umbrella for unstable angina, NSTEMI (non-ST-elevation myocardial infarction) and STEMI (ST-elevation myocardial infarction) Slides 42–43

Etiology (cause)

Plaque rupture → platelet activation + tissue factor → clotting cascade → fibrin Slide 20

Epidemiology (who)

Not covered in the lecture

Risk Factors

CAD (coronary artery disease) risk factors; HEART/TIMI (Thrombolysis in Myocardial Infarction) risk factors: diabetes, hypertension, hyperlipidemia, obesity, smoking, family history of CAD, known CAD Slides 22–23, 34, 71

Pathology

Plaque rupture with thrombus Slide 20

Clinical Manifestation

Referred pain most often to jaw/tooth/arm, also back, scapula, epigastric/left upper quadrant Slide 31

Diagnosis

Chest-pain workup. ★ Troponin I (slide 72a, shown in class, not in the posted deck): standard troponin I abnormal above 0.04 ng/mL; high-sensitivity troponin I 99th percentile 12 ng/L in women, 20 ng/L in men; troponin I is heart-specific (troponins are proteins of cardiac and skeletal muscle, none in smooth muscle); ★ a rule-OUT tool, and one draw means two (watch for a rise). Risk scores GRACE, TIMI (Thrombolysis in Myocardial Infarction), PURSUIT, HEART (History, ECG, Age, Risk factors, Troponin). ★ TIMI 3 or higher justifies an early invasive approach; HEART bands and MACE (major adverse cardiac event) percentages are not tested Slides 32–34, 71–72, 72a

Treatment/Therapy

High-intensity statin (atorvastatin, rosuvastatin) for all ACS regardless of LDL (low-density lipoprotein), started before discharge Slide 81

Mortality ★

Estimated by the risk scores; the HEART and TIMI (Thrombolysis in Myocardial Infarction) outcome percentages on slides 34 and 72 are not tested Slide 34

★ Troponin separates unstable angina (normal) from NSTEMI (elevated); oxygen only if SpO2 <91%

Name of Condition

Unstable angina (UA) Slides 44–45

Definition

Change in a patient's stable angina, considered ACS (acute coronary syndrome): occurs at rest, new-onset and activity-limiting, or increasing (more discomfort, more often) Slide 45

Etiology (cause)

Change in stable angina (plaque rupture); the Braunwald classification on slide 54 (mis-cited "APACHE II") was brushed past and is not tested Slides 45, 54

Epidemiology (who)

Not covered in the lecture

Risk Factors

TIMI (Thrombolysis in Myocardial Infarction) criteria: age ≥65; ≥3 CAD (coronary artery disease) risk factors; known stenosis >50%; aspirin in past 7 days; ≥2 angina episodes in 24 h; ST deviation ≥0.5 mm; elevated marker Slide 71

Pathology

Not covered in the lecture

Clinical Manifestation

Pain at rest; nitroglycerin usually (not always) helps Slides 46, 86

Diagnosis

Nonspecific ECG (electrocardiogram) changes (usually inverted T waves) with ★ NORMAL troponin (troponin separates UA from NSTEMI (non-ST-elevation MI)); stress-test ST depression or T inversion; nuclear stress: reversible defect = ischemia, fixed = infarction; TIMI (Thrombolysis in Myocardial Infarction) 3 or higher → early invasive approach Slides 46–47, 71–72

Treatment/Therapy

Medical emergency, same as NSTEMI: chewable aspirin, beta-blocker, IV nitrates; DAPT (dual antiplatelet therapy: aspirin + clopidogrel) ± anticoagulation; MONA (morphine, oxygen, nitroglycerin, aspirin), ★ oxygen only if SpO2 <91%. After stabilization: left heart catheterization/angiography, balloon angioplasty, PCI (percutaneous coronary intervention) with stent. Post-PCI: DAPT, statin, ACE (angiotensin-converting enzyme) inhibitor, anticoagulant if indicated; ★ stopping DAPT in the first 6 weeks → sudden stent thrombosis (slide 52 calls it a "50% risk of sudden in-stent restenosis"; the event is thrombosis and the figure has no source; the DAPT durations on slides 52 and 83 disagree and are not tested); exercise as tolerated, low-salt/low-fat diet, follow-up Slides 48–53

Mortality ★

TIMI (Thrombolysis in Myocardial Infarction) 3–7 needs ICU (intensive care unit) or emergent revascularization; the percentage table (slide 72) and Braunwald prognosis (slide 54) are not tested Slide 72

★ ST depression >1 mm and/or T-wave inversion in two or more consecutive leads with elevated troponin

Name of Condition

NSTEMI (non-ST-elevation myocardial infarction); non-ST elevation ischemia Slides 4, 56, 86

Definition

MI (myocardial infarction) diagnosed by ECG (electrocardiogram) changes + ischemic symptoms + elevated troponin/high-sensitivity troponin Slide 47

Etiology (cause)

Not covered in the lecture

Epidemiology (who)

Not covered in the lecture

Risk Factors

TIMI (Thrombolysis in Myocardial Infarction) criteria Slide 71

Pathology

Subendocardial ischemia → ST depression Slide 55

Clinical Manifestation

Signs and symptoms of ischemia; nitroglycerin may help the pain Slides 47, 86

Diagnosis

★ Slide 47: ST depression >1 mm and/or T-wave inversion in ≥2 consecutive leads + ELEVATED troponin (what separates it from unstable angina); troponin I abnormal above 0.04 ng/mL (high-sensitivity 12 ng/L women, 20 ng/L men). Slide 86's "ST inversion (>1 mm)" is a deck error (ST segments are depressed; T waves invert) Slides 47, 55, 72a, 86

Treatment/Therapy

Treated the same as unstable angina (see that card) Slides 48–53

Mortality ★

TIMI (Thrombolysis in Myocardial Infarction) 3 or higher → early invasive approach (percentages not tested) Slide 72

★ Lead groups name the artery (II, III, aVF = RCA); ST depression V1–V3 = posterior, get V7–V9; new LBBB managed as STEMI only with ongoing ischemia or instability; ECG within 10 min, door-to-balloon <90 min

Name of Condition

STEMI (ST-elevation myocardial infarction); transmural myocardial infarction (MI) Slides 57, 65

Definition

Myocardial necrosis with ST elevation in ≥2 consecutive leads not quickly reversed by nitroglycerin, reciprocal ST depression, ★ new LBBB (left bundle branch block) managed as STEMI only with ongoing ischemia, hypotension or heart failure (slide and lecture: an equivalent on its own), Q waves. Slide 65 adds "elevated cardiac markers must be present"; in class he said troponin is not required (it may not have risen yet), so this is not keyed Slide 65

Etiology (cause)

Coronary occlusion; LAD (left anterior descending) most common culprit (40–50%), RCA (right coronary artery) 30–40%, left circumflex 15–20% Slide 14

Epidemiology (who)

Not covered in the lecture

Risk Factors

CAD (coronary artery disease) risk factors Slides 22–23

Pathology

Transmural ischemia → ST elevation; ECG (electrocardiogram) evolution: hyperacute T/ST elevation (minutes–hours) → T inversion + Q (hours–1 day) → Q + coronary T (1 week) → Q wave (months) Slides 55, 64

Clinical Manifestation

Typical and referred chest pain as for ACS (acute coronary syndrome) Slides 25, 31

Diagnosis

★ ECG (electrocardiogram) within 10 min of arrival: ST elevation >1 mm in ≥2 consecutive leads. Localization: ★ inferior II/III/aVF → RCA (right coronary artery) (and/or circumflex); lateral I/aVL/V5–V6 → circumflex or LAD (left anterior descending) diagonal; anterior/septal V1–V4 → LAD (V4 is anterior); ★ posterior = ST depression V1–V3, confirmed with posterior leads V7–V9; right ventricular V1/V4R. Pathologic Q waves = infarct already happened. Slide 62's other rows and V2–V3 cut-offs are self-study Slides 61–62, 65, 68, 86

Treatment/Therapy

Chewable aspirin; activate cath team for PCI (percutaneous coronary intervention); then ticagrelor/prasugrel/clopidogrel + heparin drip; nitroglycerin (sublingual/paste/infusion); beta-blocker if no bradycardia; ★ if PCI ≥2 h away give thrombolytics within 30 min of arrival (tenecteplase most common; also alteplase, reteplase, streptokinase, anistreplase, lanoteplase); ★ door-to-balloon <90 min; GP (glycoprotein) IIb/IIIa inhibitors have fallen out of favor. PCI (angioplasty, atherectomy, stent) or CABG (coronary artery bypass graft: mammary or radial ARTERY first, great saphenous vein only if an artery cannot be used). Post-MI: ★ beta-blocker improves survival when EF is reduced; calcium channel blockers do not (the deck says "across the board"; with preserved EF the benefit is not established: REDUCE-AMI, 2025 ACC/AHA ACS guideline) (diltiazem/verapamil give no mortality benefit; they relieve angina or control rate when a beta-blocker cannot be used and are avoided with reduced EF; the deck's preserved-function mortality claim is not accurate); high-intensity statin for all ACS before discharge; ACE (angiotensin-converting enzyme) inhibitor with reduced LV function; aspirin; clopidogrel after stent; warfarin only for an akinetic apex or LV thrombus after an anterior MI (slide 83: all large anterior MIs). Oxygen only if SpO2 <91%; ★ no nitroglycerin within 24 h of a PDE (phosphodiesterase) inhibitor (ask women too: pulmonary arterial hypertension) Slides 66–70, 73–74, 76–77, 80–83

Mortality ★

Complications: post-infarction ischemia, heart failure, myocardial rupture, ventricular aneurysm, thromboembolism, pericarditis (Dressler syndrome, post-MI pericarditis), cardiogenic shock (more common with left-sided MI), arrhythmias; LV (left ventricular) involvement → higher mortality; beta-blockers improve survival Slides 12, 78, 80

★ Do NOT give nitroglycerin in a right ventricular infarct ("you will kill somebody")

Name of Condition

Right ventricular (RV) infarct Slide 63

Definition

RCA (right coronary artery) occlusion affecting the inferior and posterior left ventricular wall and septum, extending into the RV in 15–30% Slide 63

Etiology (cause)

Occlusion of the RCA (right coronary artery) Slide 63

Epidemiology (who)

RV extension in 15–30% of RCA (right coronary artery) occlusions Slide 63

Risk Factors

Not covered in the lecture

Pathology

Preload-dependent RV (right ventricle): ↓ preload reduces Frank-Starling effect → RV failure (right-sided heart failure) Slide 63

Clinical Manifestation

Not covered in the lecture

Diagnosis

STEMI chart: ST elevation V1 and V4R, reciprocal depression I and aVL; culprit RCA (right coronary artery); RCA supplies the AV (atrioventricular) node → dysrhythmias Slides 11, 62

Treatment/Therapy

★ DO NOT GIVE nitroglycerin (slide 63; said three times in class): dropping preload loses the Frank-Starling push of the RV, output falls and the patient goes into shock. Slide 73's "caution in inferior MIs (right sided) with evidence of CHF" was never read and is not keyed; the rule is for right ventricular involvement, not every inferior MI (only 15–30% of RCA occlusions reach the RV) Slides 63, 73

Mortality ★

Not covered in the lecture

★ Ventricular fibrillation is the most common cause; the first manifestation of CAD in over 20% ("one in five")

Name of Condition

Sudden cardiac death Slide 85

Definition

Not covered in the lecture

Etiology (cause)

★ Most common: ventricular fibrillation; also LVH (left ventricular hypertrophy), hypertrophic cardiomyopathy, hypoxia, electrolyte abnormalities Slide 85

Epidemiology (who)

★ First manifestation of CAD (coronary artery disease) in >20% of patients Slide 85

Risk Factors

Sudden death in a first-degree relative (listed as a CAD (coronary artery disease) risk factor) Slide 22

Pathology

Not covered in the lecture

Clinical Manifestation

Not covered in the lecture

Diagnosis

Not covered in the lecture

Treatment/Therapy

Not covered in the lecture

Mortality ★

Not covered in the lecture

★ Gold standard: ergonovine or acetylcholine provocation at angiography, relieved by nitroglycerin; calcium channel blocker first-line

Name of Condition

Vasospastic angina; Prinzmetal angina; variant angina; coronary vasospasm angina Slides 87, 89

Definition

Angina due to coronary artery vasospasm, occurring at rest and responding to nitroglycerin Slide 88

Etiology (cause)

Vasospasm in normal or diseased coronaries; drug triggers: cocaine, ephedrine, marijuana, alcohol, amphetamine, triptans Slides 88–89

Epidemiology (who)

Relatively uncommon; often age <50 Slide 88

Risk Factors

Cigarette smoking (major risk factor) Slide 89

Pathology

Vasospasm without high-grade stenosis on arteriography Slides 88, 90

Clinical Manifestation

Recurrent chest pain at rest, mostly midnight to 8 am; gradual onset/offset, 5–15 min (may last longer); typical chest pain Slides 89–90

Diagnosis

ECG (electrocardiogram): transient ST elevation during an episode (transient ischemic ST changes in multiple leads, <15 min) that resolves (slide 90, as described in class); slide 91's "T-wave inversion; maybe ST depression" is not keyed. No high-grade stenoses. ★ Gold standard: spasm on angiography provoked by ergonovine or acetylcholine, relieved by nitroglycerin Slides 90–91

Treatment/Therapy

Stop smoking; nitrates for symptoms; ★ FIRST-LINE calcium channel blockers (diltiazem, amlodipine); AVOID nonselective beta-blockers, aspirin, triptans Slide 92

Mortality ★

Not covered in the lecture

Name of Condition

Microvascular angina (formerly cardiac syndrome X); the slide also lists MINOCA (myocardial infarction with non-obstructive coronary arteries). Caveat: in standard usage MINOCA requires an infarction and microvascular angina does not; the deck (and the lecture) treat them as one, and no question asks you to separate them Slides 93–94

Definition

Angina with ST changes but normal coronary arteries on angiogram, and no infarction (slide 94's "possibly elevated biomarkers" belongs to MINOCA) Slide 94

Etiology (cause)

Proposed: endothelial dysfunction, myocardial ischemia, insulin resistance/diabetes, abnormal autonomic control, altered cardiac sensitivity, estrogen deficiency, altered pain perception Slide 95

Epidemiology (who)

More frequent in females; often associated with stress or anxiety Slide 94

Risk Factors

Stress/anxiety; insulin resistance/diabetes and estrogen deficiency (proposed mechanisms) Slides 94–95

Pathology

Proposed mechanisms as under etiology Slide 95

Clinical Manifestation

Angina with ST changes Slide 94

Diagnosis

Diagnosis of exclusion; angiography required to rule out CAD (coronary artery disease) Slide 94

Treatment/Therapy

Similar to CAD (coronary artery disease): lifestyle/risk-factor reduction, calcium channel blocker, beta-blocker, ACE (angiotensin-converting enzyme) inhibitor, statin Slide 96

Mortality ★

Not covered in the lecture

★ Slide 32 flags Brain Natriuretic Peptide with '***'

Name of Condition

Heart failure (HF); congestive heart failure (CHF) as the clinical diagnosis Slides 4, 32

Definition

Heart cannot pump blood fast enough to meet metabolic demand at rest and with effort, or does so only with abnormally high filling pressures; a clinical syndrome (constellation of signs and symptoms) from any structural or functional disorder that impairs ventricular filling or ejection; clinical HF = HF symptoms plus elevated BNP (B-type natriuretic peptide) or objective cardiogenic congestion Slides 4, 5, 26

Etiology (cause)

All HF has a cardiomyopathy etiology: ischemic cardiomyopathy (myocardial infarction, chronic ischemia, hypoperfusion/shock) vs non-ischemic (hypertension, valvular disease, most often aortic stenosis; dilated, hypertrophic, restrictive, peripartum, septic, arrhythmogenic, Takotsubo cardiomyopathy; congenital heart disease; toxins such as alcohol and chemotherapy; diabetes, thyroid disease, rheumatoid arthritis, lupus) Slide 16

Epidemiology (who)

6.7 million Americans over 20 have HF (2025); 60% of patients are over 65; 10–15% of people over 80 have HF; lifetime risk 24% (1 in 4) Slide 6

Risk Factors

Age; hypertension; coronary artery disease; diabetes; chronic tachyarrhythmias; obesity/metabolic syndrome; excess alcohol; tobacco; family history; genetic abnormality; cardiotoxic medications Slide 18

Pathology

Four mechanisms: excess preload (volume), excess afterload (resistance), decreased contractility, decreased filling; injury → remodeling (myocyte hypertrophy, collagen fibrosis) driven by neurohormones (sympathetic system and RAAS (renin-angiotensin-aldosterone system) harmful; natriuretic peptides protective), inflammation, mechanical stress; compensation: ↑heart rate, ↑contractility, ↑preload Slides 4, 19, 20, 21

Clinical Manifestation

Congestion: dyspnea, DOE (dyspnea on exertion), orthopnea (breathlessness lying flat), PND (paroxysmal nocturnal dyspnea: waking breathless at night), pulmonary/peripheral edema, S3 and S4 gallops (extra heart sounds), elevated JVP (jugular venous pressure), hepatomegaly; low perfusion: fatigue, weakness, syncope, obtundation, cool extremities, narrow pulse pressure, low sodium, renal dysfunction; warm/cold and wet/dry profiles Slides 5, 26, 28, 29

Diagnosis

Clinical diagnosis: HF signs/symptoms + elevated BNP (B-type natriuretic peptide) or cardiogenic congestion; chest X-ray (pleural effusion, cephalization, Kerley B lines (short horizontal lines at the lung edges), ↑cardiothoracic ratio); echo (most accurate structures); MUGA (multigated acquisition scan; most accurate EF (ejection fraction)); CBC (complete blood count), CMP (comprehensive metabolic panel: potassium, renal function), troponin; ECG (electrocardiogram): ischemia, LVH (left ventricular hypertrophy), right heart strain; BNP <100 rules out acute HF, >400 likely HF; NT-proBNP (N-terminal pro-BNP) >125 under 75 y, >450 over 75 y likely HF Slides 32, 33, 34, 38

Treatment/Therapy

Goals: fewer symptoms, longer survival, slower progression; GDMT (guideline-directed medical therapy): diuretics (hydrochlorothiazide, metolazone, furosemide, bumetanide), ACEi (angiotensin-converting enzyme inhibitor: lisinopril, enalapril), ARB (angiotensin receptor blocker: losartan, valsartan, irbesartan), ARNI (angiotensin receptor-neprilysin inhibitor: valsartan/sacubitril), beta blocker (metoprolol, atenolol, propranolol), SGLT2i (sodium-glucose cotransporter 2 inhibitor: dapagliflozin, empagliflozin), MRA (mineralocorticoid receptor antagonist: spironolactone, eplerenone), nitrates; avoid calcium channel blockers (deck: dihydropyridines contraindicated, non-dihydropyridines avoid); inotropes in the intensive care unit only; 2022 stages: A SGLT2i in diabetes; B SGLT2i in diabetes, ACEi (ARB if intolerant), beta blocker; ICD (implantable cardioverter-defibrillator) if LVEF (left ventricular ejection fraction) ≤35%, NYHA (New York Heart Association) II–III on optimal GDMT, life expectancy ≥1 y Slides 40, 51, 52, 53

Mortality ★

1-year post-hospitalization mortality 35%; HF causes 45% of cardiovascular deaths (47% vs 29% for heart attack in 2022); each BNP (B-type natriuretic peptide) rise of 100 → 35% higher relative risk of death; predischarge BNP <430 → lower 30-day readmission Slides 6, 38

★ Slide 8 lists 'Most common by far (70-80%)' under 'Important to know'

Name of Condition

Left heart failure (left-sided HF (heart failure)) Slide 8

Definition

Left ventricular involvement: systolic or diastolic failure; dilated, hypertrophic or restrictive cardiomyopathy; ischemic or non-ischemic; preserved or reduced EF (ejection fraction) Slide 8

Etiology (cause)

As for all HF (heart failure): a cardiomyopathy etiology, ischemic or non-ischemic Slides 8, 16

Epidemiology (who)

Most common type by far (70–80%); the main focus of the lecture Slide 8

Risk Factors

Not covered in the lecture

Pathology

Systolic dysfunction from ischemic/dilated cardiomyopathy, or diastolic dysfunction from hypertrophic cardiomyopathy (see HFrEF and HFpEF cards) Slides 25, 39

Clinical Manifestation

S3 (rapid ventricular filling sound) and S4 (atrial contraction sound); systolic: normal/low blood pressure, S3, pulmonary edema; diastolic: hypertension, S4, peripheral then pulmonary edema Slides 26, 27, 39, 56

Diagnosis

Not covered in the lecture

Treatment/Therapy

Not covered in the lecture

Mortality ★

Not covered in the lecture

★ Slide 9 lists the etiologies and worse prognosis under 'Important to know'

Name of Condition

Right heart failure (right-sided HF (heart failure)) Slides 9, 10

Definition

HF of the right ventricle: systolic or diastolic failure; dilated, hypertrophic or restrictive cardiomyopathy; ischemic (right coronary artery) or non-ischemic; preserved or reduced EF (ejection fraction) Slides 9, 10

Etiology (cause)

Chronic left-sided HF (most common: left HF → right hypertrophic → right dilated cardiomyopathy); mitral valve stenosis; PAH (pulmonary artery hypertension) Slides 9, 10

Epidemiology (who)

Same as left-sided HF Slide 10

Risk Factors

Same as left-sided HF Slide 10

Pathology

Same as left-sided HF; right ventricular failure = fluid backs up Slide 10

Clinical Manifestation

Systemic overload: peripheral edema, JVD (jugular venous distension); portal overload: nausea, loss of appetite, hepatomegaly (congestion/ascites); ± murmur: mitral stenosis (rumbling diastolic apical murmur with opening snap) or tricuspid regurgitation in PAH (pulmonary artery hypertension; holosystolic murmur at left lower sternal border) Slides 10, 27

Diagnosis

Clinical HF with JVD (jugular venous distension) suggests right-sided; echo (definitive, by EF (ejection fraction)); right heart catheterization (severity; PCWP (pulmonary capillary wedge pressure) 5–12 mmHg, pulmonary edema likely >20); ECG (electrocardiogram) right heart strain: right axis deviation, RBBB (right bundle branch block), T-wave inversion V1–V3 Slides 10, 32, 34

Treatment/Therapy

Same as left-sided HF: symptom management, treat underlying cause, heart transplant, palliative care Slide 10

Mortality ★

Prognosis much worse than left-sided HF Slide 9

Name of Condition

Combined (right- and left-sided) HF (heart failure) Slide 11

Definition

Not covered in the lecture

Etiology (cause)

Not covered in the lecture

Epidemiology (who)

Not covered in the lecture

Risk Factors

Not covered in the lecture

Pathology

Not covered in the lecture

Clinical Manifestation

Not covered in the lecture

Diagnosis

Not covered in the lecture

Treatment/Therapy

Symptom management; comfort care; transplant Slide 11

Mortality ★

Not covered in the lecture

★ Slide 56 marks the HFrEF GDMT summary 'REMEMBER!!!'

Name of Condition

Systolic heart failure; HFrEF (heart failure with reduced ejection fraction); HFimpEF (heart failure with improved ejection fraction) Slides 12, 23

Definition

Failure of systolic function (the squeeze): impaired contraction; HFrEF = LVEF (left ventricular ejection fraction) ≤40%; HFimpEF = LVEF ≤40% that improves to >40%; EF (ejection fraction) = stroke volume / end-diastolic volume × 100 Slides 12, 22, 23, 52

Etiology (cause)

Ischemic cardiomyopathy or dilated cardiomyopathy Slides 17, 25, 39, 56

Epidemiology (who)

Not covered in the lecture

Risk Factors

Not covered in the lecture

Pathology

Dilated cardiomyopathy: thin, dilated (ballooned) muscle; less muscle = poor contraction and loss of elasticity; decreased contractility Slides 13, 19

Clinical Manifestation

Normal or low blood pressure; S3 (sound of rapid filling of the dilated left ventricle); pulmonary edema Slides 26, 39, 56

Diagnosis

Reduced EF (ejection fraction, ≤40%) on echo (MUGA (multigated acquisition scan) most accurate EF); add an elevated BNP (B-type natriuretic peptide) = "slam dunk" Slides 32, 39, 52

Treatment/Therapy

GDMT (guideline-directed medical therapy): beta blocker, RAS-i (renin-angiotensin system inhibitor), MRA (mineralocorticoid receptor antagonist), SGLT2i (sodium-glucose cotransporter 2 inhibitor), prioritized for comorbidities; 2022 figure (all class 1): ARNI (angiotensin receptor-neprilysin inhibitor) in NYHA (New York Heart Association) II–III or ACEi/ARB (angiotensin-converting enzyme inhibitor / angiotensin receptor blocker) in II–IV, beta blocker, MRA, SGLT2i, diuretics as needed, hydralazine-nitrates for NYHA III–IV in African American patients; ICD (implantable cardioverter-defibrillator) if LVEF ≤35%, NYHA II–III on optimal GDMT, life expectancy ≥1 y; acute HF with EF <35% → LifeVest (wearable defibrillator) → optimize GDMT + cardiac rehab → recheck echo → ICD if not improved Slides 52, 53, 56

Mortality ★

52% of cardiac arrests in hospitalized HFrEF patients are due to ventricular arrhythmias Slide 53

★ Slide 56 marks the HFpEF GDMT summary 'REMEMBER!!!'

Name of Condition

Diastolic heart failure; HFpEF (heart failure with preserved ejection fraction) Slides 12, 23

Definition

Failure of diastolic function (the rest): impaired relaxation; HFpEF = LVEF (left ventricular ejection fraction) ≥50% Slides 12, 23, 52

Etiology (cause)

Hypertrophic cardiomyopathy (hypertension → hypertrophy) Slides 17, 25, 39, 56

Epidemiology (who)

Not covered in the lecture

Risk Factors

Not covered in the lecture

Pathology

Hypertrophic cardiomyopathy: enlarged, thickened muscle; more muscle = strong contraction but poor relaxation; decreased filling; echo LVH (left ventricular hypertrophy) = wall >10 mm Slides 13, 14, 19

Clinical Manifestation

Hypertension; S4 (strong left atrial contraction against a stiff hypertrophic left ventricle); peripheral edema → pulmonary edema Slides 26, 39, 56

Diagnosis

Preserved EF (ejection fraction, ≥50%) on echo; add an elevated BNP (B-type natriuretic peptide); ECG (electrocardiogram) LVH: tall R in V5–V6, deep S in V1–V2 Slides 23, 32, 34, 39, 52

Treatment/Therapy

Diuretics as needed; beta blocker, RAS-i (renin-angiotensin system inhibitor), MRA (mineralocorticoid receptor antagonist), SGLT2i (sodium-glucose cotransporter 2 inhibitor) for comorbidities; 2022 figure: diuretics (class 1), SGLT2i (2a), ARNI (angiotensin receptor-neprilysin inhibitor), MRA, ARB (angiotensin receptor blocker) (2b) Slides 52, 56

Mortality ★

Not covered in the lecture

★ Slide 56 marks the HFmrEF GDMT summary 'REMEMBER!!!'

Name of Condition

HFmrEF (heart failure with mildly reduced ejection fraction) Slide 23

Definition

LVEF (left ventricular ejection fraction) 41–49% Slides 23, 52, 56

Etiology (cause)

Not covered in the lecture

Epidemiology (who)

Not covered in the lecture

Risk Factors

Not covered in the lecture

Pathology

Not covered in the lecture

Clinical Manifestation

Not covered in the lecture

Diagnosis

Echo EF (ejection fraction) 41–49% Slides 23, 30

Treatment/Therapy

Diuretics as needed; beta blocker, RAS-i (renin-angiotensin system inhibitor), MRA (mineralocorticoid receptor antagonist), SGLT2i (sodium-glucose cotransporter 2 inhibitor) for comorbidities; 2022 figure: diuretics (class 1), SGLT2i (2a), ACEi (angiotensin-converting enzyme inhibitor), ARB (angiotensin receptor blocker), ARNI (angiotensin receptor-neprilysin inhibitor), MRA, beta blocker (2b) Slides 52, 56

Mortality ★

Not covered in the lecture

Name of Condition

Acute HF (heart failure): acute new-onset HF, HF exacerbation, acute on chronic HF; decompensated HF Slides 7, 30, 31

Definition

Acute = sudden, new onset or exacerbation (chronic = over 1 year); course: pre-HF (asymptomatic) → acute new-onset HF → resolution → exacerbation → chronic HF → acute on chronic HF; clinical HF is symptomatic and its diagnosis requires congestion (pulmonary and/or peripheral edema) Slides 30, 31

Etiology (cause)

Myocardial infarction, sepsis, acute renal failure, etc. Slide 53

Epidemiology (who)

Not covered in the lecture

Risk Factors

Not covered in the lecture

Pathology

Not covered in the lecture

Clinical Manifestation

Congestion (edema); crackles; Forrester subsets (deck: "Swan-Forester"; by cardiac index 2.5 L/min/m² and wedge pressure 15 mmHg): I warm-dry, II warm-wet (congestion), III cool-dry (hypoperfusion), IV cool-wet Slides 28, 30, 31

Diagnosis

BNP (B-type natriuretic peptide) rises in 1–3 h, peaks at 12 h, is degraded by neprilysin (affected by ARNI (angiotensin receptor-neprilysin inhibitor)) and by chronic kidney disease; NT-proBNP (N-terminal pro-BNP) is more stable, peaks at 24 h, detected earlier and longer; BNP <100 rules out acute HF, >900 likely acute HF; NT-proBNP cut-off 300 rules out acute HF Slides 35, 38

Treatment/Therapy

Inotropes in the ICU (intensive care unit) only: digitalis, dobutamine, norepinephrine, epinephrine, milrinone; diuretics; with EF (ejection fraction) <35% → LifeVest (wearable defibrillator) → optimize GDMT (guideline-directed medical therapy) + cardiac rehab → recheck echo → ICD (implantable cardioverter-defibrillator) if not improved Slides 40, 51, 53

Mortality ★

1-year post-hospitalization mortality 35%; each BNP (B-type natriuretic peptide) rise of 100 → 35% higher relative risk of death; predischarge BNP <430 → lower 30-day readmission Slides 6, 38

Name of Condition

High-output heart failure Slide 54

Definition

Elevated cardiac output from increased heart rate and contractility Slide 54

Etiology (cause)

Increased peripheral demand: anemia, hyperthyroidism, atrioventricular fistula Slide 54

Epidemiology (who)

Not covered in the lecture

Risk Factors

Obesity; COPD (chronic obstructive pulmonary disease); cirrhosis; Paget disease (osteitis deformans) Slide 54

Pathology

Increased demand may lead to ischemic cardiomyopathy or remodeling Slide 54

Clinical Manifestation

Heart failure syndrome: fatigue, dyspnea, edema, palpitations Slide 54

Diagnosis

Echo; CBC (complete blood count); CMP (comprehensive metabolic panel); BNP (B-type natriuretic peptide) Slide 54

Treatment/Therapy

Treat the underlying cause; diuretic Slide 54

Mortality ★

Not covered in the lecture