Cardiovascular Disorders - Full Clinical Reference
Cardiovascular disease is the number-one cause of mortality worldwide, accounting for roughly 1 in 5 deaths in the United States alone (~700,000 deaths/year) - exceeding all cancers combined. The major categories are presented below.
1. ISCHEMIC HEART DISEASE (IHD) / CORONARY ARTERY DISEASE (CAD)
Pathophysiology
IHD results from imbalance between myocardial oxygen supply and demand, almost always due to atherosclerotic narrowing of the coronary arteries. Atherosclerosis is a disease of chronic low-grade inflammation. Risk factors include:
- Traditional: Hypertension, hyperlipidemia (especially LDL), smoking, diabetes mellitus, family history, age, male sex
- Non-traditional: High-sensitivity CRP (hsCRP), lipoprotein(a) [Lp(a)], fibrinogen, obesity (visceral adiposity generates IL-6, TNF-α promoting atherogenesis)
Blood flow through coronary arteries occurs during diastole; tachycardia shortens diastole and can compromise perfusion.
Clinical Presentations
A. Stable Angina (Stable IHD)
- Predictable chest pain on exertion, relieved by rest or nitrates
- Fixed atherosclerotic plaque causing >70% stenosis
- ECG: ST depression during symptoms; normal at rest
- Dx: Stress test (exercise ECG, nuclear, stress echo), coronary angiography
- Rx: Nitrates, beta-blockers, CCBs, aspirin, statins; revascularization (PCI or CABG) if refractory
B. Unstable Angina (UA) / NSTEMI (Acute Coronary Syndrome)
- Plaque rupture with partial coronary occlusion, thrombus formation, microembolization, or vasoactive substance release causing localized spasm
- UA defined as: (1) Rest angina ≥20 min within 1 week, OR (2) New-onset class III angina within 2 months, OR (3) Previously stable angina that worsened by ≥1 CCS class in the prior 2 months
- Prolonged rest angina (>30-60 min) typically causes myocardial necrosis = NSTEMI
- Cardiac Biomarkers:
- Myoglobin: rises in 1-2 hr, remains elevated 7-12 hr; sensitive but not specific
- CK-MB: 90% accurate at 6 hr; peaks at ~24 hr; normalizes by 72 hr
- Troponin I: most specific; rises 10-14 hr after onset; sensitivity 58%/specificity 94% at 6 hr; 92%/95% at 10 hr; remains elevated for days
- High-risk features requiring admission: Age >70, prior SIHD/revascularization, ECG ischemia (ST deviation, new T-wave changes, new LBBB), ongoing chest pain >20 min, hemodynamic instability, CHF, elevated biomarkers
- ECG: ST depression or T-wave inversions in contiguous leads (can be silent)
- Rx: Antiplatelet (aspirin + P2Y12 inhibitor), anticoagulation (heparin), nitrates, beta-blockers, oxygen; early invasive strategy if high-risk; revascularization by PCI or CABG
C. ST-Elevation Myocardial Infarction (STEMI)
- Complete occlusion of a coronary artery; transmural necrosis
- ECG: ST elevation in contiguous leads; later Q waves
- Rx: Emergent reperfusion - primary PCI within 90 min (door-to-balloon); fibrinolysis if PCI unavailable within 120 min
- Complications: Arrhythmias, cardiogenic shock, papillary muscle rupture (MR), free wall rupture, ventricular septal defect, Dressler syndrome (post-MI pericarditis, weeks later)
| Marker | Rise | Peak | Return to Normal |
|---|
| Myoglobin | 1-2 hr | 6-9 hr | 12-24 hr |
| CK-MB | 3-6 hr | 24 hr | 48-72 hr |
| Troponin I | 3-6 hr | 24-48 hr | 7-10 days |
2. HEART FAILURE (HF)
Definition and Epidemiology
Heart failure is a clinical syndrome from the inability of the heart to meet the body's metabolic requirements at normal filling pressures. Over 650,000 new cases diagnosed annually in the US; mortality ~50% within 5 years. 1-month re-hospitalization rate ~25%.
Types
| Type | EF | Mechanism |
|---|
| HFrEF (Heart Failure with Reduced EF) | <45-50% | Impaired LV contraction (systolic dysfunction) |
| HFpEF (Heart Failure with Preserved EF) | >45-50% | Impaired LV filling/relaxation (diastolic dysfunction) |
Nearly equally common; HFpEF increasingly recognized.
Pathophysiology
The old hemodynamic model has been replaced by the LV remodeling concept:
- A precipitating injury (CAD, MI, hypertension, valvular disease, diabetes, anemia, alcohol) triggers LV remodeling (stretching and dilation)
- Neurohormonal activation follows: RAAS (angiotensin II, aldosterone) and SNS (catecholamines) are upregulated
- Angiotensin II causes cardiomyocyte apoptosis, hypertrophy, and ventricular fibrosis
- Aldosterone "escapes" RAAS suppression - requiring separate aldosterone blockade
- Catecholamines suppress beta-adrenergic receptors and have direct myocardial toxicity
- Inflammatory cytokines (endothelin-1, MMPs) cause cardiac fibrosis and collagen deposition
- Calcium flux alterations and shift to glycolytic metabolism impair function
Causes / Precipitants
CAD/MI, systemic hypertension, valvular heart disease, cardiomyopathy, diabetes, congenital defects, anemia, alcoholism
Clinical Features
- Dyspnea (on exertion, then at rest), orthopnea, paroxysmal nocturnal dyspnea
- Fatigue, exercise intolerance
- Fluid retention: peripheral edema, ascites, elevated JVP, S3 gallop
- Pulmonary congestion: bibasilar crackles
- Note: Pulmonary congestion may be absent even in established HF
Diagnosis
- Echocardiogram (measure EF, wall motion, diastolic function) - key test
- BNP/NT-proBNP (elevated in HF, inversely proportional to EF)
- CXR: cardiomegaly, Kerley B lines, pulmonary vascular congestion
- ECG: may show prior MI, LVH, arrhythmias
Treatment
HFrEF (Disease-Modifying Therapies - Reduce Mortality):
- ACE inhibitors or ARBs - block angiotensin II; reduce apoptosis, hypertrophy, fibrosis
- Beta-blockers (carvedilol, metoprolol succinate, bisoprolol) - reverse SNS toxicity
- Aldosterone antagonists (spironolactone, eplerenone) - needed alongside ACEi/ARBs due to aldosterone escape
- ARNI (sacubitril/valsartan - entresto) - replaces ACEi in stable HFrEF
- SGLT2 inhibitors (dapagliflozin, empagliflozin) - reduce HF hospitalizations and CV death
- Diuretics (furosemide) - symptom relief, fluid management
- Digoxin - reduces hospitalizations; no mortality benefit
- ICD - for EF <35% to prevent sudden death
- CRT (cardiac resynchronization therapy) - for LBBB with EF <35%
HFpEF: No proven mortality-reducing therapy; SGLT2 inhibitors now show benefit; diuretics for symptoms; treat underlying cause
3. HYPERTENSION
Classification (AHA/ACC 2017)
| Category | Systolic | Diastolic |
|---|
| Normal | <120 mmHg | <80 mmHg |
| Elevated | 120-129 | <80 |
| Stage 1 HTN | 130-139 | 80-89 |
| Stage 2 HTN | ≥140 | ≥90 |
| Hypertensive Crisis | >180 | >120 |
Primary (Essential) Hypertension (~95% of cases)
- No single identifiable cause
- Polygenic predisposition + environmental (salt, obesity, sedentary lifestyle, stress)
- Neurohormonal (RAAS, SNS activation), endothelial dysfunction
Secondary Hypertension (~5%)
| Cause | Clue |
|---|
| Renovascular (renal artery stenosis) | Young woman (FMD) or older male smoker; abdominal bruit |
| Primary hyperaldosteronism (Conn syndrome) | Hypokalemia, suppressed renin, elevated aldosterone |
| Pheochromocytoma | Episodic headache, sweating, palpitations, paroxysmal HTN |
| Cushing syndrome | Central obesity, striae, buffalo hump |
| Coarctation of aorta | Unequal arm/leg BP, young patient, rib notching |
| Obstructive sleep apnea | Resistant HTN, obesity, snoring; CPAP reduces BP |
| Chronic kidney disease | Elevated creatinine, proteinuria |
| Hypothyroidism / Hyperthyroidism | TSH abnormal |
Target Organ Damage
- Heart: LVH, HF, CAD, MI
- Brain: Stroke, hypertensive encephalopathy
- Kidney: Nephrosclerosis, CKD, microalbuminuria
- Eyes: Hypertensive retinopathy (AV nicking, flame hemorrhages, papilledema)
- Vessels: Accelerated atherosclerosis, aortic aneurysm
Treatment
- Lifestyle: DASH diet, weight loss, sodium restriction (<2.4 g/day), aerobic exercise, limit alcohol
- Drug therapy:
- Thiazide diuretics (chlorthalidone preferred over HCTZ), CCBs - first-line, especially in Black patients
- ACE inhibitors/ARBs - first-line in diabetes, CKD, HF, proteinuria
- Beta-blockers - preferred in CAD, HF, post-MI, arrhythmias
- Aldosterone antagonists - useful in resistant hypertension
- Hypertensive urgency (no end-organ damage): Oral agents, lower BP over 24-48 hr
- Hypertensive emergency (end-organ damage): IV agents (labetalol, nicardipine, nitroprusside); lower MAP by 25% in 1st hour
4. ARRHYTHMIAS AND CONDUCTION DISORDERS
Atrial Arrhythmias
Atrial Fibrillation (AF) - Most Common Sustained Arrhythmia
- Disorganized rapid atrial activity (350-600 impulses/min); irregular ventricular response
- Causes: Hypertension (most common), valvular disease (especially MS), hyperthyroidism, alcohol ("holiday heart"), CAD, HF, post-cardiac surgery, sleep apnea, obesity
- Risks: Stroke (5x increased risk), HF, hemodynamic compromise
- ECG: Absent P waves, irregularly irregular rhythm
- Stroke prevention: CHA₂DS₂-VASc score guides anticoagulation
- Score ≥2 (men) or ≥3 (women): oral anticoagulant indicated
- NOACs (apixaban, rivaroxaban, dabigatran) preferred over warfarin (except mechanical valves/MS)
- Rate control: Beta-blockers, CCBs (diltiazem/verapamil), digoxin
- Rhythm control: Cardioversion (electrical or pharmacologic), antiarrhythmics (flecainide, amiodarone), catheter ablation
Atrial Flutter
- Reentrant circuit in right atrium; rate ~300 bpm with 2:1 block → ventricular rate ~150 bpm
- ECG: Sawtooth flutter waves (F-waves) in II, III, aVF
- Rx: Similar to AF; catheter ablation highly effective
Ventricular Arrhythmias
Ventricular Tachycardia (VT)
- ≥3 consecutive ventricular beats at >100 bpm; wide QRS complex (>120 ms)
- Sustained VT (>30 sec or hemodynamic compromise): Cardiovert if unstable; amiodarone/lidocaine if stable
- Causes: CAD/scar, cardiomyopathy, electrolyte abnormalities, long QT, Brugada syndrome
- Treatment of recurrent VT: ICD + antiarrhythmics (amiodarone, sotalol), catheter ablation
Ventricular Fibrillation (VF)
- Chaotic ventricular activity; no effective cardiac output = cardiac arrest
- Rx: Immediate defibrillation (unsynchronized shock); CPR; ACLS protocol; ICD for secondary prevention
Long QT Syndrome
- Prolonged ventricular repolarization → risk of torsades de pointes (TdP)
- Congenital: Ion channel mutations (LQT1: KCNQ1; LQT2: KCNH2; LQT3: SCN5A)
- Acquired: Drugs (sotalol, quinidine, amiodarone, antipsychotics, macrolides), hypokalemia, hypomagnesemia
- Rx: Avoid QT-prolonging drugs; beta-blockers (LQT1, LQT2); ICD in high-risk patients
Bradyarrhythmias and Conduction Disorders
Sick Sinus Syndrome (SSS)
- Sinus node dysfunction: sinus bradycardia, sinus arrest, sinoatrial block, tachycardia-bradycardia syndrome
- Rx: Permanent pacemaker if symptomatic
Atrioventricular (AV) Block
| Degree | ECG Finding | Management |
|---|
| 1st degree | Prolonged PR >200 ms | None needed |
| 2nd degree Mobitz I (Wenckebach) | Progressive PR lengthening then dropped beat | Often benign; pacemaker if symptomatic |
| 2nd degree Mobitz II | Fixed PR, sudden dropped QRS | High risk of complete block; pacemaker indicated |
| 3rd degree (Complete) | No AV conduction; P and QRS dissociated | Emergent pacemaker |
Bundle Branch Blocks
- LBBB: QRS >120 ms; broad notched R in V5/V6, I, aVL; always investigate underlying cause (IHD, cardiomyopathy)
- RBBB: RSR' (M-shape) in V1; broad S in I, V5/V6; may be normal variant
5. VALVULAR HEART DISEASE
Aortic Stenosis (AS) - Most Common Valvular Disorder in Adults
- Causes: Calcific/degenerative (most common; elderly), bicuspid aortic valve (younger adults), rheumatic heart disease
- Pathophysiology: Pressure overload → concentric LVH → diastolic dysfunction → eventually systolic dysfunction
- Classic Triad of Symptoms (occur late, bad prognosis when they appear):
- Angina (average survival ~5 yr)
- Syncope (average survival ~3 yr)
- Heart failure (average survival ~2 yr)
- Signs: Harsh systolic ejection murmur (SEM) at RUSB radiating to carotids; diminished and delayed carotid pulse (pulsus parvus et tardus); soft/absent S2; S4
- ECG: LVH; Echo: reduced AVA, high gradient
- Rx: Valve replacement - SAVR (surgical) or TAVR (transcatheter, for high-risk/elderly); no proven medical therapy; avoid vasodilators in severe AS
Aortic Regurgitation (AR)
- Causes (Acute): Infective endocarditis, aortic dissection - surgical emergency
- Causes (Chronic): Bicuspid aortic valve, rheumatic, Marfan syndrome, aortitis (syphilis, ankylosing spondylitis), hypertension
- Pathophysiology: Volume overload → eccentric LVH → LV dilation
- Signs: High-pitched diastolic decrescendo murmur at LUSB; wide pulse pressure; bounding peripheral pulses (Corrigan water-hammer pulse); de Musset's sign (head bobbing); Quincke's pulse; Austin Flint murmur (diastolic rumble)
- Rx: Vasodilators (ACEi, nifedipine) in chronic AR; surgical repair/replacement when symptomatic or EF declining
Mitral Stenosis (MS)
- Cause: Almost exclusively rheumatic heart disease (streptococcal pharyngitis → autoimmune valve damage)
- Pathophysiology: Obstruction of LA-LV flow → elevated LA pressure → pulmonary HTN → RV failure
- Signs: Low-pitched mid-diastolic rumble at apex; opening snap (OS); loud S1; OS-S2 interval shorter = more severe; AF is common complication
- Rx: Anticoagulation if AF; diuretics; beta-blockers for rate control; balloon mitral valvuloplasty (BMV) for suitable anatomy; mitral valve replacement for severe/unsuitable anatomy
Mitral Regurgitation (MR)
- Causes (Acute): Papillary muscle rupture post-MI, infective endocarditis, chordae tendineae rupture - emergency
- Causes (Chronic): Mitral valve prolapse (most common in developed world), rheumatic, dilated cardiomyopathy, Marfan syndrome
- Signs: Holosystolic murmur at apex radiating to axilla; S3 gallop in severe MR; LV dilation on echo
- Rx: Vasodilators; surgical/transcatheter repair (MitraClip) when severe or symptomatic
Mitral Valve Prolapse (MVP)
- Myxomatous degeneration; posterior leaflet billows into LA during systole
- Most common valvular disorder overall; 2-3% of population; often benign
- Signs: Mid-systolic click + late systolic murmur; earlier with Valsalva/standing; later with squatting
- Complications: MR, arrhythmias, rarely sudden death
- Rx: Reassurance if asymptomatic; surgery if significant MR
Tricuspid and Pulmonary Valve Disease
- Tricuspid regurgitation (TR): Most commonly functional (RV dilation from pulmonary HTN); systolic murmur at LLSB that increases with inspiration; treat underlying cause
- Pulmonary stenosis (PS): Often congenital; systolic murmur at LUSB; balloon valvuloplasty if severe
Infective Endocarditis (IE)
- Infection of valvular endothelium; vegetation formation
- Organisms: Streptococcus viridans (subacute, native valve, dental), Staphylococcus aureus (acute, IV drug users, prosthetic valves), Enterococcus, HACEK group
- Risk factors: IV drug use, structural heart disease, prosthetic valves, poor dentition, intravascular catheters
- Clinical features: Fever, new regurgitant murmur, embolic phenomena (stroke, splenic infarct), Janeway lesions (painless), Osler's nodes (painful), Roth's spots (retinal), splinter hemorrhages, splenomegaly
- Duke Criteria: Major (blood cultures, echo vegetation/abscess/new valvular regurgitation) + minor criteria for diagnosis
- Dx: Blood cultures (≥3 sets before antibiotics), transesophageal echocardiogram (TEE > TTE)
- Rx: Prolonged IV antibiotics (4-6 weeks); surgery for severe valvular dysfunction, persistent bacteremia, abscess, emboli
6. CARDIOMYOPATHIES
Dilated Cardiomyopathy (DCM)
- LV and/or RV dilation with systolic dysfunction; EF typically <40%
- Causes: Idiopathic (most common, often genetic), viral myocarditis (Coxsackievirus B), alcohol, cocaine, peripartum cardiomyopathy, doxorubicin toxicity, thyroid disease, hemochromatosis, sarcoidosis
- Genetics: ~35% familial; mutations in sarcomere proteins (titin - most common, lamin A/C), cytoskeletal proteins
- Clinical: HF symptoms (dyspnea, edema), dilated LV on echo with reduced EF, functional MR, S3 gallop
- Rx: Standard HF therapy (ACEi/ARBs/ARNI, beta-blockers, aldosterone antagonists, SGLT2i, diuretics); ICD if EF <35%; cardiac transplant for refractory cases
Hypertrophic Cardiomyopathy (HCM)
- Asymmetric (usually septal) LV hypertrophy without a hemodynamic cause; sarcomere protein mutations
- Genetics: Autosomal dominant; MYH7 (beta-myosin heavy chain), MYBPC3 (myosin binding protein C) most common
- Obstructive HCM (HOCM): Dynamic LVOT obstruction due to systolic anterior motion (SAM) of mitral valve
- Clinical: Dyspnea, chest pain, syncope (exertional); harsh systolic murmur at LLSB
- Murmur increases with: Valsalva, standing (decrease preload = worse obstruction)
- Murmur decreases with: squatting, lying down (increase preload)
- Most common cause of sudden cardiac death in young athletes
- ECG: LVH, deep Q waves (pseudo-infarction) in lateral leads
- Rx: Beta-blockers or non-dihydropyridine CCBs; avoid vasodilators, digoxin, high-intensity exercise; mavacamten (cardiac myosin inhibitor) - novel therapy; septal reduction (surgical myectomy or alcohol septal ablation) for refractory obstructive disease; ICD for high-risk features
Restrictive Cardiomyopathy (RCM)
- Impaired ventricular filling with normal/near-normal systolic function; stiff, non-compliant myocardium
- Causes: Amyloidosis (most common; TTR or AL), sarcoidosis, hemochromatosis, radiation, eosinophilic heart disease (Löffler endocarditis), endomyocardial fibrosis
- Clinical: HFpEF picture; exertional dyspnea, elevated JVP, Kussmaul sign; preserved EF on echo
- Must distinguish from constrictive pericarditis (both cause similar physiology but different treatment)
- Rx: Treat underlying cause; diuretics; avoid digoxin in amyloidosis; tafamidis for TTR amyloidosis; anticoagulation if AF
Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)
- Fibrofatty replacement of RV myocardium; autosomal dominant (desmosomal gene mutations - PKP2 most common)
- Clinical: VT with LBBB morphology (RV origin), palpitations, syncope; SCD in young adults
- ECG: Epsilon wave in V1-V3; T-wave inversions in right precordial leads; prolonged QRS
- Rx: ICD; beta-blockers; catheter ablation; avoid competitive sports
7. PERICARDIAL DISEASES
Acute Pericarditis
- Inflammation of the pericardium; most common pericardial disease
- Causes: Viral (most common; Coxsackievirus A/B, EBV, echovirus), idiopathic, post-MI (Dressler syndrome), uremia, autoimmune (SLE, RA), malignancy, tuberculosis (most common worldwide cause of constrictive pericarditis)
- Clinical: Sharp pleuritic chest pain, relieved by sitting forward; worse supine; pericardial friction rub (3-component)
- ECG: Diffuse saddle-shaped ST elevation with PR depression (pathognomonic); evolution through 4 stages
- Dx: Elevated inflammatory markers (CRP, ESR); echo for effusion
- Rx: NSAIDs + colchicine (reduces recurrence); restrict activity until asymptomatic; steroids only for specific causes (autoimmune, uremic); hospitalize if: high-risk features (fever >38°C, large effusion, tamponade, immunocompromised, trauma)
Pericardial Effusion and Cardiac Tamponade
- Accumulation of fluid in pericardial space; rate of accumulation matters (acute >150 mL can cause tamponade; chronic >1L may be tolerated)
- Tamponade: External compression of the heart impairing cardiac filling
- Clinical (Beck's Triad): Hypotension, elevated JVP (distended neck veins), muffled heart sounds
- Pulsus paradoxus: >10 mmHg fall in systolic BP with inspiration (hallmark)
- ECG: Electrical alternans (alternating QRS amplitude) + sinus tachycardia
- Rx: Emergent pericardiocentesis; drainage catheter; pericardiectomy for recurrent/malignant effusions
Constrictive Pericarditis
- Fibrous scarring and calcification of pericardium impairing diastolic filling
- Causes: Post-viral, post-radiation, TB (developing world), post-cardiac surgery, post-pericarditis
- Clinical: Progressive RHF (JVD, ascites, edema); Kussmaul sign (JVP rises with inspiration - opposite of normal); pericardial knock (high-pitched early diastolic sound); normal EF on echo with pericardial thickening/calcification
- CT/MRI: Best for demonstrating pericardial thickening/calcification
- Rx: Pericardiectomy (surgical stripping) - definitive; diuretics for symptom relief
8. CONGENITAL HEART DISEASE (CHD)
CHD affects slightly <1% of live births; 12 disorders account for ~85% of cases.
| Defect | Frequency | Physiology |
|---|
| Ventricular Septal Defect (VSD) | 42% (most common) | L→R shunt; small = restrictive (may close spontaneously); large = pulmonary overcirculation → HTN |
| Atrial Septal Defect (ASD) | 10% | L→R shunt; secundum type most common; may present in adulthood with AF, dyspnea |
| Pulmonary Stenosis (PS) | 8% | RV outflow obstruction; often isolated, favorable prognosis |
| Patent Ductus Arteriosus (PDA) | 7% | Failure of DA to close; continuous "machine murmur"; associated with prematurity, rubella |
| Tetralogy of Fallot (ToF) | 5% | 4 defects: VSD + RVOT obstruction + RVH + overriding aorta; cyanotic; boot-shaped heart on CXR |
| Coarctation of Aorta | 5% | Narrowing of aorta (usually post-ductal); HTN in arms + lower BP in legs; rib notching on CXR |
| Transposition of Great Arteries | 4% | Aorta from RV, PA from LV; requires mixing lesion to survive; prostaglandin E1 + urgent Jatene procedure |
| Tricuspid Atresia | 1% | No tricuspid valve; requires patent foramen ovale and often VSD |
Eisenmenger Syndrome: Uncorrected L→R shunt → pulmonary vascular disease → reversed R→L shunt → cyanosis; precludes surgical correction
9. HYPERTENSIVE HEART DISEASE
- Sustained hypertension → increased afterload → concentric LVH (pressure overload)
- LVH is an independent risk factor for MI, HF, stroke, sudden death
- Systemic hypertensive heart disease: LVH; diastolic dysfunction; eventually systolic dysfunction and HF
- Pulmonary hypertensive heart disease (Cor Pulmonale): Pulmonary HTN → RV pressure overload → RVH → RV failure
- Causes of pulmonary HTN: Chronic lung disease (COPD, IPF), recurrent PE, primary pulmonary arterial hypertension (PAH), left heart disease, connective tissue disease
- PAH Treatment: Endothelin receptor antagonists (bosentan, ambrisentan), PDE5 inhibitors (sildenafil, tadalafil), prostacyclin analogues (epoprostenol), soluble guanylate cyclase stimulators (riociguat)
10. AORTIC DISEASES
Aortic Aneurysm
- Thoracic Aortic Aneurysm (TAA): Associated with cystic medial necrosis, Marfan syndrome, Ehlers-Danlos, bicuspid aortic valve, syphilis (luetic aortitis), aortitis
- Abdominal Aortic Aneurysm (AAA): >90% infrarenal; associated with atherosclerosis; risk factors: male sex, smoking, age >65
- Screening: one-time abdominal ultrasound for men ≥65 who have ever smoked
- Repair: open surgery or EVAR when ≥5.5 cm (men) or ≥5.0 cm (women), or expanding >0.5-1 cm/year, or symptomatic
- Rupture: Sudden tearing abdominal/back pain, hypotension, pulsatile mass; 80% mortality
Aortic Dissection
- Intimal tear → blood enters media creating false lumen
- Risk factors: Hypertension (most common), Marfan syndrome, bicuspid aortic valve, aortitis, pregnancy, cocaine
- Stanford Classification:
- Type A: involves ascending aorta - surgical emergency
- Type B: descending aorta only - medical management (IV beta-blockers first, then vasodilators); endovascular repair for complications
- Clinical: Sudden tearing/ripping chest pain radiating to the back; unequal BP between arms; aortic regurgitation murmur (Type A); neurological deficits
- Dx: CT angiography of chest (gold standard in stable); TEE (unstable)
- Rx Type A: Emergency surgery; avoid fibrinolytics; control HR and BP
11. PERIPHERAL VASCULAR DISEASE (PVD)
Peripheral Arterial Disease (PAD)
- Atherosclerotic narrowing of non-coronary arteries; lower extremities most commonly affected
- Risk factors: Smoking (strongest modifiable), diabetes, hypertension, hyperlipidemia, male sex, age; hsCRP independently predicts PAD
- Note: Lp(a) is an atherogenic LDL subspecies that impairs fibrinolysis and may contribute to PAD
- Initial data suggested men develop IC ~10 years before women but more recent studies do NOT support gender-based timing differences
- Clinical: Intermittent claudication (reproducible leg pain/cramping with exertion, relieved by rest); critical limb ischemia (rest pain, non-healing ulcers, gangrene)
- ABI (Ankle-Brachial Index): ≤0.9 = PAD; ≤0.4 = critical limb ischemia; >1.4 = non-compressible vessels (diabetes/CKD)
- Rx: Lifestyle modification; antiplatelet therapy (aspirin or clopidogrel); statins; cilostazol (claudication); revascularization (PTA/stenting or bypass) for critical limb ischemia or disabling claudication
Deep Vein Thrombosis (DVT) and Pulmonary Embolism (PE)
- See Virchow's triad: stasis, endothelial injury, hypercoagulability
- DVT: Unilateral leg swelling, pain, erythema, warmth; Homan's sign unreliable
- PE: Dyspnea, pleuritic chest pain, hemoptysis, tachycardia; massive PE → hypotension/shock
- Dx: D-dimer (sensitive, not specific); Doppler ultrasound (DVT); CTPA (gold standard for PE); V/Q scan if contrast contraindicated
- ECG in PE: Sinus tachycardia (most common); S1Q3T3; right heart strain pattern
- Rx: Anticoagulation with LMWH/heparin bridging to DOAC or warfarin; thrombolysis for massive PE; catheter-directed therapy; IVC filter if anticoagulation contraindicated
12. MYOCARDITIS
- Inflammatory disease of myocardium; most commonly viral
- Causes: Viral (Coxsackievirus B, parvovirus B19, HIV, COVID-19), autoimmune (giant cell myocarditis - aggressive), sarcoidosis, drug-induced (immune checkpoint inhibitors increasingly recognized), Chagas disease (T. cruzi - most common infective cause worldwide)
- Clinical: Chest pain, dyspnea, palpitations, arrhythmias; mimics ACS; mild to fulminant
- Dx: Elevated troponin; ECG (diffuse ST changes); echo (regional or global LV dysfunction); MRI (gold standard - late gadolinium enhancement); endomyocardial biopsy (Dallas criteria - definitive but low sensitivity)
- Rx: Supportive; treat HF; immunosuppression for giant cell/autoimmune myocarditis; IVIG in selected pediatric cases; MCS (mechanical circulatory support) for cardiogenic shock
13. CARDIAC TUMORS
Primary Cardiac Tumors (Rare)
| Tumor | Features |
|---|
| Myxoma (most common primary) | Left atrium (75%); gelatinous; "ball-valve" obstruction; constitutional symptoms; tumor "plop" sound; emboli |
| Lipoma | Subendocardial or epicardial; usually incidental |
| Papillary fibroelastoma | Valvular; embolic risk |
| Rhabdomyoma | Most common in children; associated with tuberous sclerosis |
| Angiosarcoma | Most common malignant primary tumor; right atrium; hemorrhagic pericardial effusion |
Metastatic Cardiac Tumors
- Far more common than primary tumors
- Most common sources: lung, breast, esophagus, melanoma (highest tendency), lymphoma, leukemia
- Pericardial effusion most common manifestation
Summary Table: Key Cardiovascular Disorders
| Disorder | Key Pathophysiology | Hallmark Finding | First-Line Treatment |
|---|
| Stable angina | Fixed coronary stenosis >70% | ST depression on stress test | Beta-blockers, nitrates, aspirin, statins |
| NSTEMI | Partial coronary occlusion | Elevated troponin, no ST elevation | Antiplatelet + anticoagulation + PCI |
| STEMI | Complete coronary occlusion | ST elevation | Primary PCI within 90 min |
| HFrEF | LV systolic dysfunction | EF <40%, S3 gallop | ACEi/ARNI + BB + MRA + SGLT2i |
| HFpEF | LV diastolic dysfunction | EF >50%, BNP elevated | Diuretics, SGLT2i, treat cause |
| Essential HTN | Multifactorial | BP ≥130/80 | Lifestyle + thiazide/CCB/ACEi/ARB |
| AF | Disorganized atrial activity | Irregularly irregular, no P waves | Rate control + anticoagulation |
| Aortic stenosis | Calcified/obstructed valve | Systolic ejection murmur | SAVR or TAVR |
| HCM | Sarcomere mutation, LVH | Murmur worsens with Valsalva | Beta-blockers; avoid vasodilators |
| DCM | LV dilation, systolic dysfunction | Echo: dilated LV, reduced EF | HF therapy; ICD if EF <35% |
| Acute pericarditis | Pericardial inflammation | Friction rub, saddle-shaped ST elevation | NSAIDs + colchicine |
| Cardiac tamponade | Pericardial fluid compressing heart | Beck's triad + pulsus paradoxus | Emergent pericardiocentesis |
| Aortic dissection Type A | Intimal tear, ascending aorta | Tearing chest pain, unequal BP | Emergency surgery |
| IE | Valvular infection/vegetation | Fever + new murmur + emboli | IV antibiotics 4-6 weeks ± surgery |
| VSD | L→R shunt | Harsh holosystolic murmur, LLSB | Surgical closure if large/symptomatic |
| Tetralogy of Fallot | VSD + RVOT obstruction + RVH + overriding aorta | Cyanosis, boot-shaped heart | Surgical repair |