All Cardiovascular disorders

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Here is a full clinical reference on all major cardiovascular disorders, organized by category, synthesized from Robbins & Cotran Pathologic Basis of Disease, Fuster & Hurst's The Heart 15th Ed., Braunwald's Heart Disease, and Textbook of Family Medicine 9e.

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)
MarkerRisePeakReturn to Normal
Myoglobin1-2 hr6-9 hr12-24 hr
CK-MB3-6 hr24 hr48-72 hr
Troponin I3-6 hr24-48 hr7-10 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

TypeEFMechanism
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:
  1. A precipitating injury (CAD, MI, hypertension, valvular disease, diabetes, anemia, alcohol) triggers LV remodeling (stretching and dilation)
  2. Neurohormonal activation follows: RAAS (angiotensin II, aldosterone) and SNS (catecholamines) are upregulated
  3. Angiotensin II causes cardiomyocyte apoptosis, hypertrophy, and ventricular fibrosis
  4. Aldosterone "escapes" RAAS suppression - requiring separate aldosterone blockade
  5. Catecholamines suppress beta-adrenergic receptors and have direct myocardial toxicity
  6. Inflammatory cytokines (endothelin-1, MMPs) cause cardiac fibrosis and collagen deposition
  7. 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)

CategorySystolicDiastolic
Normal<120 mmHg<80 mmHg
Elevated120-129<80
Stage 1 HTN130-13980-89
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%)

CauseClue
Renovascular (renal artery stenosis)Young woman (FMD) or older male smoker; abdominal bruit
Primary hyperaldosteronism (Conn syndrome)Hypokalemia, suppressed renin, elevated aldosterone
PheochromocytomaEpisodic headache, sweating, palpitations, paroxysmal HTN
Cushing syndromeCentral obesity, striae, buffalo hump
Coarctation of aortaUnequal arm/leg BP, young patient, rib notching
Obstructive sleep apneaResistant HTN, obesity, snoring; CPAP reduces BP
Chronic kidney diseaseElevated creatinine, proteinuria
Hypothyroidism / HyperthyroidismTSH 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

DegreeECG FindingManagement
1st degreeProlonged PR >200 msNone needed
2nd degree Mobitz I (Wenckebach)Progressive PR lengthening then dropped beatOften benign; pacemaker if symptomatic
2nd degree Mobitz IIFixed PR, sudden dropped QRSHigh risk of complete block; pacemaker indicated
3rd degree (Complete)No AV conduction; P and QRS dissociatedEmergent 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.
DefectFrequencyPhysiology
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 Aorta5%Narrowing of aorta (usually post-ductal); HTN in arms + lower BP in legs; rib notching on CXR
Transposition of Great Arteries4%Aorta from RV, PA from LV; requires mixing lesion to survive; prostaglandin E1 + urgent Jatene procedure
Tricuspid Atresia1%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)

TumorFeatures
Myxoma (most common primary)Left atrium (75%); gelatinous; "ball-valve" obstruction; constitutional symptoms; tumor "plop" sound; emboli
LipomaSubendocardial or epicardial; usually incidental
Papillary fibroelastomaValvular; embolic risk
RhabdomyomaMost common in children; associated with tuberous sclerosis
AngiosarcomaMost 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

DisorderKey PathophysiologyHallmark FindingFirst-Line Treatment
Stable anginaFixed coronary stenosis >70%ST depression on stress testBeta-blockers, nitrates, aspirin, statins
NSTEMIPartial coronary occlusionElevated troponin, no ST elevationAntiplatelet + anticoagulation + PCI
STEMIComplete coronary occlusionST elevationPrimary PCI within 90 min
HFrEFLV systolic dysfunctionEF <40%, S3 gallopACEi/ARNI + BB + MRA + SGLT2i
HFpEFLV diastolic dysfunctionEF >50%, BNP elevatedDiuretics, SGLT2i, treat cause
Essential HTNMultifactorialBP ≥130/80Lifestyle + thiazide/CCB/ACEi/ARB
AFDisorganized atrial activityIrregularly irregular, no P wavesRate control + anticoagulation
Aortic stenosisCalcified/obstructed valveSystolic ejection murmurSAVR or TAVR
HCMSarcomere mutation, LVHMurmur worsens with ValsalvaBeta-blockers; avoid vasodilators
DCMLV dilation, systolic dysfunctionEcho: dilated LV, reduced EFHF therapy; ICD if EF <35%
Acute pericarditisPericardial inflammationFriction rub, saddle-shaped ST elevationNSAIDs + colchicine
Cardiac tamponadePericardial fluid compressing heartBeck's triad + pulsus paradoxusEmergent pericardiocentesis
Aortic dissection Type AIntimal tear, ascending aortaTearing chest pain, unequal BPEmergency surgery
IEValvular infection/vegetationFever + new murmur + emboliIV antibiotics 4-6 weeks ± surgery
VSDL→R shuntHarsh holosystolic murmur, LLSBSurgical closure if large/symptomatic
Tetralogy of FallotVSD + RVOT obstruction + RVH + overriding aortaCyanosis, boot-shaped heartSurgical repair

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