Cardiovascular Pathology

⚡ Ischemic Heart Disease

Epidemiology — leading cause of death in the US; most common in middle‑aged men and postmenopausal women.
Pathophysiology — mismatch between myocardial O₂ supply and demand; usually due to coronary atherosclerosis.

                    Angina = transient ischemia without necrosis; MI = irreversible coagulative necrosis.

                

Stable angina — fixed atherosclerosis (>75% stenosis); triggered by exertion/emotion; relieved by rest or nitroglycerin; ECG: ST depression.
Prinzmetal (variant) — coronary vasospasm; occurs at rest; relieved by nitroglycerin; ECG: transient ST elevation.
Unstable angina — nonocclusive thrombus on plaque; increasing frequency/duration; high risk for MI.
Myocardial infarction (MI) — coagulative necrosis from ischemia; 90% due to thrombotic occlusion.

LAD 45%→ RCA 35%→ LCx 15%

Marker	Elevation	Peak	Normalization
CK‑MB	4‑8 h	18 h	2‑3 d
Troponin I/T	3‑6 h	16 h	7‑10 d
LDH	24 h	3‑6 d	8‑14 d

Gross changes — 0‑12h: none; 12‑24h: pallor; 1‑7d: yellow pallor; 7‑10d: red border; 6‑8w: white scar.
Microscopic — 1‑4h: wavy fibers; 4h‑3d: coagulative necrosis; 1‑3d: neutrophils; 3‑7d: macrophages; 7‑10d: granulation; 3‑8w: collagen scar.
Complications — arrhythmias, CHF, cardiogenic shock (>40‑50% necrosis), mural thrombus, pericarditis, ventricular aneurysm, rupture (3‑7d).
Sudden cardiac death — <1h symptoms; usually V‑fib; CAD (80%) or HCM, MVP, AS.
Chronic ischemic HD — progressive CHF from replacement fibrosis and loss of hypertrophied myocytes.

Definition — cardiac output insufficient to meet metabolic demand; final common pathway of many cardiac diseases.
Forward failure — decreased organ perfusion. Backward failure — passive congestion.

Left‑sided HF — causes: IHD, HTN, mitral/aortic disease.
↑ heart weight, LVH + dilatation.
Lungs: heavy, edematous.
Symptoms: dyspnea, orthopnea, PND, rales, S3 gallop.
Micro: myocyte hypertrophy (pleiotropic nuclei); alveolar hemosiderin‑laden macrophages (“heart failure cells”).

Right‑sided HF — most common cause = left‑sided HF; also pulmonic/tricuspid disease, cor pulmonale.
JVD, hepatosplenomegaly, dependent edema, ascites, pleural effusions.
RV hypertrophy + dilatation.
Chronic passive liver congestion → cardiac cirrhosis (long‑standing).

Lung disease→ pulmonary HTN→ RV pressure ↑→ RVH→ right‑sided HF

                    Orthopnea severity often quantified by number of pillows needed (“three‑pillow orthopnea”).

                

Bicuspid aortic valve — most common congenital defect; NOTCH1 mutations; stenosis > insufficiency; risk: endocarditis, aortic dissection.
Degenerative calcific AS — age‑related dystrophic calcification; outflow side of cusps; concentric LVH; risk of sudden death.
Mitral valve prolapse — myxomatous degeneration; mid‑systolic click; Marfan association; complications: endocarditis, chordal rupture, sudden death (rare).
Carcinoid heart disease — right‑sided endocardial fibrosis (serotonin from liver metastases); 5‑HIAA ↑ in urine; flushing, diarrhea, wheezing.

Endocarditis type	Organism	Valve	Features
Acute	S. aureus	Normal	Destructive vegetations, high mortality (10‑40%)
Subacute	Viridans group strep	Damaged	Indolent, <10% mortality

Infective endocarditis — risk: rheumatic, MVP, bicuspid, congenital, prosthetic, IVDU, dental.
Clinical: fever, murmur, Roth spots, Osler nodes, Janeway lesions, splinter hemorrhages.
Rheumatic heart disease — post‑strep (Group A β‑hemolytic); type II hypersensitivity; Jones criteria (2 major or 1 major + 2 minor).
Acute: Aschoff bodies (macrophages, Anitschkow cells), fibrinous pericarditis, mitral/aortic vegetations.
Chronic: valve fibrosis, commissural fusion, chordae shortening → stenosis/regurgitation.
Noninfective (marantic) — sterile vegetations; SLE (Libman‑Sacks), antiphospholipid; embolism risk.

Definition — inflammatory infiltrate with myocyte damage; may be asymptomatic or cause acute HF / dilated cardiomyopathy / sudden death.
Infectious causes — Coxsackie A/B, enteroviruses, T. cruzi (Chagas), Toxoplasma, B. burgdorferi (Lyme).
Noninfectious — SLE, RA, drug hypersensitivity.

                    Chagas disease → myocarditis with intracellular amastigotes; endemic in Latin America.

                

Epidemiology — most common childhood heart disease; 90% idiopathic; 5% genetic (trisomies, Turner), viral (rubella), drugs/alcohol.

Right‑to‑left (cyanotic) — early cyanosis.
• Tetralogy of Fallot (most common cyanotic) — RVOT stenosis, RVH, VSD, overriding aorta; clubbing, polycythemia.
• Transposition of great arteries — aorta from RV, PA from LV; requires mixing (VSD/ASD/PDA).
• Pulmonary atresia, tricuspid atresia, truncus arteriosus.

Left‑to‑right (acyanotic) — late cyanosis (Eisenmenger).
• VSD (second most common defect) — small: may close; large → Eisenmenger.
• ASD (ostium secundum most common) — paradoxical emboli.
• PDA — prematurity, rubella; machinery murmur; keep open with PGE₂, close with indomethacin.

Coarctation — preductal (infantile): Turner, PDA, lower‑extremity cyanosis; postductal (adult): upper‑extremity HTN, weak femoral pulses, rib notching.
Complications: CHF, intracerebral hemorrhage, dissecting aneurysm.

Preductal→proximal to DA→PDA dependent | Postductal→distal to DA→rib notching

Dilated (DCM) — most common; all 4 chambers dilated; systolic dysfunction; EF ↓. Causes: genetic (20‑50%), alcohol, doxorubicin, viral (Coxsackie B), Chagas, iron overload, pregnancy. Micro: myocyte hypertrophy + interstitial fibrosis; poor prognosis (5‑year survival 25%).
Hypertrophic (HCM) — autosomal dominant (sarcomere mutations); asymmetrical septal hypertrophy; diastolic dysfunction; myocyte disarray; sudden death in athletes; outflow obstruction during exercise.
Restrictive (RCM) — diastolic restriction; amyloidosis, sarcoidosis, endomyocardial fibroelastosis, Loeffler. Ventricles not dilated; normal wall thickness.
Arrhythmogenic RV — desmosomal mutations; fatty infiltration of RV; thinning, arrhythmias.

HCM is a common cause of sudden cardiac death in young athletes — exertion collapses the outflow tract.

Primary — rare; most benign; malignant: sarcomas, lymphomas.
Myxoma — most common adult tumor; left atrium (fossa ovalis); 3rd‑6th decade; Carney complex (10%, AD); stellate cells in myxoid stroma; complications: emboli, ball‑valve obstruction.
Rhabdomyoma — most common pediatric tumor; associated with tuberous sclerosis (TSC1/TSC2, hamartin/tuberin).

Acute pericarditis — fibrinous (viral, uremia) or fibrinopurulent (bacterial).
Chronic pericarditis — adhesions; constrictive physiology.
Pericardial effusion — serous (HF, hypoalbuminemia), serosanguineous (trauma, malignancy, rupture), chylous (thoracic duct injury).
Tumors — primary (synovial sarcoma, mesothelioma, solitary fibrous, germ cell); metastases from breast, lung.

Friction rub is classic for pericarditis; most common 2‑3 days post‑MI (Dressler syndrome: type II autoimmune).