Explain heart pathology with pictures

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Heart Pathology - A Comprehensive Overview with Pictures

Source: Robbins & Kumar Basic Pathology and Robbins, Cotran & Kumar Pathologic Basis of Disease

Overview

Heart disease is the leading cause of death globally, responsible for over 7.5 million deaths per year. The major categories of cardiac pathology are:

Ischemic Heart Disease (IHD)
Hypertensive Heart Disease
Valvular Heart Disease
Cardiomyopathies
Congenital Heart Disease
Pericardial Disease / Myocarditis

1. Ischemic Heart Disease (IHD)

IHD is caused by an imbalance between myocardial oxygen supply and demand. Over 90% of cases are caused by atherosclerotic coronary artery disease (CAD). The clinical spectrum includes:

Syndrome	Mechanism
Stable angina	Fixed atherosclerotic narrowing; pain on exertion
Unstable angina	Plaque rupture + partial thrombosis; pain at rest
Myocardial Infarction (MI)	Complete occlusion → cardiomyocyte necrosis
Sudden cardiac death	Lethal ventricular fibrillation from ischemia
Chronic IHD / CHF	Progressive pump failure from accumulated ischemic damage

Pathogenesis pathway:

Pathways in the progression of ischemic heart disease - from coronary artery disease through fixed obstruction or acute plaque/thrombosis, leading to myocardial infarction, chronic IHD, congestive heart failure, and sudden cardiac death

FIG. 9.15 - Robbins Basic Pathology: Pathways in the progression of ischemic heart disease.

Myocardial Infarction (MI)

MI = necrosis of heart muscle from ischemia. The sequence of events:

Atheromatous plaque erodes or ruptures, exposing subendothelial collagen
Platelet aggregation + thromboxane A2 release → vasospasm
Coagulation cascade activation → growing thrombus
Within minutes, the thrombus completely occludes the coronary lumen

Patterns of infarction depend on which vessel is occluded and whether flow is restored:

Diagram of transmural vs nontransmural infarcts showing patterns from permanent LAD, LCX, or RCA occlusion vs transient obstruction, global hypotension, and microinfarcts

FIG. 9.9 - Robbins Basic Pathology: Dependence of MI on location and nature of diminished perfusion. Left = transmural infarcts from complete occlusion. Right = nontransmural patterns from partial or transient occlusion.

Morphologic evolution of MI (gross and microscopic):

Time	Gross	Microscopy
0-4 hours	None visible	Waviness of fibers at border
4-12 hours	Occasional dark mottling	Coagulation necrosis begins; edema, hemorrhage
12-24 hours	Dark mottling	Coagulation necrosis, pyknosis of nuclei, neutrophilic infiltrate
1-3 days	Yellow-tan center	Ongoing necrosis, dense neutrophil infiltrate
3-7 days	Hyperemic border; soft yellow-tan center	Macrophage phagocytosis at infarct border
7-10 days	Maximally soft, yellow	Granulation tissue with neovascularization
2-8 weeks	Gray-white fibrosis progressing	Scar collagen deposition
>2 months	Dense white scar	Dense fibrosis - complete scar

Gross pathology specimen - acute MI stained with triphenyl tetrazolium chloride (TTC):

Cross section of heart showing acute myocardial infarct of posterolateral left ventricle as pale unstained area (arrow), old anterior scar (arrowhead), and myocardial hemorrhage from ventricular rupture (asterisk)

FIG. 9.10 - Robbins Basic Pathology: Acute MI of the posterolateral LV demonstrated by lack of TTC staining in areas of necrosis (arrow = acute infarct, pale/yellow). White arrowhead = old scar from remote infarction. Asterisk = myocardial hemorrhage from ventricular rupture (cause of death).

Complications of MI include:

Contractile dysfunction - cardiogenic shock
Papillary muscle rupture → acute mitral regurgitation
Ventricular wall rupture (3-7 days, peak risk) → cardiac tamponade
Ventricular septal defect (rupture of necrotic septum)
Mural thrombus → systemic emboli
Ventricular aneurysm → paradoxical bulging, arrhythmias
Arrhythmias → VF is the most common cause of death in the first 24 hours

2. Hypertensive Heart Disease

Sustained hypertension imposes pressure overload on the left ventricle, driving concentric hypertrophy. Key features:

LV wall thickness >2.0 cm (normal 1.2-1.4 cm)
Heart weight >500 g (normal ~320-360 g in a 60-70 kg person)
Microscopy: increased myocyte transverse diameter, "boxcar nuclei" (prominent nuclear enlargement), interstitial fibrosis
Diastolic dysfunction (stiff LV) precedes systolic dysfunction
Late-stage: LV dilation and congestive heart failure

Right-sided hypertensive heart disease = cor pulmonale, caused by pulmonary hypertension from diseases like COPD, interstitial fibrosis, or recurrent PE.

3. Valvular Heart Disease

Valves can fail in two ways:

Stenosis - valve fails to open fully → obstructs forward flow
Insufficiency / Regurgitation - valve fails to close fully → backflow

Most common causes of acquired valve disease:

Valve	Common Causes
Mitral stenosis	Rheumatic heart disease
Mitral regurgitation	MVP, endocarditis, ischemic papillary muscle dysfunction
Aortic stenosis	Senile calcification, bicuspid AV, rheumatic disease
Aortic regurgitation	Infective endocarditis, Marfan syndrome, rheumatic disease

Calcific Degenerative Valve Disease (gross pathology):

Four gross pathology images: A - calcific aortic stenosis of normal trileaflet valve with calcium heaped in sinuses of Valsalva; B - calcific stenosis on bicuspid valve with raphe; C and D - mitral annular calcification with nodules at leaflet margins and extension into myocardium

FIG. 9.17 - Robbins Basic Pathology: Calcific valvular degeneration. (A) Aortic stenosis - calcific nodules in sinuses of Valsalva, commissures NOT fused (unlike rheumatic). (B) Bicuspid aortic valve with raphe (arrow). (C-D) Mitral annular calcification, with extension into myocardium (can impinge on the conduction system).

Rheumatic heart disease is caused by cross-reactive antibodies after Group A Streptococcal pharyngitis (molecular mimicry). The mitral valve is most commonly affected. Acute features include:

Aschoff bodies (foci of fibrinoid necrosis with multinucleated giant cells) - pathognomonic
Small verrucous vegetations along valve closure line

Chronic changes: leaflet thickening, commissural fusion, chordal shortening → "fish-mouth" or "buttonhole" mitral stenosis orifice.

4. Cardiomyopathies

Cardiomyopathies are diseases of the myocardium itself. There are three major patterns:

Side-by-side comparison of the three types:

Diagram comparing normal heart with dilated, hypertrophic, and restrictive cardiomyopathy - showing four-chamber anatomy including atrial and ventricular dilation and wall thickness changes for each type

FIG. 9.23 - Robbins Basic Pathology: Three major forms of cardiomyopathy. DCM = systolic dysfunction. HCM and Restrictive = diastolic dysfunction.

Dilated vs Hypertrophic - Causes, Pathology, and Clinical Features:

Comparison diagram of dilated cardiomyopathy (non-genetic causes: myocarditis/peripartum/toxic/idiopathic; genetic 20-50% cytoskeletal) vs hypertrophic cardiomyopathy (genetic 100%, sarcomeric proteins), showing gross and microscopic pathology and shared clinical outcomes of heart failure, sudden death, AF, stroke

FIG. 12.33B - Robbins Pathologic Basis of Disease: Dilated vs Hypertrophic Cardiomyopathy.

Dilated Cardiomyopathy (DCM)

Most common (90% of all cardiomyopathies)
Progressive four-chamber dilation + systolic (contractile) dysfunction
Causes: genetic (titin, dystrophin, β-myosin mutations), myocarditis (viral), alcohol, peripartum, doxorubicin toxicity
Gross: flabby, enlarged heart; mural thrombi common → embolic stroke risk
Micro: variable myocyte hypertrophy + interstitial fibrosis
Treatment: heart failure therapy; eventual transplant

Hypertrophic Cardiomyopathy (HCM)

100% genetic - mutations in sarcomeric proteins (β-MHC, cardiac troponin T, myosin binding protein C)
Massive asymmetric septal hypertrophy → banana-shaped LV cavity → dynamic outflow obstruction
Micro: myocyte disarray (chaotically arranged myocytes) - pathognomonic
Most common cause of sudden cardiac death in young athletes (<35 years)
Diastolic dysfunction (stiff, non-compliant LV)

Restrictive Cardiomyopathy

Least common; ventricular walls are stiff, impeding diastolic filling
Causes: amyloidosis, sarcoidosis, post-radiation fibrosis, hemochromatosis
Normal/near-normal systolic function; severely impaired diastolic filling
Bilateral atrial dilation is characteristic

5. Congenital Heart Disease

Congenital heart disease (CHD) affects ~1% of live births. The top 12 lesions account for 85% of all CHD:

Malformation	Incidence per million live births	% of CHD
Ventricular septal defect (VSD)	4482	42%
Atrial septal defect (ASD)	1043	10%
Pulmonary stenosis	836	8%
Patent ductus arteriosus (PDA)	781	7%
Tetralogy of Fallot	577	5%
Coarctation of aorta	492	5%
AV septal defect	396	4%
Aortic stenosis	388	4%
Transposition of great arteries	388	4%

Key Lesions Explained

Left-to-right shunts (acyanotic initially; may become cyanotic late via Eisenmenger syndrome):

VSD - most common; harsh holosystolic murmur; spontaneous closure common in small VSDs
ASD - fixed split S2; pulmonary overcirculation; thromboembolism risk
PDA - continuous "machinery" murmur; closes with indomethacin (inhibits prostaglandin)

Right-to-left shunts (cyanotic from birth):

Tetralogy of Fallot (TOF): 4 components - (1) VSD, (2) pulmonary stenosis, (3) aorta overriding the VSD, (4) right ventricular hypertrophy. Classic "boot-shaped heart" on CXR. Presents with cyanosis, "tet spells," squatting (increases SVR).
Transposition of the great arteries (TGA): Aorta arises from RV, pulmonary artery from LV → two parallel circuits incompatible with life unless ASD/VSD/PDA exists. "Egg on a string" CXR.

Obstructive lesions:

Coarctation of the aorta: Segmental narrowing, usually postductal (near ligamentum arteriosum). Presents with upper-body hypertension, weak femoral pulses, rib notching on CXR from dilated intercostal collaterals.

6. Myocarditis

Myocarditis = inflammatory disease of the myocardium.

Most common cause: Viral (Coxsackievirus B, parvovirus B-19, HIV, COVID-19)
Chagas disease (Trypanosoma cruzi) - most common cause worldwide in South America
Autoimmune: giant cell myocarditis (rapidly fatal without transplant), sarcoidosis
Presents with: sudden onset heart failure in a previously healthy young person, chest pain mimicking MI, arrhythmias
Diagnosis: cardiac MRI (late gadolinium enhancement) + endomyocardial biopsy
Dallas criteria (biopsy): myocyte necrosis + adjacent inflammatory infiltrate

Summary Table

Category	Hallmark Pathology	Key Feature
Ischemic / MI	Coagulation necrosis → scar	Pale/yellow area on TTC stain
Hypertensive	LV concentric hypertrophy	Boxcar nuclei, wall >2 cm
Valvular (calcific)	Calcium in cusps/annulus	Aortic > mitral; commissures not fused
Valvular (rheumatic)	Aschoff bodies, commissural fusion	"Fish-mouth" mitral orifice
DCM	4-chamber dilation, interstitial fibrosis	Systolic dysfunction
HCM	Asymmetric septal hypertrophy, myocyte disarray	#1 cause SCD in young athletes
Restrictive	Stiff ventricle, atrial dilation	Amyloidosis most common cause
TOF	VSD + PS + overriding aorta + RVH	Cyanosis, tet spells, boot-shaped heart
Myocarditis	Myocyte necrosis + inflammation	Coxsackie B virus most common

Sources: Robbins & Kumar Basic Pathology (9780323790185) and Robbins, Cotran & Kumar Pathologic Basis of Disease (9780443264528)

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