# Cardiac Pathology

> Cardiac pathology for FMGE Pathology, covering MI timeline and complications, rheumatic fever Aschoff bodies, endocarditis organisms and cardiomyopathies.

- Canonical URL: https://prepelephant.com/topics/fmge/pathology/cardiac-pathology
- Exam / course: FMGE · Subject: Pathology
- Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team
- First published: 2026-10-02
- Last updated: 2026-10-02
- How to cite: "Cardiac Pathology", PrepElephant, https://prepelephant.com/topics/fmge/pathology/cardiac-pathology

## Direct answer

Cardiac pathology for FMGE centres on ischaemic heart disease — angina syndromes, the infarction timeline and its complications — rheumatic heart disease with Aschoff bodies, infective endocarditis with its peripheral stigmata, and the three cardiomyopathies. Myocardial infarction shows coagulative necrosis with neutrophil infiltration, granulation tissue then fibrosis; troponin I is the definitive marker. Each disease carries pathognomonic cells, organisms or murmurs that convert directly into single-best-answer marks.

## What you must remember

- Angina: stable from fixed stenosis above about 70 per cent with exertional ST depression; unstable from plaque rupture with non-occlusive thrombosis; Prinzmetal vasospasm with rest ST elevation treated by calcium channel blockers.
- MI timeline: coagulative necrosis by four to twelve hours, neutrophil peak at one to three days, granulation tissue from the first week, grey-white scar by six weeks. Troponin I is most specific and stays raised about ten days; CK-MB normalises by 72 hours, so it detects reinfarction.
- MI complications: arrhythmia is the commonest early cause of death; cardiogenic shock; papillary muscle, septal and free-wall rupture at three to seven days; ventricular aneurysm with dyskinesia and persistent ST elevation; Dressler syndrome, autoimmune fibrinous pericarditis at two to ten weeks.
- Rheumatic fever follows group A streptococcal pharyngitis via molecular mimicry; Jones criteria; Aschoff bodies with Anitschkow caterpillar cells are pathognomonic; chronic disease chiefly stenoses the mitral valve into a fish-mouth orifice.
- Infective endocarditis: acute Staphylococcus aureus in intravenous users with large tricuspid vegetations; subacute viridans streptococci after dental work; splinter haemorrhages, painful Osler nodes, painless Janeway lesions and Roth spots; three blood culture sets before antibiotics; embolic stroke, mycotic aneurysm and valve destruction complicate; marantic and Libman-Sacks vegetations are sterile.
- Cardiomyopathies: dilated — commonest, four-chamber dilatation with low ejection fraction from alcohol, viral myocarditis or the peripartum state; hypertrophic — autosomal dominant sarcomere mutation with asymmetric septal hypertrophy, dynamic outflow obstruction and sudden death in young athletes, treated with beta blockers; restrictive — amyloid, sarcoid, haemochromatosis and tropical endomyocardial fibrosis.
- Tumours: left atrial myxoma mimicking mitral stenosis with positional syncope; rhabdomyoma in tuberous sclerosis; metastases are the commonest cardiac tumours overall.

## Common confusion

Papillary muscle rupture (new mitral murmur with pulmonary oedema), septal rupture (harsh pansystolic murmur with thrill) and free-wall rupture (tamponade) all cluster at three to seven days — timing plus murmur separates them. Osler nodes are painful and immune-complex mediated; Janeway lesions painless and septic. Hypertrophic cardiomyopathy preserves systolic function but kills young athletes, while dilated disease fails systolically.

## Exam-focused takeaway

FMGE converts the MI timeline into histology-at-hours questions and complications into day-specific vignettes; learn troponin and CK-MB kinetics together. Rheumatic questions ask for the Aschoff body or major Jones criteria; endocarditis stems expect organism plus the culture rule. Indian pericarditis questions favour tuberculosis as the cause of constrictive disease.

## Frequently asked questions

### Which enzyme detects reinfarction?
CK-MB, which normalises within about 72 hours so a second rise shows new necrosis; troponin I stays elevated up to ten days and masks it.

### What is an Aschoff body?
The pathognomonic granuloma of rheumatic carditis — perivascular fibrinoid necrosis with Anitschkow caterpillar cells and giant cells; chronic disease instead shows valve fibrosis with commissural fusion.

### Which organism causes subacute endocarditis after dental work?
Viridans group streptococci colonising previously damaged valves; three blood culture sets before antibiotics remain standard.

### Why does mitral disease dominate rheumatic fever?
Left-sided high-pressure flow plus immune cross-reactivity fuse the commissures and thicken chordae into a fish-mouth stenosis; mixed stenosis and regurgitation is common, aortic valve next.

### What defines hypertrophic cardiomyopathy?
Autosomal dominant sarcomere mutation causing asymmetric septal hypertrophy with dynamic outflow obstruction worsened by dehydration and inotropes; sudden death threatens the young, and beta blockers come first.