Cardiovascular System for NEET PG Pathology: Atherosclerosis, Aneurysm, MI, Rheumatic Fever, Endocarditis, Cardiomyopathy, Congenital Heart Disease

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🎯 Exam priority: High. Expect: infarct age from the histology, TTC staining, Aschoff bodies and the Jones criteria, Osler vs Janeway, Libman-Sacks vs marantic vegetations, HCM genetics and disarray, the commonest cardiac tumour, and TOF/VSD/ASD/PDA/coarctation clues.

CBME mapping: PA 26.1–26.10. Haemodynamics (thrombosis, embolism, infarction in general) is in article 3; amyloid heart in article 6.

Infarct timeline, valve vegetations, vessels, cardiomyopathy, tumours and congenital heart disease. Drawn by TrackNation.

Arteries and Aneurysms

• Arteriosclerosis = arterial wall thickening with lost elasticity. Three forms: atherosclerosis (intimal plaques in large and medium arteries), arteriolosclerosis (small arteries and arterioles thickened by cell proliferation or hyaline deposition) and Mönckeberg medial calcific sclerosis (calcified media of muscular arteries).

• Atheroma: monocytes become macrophages, take up lipoprotein through scavenger receptors and turn into foam cells — the hallmark of the early plaque. A mature plaque has a lipid core under a fibrous cap of smooth muscle and collagen. A vulnerable plaque has a thin cap and a big lipid core and is the one that ruptures.

• Abdominal aortic aneurysm: diameter ≥ 3 cm, usually infrarenal. Smoking is the strongest risk factor. Repair when > 5.5 cm in men or > 5 cm in women. Mycotic (infected) aneurysm: S. aureus first, then Salmonella.

• Aortic dissection: blood surges through an intimal tear and splits intima from media, making a false lumen. Hypertension is a key contributor. Peak age 50–65 in general but 20–40 in Marfan or Ehlers-Danlos. Stanford A involves the ascending aorta; B is confined to the descending aorta beyond the left subclavian.

• Primary (essential) hypertension is about 85% of cases; the rest are secondary (for example primary aldosteronism, renal disease).

Ischaemic Heart Disease

• Spectrum: unstable angina (ischaemia, troponin below the 99th percentile) → NSTEMI (subendocardial; troponin up, no ST elevation) → STEMI. MI = troponin rise above the 99th percentile plus ischaemic symptoms, ECG change or imaging evidence.

• Type 1 MI: plaque rupture, erosion or fissuring with thrombus. Type 2: supply-demand mismatch (for example coronary spasm or a demand surge). Transmural infarcts span epicardium to endocardium.

• Infarct age on histology (autopsy series): < 4 h wavy fibres with a few neutrophils; 4–12 h coagulative necrosis; 7–10 days granulation tissue at the edge; > 6 weeks fibrous scar. Gross changes need 24–48 h, so very early infarcts are found with TTC stain: living muscle turns brick red (dehydrogenase activity); the infarct stays pale.

• Site clues: right ventricular infarction usually means proximal right coronary artery occlusion. Papillary muscle dysfunction gives a soft apical murmur of mitral regurgitation; a friction rub on days 2–3 after STEMI is common.

Rheumatic Fever and Endocarditis

• Rheumatic fever: a non-suppurative complication of group A streptococcal pharyngitis — arthritis, carditis, subcutaneous nodules, erythema marginatum, chorea (modified Jones criteria). Evidence of preceding infection: throat culture/antigen or ASO > 320 U.

• Aschoff bodies (granulomatous collections of leukocytes, myocytes and collagen) form in the myocardium. Carditis is a pancarditis, but valvulitis is its most consistent feature. Acute: mitral regurgitation; chronic rheumatic heart disease: mitral stenosis, then aortic disease. Sydenham chorea reflects basal ganglia involvement.

• Infective endocarditis: S. aureus attacks even normal valves; viridans streptococci follow dental bacteraemia (even toothbrushing with gingivitis). Mostly left-sided; 5–10% right-sided (tricuspid, pulmonary), much commoner in IV drug users. HACEK organisms are a minority. Signs: Roth spots (retina), Osler nodes (painful, finger tips), Janeway lesions (painless, palms and soles), splinter haemorrhages.

Myocardium, Pericardium and Tumours

• Dilated cardiomyopathy: genetic, or acquired — coxsackievirus B, Trypanosoma cruzi, alcohol, cardiotoxic chemotherapy. The commonest cardiomyopathy of childhood.

• Hypertrophic cardiomyopathy: usually a sarcomere gene mutation. Asymmetric hypertrophy of the basal septum; histology shows myocyte hypertrophy, myocyte disarray and fibrosis. Systolic murmur louder with Valsalva; syncope and sudden death.

• Restrictive cardiomyopathy: stiff walls that impede filling with near-normal systolic function — amyloidosis, sarcoidosis, haemochromatosis, Fabry, and endomyocardial fibrosis (children and young adults in the tropics).

• Pericarditis: mostly viral or idiopathic in the West, TB where TB is endemic; also uraemia, MI, cancer. Constrictive pericarditis = fibrous scarring fuses both layers. Tamponade = compression by fluid or blood.

• Cardiac tumours: metastases are far commoner than primaries. Myxoma is the commonest primary, usually in the left atrium; about 15% of pedunculated ones give a "tumour plop". Rhabdomyoma is the commonest in children — up to 90% have tuberous sclerosis.

Congenital Heart Disease

• The commonest congenital anomaly, in almost 1% of live births.

• VSD: about 20% of defects; loud harsh holosystolic murmur at the lower left sternal border. A large shunt raises pulmonary resistance until flow reverses — Eisenmenger syndrome.

• ASD (secundum, at the fossa ovalis): wide, fixed splitting of S2; paradoxical emboli later. PDA: continuous murmur and bounding pulses; a COX inhibitor (ibuprofen or indomethacin) may close it in preterm babies.

• Tetralogy of Fallot — the commonest cyanotic lesion (twice TGA): large VSD, RV outflow obstruction, RV hypertrophy, overriding aorta. Boot-shaped heart; right aortic arch in 25%. TGA: egg-on-a-string shadow with a narrow mediastinum.

• Coarctation: in 10–20% of Turner syndrome; arm hypertension with weak, delayed femoral pulses; collateral intercostal arteries notch ribs 3–8 (rarely before age 5).

Traps the Examiner Sets

• Osler = Ouch (painful); Janeway = painless.

• Libman-Sacks (SLE) and marantic vegetations are sterile; infective ones are not.

• Acute rheumatic carditis → mitral regurgitation; chronic → mitral stenosis.

• TTC: pale = dead; brick red = alive.

• Commonest primary cardiac tumour: myxoma (adult, left atrium); in children: rhabdomyoma (tuberous sclerosis).

Memory Hooks & Shortcuts

Shortcuts to lock in this article's numbers and lists. Each one only re-packages facts proven above.

• 🧠 Osler = Ouch; Janeway = painless (J for 'just a spot') — IE skin signs

• 🧠 Wavy at 4, Necrosis by 12, Granulation at 10 days, Scar at 6 weeks — infarct dating

• 🧠 TTC: Tissue That's Caput stays pale — TTC staining

• 🧠 Libman-Sacks = Lupus; Marantic = Malignancy (mucin) — sterile vegetations

• 🧠 Myxoma Mostly in the left atriuM — myxoma

• 🧠 Rhabdo for babies with tubers (tuberous sclerosis) — rhabdomyoma

• 🧠 Turner turns the aorta tight (coarctation) — coarctation

Rapid-Revision Cards

• Arteriolosclerosis

  Small arteries/arterioles: hyaline or cell proliferation.

• Mönckeberg

  Calcified media of muscular arteries.

• Early plaque hallmark

  Foam cells (lipid-laden macrophages).

• Vulnerable plaque

  Thin fibrous cap, big lipid core.

• AAA

  ≥ 3 cm, infrarenal; smoking; repair > 5.5 cm (men).

• Mycotic aneurysm

  S. aureus, then Salmonella.

• Stanford A vs B

  A = ascending aorta; B = descending only.

• Infarct < 4 h

  Wavy fibres, few neutrophils.

• Infarct 4–12 h

  Coagulative necrosis.

• Infarct 7–10 d

  Granulation tissue at the edge.

• Infarct > 6 wk

  Fibrous scar.

• TTC stain

  Brick red = alive; pale = infarct.

• Type 1 vs 2 MI

  1 = plaque rupture; 2 = supply-demand.

• Aschoff body

  Rheumatic carditis; myocardium.

• Rheumatic valve

  Acute MR; chronic mitral stenosis.

• ASO in ARF

  > 320 U.

• Osler vs Janeway

  Osler painful finger tips; Janeway painless palms/soles.

• IV drug user IE

  Right-sided (tricuspid).

• Libman-Sacks

  SLE; sterile; closure line.

• Marantic

  Mucin-producing cancer; sterile; embolise.

• HCM

  Sarcomere genes; septum; disarray; Valsalva ↑ murmur.

• RCM causes

  Amyloid, sarcoid, haemochromatosis, EMF.

• Myxoma

  Commonest primary; left atrium; tumour plop.

• Rhabdomyoma

  Children; tuberous sclerosis.

• TOF

  VSD, RVOT block, RVH, overriding aorta; boot heart.

• ASD

  Wide fixed split S2.

• Coarctation

  Turner; weak femorals; rib notching.

Sources

Facts in this article were checked against these documents.

• MSD Manual Professional: Atherosclerosis; Abdominal Aortic Aneurysms; Aortic Dissection; Hypertension; Heart Failure — Merck & Co. (MSD Manuals), reviewed 2024–26 (link)

• MSD Manual Professional: Acute Coronary Syndromes; Acute Myocardial Infarction; Infective and Noninfective Endocarditis; Rheumatic Fever; Dilated, Hypertrophic and Restrictive Cardiomyopathy; Pericarditis; Cardiac Tumors — Merck & Co. (MSD Manuals), reviewed 2025–26 (link)

• MSD Manual Professional: Congenital Cardiovascular Anomalies (overview, VSD, ASD, PDA, Tetralogy of Fallot, TGA, Coarctation) — Merck & Co. (MSD Manuals), reviewed 2023–26 (link)

• Standard Treatment Workflow: Acute Rheumatic Fever — ICMR, 2022

• Medical Subject Headings (scope notes) — US National Library of Medicine, 2026 (link)

• Varun KB et al. Comparison of histopathological and triphenyl tetrazolium chloride test in diagnosing myocardial infarction: an autopsy study. F1000Research (CC BY 4.0) — F1000Research, 2024 (link)

• Competency Based Undergraduate Curriculum, Pathology (PA 26) — National Medical Commission, 2024

Test Yourself: Practice Questions

Thirty-four questions in NEET PG style, most of them clinical vignettes.

Practice Questions (NEET PG pattern)

Original questions written in the style of the exam: +4 for a correct answer, −1 for a wrong one. Every answer was checked against the sources listed above. NEET PG papers are not published by NBEMS, so these are not past-paper questions.

Q1. A kidney biopsy shows small arteries and arterioles whose walls are thickened by hyaline deposition. This lesion is

• (a) fibromuscular dysplasia

• (b) arteriolosclerosis

• (c) Mönckeberg medial calcific sclerosis

• (d) atherosclerosis

Q2. Sections of a muscular artery show calcification confined to the tunica media, with the intima spared. The condition is

• (a) Buerger disease

• (b) atherosclerosis

• (c) arteriolosclerosis

• (d) Mönckeberg medial calcific sclerosis

Q3. The cell that is the hallmark of the early atherosclerotic plaque is the

• (a) plasma cell

• (b) Langhans giant cell

• (c) eosinophil

• (d) foam cell (lipid-laden macrophage)

Q4. Which plaque is most likely to rupture and cause an acute coronary event?

• (a) a fatty dot without a core

• (b) heavily calcified small plaque

• (c) thick fibrous cap with a small lipid core

• (d) thin fibrous cap with a large lipid core

Q5. A 72-year-old smoker has a pulsatile abdominal mass. Ultrasound shows an infrarenal aortic diameter of 3.8 cm. The single strongest risk factor for this lesion is

• (a) syphilis

• (b) diabetes

• (c) female sex

• (d) smoking

Q6. The organism most often responsible for a mycotic (infected) aortic aneurysm is

• (a) Candida

• (b) Staphylococcus aureus

• (c) Streptococcus pyogenes

• (d) Treponema pallidum

Q7. A 30-year-old with Marfan syndrome has abrupt tearing chest pain. Imaging shows an intimal flap and double lumen involving the ascending aorta. This is

• (a) Stanford type A aortic dissection

• (b) abdominal aortic aneurysm

• (c) Stanford type B dissection

• (d) pulmonary embolism

Q8. The basic lesion of aortic dissection is

• (a) a saccular outpouching of all three layers

• (b) an intimal tear with blood splitting intima from media (false lumen)

• (c) a full-thickness wall rupture

• (d) medial calcification

Q9. A man with severe chest pain dies within 3 hours. The most likely microscopic finding in the infarcted myocardium is

• (a) wavy fibres with a few neutrophils

• (b) dense fibrous scar

• (c) granulation tissue

• (d) macrophages full of haemosiderin only

Q10. At autopsy, the margin of a myocardial infarct shows well-formed granulation tissue. The infarct is most likely about

• (a) 2 hours old

• (b) 7–10 days old

• (c) 12 hours old

• (d) 6 months old

Q11. A heart slice is immersed in triphenyl tetrazolium chloride (TTC). A pale unstained area against brick-red muscle means

• (a) normal myocardium

• (b) fatty infiltration

• (c) infarcted myocardium that has lost dehydrogenase activity

• (d) fixation artefact

Q12. An MI caused by coronary plaque rupture with thrombosis is classified as

• (a) type 3

• (b) type 2

• (c) type 5

• (d) type 1

Q13. A patient has rest angina for 30 minutes; ECG has no ST elevation and troponin stays below the 99th percentile. The diagnosis is

• (a) unstable angina

• (b) STEMI

• (c) NSTEMI

• (d) type 2 MI

Q14. An infarct of the right ventricle most often results from occlusion of the

• (a) left anterior descending artery

• (b) left main coronary artery

• (c) diagonal branch

• (d) proximal right coronary artery

Q15. Two to three weeks after a sore throat, a child develops migratory polyarthritis and an apical pansystolic murmur. Which antibody titre supports preceding streptococcal infection?

• (a) anti-dsDNA

• (b) anti-CCP

• (c) ANCA

• (d) ASO above 320 units

Q16. Heart tissue from a child who died of acute rheumatic carditis shows granulomatous collections of leukocytes, myocytes and collagen. These are

• (a) Aschoff bodies

• (b) Anitschkow cells alone

• (c) Mallory bodies

• (d) Langhans giant cells

Q17. The commonest valve lesion of chronic rheumatic heart disease is

• (a) mitral stenosis

• (b) tricuspid stenosis alone

• (c) pulmonary stenosis

• (d) aortic coarctation

Q18. The most consistent feature of rheumatic carditis, without which the diagnosis should be reconsidered, is

• (a) valvulitis

• (b) myocardial abscess

• (c) heart block

• (d) pericardial effusion

Q19. A patient with fever and a murmur has painful red nodules on the finger pads. These are

• (a) Osler nodes

• (b) splinter haemorrhages

• (c) Janeway lesions

• (d) Roth spots

Q20. A person who injects drugs has septic pulmonary emboli. The valve most likely involved by endocarditis is the

• (a) tricuspid valve

• (b) mitral valve

• (c) a prosthetic mitral valve

• (d) aortic valve

Q21. An organism able to cause endocarditis on a previously normal valve is

• (a) Staphylococcus aureus

• (b) Lactobacillus

• (c) Staphylococcus epidermidis on a native valve

• (d) Corynebacterium diphtheriae

Q22. A woman with SLE has small sterile vegetations along the closure line of the mitral leaflets. These are

• (a) Libman-Sacks lesions

• (b) marantic vegetations

• (c) Lambl excrescences

• (d) infective vegetations

Q23. A man with metastatic pancreatic adenocarcinoma has a systemic arterial embolus; echo shows valve vegetations and blood cultures are negative. The lesion is

• (a) Libman-Sacks endocarditis

• (b) rheumatic valvulitis

• (c) carcinoid heart disease

• (d) marantic (non-bacterial thrombotic) endocarditis

Q24. A young athlete collapses and dies. Autopsy shows asymmetric thickening of the basal interventricular septum and microscopic myocyte disarray. The usual cause is

• (a) a sarcomere protein gene mutation

• (b) amyloid deposition

• (c) alcohol

• (d) coxsackievirus myocarditis

Q25. Which of these is a recognised infectious cause of dilated cardiomyopathy?

• (a) Mycobacterium leprae

• (b) Treponema pallidum

• (c) Trypanosoma cruzi

• (d) Entamoeba histolytica

Q26. Restrictive cardiomyopathy with stiff ventricles and near-normal systolic function is classically caused by

• (a) sarcomere gene mutation

• (b) coxsackievirus B

• (c) chronic alcohol use

• (d) amyloidosis

Q27. In a country where tuberculosis is endemic, the commonest cause of pericarditis is

• (a) tuberculosis

• (b) uraemia

• (c) radiation

• (d) viral infection

Q28. A woman has a murmur like mitral stenosis whose loudness varies with body position; echo shows a pedunculated left atrial mass. The likely tumour is

• (a) rhabdomyoma

• (b) fibroma

• (c) myxoma

• (d) angiosarcoma

Q29. An infant with multiple cardiac tumours in the ventricular walls is most likely to have which underlying syndrome?

• (a) tuberous sclerosis

• (b) Down syndrome

• (c) Marfan syndrome

• (d) Turner syndrome

Q30. A cyanotic infant's chest X-ray shows a boot-shaped heart with reduced pulmonary markings. The four components of the lesion are

• (a) ASD, PDA, LVH, coarctation

• (b) VSD, ASD, PDA, TGA

• (c) mitral stenosis, AR, TR, PS

• (d) VSD, RV outflow obstruction, RV hypertrophy, overriding aorta

Q31. A child with an uncorrected large VSD later becomes cyanosed as pulmonary resistance rises and the shunt reverses. This is

• (a) Eisenmenger syndrome

• (b) Ebstein anomaly

• (c) tetralogy of Fallot

• (d) transposition

Q32. Wide and fixed splitting of the second heart sound is typical of

• (a) patent ductus arteriosus

• (b) ventricular septal defect

• (c) coarctation

• (d) atrial septal defect

Q33. A preterm infant has bounding pulses and a continuous murmur at the upper left sternal border. Medical closure is attempted with

• (a) a cyclo-oxygenase inhibitor such as ibuprofen or indomethacin

• (b) a beta-blocker

• (c) digoxin

• (d) prostaglandin E1

Q34. A girl with Turner syndrome has hypertension in the arms with weak, delayed femoral pulses. The likely cardiovascular lesion is

• (a) coarctation of the aorta

• (b) Ebstein anomaly

• (c) tetralogy of Fallot

• (d) patent ductus arteriosus

Active Recall

From memory: distinguish the three forms of arteriosclerosis; describe the atheroma and vulnerable plaque; define AAA and dissection; date an infarct from histology and explain TTC staining; describe rheumatic fever, Aschoff bodies and its valve lesions; compare infective, Libman-Sacks and marantic vegetations; summarise DCM, HCM and RCM; name the commonest cardiac tumours; and give the clues for VSD, ASD, PDA, TOF and coarctation.