PA26.1-10 | Cardiovascular System — Glossary

Chromosomal microdeletion causing DiGeorge/velocardiofacial syndrome; associated with conotruncal cardiac defects including Tetralogy of Fallot and truncus arteriosus.

A four-stage (A-D) structural/progressive staging of heart failure from risk factors only (Stage A) to refractory end-stage disease (Stage D); stages are unidirectional.

The clinical spectrum of unstable angina, NSTEMI, and STEMI, all sharing the common mechanism of acute plaque disruption with coronary thrombosis.

Infective endocarditis caused by highly virulent organisms (most commonly S. aureus) that attack previously normal valves, producing large destructive vegetations and a rapidly progressive clinical course.

Disruption of an atheromatous plaque — by rupture or endothelial erosion — that exposes thrombogenic material to blood, triggering coronary thrombosis and ACS.

A systemic inflammatory disease occurring 2–4 weeks after group-A streptococcal pharyngitis, mediated by molecular mimicry; affects heart, joints, brain, and skin.

Deposition of amyloid fibrils (AL or transthyretin type) in the myocardial interstitium causing restrictive cardiomyopathy; identified by apple-green birefringence on Congo red staining under polarised light.

Localised, permanent dilation of a blood vessel to ≥1.5× its normal diameter; may be true (all three wall layers) or false (haematoma contained by adventitia alone).

The commonest primary malignant cardiac tumour (right atrium); also occurs in liver (vinyl chloride), breast/skin (post-irradiation lymphoedema); composed of atypical endothelial cells lining irregular anastomosing channels.

A modified macrophage pathognomonic of rheumatic carditis; characterised by a nucleus in which chromatin condenses into a central wavy bar resembling a caterpillar on longitudinal section.

Entry of blood through an intimal tear into the degenerated aortic media, creating a false lumen that propagates proximally/distally; classified Stanford A (ascending) or B (descending).

Thickening and hardening of small arteries and arterioles; two patterns: hyaline (benign HTN, diabetes) and hyperplastic/onion-skin (malignant hypertension).

Generic term for thickening and loss of elasticity of arterial walls; encompasses atherosclerosis, arteriolosclerosis, and Mönckeberg medial calcific sclerosis.

The pathognomonic granuloma-like lesion of rheumatic myocarditis, consisting of a central zone of fibrinoid necrosis surrounded by Anitschkov cells (caterpillar cells) and peripheral lymphocytes; found in the myocardial interstitium.

A multinucleate form of the Anitschkov cell found within Aschoff bodies; analogous to giant cells in other granulomatous conditions.

Chronic intimal disease of large and medium arteries characterised by lipid deposition, inflammation, and fibrous plaque formation; the leading cause of ischaemic heart disease and stroke.

Intermittent prolapse of a pedunculated left atrial myxoma through the mitral valve opening, causing positional syncope and dyspnoea — clinically mimicking mitral stenosis.

The three classic clinical signs of cardiac tamponade: hypotension, elevated jugular venous pressure (distended neck veins), and muffled/distant heart sounds.

Small saccular aneurysm at branch points of the circle of Willis due to congenital absence of the tunica media; rupture causes subarachnoid haemorrhage; associated with ADPKD.

A natriuretic hormone secreted by ventricular cardiomyocytes in response to increased wall stress; promotes natriuresis and vasodilation; markedly elevated in heart failure and used as a diagnostic biomarker.

The characteristic chest X-ray appearance in Tetralogy of Fallot showing an upturned cardiac apex (from RVH), small pulmonary bay, and reduced pulmonary vascular markings.

Involuntary loss of fat and lean body mass in chronic heart failure, driven by cytokine-mediated catabolism (TNF-α, IL-6), reduced mesenteric perfusion causing malabsorption, and anorexia from hepatic distension.

Centrilobular fibrosis progressing to bridging fibrosis in the liver, resulting from long-standing chronic passive congestion in severe right heart failure; a form of cirrhosis with 'reverse lobulation'.

The commonest primary cardiac tumour in adults; arises most frequently in the left atrium near the fossa ovalis; composed of stellate myxoma cells in an abundant myxoid stroma; presents with obstruction, embolism, or constitutional features.

Life-threatening compression of the heart by rapid pericardial fluid accumulation causing obstructive shock; characterised by Beck's triad (hypotension, raised JVP, muffled heart sounds) and pulsus paradoxus.

Cardiac-specific isoforms of the contractile regulatory proteins troponin I and T; released from necrotic myocytes and detectable in serum 3–6 hours post-MI. The most sensitive and specific biomarkers for myocardial injury.

Pump failure due to massive myocardial loss (≥40% of LV), causing inadequate cardiac output, hypotension, end-organ hypoperfusion, and high mortality.

Primary disease of the myocardium not caused by ischaemia, hypertension, valvular disease, or congenital anomalies; classified as dilated, hypertrophic, or restrictive based on functional pattern.

Bidirectional dysfunction in which cardiac failure impairs renal perfusion and venous drainage, reducing GFR and worsening fluid retention; RAAS activation perpetuates both.

TB-specific pericarditis showing central caseation with epithelioid granulomas and Langhans giant cells; the type most prone to organise into constrictive disease.

Death of hepatocytes in Zone 3 (perivenular zone) of the hepatic acinus, due to combined venous congestion and relative ischaemia; characteristic of right heart failure.

Tiny (<1 mm) aneurysm in small perforating brain arteries (basal ganglia, thalamus, pons) due to chronic hypertension and lipohyalinosis; rupture causes hypertensive intracerebral haemorrhage.

The MB isoform of creatine kinase; elevated in MI within 4–8 hours and returning to normal by 48–72 hours; clinically important for detecting reinfarction when troponin remains elevated.

The histological pattern of cell death in infarcted myocardium: preservation of cellular outlines ('ghost' cells) with pyknotic nuclei and eosinophilic cytoplasm; the dominant finding from 12h to several days.

Discrete narrowing of the aortic lumen, usually near the ductus arteriosus; causes upper body hypertension and diminished lower body pulses; associated with Turner syndrome and bicuspid aortic valve.

Adhesion and fibrotic fusion of the valve leaflet edges at the commissures (junctions), the key mechanism producing the narrowed orifice of rheumatic mitral stenosis.

Thickening of the ventricular wall with a normal or reduced cavity, caused by pressure overload (e.g. hypertension, aortic stenosis); sarcomeres are added in parallel.

Structural cardiac malformations present at birth due to abnormal fetal cardiac development, resulting from genetic, environmental, or multifactorial causes.

Biventricular failure in which both pulmonary and systemic venous congestion are present simultaneously.

Dense fibro-calcific encasement of the heart following chronic pericardial inflammation (TB commonest in India), preventing diastolic filling of all four chambers; treated by pericardiectomy.

Intensely eosinophilic transverse bands in myocytes formed by hypercontracted sarcomeres; the pathological hallmark of reperfusion injury, caused by calcium overload when oxygenated blood re-enters ischaemic cells.

Right heart failure resulting from pulmonary hypertension caused by primary lung disease (e.g. COPD, pulmonary fibrosis), without left heart failure as the primary driver.

Loss of SMCs, fragmentation of elastic fibres, and mucoid/myxoid change in the aortic media; the pathological substrate for aortic dissection; characteristic of Marfan syndrome and hypertension.

Histological hallmark of Marfan syndrome aortopathy: elastin/collagen matrix disruption due to fibrillin-1 deficiency (FBN1 mutation) → TGF-β dysregulation → medial degeneration → aortic root dilation and dissection.

A significant rise and/or fall in serial troponin measurements, used to distinguish acute MI (dynamic troponin change) from chronic myocardial injury (persistently elevated but stable troponin).

Heart failure in which ventricular contractility and ejection fraction are preserved (≥ 50%) but impaired relaxation and reduced compliance elevate filling pressures and cause symptoms.

Cardiomyopathy characterised by systolic failure and four-chamber dilatation with thin, flabby walls; causes include idiopathic/genetic, alcohol, peripartum, doxorubicin, and viral myocarditis.

Dilated cardiomyopathy caused by cumulative doxorubicin (Adriamycin) toxicity; mediated by free-radical mitochondrial damage; irreversible above a cumulative dose of ~550 mg/m².

Autoimmune pericarditis occurring 2–10 weeks after acute myocardial infarction, mediated by anti-myocardial antibodies; presents as recurrent pericarditis with effusion.

An autoimmune post-MI pericarditis occurring weeks to months after MI, caused by antibodies directed against necrotic myocardial antigens; presents with fever, pericardial effusion, and elevated inflammatory markers.

Modified diagnostic criteria (2000) for infective endocarditis, classifying cases as definite (2 major, or 1 major + 3 minor, or 5 minor), possible, or rejected based on microbiology and echocardiographic findings.

Thinning of the ventricular wall with dilatation of the cavity, caused by volume overload or dilated cardiomyopathy; sarcomeres are added in series.

Reversal of a left-to-right shunt to right-to-left due to severe pulmonary hypertension caused by longstanding increased pulmonary blood flow; results in late-onset cyanosis and is a contraindication to surgical closure.

The commonest cause of restrictive cardiomyopathy in India and tropical Africa; characterised by dense fibrous obliteration of ventricular apices and subvalvular regions, causing diastolic heart failure.

A pulsatile haematoma contained only by the adventitia and/or perivascular tissue — not by a complete vessel wall; caused by arterial wall breach (trauma, iatrogenic, anastomotic leak).

Earliest macroscopic atherosclerotic lesion — flat, yellow intimal discolouration composed of subendothelial foam cells; present from adolescence; potentially reversible.

Pericarditis characterised by a fibrin-rich exudate that forms shaggy strands on both pericardial surfaces; classically called 'bread-and-butter' pericarditis due to its gross appearance.

Superficial layer of the atheromatous plaque composed of SMCs, macrophages, and dense collagen matrix; provides structural integrity; thinning of this cap confers plaque vulnerability.

The gross appearance of a chronically rheumatic stenotic mitral valve, in which fused commissures and thickened leaflets create a fixed, slit-like orifice resembling a fish's mouth.

Macrophage engorged with oxidised LDL via scavenger receptors; the cellular hallmark of the fatty streak and atheromatous plaque; appears as a large cell with a vacuolated (foamy) cytoplasm on histology.

The intrinsic property of cardiac muscle whereby increased sarcomere stretch (via increased end-diastolic volume) results in greater force of contraction and stroke volume, up to an optimal fibre length.

Rupture of the necrotic ventricular wall, typically days 3–7 post-MI during maximal neutrophilic digestion, causing haemopericardium, cardiac tamponade, and usually sudden death.

Benign, exquisitely painful tumour of the glomus body (arteriovenous thermoregulatory unit); classic site is subungual; histology shows nests of small round glomus cells around dilated vascular channels.

Vascular connective tissue — capillary loops, fibroblasts, and macrophages — that replaces necrotic myocardium at 1–2 weeks; the stage of repair between neutrophilic digestion and mature collagen scar formation.

The commonest benign vascular tumour; types include capillary (children, involutes spontaneously), cavernous (large blood-filled spaces, liver common site), and lobular capillary (pyogenic granuloma).

Clinical syndrome in which the heart cannot deliver sufficient cardiac output to meet the metabolic demands of the body, or can only do so at abnormally elevated filling pressures.

Alveolar macrophages containing haemosiderin granules, derived from phagocytosis of extravasated red blood cells in chronically congested alveoli; pathognomonic of chronic passive pulmonary congestion; demonstrated by Perl's Prussian blue stain.

A histological grading system (Grades 1–6) for pulmonary vascular disease in congenital heart disease; Grades 1–2 are reversible, Grade 4+ are irreversible.

Human Herpesvirus 8 (Kaposi sarcoma-associated herpesvirus); the necessary aetiological agent of Kaposi sarcoma in all four clinical forms.

A form of heart failure in which cardiac output is elevated or normal but insufficient to meet abnormally high metabolic demand (e.g. severe anaemia, thyrotoxicosis, beri-beri).

Cardiomyopathy caused by sarcomere gene mutations (usually MYH7 or MYBPC3) characterised by asymmetric septal hypertrophy, myofibre disarray, diastolic dysfunction, and risk of sudden death.

Microbial infection of the cardiac endocardium, typically the valve leaflets, producing vegetations composed of fibrin, platelets, bacteria, and inflammatory cells.

A group of syndromes caused by inadequate myocardial oxygen supply relative to demand, almost always due to coronary artery atherosclerosis.

Non-tender, haemorrhagic macular lesions on the palms and soles in infective endocarditis; result from septic microemboli lodging in skin capillaries; represent a vascular phenomenon in Duke criteria.

Diagnostic criteria for acute rheumatic fever: diagnosis requires 2 major (CASES) or 1 major + 2 minor criteria, plus evidence of preceding streptococcal infection.

Low-grade endothelial malignancy caused by HHV-8; four clinical forms including AIDS-related (epidemic) which is the most common AIDS-defining malignancy; histology shows spindle cells, slit-like vascular channels, and haemosiderin.

Physical law stating wall tension = pressure × radius / wall thickness; explains why aneurysm dilation is self-reinforcing and rupture risk rises exponentially with increasing size.

Branch of the left main coronary artery supplying the anterior left ventricular wall, apex, anterior two-thirds of interventricular septum, and bundle branches; occlusion causes anterior MI.

An abnormal communication between the left and right sides of the heart through which blood flows from the high-pressure left side to the lower-pressure right side, increasing pulmonary blood flow.

Sterile vegetations on both the atrial and ventricular surfaces of heart valves (distinctive bilateral distribution) in systemic lupus erythematosus; caused by immune complex deposition.

Dynamic obstruction of the left ventricular outflow tract in HOCM by asymmetric septal hypertrophy and systolic anterior motion of the mitral valve; worsens with reduced preload or increased contractility.

A roughened, irregular fibrotic plaque on the posterior left atrial wall at the jet-stream impact zone of mitral regurgitation; pathognomonic of chronic rheumatic heart disease.

Narrowing of the mitral valve orifice, most commonly from chronic rheumatic heart disease; characterised by leaflet thickening, commissural fusion, and chordal shortening producing a fish-mouth or buttonhole orifice.

A pathogenic mechanism in which antibodies or T cells generated against a foreign antigen (e.g., streptococcal M-protein) cross-react with structurally similar self-antigens (e.g., cardiac myosin), causing autoimmune tissue damage.

Dystrophic calcification of the media of muscular arteries without luminal narrowing or atheromatous change; incidental X-ray finding in elderly and diabetics.

A thrombus forming on the akinetic endocardium overlying an infarcted segment; risk of systemic embolism; common with large anterior MI.

Arterial aneurysm caused by infective destruction of the vessel wall, typically via septic emboli from infective endocarditis; can affect any artery; often multiple; prone to rupture.

Progressive geometric and structural changes in the failing heart including cardiomyocyte loss, interstitial fibrosis, and chamber dilatation; self-perpetuating and driven by neurohormonal activation (angiotensin II, TGF-β).

Inflammatory disease of the myocardium, most commonly viral (Coxsackievirus B), characterised on histology by interstitial lymphocytic infiltration and myocyte necrosis (Dallas criteria); can progress to DCM.

Pathognomonic microscopic finding in HCM showing myocytes arranged in haphazard whorled patterns instead of the normal parallel arrays; reflects abnormal sarcomere assembly.

Stellate or globular cells with pale nuclei and scant cytoplasm, scattered in myxoid (mucopolysaccharide-rich) stroma; the defining histological element of cardiac myxoma.

Sterile vegetations on otherwise normal valves in hypercoagulable or cachectic states (malignancy, sepsis, burn); composed of bland fibrin-platelet thrombi without inflammatory cells or microorganisms.

Non-ST-elevation MI: partial or transient coronary occlusion causing subendocardial necrosis, with troponin rise but no ST elevation on ECG.

Macroscopic appearance of the liver in chronic right heart failure; the cut surface shows a mottled red-and-yellow pattern resembling a nutmeg, caused by centrilobular congestion (red) surrounded by fatty or preserved periportal hepatocytes (yellow).

A four-class functional classification of heart failure based on symptom severity: Class I (no limitation) to Class IV (symptoms at rest).

Dyspnoea (breathlessness) occurring on lying flat, relieved by sitting up; caused by redistribution of fluid from peripheral tissues into the pulmonary circulation in left heart failure.

Tender, painful subcutaneous nodules at the fingertips and toe pads in infective endocarditis; caused by immune complex deposition and microemboli; represent an immunological phenomenon in Duke criteria.

LDL modified by reactive oxygen species in the arterial intima; more atherogenic than native LDL — it is taken up by macrophage scavenger receptors (bypassing feedback inhibition), is proinflammatory, and inhibits eNOS.

Simultaneous inflammation of all three layers of the heart (pericardium, myocardium, endocardium); occurs in acute rheumatic fever and some viral myocarditides.

Small, frond-like benign cardiac tumour arising on valve surfaces (usually aortic), resembling a sea anemone; risk of systemic embolism despite benign histology.

Rupture of a necrotic papillary muscle — most often the posteromedial — causing acute severe mitral regurgitation; a mechanical complication of MI presenting with a new mitral regurgitation murmur and acute pulmonary oedema.

A venous thrombus that crosses a cardiac right-to-left communication (ASD, VSD, PFO) to enter the systemic arterial circulation, potentially causing stroke or peripheral arterial occlusion.

Sudden severe breathlessness waking the patient from sleep, 1-2 hours after lying down; caused by gradual mobilisation of dependent oedema into the pulmonary circulation during sleep.

Failure of the ductus arteriosus to close after birth, creating a communication between the aorta and pulmonary artery; commonly associated with prematurity and congenital rubella.

Cytokine released by activated macrophages and platelets in atherogenesis; drives migration of medial smooth muscle cells into the intima and their subsequent proliferation.

Excess fluid (>50 mL) in the pericardial cavity; classified as serous (transudate), serosanguineous, or chylous depending on composition and cause.

Surgical stripping or resection of the thickened, constrictive pericardium; the only definitive treatment for constrictive pericarditis.

Needle aspiration of fluid from the pericardial sac; the emergency treatment for cardiac tamponade.

Inflammation of the pericardium (visceral + parietal layers), classified by etiology (infective, immune, neoplastic) and morphology (serous, fibrinous, purulent, haemorrhagic, caseous).

Dilated cardiomyopathy arising in the last month of pregnancy or within 5 months postpartum; mechanisms include immune activation and prolactin-mediated myocyte injury.

Accumulation of fluid in the pulmonary interstitium and/or alveoli due to elevated pulmonary capillary hydrostatic pressure, as seen in left heart failure.

The resistance to blood flow offered by the pulmonary vasculature; normally much lower than systemic vascular resistance; elevated in pulmonary hypertension.

An inspiratory fall in systolic blood pressure exceeding 10 mmHg; a hallmark of cardiac tamponade, reflecting exaggerated septal shift impeding left ventricular filling during inspiration.

A neurohormonal cascade activated by reduced renal perfusion pressure; produces angiotensin II (vasoconstriction) and aldosterone (sodium and water retention), increasing preload and afterload.

Additional myocardial damage that paradoxically occurs when ischaemic tissue is reperfused, mediated by calcium overload, reactive oxygen species, and mitochondrial permeability transition pore opening.

Ross's unifying theory of atherogenesis: repeated endothelial injury triggers LDL entry/oxidation, monocyte recruitment, foam cell formation, and SMC proliferation — producing the fibrous atheromatous plaque.

Cardiomyopathy characterised by impaired ventricular filling due to increased wall stiffness (reduced compliance), with normal or near-normal systolic function; caused by amyloid, endomyocardial fibrosis, or sarcoidosis.

The commonest cardiac tumour in infants and children; hamartomatous, associated with tuberous sclerosis; histologically characterised by large vacuolated 'spider cells'.

Erosion of the inferior rib margins (ribs 3–9) seen on chest X-ray in postductal coarctation of the aorta, caused by enlarged intercostal collateral arteries.

Supplies the right ventricle, inferior and posterior walls of the left ventricle (in right-dominant systems), AV node, and usually SA node; occlusion causes inferior MI and may produce heart block.

An abnormal communication allowing deoxygenated blood from the right heart to enter the systemic circulation, causing central cyanosis from birth.

Extension of IE infection into the fibrous valve annulus and surrounding structures; commonest with S. aureus acute IE; may involve the cardiac conduction system causing heart block.

Retinal haemorrhages with pale white centres seen on fundoscopy in infective endocarditis; caused by immune complex vasculitis of retinal capillaries; classified as an immunological Duke minor criterion.

Fragments of infected vegetation that detach and travel in the bloodstream, seeding distant organs with infection; in left-sided IE, cause brain abscess, renal abscess, and mycotic aneurysms; in right-sided IE, cause pulmonary abscesses.

Large, glycogen-distended myocytes with cytoplasmic strands radiating to the cell membrane; the hallmark histological finding of cardiac rhabdomyoma.

Surgical classification of aortic dissection: Type A involves the ascending aorta regardless of extent (surgical emergency); Type B is confined to the descending aorta (medical management unless complicated).

ST-elevation MI: complete coronary occlusion causing transmural myocardial infarction, with ST elevation on ECG; requires emergency reperfusion.

Angiosarcoma arising in the setting of chronic post-mastectomy lymphoedema of the upper limb; the chronic lymphatic stasis is thought to create an angiogenic microenvironment.

Infective endocarditis caused by low-virulence organisms (most commonly S. viridans) that colonise previously damaged valves, producing smaller vegetations and an indolent course over weeks to months.

Bleeding into the subarachnoid space, most commonly from a ruptured berry aneurysm; presents as sudden-onset 'thunderclap' headache ('worst headache of my life').

Myocardial necrosis confined to the inner one-third to one-half of the ventricular wall, most vulnerable due to high wall tension and distance from epicardial vessels.

Unexpected death within 1 hour of symptom onset from a cardiac cause, most often ventricular fibrillation triggered by acute ischaemia; IHD is the underlying cause in >80% of adult SCDs.

Involuntary, purposeless, jerky movements occurring as a major Jones criterion in ARF; caused by cross-reactive antibodies against neuronal antigens in the caudate nucleus; may appear months after the initial streptococcal infection.

Endarteritis obliterans of the vasa vasorum of the thoracic aorta in tertiary syphilis → medial ischaemia → aneurysm of the ascending aorta/arch → aortic regurgitation and coronary ostial stenosis.

Abnormal forward movement of the anterior mitral leaflet toward the interventricular septum during systole in HOCM, caused by Venturi effect of high-velocity LVOT flow; worsens outflow obstruction.

Heart failure characterised by impaired ventricular contractility and reduced ejection fraction (< 40%), typically with ventricular dilatation.

A sudden episode of severe cyanosis in Tetralogy of Fallot triggered by reduced pulmonary blood flow; relieved by squatting, which raises systemic vascular resistance.

The commonest cyanotic congenital heart defect, comprising VSD, overriding aorta, pulmonary stenosis, and RVH — all arising from anterior malalignment of the infundibular septum.

Full-thickness myocardial necrosis spanning the ventricular wall; associated with complete coronary occlusion, ST elevation, and pathological Q waves.

Cyanotic congenital defect in which the aorta arises from the RV and the pulmonary artery from the LV, creating two parallel circulations; the commonest cyanotic CHD presenting in the neonatal period.

Dilation involving all three layers of the vessel wall (intima, media, adventitia); examples include atherosclerotic AAA, syphilitic aortitis aneurysm, and berry aneurysm.

ACS without myocardial necrosis — rest pain, new-onset angina, or crescendo angina caused by partial coronary thrombosis; troponin is normal.

Transient coronary vasospasm causing severe, often complete, coronary occlusion at rest; produces transient ST elevation that fully resolves; treated with calcium-channel blockers.

A mass of fibrin, platelets, bacteria, inflammatory cells, and necrotic debris adherent to the valve surface in infective endocarditis; may be bulky and destructive (acute IE) or smaller and wart-like (subacute IE).

Thin-walled fibrous outpouching of the left ventricular wall formed from a healed transmural infarct scar; bulges paradoxically during systole and predisposes to heart failure, arrhythmia, and mural thrombus.

The most common congenital heart defect; a hole in the interventricular septum allowing left-to-right shunting of blood.

Small (1–2 mm), warty, sterile vegetations along the line of valve closure in acute rheumatic endocarditis; composed of fibrin deposits over inflamed, denuded endothelium.

Thin-cap fibroatheroma with a large necrotic lipid core, few SMCs, and abundant macrophages; prone to rupture even with <50% stenosis; responsible for most acute coronary events.

The earliest microscopic sign of MI (0–12h): elongated, undulating myocytes at the border of the infarct, caused by passive stretching of necrotic cells adjacent to contracting viable myocardium.