IM1.1-27 | Heart Failure — Glossary

A unidirectional structural staging system for heart failure: Stage A (risk factors, no structural disease), Stage B (structural disease, no symptoms), Stage C (structural disease + symptoms), Stage D (advanced refractory HF requiring specialised interventions). Complements NYHA classification.

A drug class that inhibits the angiotensin-converting enzyme, blocking conversion of angiotensin I to angiotensin II. Reduces vasoconstriction, preload, afterload, aldosterone-mediated sodium retention, and adverse cardiac remodelling. First-line in HFrEF. Adverse effect: dry cough (10–15%), hyperkalaemia, worsening renal function.

A clinical emergency defined by new or worsening HF symptoms (dyspnoea, oedema) requiring urgent hospitalisation. Managed by clinical profiling (Wet/Dry × Warm/Cold) to guide treatment: IV diuretics and vasodilators (Wet-Warm), inotropes (Wet-Cold), fluid challenge (Dry-Cold).

CHD lesions with left-to-right shunts (VSD, ASD, PDA) or outflow obstruction without shunting. No cyanosis because deoxygenated blood does not reach the systemic circulation. Pulmonary overcirculation is the major haemodynamic consequence.

The resistance against which the ventricle must contract to eject blood; primarily determined by systemic vascular resistance (left ventricle) and pulmonary vascular resistance (right ventricle). Increased afterload reduces stroke volume in a failing heart.

Administration of amoxicillin 2 g orally 30–60 minutes before invasive dental procedures in the highest-risk patients: prosthetic valve, prior IE, unrepaired cyanotic CHD, repaired CHD with prosthetic material within 6 months. No longer recommended for all valvular heart disease.

Incompetence of the aortic valve causing regurgitation of blood from the aorta back into the left ventricle during diastole; characterised by an early diastolic decrescendo murmur at the left sternal border (Erb's point), collapsing pulse, wide pulse pressure, and displaced apex from LV volume overload.

The cross-sectional area of the aortic valve orifice; calculated by echocardiography using the continuity equation. Severe aortic stenosis: AVA ≤1.0 cm², mean gradient ≥40 mmHg, peak velocity ≥4.0 m/s.

The outermost and lowest point of visible or palpable cardiac impulse, normally in the 5th intercostal space at the mid-clavicular line; displacement beyond this position indicates left ventricular dilatation; character (heaving, diffuse, thrusting) indicates the type of LV loading.

The combination drug sacubitril/valsartan (Entresto). Blocks angiotensin II receptor (ARB) and inhibits neprilysin (raises natriuretic peptide levels). Showed 20% greater reduction in cardiovascular mortality than enalapril in PARADIGM-HF. Preferred over ACEi alone in HFrEF if tolerated. Do NOT combine with ACEi (angioedema risk); 36-hour washout from ACEi required.

The most common arrhythmia in heart failure; present in 30–50% of patients; caused by atrial pressure overload, fibrosis, and reentry circuits; decompensates HF by loss of atrial kick and tachycardia-induced reduction in diastolic filling; requires rate control (beta-blockers, digoxin) and anticoagulation (DOAC if non-valvular AF, CHA₂DS₂-VASc ≥2 in men).

A cardiac peptide released by ventricular cardiomyocytes in response to increased wall stress (elevated preload and afterload). BNP >100 pg/mL (or NT-proBNP >300 pg/mL) supports the diagnosis of heart failure. Serial measurements guide diuretic therapy.

The three classic signs of cardiac tamponade: (1) raised jugular venous pressure, (2) hypotension, and (3) muffled heart sounds; reflects the haemodynamic consequence of pericardial fluid compressing the cardiac chambers and reducing cardiac output.

Only three beta-blockers have proven mortality benefit in HFrEF: carvedilol (non-selective beta-1/2/alpha-1), bisoprolol (selective beta-1), and metoprolol succinate CR/XL. Must be started low and uptitrated slowly. Do NOT initiate in acute decompensation; do NOT abruptly stop in a patient already taking them.

The most common CHD in adults (prevalence 1–2%). Two aortic valve leaflets instead of three. Associated with accelerated degenerative aortic stenosis (2nd–6th decade), regurgitation, endocarditis, and aortic root dilation (aortopathy). Associated with coarctation of the aorta in ~20% of cases.

For IE diagnosis: ≥3 sets (1 aerobic + 1 anaerobic bottle per set) from separate peripheral venipuncture sites, 10 mL blood per bottle, collected before antibiotics. Never from a central line. Prolonged incubation (14–21 days) for HACEK/culture-negative IE.

Natriuretic peptides secreted by ventricular cardiomyocytes in response to elevated wall stress; promote natriuresis and vasodilation as counter-regulation to RAAS; elevated in heart failure (NT-proBNP diagnostic cut-off ≥125 pg/mL; acute HF thresholds: >450 (<50 yr), >900 (50–75 yr), >1800 (>75 yr)); key diagnostic biomarker.

Biventricular pacing device that corrects interventricular and intraventricular electrical dyssynchrony; indicated in HFrEF (LVEF ≤35%), left bundle branch block morphology with QRS ≥150 ms, NYHA Class II–III on optimal medical therapy; reverses remodelling, improves LVEF, reduces mortality.

The definitive treatment for end-stage HF refractory to all other therapies. Indications: NYHA IV, peak VO₂ <12–14 mL/kg/min, refractory cardiogenic shock. Contraindicated in irreversible pulmonary hypertension (PVR >6 Wood units), active malignancy, active infection. Five-year survival ~70%.

The bidirectional interaction between cardiac and renal dysfunction: reduced cardiac output reduces renal perfusion (CRS Type 1 — acute); CKD causes fluid retention and RAAS activation worsening HF (CRS Type 4 — chronic); managing both simultaneously requires careful titration of diuretics and RAAS inhibitors.

The widest cardiac diameter divided by the widest internal thoracic diameter on a PA chest radiograph. CTR >0.5 is defined as cardiomegaly.

A validated scoring tool for estimating annual stroke risk in atrial fibrillation: Congestive HF (1), Hypertension (1), Age ≥75 (2), Diabetes (1), Stroke/TIA (2), Vascular disease (1), Age 65–74 (1), Sex female (1); score ≥2 in men or ≥3 in women warrants oral anticoagulation.

Narrowing of the aortic isthmus, typically just distal to the left subclavian artery. Presents in adults as upper limb hypertension, radio-femoral delay, back murmur (intercostal collaterals), and rib notching on CXR (dilated intercostal arteries). Associated with bicuspid aortic valve (20%) and intracranial berry aneurysms (5–10%).

A pulse with a rapid forceful upstroke followed by sudden collapse; indicates a large stroke volume ejected into a low-resistance circuit; best appreciated by elevating the patient's arm and palpating at the radial artery; classic sign of aortic regurgitation.

Right ventricular hypertrophy and eventual failure secondary to chronic elevated pulmonary vascular resistance from primary pulmonary disease (COPD, pulmonary hypertension, ILD); the most important cause of isolated right heart failure; diagnosed by ECG (right axis deviation, P pulmonale), CXR (enlarged right heart, prominent pulmonary arteries), and echo.

CHD lesions with right-to-left shunts, causing deoxygenated blood to enter the systemic circulation directly. Characterised by central cyanosis (lips, tongue, mucous membranes), digital clubbing, and secondary polycythaemia. Examples: Tetralogy of Fallot, Eisenmenger syndrome, TGA.

Impaired relaxation and filling of the left ventricle during diastole, assessed by echocardiographic Doppler indices: E/A ratio, E/e' ratio, left atrial volume index. E/e' >14 indicates elevated filling pressures.

A cardiac glycoside that inhibits Na+/K+-ATPase, increasing intracellular calcium (positive inotropy) and enhancing vagal tone (negative chronotropy/dromotropy). In HFrEF: reduces hospitalisation and symptoms but NOT mortality (DIG trial). Target serum level 0.5–0.9 ng/mL. Narrow therapeutic index; toxicity exacerbated by hypokalaemia.

Echocardiographic evidence of endocardial involvement meeting a Duke major criterion: oscillating intracardiac mass on a valve, paravalvular abscess, new prosthetic valve dehiscence, or new valvular regurgitation.

Ratio of early mitral inflow velocity (E) to early diastolic mitral annular velocity (e') by tissue Doppler echocardiography. A surrogate for left atrial filling pressure. E/e' >14 suggests elevated filling pressures consistent with HFpEF or grade II–III diastolic dysfunction.

The end-stage complication of a large unrepaired left-to-right shunt (VSD, ASD, PDA) in which progressive pulmonary arterial hypertension causes pulmonary vascular resistance to equal or exceed systemic vascular resistance, reversing the shunt to right-to-left. Results in central cyanosis, clubbing, and polycythaemia. Closure of the underlying defect is absolutely contraindicated once Eisenmenger is established.

The proportion of end-diastolic volume ejected with each heartbeat; EF = stroke volume / end-diastolic volume × 100%. Normal LVEF ≥55–60%. Measured by Simpson's biplane volumetric method on 2D echocardiography.

A characteristic auscultatory sign of atrial septal defect in which the normal respiratory variation in S2 splitting is abolished. The A2-P2 interval remains constant throughout the respiratory cycle because the ASD ensures equal RV filling regardless of phase, preventing the normal inspiratory widening.

A low-pitched, late-diastolic (presystolic) sound produced by atrial contraction into a stiff, non-compliant left ventricle; signifies diastolic dysfunction; heard at the apex with the bell; absent in atrial fibrillation.

Clinical criteria for diagnosing heart failure: requires 2 major or 1 major + 2 minor criteria. Major criteria include PND, raised JVP, pulmonary rales, cardiomegaly, acute pulmonary oedema, S3 gallop, hepatojugular reflux.

The intrinsic cardiac property whereby increasing ventricular end-diastolic volume (preload) stretches sarcomeres and increases stroke volume within physiological limits; a compensatory response in early heart failure that maintains output at the cost of elevated filling pressures.

Pan-systolic regurgitation at the mitral valve in the absence of primary valvular pathology, caused by annular dilatation from left ventricular dilatation in dilated cardiomyopathy; important to recognise as a secondary consequence of HFrEF rather than a primary valvular disease.

The combination of four evidence-based pharmacological drug classes for HFrEF: ACEi/ARNI, beta-blocker (carvedilol/bisoprolol/metoprolol succinate), mineralocorticoid receptor antagonist (spironolactone/eplerenone), and SGLT2 inhibitor. All four should be used unless contraindicated.

A group of slow-growing fastidious gram-negative rods that cause culture-negative IE: Haemophilus, Aggregatibacter (formerly Actinobacillus), Cardiobacterium, Eikenella, Kingella. Require prolonged blood culture incubation (14–21 days). Typically subacute, native valve IE.

A clinical syndrome in which the heart is unable to pump sufficient blood to meet the body's metabolic demands, or can do so only at abnormally elevated filling pressures; characterised by symptoms of dyspnoea, fatigue, and fluid retention and by structural or functional cardiac abnormality.

Heart failure where the LVEF is ≥50%, with evidence of diastolic dysfunction and elevated filling pressures; associated with hypertension, diabetes, obesity, and atrial fibrillation; no mortality-reducing pharmacotherapy proven; diuretics for congestion.

Heart failure where the left ventricular ejection fraction is ≤40%; formerly called 'systolic heart failure'; characterised by LV dilatation, reduced contractility, and elevated filling pressures; treated with ACE inhibitors/ARBs, beta-blockers, and aldosterone antagonists (the evidence-based triad).

A clinical test in which sustained right upper quadrant compression for 10–15 seconds causes a sustained rise in JVP of more than 4 cm; a positive HJR confirms elevated central venous pressure and right heart congestion.

Heart failure with mildly reduced ejection fraction; LVEF 41–49%. An intermediate category that may represent a transitional state between HFrEF and HFpEF.

Heart failure with LVEF 41–49%; an intermediate phenotype with mixed systolic and diastolic features; emerging evidence supports HFrEF-type pharmacotherapy.

Heart failure with preserved ejection fraction; LVEF ≥50%. Characterised by diastolic dysfunction and elevated filling pressures with preserved systolic function. Common in elderly women with hypertension.

Heart failure with LVEF ≥50%; characterised by diastolic dysfunction (impaired relaxation/compliance), concentric LV hypertrophy, and risk factor-driven aetiology (hypertension, diabetes, obesity, AF); SGLT2 inhibitors now evidence-based.

Heart failure with reduced ejection fraction; LVEF ≤40%. Characterised by systolic dysfunction. Neurohormonal agents (ACE inhibitors, beta-blockers, MRA) have strong evidence-based mortality benefit in this category.

Heart failure with LVEF ≤40%; characterised by systolic dysfunction, ventricular dilatation, and eccentric hypertrophy; the phenotype for which ACE inhibitors, beta-blockers, MRA, and SGLT2 inhibitors have the strongest mortality-reduction evidence.

A device implanted to detect and terminate malignant ventricular arrhythmias (VT/VF) with internal shocks; indicated for primary prevention of sudden cardiac death in HFrEF with LVEF ≤35% despite ≥3 months of optimal medical therapy, NYHA Class II–III; reduces sudden cardiac death.

A device for primary prevention of sudden cardiac death in HFrEF patients with LVEF ≤35% + NYHA II–III after ≥3 months of GDMT. Reduces all-cause mortality by ~23% (SCD-HeFT). Not indicated in end-stage NYHA IV or when life expectancy <1 year.

A life-threatening infection of the endocardial surface of the heart, most commonly involving the cardiac valves. Produces vegetations composed of fibrin, platelets, and bacteria. Classified as acute (fulminant, S. aureus) or subacute (indolent, S. viridans).

Removal of a measured volume of blood with simultaneous replacement of the same volume of IV normal saline, performed in Eisenmenger patients with symptomatic hyperviscosity (Hct >65%). The isovolaemic replacement prevents haemodynamic compromise that would occur with simple volume removal.

Non-tender, flat, haemorrhagic macules on the palms or soles caused by septic microemboli. More characteristic of acute IE (Staphylococcus aureus).

The pressure in the internal jugular vein, which reflects right atrial pressure directly; measured as the vertical height of the uppermost venous pulsation above the sternal angle of Louis; normal ≤4 cm at 45°; elevated JVP signals right heart congestion.

The pulsatile pattern visible in the internal jugular vein comprising: a wave (atrial contraction), x descent (atrial relaxation), v wave (passive atrial filling during ventricular systole), and y descent (tricuspid valve opening with early ventricular filling); each component carries diagnostic information.

Horizontal, dense, short (1–2 cm) lines at the lung periphery on CXR, representing fluid in interlobular septa (interstitial pulmonary oedema). Indicate pulmonary capillary wedge pressure approximately 18–25 mmHg.

The sounds heard with the stethoscope over the brachial artery during sphygmomanometry; Phase I (appearance of tapping sounds) marks systolic BP; Phase V (disappearance of sounds) marks diastolic BP in most circumstances; Phase IV (muffling) is used in aortic regurgitation and pregnancy.

Paradoxical rise in JVP during inspiration (normally the JVP falls with inspiration); seen in cardiac tamponade and constrictive pericarditis; reflects impaired right-heart filling due to a fixed or restricted pericardial space.

A conduction abnormality with QRS duration ≥120 ms; broad notched R waves in lateral leads (I, V5–V6), deep S in V1, absent septal Q waves in lateral leads. LBBB + LVEF ≤35% + QRS ≥150 ms indicates ventricular dyssynchrony and is the key criterion for cardiac resynchronisation therapy (CRT).

A mechanical ventricular assist pump for end-stage HFrEF used as: bridge to transplantation (BTT) or destination therapy (DT) in non-transplant candidates. Complications include device thrombosis, stroke, drive-line infection, and right heart failure.

A potent diuretic acting on the Na-K-2Cl cotransporter in the thick ascending limb of Henle. The cornerstone of symptomatic congestion relief in heart failure. Does NOT reduce mortality. Dose 20–80 mg OD/BD PO; 20–40 mg IV for acute decompensation. Causes hypokalaemia, hypomagnesaemia, and ototoxicity at high doses.

Spironolactone or eplerenone; blocks aldosterone at the mineralocorticoid receptor, reducing renal sodium retention and myocardial fibrosis. Spironolactone 25–50 mg OD in HFrEF. Monitor potassium and creatinine. Contraindicated if eGFR <30 or K+ >5.0 mmol/L.

Narrowing of the mitral valve orifice, most commonly from rheumatic heart disease; characterised by mid-diastolic rumble with opening snap, loud S1, tapping apex beat, and downstream pulmonary hypertension; remains prevalent in India due to ongoing streptococcal disease burden.

The cross-sectional area of the mitral valve orifice measured by echocardiography (planimetry or pressure half-time method). Severity of mitral stenosis: mild >1.5 cm², moderate 1.0–1.5 cm², severe <1.0 cm².

A validated diagnostic framework for infective endocarditis incorporating two major criteria (positive blood cultures, echocardiographic evidence) and five minor criteria. Definite IE requires 2 major, or 1 major + 3 minor, or 5 minor criteria.

An infected aneurysmal dilation of an arterial wall at a site of septic embolism; most dangerous when intracranial. Detected by CT or MR angiography. Risk of rupture with subarachnoid haemorrhage.

A state of chronic myocardial dysfunction due to persistent ischaemia, where myocardium is viable but non-contractile. Detected as reversible perfusion defects on nuclear myocardial perfusion imaging. May recover function after revascularisation.

A sterile platelet-fibrin thrombus that forms on disrupted valvular endothelium due to turbulent flow; serves as the nidus onto which bacteria adhere during bacteraemia to initiate infective endocarditis.

The predisposition of congenitally abnormal valves and endocardium to form sterile platelet-fibrin thrombi at sites of turbulent flow — the nidus for infective endocarditis. This underlies the indication for endocarditis prophylaxis in high-risk CHD lesions.

The N-terminal cleavage fragment of pro-BNP; biologically inactive but measurable, with a longer half-life than BNP. Age-adjusted thresholds for HF diagnosis: >450 pg/mL (<50 yr), >900 pg/mL (50–75 yr), >1800 pg/mL (>75 yr).

New York Heart Association classification of heart failure severity based on functional limitation: Class I (no symptoms at ordinary activity), Class II (mild symptoms on ordinary exertion), Class III (symptoms on less-than-ordinary exertion), Class IV (symptoms at rest or minimal activity).

A four-class clinical grading system for heart failure symptom severity based on exercise tolerance: Class I (no limitation), Class II (slight limitation — ordinary activity causes symptoms), Class III (marked limitation — less-than-ordinary activity causes symptoms), Class IV (symptoms at rest).

A high-pitched early diastolic sound produced by the sudden tensing of the thickened, pliable mitral valve leaflets as they open in mitral stenosis; heard at the apex and lower left sternal border; a shorter OS-to-S2 interval indicates higher left atrial pressure and more severe stenosis.

Breathlessness that worsens on lying flat, relieved by sitting or standing; reflects redistribution of dependent interstitial fluid into the pulmonary circulation on recumbency, increasing pulmonary venous pressure; quantified by the number of pillows required to sleep comfortably.

Tender, raised, erythematous nodules on the pulps of the fingers or toes, caused by immune complex deposition and vasculitis in infective endocarditis. More characteristic of subacute IE (streptococcal).

A thrombus that originates in the venous circulation (typically deep veins) but crosses from the right to the left atrium via a patent foramen ovale (PFO) or ASD and then embolises to the systemic arterial circulation, causing stroke or peripheral embolism.

A sustained outward lift of the left parasternal region of the chest during systole, felt by placing the heel of the hand over the 3rd–5th intercostal spaces at the left sternal border; indicates right ventricular hypertrophy, typically from pulmonary hypertension.

An extension of endocarditic infection beyond the valve annulus into the fibrous skeleton of the heart; most common in aortic valve IE. Manifests as new conduction defects (PR prolongation, BBB) on ECG. A major surgical indication.

Episodes of sudden, severe breathlessness that wake the patient from sleep, typically 1–3 hours after lying down; represents a more severe variant of orthopnoea; the patient must sit upright or stand for relief; a symptom of significant left heart failure.

Persistence of the foetal ductus arteriosus connecting the aorta to the pulmonary artery beyond 3 months of life. Produces a continuous 'machinery' murmur at the left infraclavicular area and bounding pulses (wide pulse pressure). Causes pulmonary overcirculation and Eisenmenger if large and unrepaired.

A persistent opening in the interatrial septum at the fossa ovalis, present in ~25% of adults. In most it is haemodynamically insignificant, but PFO is associated with cryptogenic stroke (paradoxical embolism) in young adults. Detected by bubble contrast echocardiography.

A catheter-based technique using an Inoue balloon to dilate a stenosed mitral valve. Preferred intervention for suitable rheumatic mitral stenosis (Wilkins score ≤8, no significant MR, no LA thrombus).

A dilated cardiomyopathy presenting in the last month of pregnancy or within 5 months postpartum (extended to 12 months in some guidelines) in women with no prior cardiac disease; LVEF <45%; implicated mechanisms include abnormal prolactin cleavage causing endothelial toxicity; bromocriptine is an adjunctive aetiology-specific therapy.

The ventricular filling pressure at the end of diastole (represented by end-diastolic volume or LVEDP); determined by venous return and ventricular compliance. Elevated preload causes upstream venous congestion (pulmonary in LHF, systemic in RHF).

The resistance to blood flow through the pulmonary arterial circulation, measured in Wood units (mmHg per L/min). Normal PVR is <3 Wood units. Progressively elevated PVR in unrepaired left-to-right shunts leads to Eisenmenger syndrome when PVR exceeds systemic vascular resistance.

A pulse abnormality in which the strength of alternate beats in regular sinus rhythm alternates between stronger and weaker; a sign of severe left ventricular systolic dysfunction reflecting the ventricle's inability to maintain a consistent stroke volume beat-to-beat.

An exaggerated inspiratory fall in systolic blood pressure of more than 10 mmHg; the cardinal sign of cardiac tamponade (also occurs in severe bronchospasm and constrictive pericarditis); measured by sphygmomanometry by noting the pressure difference between expiratory-only and all-cycle Korotkoff sounds.

The ratio of pulmonary (Qp) to systemic (Qs) blood flow. Normal = 1:1. In left-to-right shunts, Qp:Qs >1 (pulmonary overcirculation). A Qp:Qs ≥1.5:1 with PVR <3 Wood units is the threshold favouring defect closure.

A neurohormonal cascade activated by reduced renal perfusion in heart failure: renin converts angiotensinogen to angiotensin I; ACE converts Ang I to angiotensin II; Ang II causes vasoconstriction, aldosterone release (→ sodium/water retention), and cardiac/vascular fibrosis; targeted by ACE inhibitors, ARBs, and MRAs.

A sign of coarctation of the aorta in which the femoral pulse is palpated appreciably later than the radial pulse, because blood reaches the lower limbs via slow collateral circulation around the obstruction rather than directly through the narrowed aorta.

Improvement in LV geometry and function — increased LVEF, reduced LV end-diastolic dimension — occurring with GDMT in HFrEF. Represents a key therapeutic goal; patients who achieve LVEF normalisation (>50%) have significantly better prognosis.

A radiological sign of coarctation of the aorta — erosions on the inferior surface of the 3rd–8th ribs bilaterally, caused by dilated intercostal collateral arteries that form to bypass the coarctation. Best seen on PA chest X-ray.

Boat-shaped retinal haemorrhages with a pale centre, caused by septic emboli to the retinal vasculature; a peripheral sign of infective endocarditis visible on fundoscopy.

Infected emboli arising from right-sided valve vegetations (tricuspid or pulmonary) that lodge in the pulmonary circulation. Produce bilateral peripheral wedge-shaped or cavitating opacities on CXR/CT. Classic complication of right-sided IE in IVDU.

Sodium-glucose cotransporter-2 inhibitors (empagliflozin, dapagliflozin) originally developed for type 2 diabetes; reduce cardiovascular death and HF hospitalisation in HFrEF regardless of diabetes status. Also show benefit in HFpEF. Mechanism includes osmotic diuresis, natriuresis, and possible direct myocardial effects. Dose: 10 mg OD.

Dietary sodium intake <2 g/day (equivalent to <5 g table salt/day) is recommended in symptomatic heart failure (NYHA II–IV). Reduces fluid retention and augments the effect of diuretic therapy.

Voltage criteria for left ventricular hypertrophy on ECG: S wave in V1 + R wave in V5 or V6 >35 mm (in adults >35 years). Specific but not sensitive for LVH.

Dark linear streaks under the fingernails or toenails caused by microemboli in the nail bed vasculature; more specific for IE when proximal (distal position may be traumatic).

An oral/GI streptococcus causing subacute infective endocarditis; associated with colonic adenoma and adenocarcinoma in up to 25–80% of cases. Every patient with S. bovis IE must be referred for colonoscopy.

The most common cyanotic CHD, comprising four features: ventricular septal defect, overriding aorta, right ventricular outflow tract obstruction, and right ventricular hypertrophy. Causes right-to-left shunting and central cyanosis. CXR shows boot-shaped heart. Most cases are surgically repaired in infancy; adults present with residual complications (pulmonary regurgitation, RV dilatation).

A low-pitched, early-diastolic sound produced by sudden deceleration of the blood column during rapid ventricular filling in a dilated, non-compliant ventricle; heard at the apex with the bell in left lateral decubitus; the most specific clinical sign of elevated LV filling pressure and reduced LVEF.

An echocardiographic technique with superior sensitivity for IE detection (87–100%) compared to transthoracic echo (50–63%). Mandatory when TTE is non-diagnostic, prosthetic valve IE is suspected, or perivalvular complications are sought.

A CXR sign of early left heart failure in which upper lobe pulmonary vessels are larger than lower lobe vessels (reversed from normal), reflecting equalisation and then reversal of normal hydrostatic gradient due to elevated pulmonary venous pressure.

A mass of fibrin, platelets, bacteria, and inflammatory cells on the endocardial surface of a valve or supporting structure, the hallmark pathological lesion of infective endocarditis. Vegetations cause local valve destruction and can embolise.

Structural and functional changes in the heart in response to chronic pressure/volume overload and neurohormonal activation; eccentric hypertrophy (chamber dilation, sarcomere replication in series) in HFrEF; concentric hypertrophy (wall thickening, sarcomere replication in parallel) in HFpEF; reversal by ACE-I, beta-blockers, and CRT is a therapeutic goal.

The preferred site for intramuscular injection in adults. Located over gluteus medius and minimus. Identified by placing the heel of the hand on the greater trochanter, index finger on ASIS, middle finger along the iliac crest — inject in the V-space. Has the highest muscle mass and fewest blood vessels/nerves among IM sites.

An echocardiographic scoring system for mitral valve morphology in rheumatic mitral stenosis. Scores leaflet mobility, thickening, calcification, and subvalvular apparatus, each 1–4. Total ≤8 indicates favourable anatomy for percutaneous mitral balloon valvotomy (PMBV).