IM2.1-24 | Acute Myocardial Infarction and Ischemic Heart Disease — Glossary

A mnemonic for reversible causes of cardiac arrest: 4Hs — Hypoxia, Hypovolaemia, Hypo/Hyperkalaemia (metabolic), Hypothermia; 4Ts — Tension pneumothorax, Tamponade (cardiac), Toxins, Thrombosis (pulmonary or coronary); identifying and treating these causes is mandatory in every PEA or refractory VF arrest.

A regular wide-complex rhythm at 60–100 bpm occurring in the first 12–24 hours post-MI or after successful reperfusion; a 'reperfusion arrhythmia'; haemodynamically well-tolerated; does not require antiarrhythmic treatment; distinguished from VT by rate (≤100 bpm).

Sudden complete occlusion of a coronary stent by thrombus, typically caused by premature discontinuation of dual antiplatelet therapy; presents as STEMI within days to weeks of stenting; carries 15–45% mortality; requires emergency PCI.

A structured resuscitation protocol for monitored cardiac arrest that adds rhythm identification, defibrillation (for VF/pulseless VT), IV drug therapy (adrenaline, amiodarone), advanced airway management, and identification of reversible causes (4Hs and 4Ts) to the foundation of high-quality BLS.

Separation of the aortic wall layers by a haematoma, typically beginning at an intimal tear; type A involves the ascending aorta (surgical emergency); mimics ACS but is a contraindication to thrombolysis; clinical clues: tearing quality, maximal at onset, back radiation, unequal arm blood pressures, pulse deficits, aortic regurgitation murmur.

Apolipoprotein B; the structural protein of LDL, VLDL, IDL, and Lp(a); each atherogenic particle carries exactly one ApoB-100 molecule; ApoB measurement directly quantifies atherogenic particle number and is a superior risk marker in atherogenic dyslipidaemia where LDL-C underestimates particle burden; target ApoB <80 mg/dL in very high risk.

A lipid pattern characterised by elevated triglycerides, low HDL, and small dense LDL; commonly seen in metabolic syndrome and type 2 diabetes; more atherogenic per unit LDL-C than isolated hypercholesterolaemia.

A chronic inflammatory disease of large and medium-sized arteries characterised by subintimal accumulation of lipid, inflammatory cells, smooth muscle cells, and fibrous matrix; the pathological basis of IHD, stroke, and peripheral arterial disease.

A sequence of emergency interventions for cardiac arrest comprising chest compressions (30:2 ratio with rescue breaths) at a depth of 5–6 cm and rate of 100–120/min, aimed at maintaining cerebral and coronary perfusion until defibrillation and advanced care are available.

A vagal reflex triggered by ischaemia of the inferior myocardial wall (supplied by the RCA); manifests as bradycardia, hypotension, nausea, and epigastric pain; responsible for atypical presentations of inferior STEMI that mimic acute abdomen.

The Rating of Perceived Exertion scale (6–20 points); RPE 12–14 ('somewhat hard') corresponds to moderate-intensity exercise appropriate for Phase II cardiac rehabilitation; used when heart rate monitoring is unavailable or when beta-blockers blunt the heart rate response to exercise.

A 4-level grading system for stable angina severity based on the level of exertion that triggers symptoms: Class I (ordinary activity; heavy exertion only), Class II (slight limitation; walking >2 blocks or climbing >1 flight), Class III (marked limitation; walking 1–2 blocks or 1 flight), Class IV (inability to perform any activity without discomfort; rest angina).

A structured multidisciplinary programme of supervised exercise training, risk factor modification, patient education, and psychosocial support for patients after ACS, cardiac surgery, or heart failure; associated with 26% reduction in cardiovascular mortality and 18% reduction in hospital readmissions (Cochrane 2016).

A state of acute circulatory failure due to impaired cardiac output, defined as sustained hypotension (systolic BP <90 mmHg for >30 minutes) with evidence of impaired tissue perfusion (cold extremities, oliguria, confusion); Killip class IV; carries ~67% 30-day mortality without mechanical support.

The ratio of the maximum transverse cardiac diameter to the maximum transverse thoracic diameter on a PA chest X-ray; normal <0.5; CTR >0.5 indicates cardiomegaly. Not reliably measured on AP (supine) films due to magnification artifact.

A systematic approach to identifying undiagnosed FH cases in first-degree relatives of a diagnosed FH proband; recommended by ESC/EAS and British Heart Foundation guidelines; cost-effective because each proband has a 50% probability of transmitting the mutation to each offspring; early detection enables preventive statin therapy before CAD develops.

A validated scoring system for estimating stroke risk in atrial fibrillation: Congestive heart failure (1), Hypertension (1), Age ≥75 (2), Diabetes (1), Stroke/TIA history (2), Vascular disease (1), Age 65–74 (1), Sex female (1); score ≥2 in males or ≥3 in females = oral anticoagulation recommended.

The AHA 5-link model for maximising cardiac arrest survival: (1) recognition and emergency activation, (2) early CPR, (3) rapid defibrillation, (4) advanced resuscitation (ACLS), (5) post-resuscitation care; survival decreases by 7–10% for every minute of delayed defibrillation in VF.

A cardiac-specific isoenzyme of creatine kinase; rises 3–6 hours after MI, peaks at 12–24 hours, and returns to baseline within 48–72 hours; superseded by troponin for initial MI diagnosis but retains utility for detecting reinfarction — a new rise after baseline normalisation indicates a new MI event.

The proportion of resuscitation time during which chest compressions are actively delivered; target >60%, ideally >80%; minimised by reducing all pauses (pulse checks, rhythm analysis, drug delivery) to ≤5–10 seconds; an important quality indicator of CPR performance.

A pattern of stable angina becoming progressively more frequent, more severe, occurring at lower exertion thresholds, or beginning to occur at rest; represents a transition from stable to unstable plaque behaviour and constitutes a form of unstable angina requiring urgent evaluation.

An ECG pattern representing a STEMI equivalent: tall symmetric T-waves with upsloping ST depression at the J-point in V1–V6, with ST elevation in aVR; indicates acute proximal LAD occlusion without classic ST elevation; requires immediate reperfusion.

A late pericarditis complication occurring 2–8 weeks after MI, caused by an autoimmune inflammatory reaction to myocardial antigens released during infarction; presents with fever, pleuritic chest pain, and pericardial friction rub; treated with NSAIDs or colchicine.

Combination of aspirin (COX-1 inhibitor) and a P2Y12 receptor inhibitor (ticagrelor, clopidogrel, or prasugrel); standard treatment for all ACS patients; maintained for at least 12 months after coronary stenting to prevent in-stent thrombosis; duration adjusted by DAPT or PRECISE-DAPT score based on ischaemic vs bleeding risk balance.

Impairment of the endothelium's vasoprotective functions (nitric oxide production, anti-adhesion, anti-coagulation) triggered by oxidised LDL, hypertension, hyperglycaemia, or smoking; the initiating step in atherogenesis.

A selective mineralocorticoid receptor antagonist (aldosterone antagonist); indicated post-MI in patients with LVEF ≤40% plus heart failure or diabetes (EPHESUS trial — 15% mortality reduction); started within 3–14 days; contraindicated if creatinine >2.5 mg/dL (M) or >2.0 mg/dL (F), or potassium >5.0 mmol/L.

Features on EST predicting left main or three-vessel CAD and possible survival benefit from revascularisation: ST depression ≥2 mm, multi-territory ST changes, early positive (stage 1), exercise-induced hypotension (SBP fall ≥10 mmHg), failure to reach 85% predicted maximal heart rate, sustained VT.

An intestinal cholesterol absorption inhibitor that blocks the NPC1L1 transporter at the brush border enterocyte; reduces LDL-C by 18–24% as add-on to statin therapy; IMPROVE-IT trial demonstrated modest but significant cardiovascular event reduction when added to simvastatin in post-ACS patients.

A genetic disorder of LDL receptor function (most commonly due to LDLR gene mutations) causing severely elevated LDL-C from birth; heterozygous FH (LDL 5–10 mmol/L, incidence 1:500) causes premature CAD in the 5th–6th decade without treatment; diagnosed by Dutch Lipid Clinic Network or Simon Broome criteria.

A class of drugs (fenofibrate, gemfibrozil) that activate PPARα nuclear receptors, increasing LPL expression (faster TG hydrolysis), reducing VLDL synthesis, and raising HDL-C; primary indication is severe hypertriglyceridaemia (TG >500 mg/dL — pancreatitis prevention); gemfibrozil + statin combination significantly increases myopathy risk and should be avoided.

A framework for prescribing individualised exercise in cardiac rehabilitation: Frequency (3–5 sessions/week), Intensity (50–80% heart rate reserve or RPE 12–14 on Borg scale), Type (aerobic — walking, cycling, swimming; plus resistance training after 4 weeks), Time (20–45 minutes per session, progressing gradually).

A lipid-laden macrophage formed when macrophages in the subintimal space engulf oxidised LDL via unregulated scavenger receptors; the hallmark of the fatty streak and the core cellular element of the atherosclerotic plaque.

A synthetic selective factor Xa inhibitor given as a once-daily subcutaneous injection (2.5 mg); recommended by ESC as preferred anticoagulant in NSTE-ACS for its superior bleeding profile versus enoxaparin (OASIS-5); must be supplemented with UFH during PCI to prevent catheter thrombosis.

A phenotypic classification of hyperlipoproteinaemias (Types I–V) based on the elevated lipoprotein fraction; Type IIa (elevated LDL — FH), Type IIb (elevated LDL + VLDL — combined hyperlipidaemia), Type IV (elevated VLDL — hypertriglyceridaemia); largely superseded in clinical practice by risk-based management but retains use in describing severe or genetic dyslipidaemias.

The compensatory outward expansion of the arterial wall during early plaque growth, preserving luminal diameter despite increasing plaque volume; explains why large lipid-rich plaques may not cause haemodynamically significant stenosis and may rupture without prior warning on stress testing.

A class of intravenous antiplatelet agents (abciximab, eptifibatide, tirofiban) that block fibrinogen binding to platelet GPIIb/IIIa receptors, preventing the final common pathway of platelet aggregation; current role limited to bailout in high-thrombus-burden PCI; not indicated for routine pre-PCI administration.

Global Registry of Acute Coronary Events score; predicts in-hospital and 6-month mortality in ACS using age, heart rate, systolic BP, serum creatinine, Killip class, cardiac arrest at admission, ST deviation, and troponin; superior to TIMI for mortality prediction.

High-density lipoprotein cholesterol; mediates reverse cholesterol transport from peripheral tissues (including plaques) to the liver via ApoA-I and ABCA1; low HDL is an independent cardiovascular risk factor.

A highly sensitive assay for cardiac troponin I or T that detects concentrations below 1 ng/L; enables earlier rule-in and rule-out of myocardial injury using 0h/1h or 0h/2h serial protocols; the current gold-standard biomarker for NSTEMI diagnosis.

3-hydroxy-3-methylglutaryl-CoA reductase; the rate-limiting enzyme of the mevalonate pathway for hepatic cholesterol synthesis; the pharmacological target of statin drugs; inhibition reduces intracellular cholesterol → upregulates LDL receptor expression → increases circulating LDL clearance.

A large international case-control study of 15,152 MI cases and 14,820 controls in 52 countries; identified nine modifiable risk factors (smoking, dyslipidaemia, hypertension, diabetes, abdominal obesity, psychosocial stress, lack of fruits/vegetables, physical inactivity, alcohol) that together account for >90% of population-attributable risk for MI.

A spectrum of clinical syndromes resulting from imbalance between myocardial oxygen supply and demand, most commonly due to atherosclerotic coronary artery disease; includes stable angina, unstable angina, NSTEMI, and STEMI.

A 4-class clinical staging system for acute MI severity based on physical examination findings: Class I (no heart failure signs), Class II (mild heart failure — basal rales, S3), Class III (severe heart failure — pulmonary oedema), Class IV (cardiogenic shock — hypotension + poor perfusion); used in the GRACE score for risk stratification.

Chest X-ray correlates of Killip class: Killip I = clear lung fields; Killip II = upper lobe diversion and/or Kerley B lines; Killip III = bilateral perihilar bat-wing alveolar oedema; Killip IV = above + hypotension and cardiogenic shock.

Low-density lipoprotein cholesterol; the primary atherogenic lipoprotein; enters the arterial intima, undergoes oxidative modification, and initiates foam cell formation; the principal target of pharmacological and lifestyle lipid-lowering therapy.

The fraction of end-diastolic volume ejected with each heartbeat; measured by echocardiography; normal ≥55%; LVEF ≤40% defines heart failure with reduced ejection fraction (HFrEF) requiring ACE inhibitor/ARB plus beta-blocker; predicts prognosis after MI.

The gesture of placing a clenched fist over the sternum to describe the character of ischaemic chest pain; indicative of a diffuse, pressure-like, poorly localised discomfort consistent with myocardial ischaemia.

A modified LDL particle with an additional apo(a) protein linked to ApoB-100; independently atherogenic and prothrombotic (inhibits fibrinolysis); genetically determined and not reduced by statins; elevated Lp(a) >50 mg/dL confers increased cardiovascular risk.

A patient-centred counselling approach for behaviour change that uses open questions, reflective listening, affirmation, and exploration of discrepancy between current behaviour and stated goals; evidence-based for smoking cessation, dietary change, and medication adherence in chronic disease.

Calculated as total cholesterol minus HDL cholesterol; captures all atherogenic lipoproteins (LDL, VLDL, IDL, Lp(a)); preferred over LDL-C when triglycerides are elevated (>400 mg/dL renders Friedewald-calculated LDL unreliable); target = LDL-C target + 30 mg/dL.

An acute coronary syndrome with myocardial necrosis (troponin elevation) but without ST elevation; ECG may show ST depression, T-wave inversion, or be non-diagnostic; typically caused by subtotal coronary occlusion; managed with risk-stratified early invasive strategy.

Mechanical complication of MI (typically inferior STEMI, posteromedial papillary muscle) occurring 2–5 days post-infarction; presents as new acute mitral regurgitation — a harsh pansystolic murmur at the apex with acute pulmonary oedema; surgical emergency.

A monoclonal antibody (evolocumab, alirocumab) targeting PCSK9, the hepatic protease that degrades LDL receptors; inhibition preserves more LDL receptors on the hepatocyte surface, dramatically increasing LDL clearance (50–60% additional LDL reduction on top of statin); indicated for very high-risk patients not achieving LDL target on maximal statin + ezetimibe.

ECG findings in acute pericarditis: diffuse concave (saddle-shaped) ST elevation in multiple lead territories without a single-vessel distribution; PR depression (particularly in limb leads) is near-pathognomonic; absence of reciprocal ST depression; evolves through four stages over days to weeks.

A STEMI reperfusion approach combining early thrombolysis (at non-PCI-capable hospital) with routine transfer for coronary angiography and PCI within 3–24 hours; recommended when primary PCI cannot be achieved within 120 minutes of first medical contact; includes rescue PCI for failed thrombolysis.

Disruption of the fibrous cap of a vulnerable plaque, exposing the thrombogenic lipid core to flowing blood; the most common triggering mechanism for acute coronary syndromes, initiating platelet aggregation and thrombus formation.

Cardiovascular benefits of statins beyond LDL-C reduction, including: anti-inflammatory effects (reduced hsCRP, IL-6), endothelial stabilisation (increased nitric oxide bioavailability), plaque stabilisation (reduced macrophage activity, thicker fibrous cap), and antithrombotic effects (reduced tissue factor); contribute to early cardiovascular benefit seen within days to weeks of statin initiation.

Rupture of the interventricular septum due to anterior MI (LAD territory) occurring 2–5 days post-MI; presents as new harsh pansystolic murmur at the left sternal border with left-to-right shunt on colour Doppler echo and haemodynamic deterioration; managed with surgical or transcatheter closure; mortality ~90% without repair.

STEMI involving the posterior left ventricular wall, caused by RCA or LCx occlusion; ECG shows ST depression in V1–V3 (mirror-image of posterior elevation) with tall R-waves; confirmed by ST elevation ≥0.5 mm in posterior leads V7–V9; treated with immediate reperfusion like any other STEMI.

Mechanical recanalization of the culprit coronary artery using balloon angioplasty and stenting as the primary reperfusion strategy in STEMI; preferred over thrombolysis when achievable within 120 minutes of first medical contact; door-to-balloon target ≤90 minutes; achieves TIMI 3 flow in >90% of cases.

A cardiac arrest state characterised by organised electrical activity on the ECG without a palpable pulse; managed with CPR + adrenaline and active search for reversible causes (4Hs and 4Ts); no defibrillation indicated (non-shockable rhythm).

ST depression occurring in leads geometrically opposite to the territory of ST elevation in STEMI; serves as confirmatory evidence of true STEMI; example: inferior STEMI (elevation in II, III, aVF) produces reciprocal ST depression in I and aVL.

A randomised controlled trial of icosapentaenoic acid (EPA, 4 g/day) versus placebo in 8,179 statin-treated patients with TG 135–499 mg/dL and established CVD or diabetes; achieved 25% relative risk reduction in major adverse cardiovascular events at 4.9 years; established prescription-dose EPA as an adjunct to statin therapy for cardiovascular risk reduction in elevated TG.

Segmental reduction (hypokinesia), absence (akinesia), or paradoxical outward movement (dyskinesia) of left ventricular wall segments on echocardiography, corresponding to the territory supplied by the ischaemic or infarcted coronary artery.

Percutaneous coronary intervention performed after failed pharmacological thrombolysis, defined as <50% ST segment resolution at 60–90 minutes post-thrombolysis; indicated for persistent ischaemia after failed fibrinolysis; prevents further myocardial necrosis and reduces mortality compared to repeat thrombolysis.

The resumption of organised cardiac activity producing a palpable pulse, following cardiac arrest; confirmed by carotid or femoral pulse check; triggers transition from CPR to post-resuscitation care (12-lead ECG, TTM, ICU admission).

Severe skeletal muscle breakdown causing CK >40× upper reference limit, myoglobinuria (urine dipstick positive for haemoglobin in the absence of RBCs), and acute kidney injury from myoglobin-induced tubular toxicity; a rare (<0.1%) but life-threatening complication of statin therapy; requires immediate drug discontinuation and aggressive IV fluid resuscitation.

Infarction of the right ventricular free wall due to RCA occlusion proximal to the RV marginal branches; presents with the triad of hypotension, elevated JVP, and clear lung fields in inferior STEMI; diagnosed by ST elevation in right-sided lead V4R; managed with IV fluids, not diuretics.

A low-pitched third heart sound occurring in early diastole (after S2), caused by rapid ventricular filling in a dilated, poorly compliant ventricle; pathological in adults; a sign of left ventricular failure and correlates with Killip class II or higher in ACS.

A late diastolic (presystolic) heart sound caused by atrial contraction into a stiff, non-compliant ventricle; common in hypertensive heart disease and acute myocardial ischaemia; indicates LV diastolic dysfunction but is not specific to acute HF.

Cell-surface receptors on macrophages that bind and internalise oxidised LDL; unlike the classic LDL receptor, scavenger receptors are not subject to downregulation by intracellular cholesterol accumulation, leading to unregulated lipid uptake and foam cell formation.

A mnemonic for structured pain history: Site, Onset, Character, Radiation, Associated symptoms, Timing, Exacerbating/relieving factors, Severity; used to systematically characterise chest pain and discriminate cardiac from non-cardiac causes.

A spectrum of muscle adverse effects of statin therapy from myalgia (pain without CK elevation) through myositis (pain + CK 3–10× ULN) to rhabdomyolysis (CK >40× ULN + myoglobinuria + AKI); management depends on CK level and symptom severity; incidence increases with high dose, CYP3A4 inhibitor co-administration, hypothyroidism, and renal impairment.

An acute coronary syndrome caused by complete occlusion of an epicardial coronary artery; defined by new ST elevation ≥2 mm in ≥2 contiguous precordial leads or ≥1 mm in ≥2 contiguous limb leads (or new LBBB) plus troponin elevation; requires emergency reperfusion.

The process of identifying the culprit coronary artery based on the distribution of ST elevation in a 12-lead ECG: inferior leads (II, III, aVF) → RCA; precordial leads V1–V4 → LAD; lateral leads (I, aVL, V5–V6) → LCx; posterior leads V7–V9 → RCA or LCx; right-sided lead V4R → RV infarction.

Cooling comatose post-cardiac arrest patients to a core temperature of 32–36°C for 24 hours; shown to improve neurological survival after VF arrest (TTM trial); replaces 'therapeutic hypothermia' (strict 33°C target) with a broader 32–36°C target; avoided in severe cardiogenic shock.

Firm irregular lipid deposits in the Achilles, patellar, and extensor hand tendons; virtually pathognomonic of familial hypercholesterolaemia; caused by prolonged severely elevated LDL-C leading to cholesterol deposition in tendons.

A vulnerable atherosclerotic plaque characterised by a large necrotic lipid core and a fibrous cap thinner than 65 µm; highly susceptible to rupture and the precursor to most acute myocardial infarctions.

Pharmacological dissolution of coronary thrombus in STEMI using agents that activate plasminogen to plasmin (fibrinolytic cascade); indicated when primary PCI is not available within 120 minutes of first medical contact; door-to-needle target ≤30 minutes; agents: streptokinase, alteplase, tenecteplase, reteplase.

A reversible, direct-acting oral P2Y12 ADP receptor antagonist; loading dose 180 mg, maintenance 90 mg BD; preferred P2Y12 inhibitor in ACS (PLATO trial superiority over clopidogrel); contraindicated in prior intracranial haemorrhage and active bleeding; may cause dyspnoea (reversible, not bronchospasm).

A validated 7-point scoring system for NSTE-ACS that stratifies 14-day risk of death, MI, or urgent revascularisation; incorporates age, risk factors, prior coronary stenosis, ST deviation, anginal events, and troponin elevation.

Myocardial necrosis (troponin elevation) caused by ischaemia from conditions other than plaque rupture — e.g., severe tachyarrhythmia, hypotension, severe anaemia, vasospasm, coronary embolism — where myocardial oxygen demand exceeds supply; managed by treating the underlying cause, not with thrombolysis or PCI.

An acute coronary syndrome presenting as rest angina, new severe exertional angina, or crescendo angina, in which troponin is NOT elevated; ischaemia is transient without permanent myocardial necrosis; requires urgent investigation and treatment.

A partial agonist at the α4β2 nicotinic acetylcholine receptor; first-line pharmacotherapy for smoking cessation; doubles the quit rate at 12 months compared to placebo; safe in patients with established cardiovascular disease (EAGLES trial); may cause nausea — take with food.

A chaotic, disorganised cardiac rhythm with no effective cardiac output; the most common initial rhythm in witnessed sudden cardiac death; requires immediate CPR and defibrillation; survival probability decreases approximately 10% per minute without defibrillation.

A mechanical complication of large anterior MI (septal territory of LAD) due to rupture of the interventricular septum; presents as a harsh pansystolic murmur at the left sternal border with haemodynamic deterioration; distinguished from MR by murmur location and echocardiography; surgical repair required.

The pattern of myocardial necrosis progressing from the subendocardium (most ischaemia-vulnerable) to the epicardium over 3–6 hours of coronary occlusion; underlies the 'time is muscle' principle of ACS management — earlier reperfusion salvages more myocardium.

A post-ischaemic ECG pattern of deep symmetric T-wave inversions (type B) or biphasic T-waves (type A) in V2–V3, indicating critical proximal LAD stenosis that has transiently reperfused; the patient may be pain-free; stress testing is contraindicated — requires direct coronary angiography.

A clinical prediction rule for estimating pre-test probability of pulmonary embolism; incorporates clinical signs of DVT, likelihood of PE vs alternative diagnosis, heart rate >100, immobilisation, prior DVT/PE history, haemoptysis, and malignancy; scores <2 = low, 2–6 = moderate, >6 = high probability.