Lesson 1Atrial arrhythmogenesis and thromboembolism in chronic atrial fibrillation: atrial remodelling, stasis, and stroke riskDetails how chronic atrial fibrillation alters atrial structure and function, promotes blood stasis, and increases thromboembolic risk, integrating remodelling biology with clinical stroke prediction, imaging, and anticoagulation strategies.
Electrical and structural atrial remodellingLoss of atrial kick and haemodynamic impactLeft atrial appendage stasis and clotCHA₂DS₂-VASc and bleeding risk scoresImaging of atrial thrombus and flowPathophysiology of cardioembolic strokeLesson 2Ischaemia pathophysiology in ST-elevation myocardial infarction (STEMI): plaque rupture, thrombosis, transmural infarction and inferior wall-specific anatomyCovers the sequence from plaque rupture to thrombotic occlusion and transmural infarction in STEMI, emphasising coronary anatomy, inferior wall vulnerability, right ventricular involvement, and implications for symptoms, ECG, and therapy.
Plaque rupture and thrombosis cascadeComplete occlusion and wavefront necrosisTransmural injury and ST-elevation patternsInferior wall blood supply and variantsRight ventricular infarction physiologyReperfusion injury and salvageable myocardiumLesson 3Interaction of common comorbidities (hypertension, diabetes, CKD, prior stroke, smoking, hyperlipidaemia) with cardiac pathophysiologyIntegrates how hypertension, diabetes, CKD, prior stroke, smoking, and hyperlipidaemia interact with cardiac structure, vessels, and haemostasis, accelerating atherosclerosis, remodelling, arrhythmias, and heart failure progression.
Hypertension and pressure overload LVHDiabetes, microvascular disease, and HFCKD, uraemic toxins, and volume overloadHyperlipidaemia and atherosclerotic burdenSmoking, endothelial injury, and thrombosisPrior stroke and cardio-cerebral interplayLesson 4Limitations of pathophysiologic models and translation to patients with multimorbidity and advanced ageDiscusses why classic pathophysiologic models may fail in older adults and multimorbid patients, highlighting altered reserves, polypharmacy, frailty, and competing risks that complicate diagnosis, risk prediction, and treatment choices.
Physiologic ageing and reduced reserveAtypical presentations in older patientsMultimorbidity and competing mechanismsPolypharmacy and altered drug responseRisk scores in heterogeneous populationsIndividualising goals and shared decisionsLesson 5Pharmacologic mechanisms: ACEi/ARB/ARNI, beta blockers, MRAs, SGLT2 inhibitors, antiplatelet and anticoagulant agents, reperfusion therapies and their physiologic effectsReviews mechanisms of major cardiovascular drug classes, linking receptor targets and signalling pathways to haemodynamic, neurohormonal, and antithrombotic effects, and explaining how these translate into symptom relief and outcome benefits.
RAAS blockade with ACEi, ARB, and ARNIBeta-blockers and sympathetic modulationMRAs and aldosterone-driven remodellingSGLT2 inhibitors and cardiorenal effectsAntiplatelet pathways and platelet inhibitionAnticoagulants and coagulation cascade targetsLesson 6Haemodynamic consequences of reduced LVEF: preload, afterload, contractility, and congestion explaining dyspnoea, orthopnoea, JVP, crackles, oedemaExplains how reduced left ventricular ejection fraction alters preload, afterload, and contractility, producing congestion and low output, and connects these changes to bedside signs such as dyspnoea, orthopnoea, JVP elevation, crackles, and oedema.
Frank–Starling curve in systolic failureAfterload, arterial tone, and LV performanceNeurohormonal responses to low outputPulmonary venous hypertension and dyspnoeaSystemic venous congestion and oedemaJVP, hepatojugular reflux, and exam cluesLesson 7Physiologic basis for diagnostic test findings: ECG changes (LVH, inferior ST-elevations, AF), echo findings in HFrEF and wall-motion abnormalities, biomarkers (troponin, BNP/NT-proBNP)Explores how underlying cardiac physiology produces characteristic ECG, echocardiographic, and biomarker patterns, enabling learners to interpret LVH, ischaemia, atrial fibrillation, and heart failure findings in a mechanistic, clinically useful way.
Voltage criteria and repolarisation in LVHInferior ST-elevation and coronary anatomyAF mechanisms and ECG irregularityEcho features of HFrEF and wall motionTroponin kinetics and myocardial necrosisBNP/NT-proBNP and wall stress physiologyLesson 8Cardiac remodelling and systolic dysfunction mechanisms leading to heart failure with reduced ejection fraction (HFrEF)Describes molecular, cellular, and structural processes driving cardiac remodelling and systolic dysfunction in HFrEF, including neurohormonal activation, myocyte injury, fibrosis, and chamber dilation, and how these changes worsen pump performance.
Myocyte loss, apoptosis, and necrosisHypertrophy, dilation, and geometry changeFibrosis, stiffness, and conduction delayNeurohormonal drivers of remodellingMitral regurgitation from LV dilationReverse remodelling with guideline therapy
