Lesson 1Atrial arrhythmogenesis and thromboembolism in chronic atrial fibrillation: atrial remodelling, stasis, and stroke riskExplores how persistent atrial fibrillation modifies atrial architecture and performance, fosters blood stagnation, and heightens the risk of thromboembolism, combining insights into remodelling processes with clinical tools for stroke forecasting, imaging techniques, and anticoagulation approaches.
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 anatomyExamines the progression from plaque disruption to thrombotic blockage and full-thickness infarction in STEMI, highlighting coronary vascular layout, the susceptibility of the inferior wall, right ventricular participation, and their effects on symptoms, ECG findings, and therapeutic interventions.
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 pathophysiologyExamines the ways in which hypertension, diabetes, chronic kidney disease, previous stroke, smoking, and hyperlipidaemia influence cardiac anatomy, vasculature, and clotting mechanisms, hastening the development of atherosclerosis, remodelling, arrhythmias, and the advancement of heart failure.
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 ageAnalyses the shortcomings of traditional pathophysiologic frameworks in elderly patients with multiple conditions, underscoring diminished physiological reserves, multiple medications, frailty, and overlapping risks that hinder accurate diagnosis, risk assessment, and selection of treatments.
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 effectsSurveys the actions of principal cardiovascular medication categories, associating receptor sites and signalling routes with haemodynamic, neurohormonal, and anti-clotting outcomes, and clarifying how these contribute to alleviating symptoms and enhancing clinical results.
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, oedemaDescribes how diminished left ventricular ejection fraction disrupts preload, afterload, and contractility, resulting in congestion and reduced cardiac output, and relates these alterations to clinical indicators like dyspnoea, orthopnoea, elevated JVP, 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)Investigates how fundamental cardiac physiology generates distinctive ECG, echocardiographic, and biomarker profiles, allowing learners to analyse LVH, ischaemia, atrial fibrillation, and heart failure observations through a mechanistic lens for practical clinical application.
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)Outlines the molecular, cellular, and anatomical mechanisms propelling cardiac remodelling and systolic impairment in HFrEF, encompassing neurohormonal stimulation, myocyte damage, fibrosis, and chamber expansion, and their role in deteriorating pump efficiency.
Myocyte loss, apoptosis, and necrosisHypertrophy, dilation, and geometry changeFibrosis, stiffness, and conduction delayNeurohormonal drivers of remodellingMitral regurgitation from LV dilationReverse remodelling with guideline therapy
