Lesson 1Atrial arrhythmogenesis and thromboembolism in chronic atrial fibrillation: atrial remodelling, stasis, and stroke riskExplains how chronic atrial fibrillation changes atrial structure and function, causes blood stasis, and raises thromboembolic risk, combining remodelling biology with clinical stroke prediction, imaging, and anticoagulation approaches.
Electrical and structural atrial remodelingLoss of atrial kick and hemodynamic 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 process from plaque rupture to thrombotic blockage and transmural infarction in STEMI, focusing on coronary anatomy, inferior wall risks, right ventricular involvement, and effects on symptoms, ECG, and treatment.
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 pathophysiologyShows how hypertension, diabetes, CKD, prior stroke, smoking, and hyperlipidaemia affect cardiac structure, vessels, and clotting, speeding up atherosclerosis, remodelling, arrhythmias, and heart failure worsening.
Hypertension and pressure overload LVHDiabetes, microvascular disease, and HFCKD, uremic toxins, and volume overloadHyperlipidemia 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 standard pathophysiologic models may not work well in elderly and multimorbid patients, noting reduced reserves, multiple medicines, frailty, and competing risks that complicate diagnosis, risk assessment, and treatment choices.
Physiologic aging and reduced reserveAtypical presentations in older patientsMultimorbidity and competing mechanismsPolypharmacy and altered drug responseRisk scores in heterogeneous populationsIndividualizing goals and shared decisionsLesson 5Pharmacologic mechanisms: ACEi/ARB/ARNI, beta blockers, MRAs, SGLT2 inhibitors, antiplatelet and anticoagulant agents, reperfusion therapies and their physiologic effectsReviews how major cardiovascular drug classes work, linking receptor targets and pathways to haemodynamic, neurohormonal, and anti-clotting effects, and how these lead to symptom relief and better outcomes.
RAAS blockade with ACEi, ARB, and ARNIBeta-blockers and sympathetic modulationMRAs and aldosterone-driven remodelingSGLT2 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 low left ventricular ejection fraction affects preload, afterload, and contractility, causing congestion and low output, and links these to clinical signs like dyspnoea, orthopnoea, raised JVP, crackles, and oedema.
Frank–Starling curve in systolic failureAfterload, arterial tone, and LV performanceNeurohormonal responses to low outputPulmonary venous hypertension and dyspneaSystemic venous congestion and edemaJVP, 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)Shows how cardiac physiology creates typical ECG, echo, and biomarker patterns, helping interpret LVH, ischaemia, atrial fibrillation, and heart failure findings in a practical, mechanism-based way.
Voltage criteria and repolarization 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 changes driving cardiac remodelling and systolic dysfunction in HFrEF, including neurohormonal activation, myocyte damage, fibrosis, chamber dilation, and reduced pump function.
Myocyte loss, apoptosis, and necrosisHypertrophy, dilation, and geometry changeFibrosis, stiffness, and conduction delayNeurohormonal drivers of remodelingMitral regurgitation from LV dilationReverse remodeling with guideline therapy
