Lesson 1Atrial arrhythmogenesis and thromboembolism in chronic atrial fibrillation: atrial remodeling, stasis, and stroke riskExplains how long-term atrial fibrillation changes the heart's atrial structure and function, causes blood to pool, and raises clot and stroke risks, combining biology of changes with clinical tools for predicting strokes, imaging, and blood-thinning treatments.
Electrical and structural atrial changesLoss of atrial push and blood flow effectsLeft atrial pouch pooling and clotsCHA₂DS₂-VASc and bleeding risk toolsImaging clots and blood flowBiology of heart-related strokesLesson 2Ischaemia pathophysiology in ST-elevation myocardial infarction (STEMI): plaque rupture, thrombosis, transmural infarction and inferior wall-specific anatomyCovers the process from plaque breaking to clot blockage and full-wall heart damage in STEMI, focusing on heart vessel layout, lower wall weaknesses, right ventricle involvement, and effects on symptoms, ECG readings, and treatments.
Plaque break and clot formation chainFull blockage and wave of cell deathFull-wall damage and ST-lift patternsLower wall blood supply and variationsRight ventricle damage biologyReopening injury and savable heart tissueLesson 3Interaction of common comorbidities (hypertension, diabetes, CKD, prior stroke, smoking, hyperlipidaemia) with cardiac pathophysiologyShows how high blood pressure, diabetes, kidney disease, past strokes, smoking, and high fats interact with heart structure, vessels, and clotting, speeding up artery hardening, heart changes, irregular beats, and heart failure worsening.
High blood pressure and pressure strain on left heart thickeningDiabetes, small vessel disease, and heart failureKidney disease, waste toxins, and fluid overloadHigh fats and artery clogging loadSmoking, vessel lining damage, and clotsPast stroke and heart-brain connectionsLesson 4Limitations of pathophysiologic models and translation to patients with multimorbidity and advanced ageDiscusses why standard disease models may not work well for older people with many health issues, pointing out reduced body reserves, multiple medicines, weakness, and other risks that make diagnosis, risk guessing, and treatment harder.
Body ageing and lower reservesUnusual signs in older patientsMany illnesses and overlapping causesMultiple drugs and changed medicine effectsRisk tools in mixed groupsPersonalising aims and joint choicesLesson 5Pharmacologic mechanisms: ACEi/ARB/ARNI, beta blockers, MRAs, SGLT2 inhibitors, antiplatelet and anticoagulant agents, reperfusion therapies and their physiologic effectsLooks at how main heart drug groups work, connecting targets and pathways to blood flow, hormone, and anti-clot effects, and how these lead to better symptoms and results.
RAAS block with ACEi, ARB, and ARNIBeta-blockers and nerve system controlMRAs and hormone-driven heart changesSGLT2 blockers and heart-kidney effectsAntiplatelet paths and clot preventionAnticoagulants and clotting chain targetsLesson 6Haemodynamic consequences of reduced LVEF: preload, afterload, contractility, and congestion explaining dyspnoea, orthopnoea, JVP, crackles, oedemaExplains how lower left heart pumping changes preload, afterload, and squeezing power, causing fluid buildup and low output, linking to signs like shortness of breath, lying-down breathing trouble, neck vein rise, lung noises, and swelling.
Frank–Starling curve in pump failureAfterload, vessel tone, and left heart workHormone responses to low outputLung vein high pressure and breathlessnessBody vein fluid buildup and swellingNeck vein, liver push, and exam signsLesson 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 heart biology creates typical ECG, heart scan, and marker patterns, helping interpret left heart thickening, lack of blood, irregular beats, and failure signs in a practical way.
Voltage signs and recovery in left heart thickeningLower ST-lift and vessel layoutAF causes and ECG unevennessHeart scan signs of HFrEF and wall movementTroponin timing and heart cell deathBNP/NT-proBNP and wall strain biologyLesson 8Cardiac remodelling and systolic dysfunction mechanisms leading to heart failure with reduced ejection fraction (HFrEF)Describes cell, tissue, and structure processes causing heart remodelling and pump weakness in HFrEF, including hormone activation, cell damage, scarring, chamber widening, and how these harm pumping.
Heart cell loss, death, and breakdownThickening, widening, and shape shiftsScarring, stiffness, and beat delaysHormone causes of remodellingValve leak from left chamber wideningReversing changes with standard treatments
