Lesson 1Atrial arrhythmogenesis and thromboembolism in chronic atrial fibrillation: atrial remodeling, stasis, and stroke riskThis lesson explains how long-term atrial fibrillation changes the heart's upper chambers, causes blood to pool, and raises clot and stroke risks, combining biology with tools for predicting strokes, imaging, and blood-thinning treatments suitable for Eritrean patients.
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 2Ischemia pathophysiology in ST-elevation myocardial infarction (STEMI): plaque rupture, thrombosis, transmural infarction and inferior wall-specific anatomyThis lesson covers the process from artery plaque breaking to full blockage and deep heart muscle damage in STEMI, focusing on blood vessel layout, risks in the lower heart wall, right ventricle effects, and how this affects signs, heart tracings, and care in local settings.
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, hyperlipidemia) with cardiac pathophysiologyThis lesson shows how high blood pressure, diabetes, kidney disease, past strokes, smoking, and high fats in blood affect heart structure, vessels, and clotting, speeding up artery hardening, heart changes, irregular beats, and heart failure in Eritrean contexts.
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 ageThis lesson discusses why standard heart disease models may not fit older or multi-ill patients in Eritrea, noting reduced body reserves, many medicines, weakness, and other risks that make diagnosis, prediction, and treatment more challenging.
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 effectsThis lesson reviews how key heart medicines work, from blocking hormones to calming nerves and preventing clots, linking their actions to blood flow improvements, hormone balance, and clot prevention, and how they ease symptoms and better outcomes in practice.
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 6Hemodynamic consequences of reduced LVEF: preload, afterload, contractility, and congestion explaining dyspnea, orthopnea, JVP, crackles, edemaThis lesson describes how weak heart pumping affects blood filling, resistance, and squeezing, causing fluid buildup and poor flow, and links these to signs like shortness of breath, lying-flat discomfort, neck vein swelling, lung sounds, and swelling in legs.
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)This lesson explores how heart changes create specific patterns on heart tracings, ultrasound images, and blood tests, helping interpret thickened heart walls, blocked arteries, irregular beats, weak pumping, and failure signs in a practical way for clinicians.
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 remodeling and systolic dysfunction mechanisms leading to heart failure with reduced ejection fraction (HFrEF)This lesson details cell and tissue changes causing heart reshaping and weak squeezing in HFrEF, including hormone surges, cell death, scarring, and chamber widening, and how these reduce heart efficiency over time in affected individuals.
Myocyte loss, apoptosis, and necrosisHypertrophy, dilation, and geometry changeFibrosis, stiffness, and conduction delayNeurohormonal drivers of remodelingMitral regurgitation from LV dilationReverse remodeling with guideline therapy
