Summary These comprehensive notes cover MBChB-level cardiovascular pathology, focusing on common diseases affecting the heart and blood vessels. Topics include
Summary These comprehensive notes cover MBChB-level cardiovascular pathology, focusing on common diseases affecting the heart and blood vessels. Topics include atherosclerosis, ischemic heart disease, valvular disorders, cardiomyopathies, and congenital anomalies, providing detailed information essential for examination preparation. This document outlines definitions, risk factors, pathogenesis, morphology, clinical manifestations, and complications for a thorough understanding of each condition. Key Points - Atherosclerosis is a chronic inflammatory disease of arteries, driven by endothelial injury and lipid accumulation, leading to the formation of fibrofatty plaques and significant cardiovascular complications. - Ischemic heart disease, primarily caused by coronary atherosclerosis, manifests as angina or myocardial infarction, with distinct pathological changes over time and various life-threatening complications. - Valvular heart diseases, such as those arising from rheumatic fever or degenerative calcification, involve stenosis or regurgitation, profoundly affecting cardiac function and often leading to heart failure or emboli. - Cardiomyopathies are primary myocardial diseases, classified into dilated, hypertrophic, and restrictive types, each presenting with unique structural and functional abnormalities that can result in heart failure, arrhythmias, or sudden death. - Congenital heart defects range from simple shunts to complex structural anomalies, impacting blood flow and oxygenation, necessitating early diagnosis and often surgical intervention to prevent long-term complications like Eisenmenger syndrome. Detailed Notes TOPIC 1: ATHEROSCLEROSIS & ARTERIOSCLEROSIS Definitions - Arteriosclerosis – General term for hardening and loss of elasticity of arterial walls - Atherosclerosis – Most important form; a chronic inflammatory disease of large and medium arteries characterized by formation of atheromatous plaques in the intima Risk Factors Non-modifiable: - Age (men 45, women 55) - Male sex - Family history/genetics - Race Modifiable: - Hypertension - Hyperlipidemia (high LDL, low HDL) - Diabetes mellitus - Cigarette smoking - Obesity - Sedentary lifestyle - Homocysteinemia Pathogenesis — Response to Injury Hypothesis 1. Endothelial injury/dysfunction caused by: hypertension, smoking, hyperlipidemia, toxins 2. Increased permeability → LDL enters intima → oxidized to ox-LDL 3. Endothelium expresses adhesion molecules (VCAM-1, ICAM-1) 4. Monocytes adhere and migrate into intima → become macrophages 5. Macrophages engulf ox-LDL → become foam cells → fatty streak (earliest lesion, reversible) 6. Macrophages release cytokines and growth factors → stimulate smooth muscle cell (SMC) migration from media to intima 7. SMCs proliferate and produce extracellular matrix (collagen, proteoglycans) 8. Formation of fibrofatty plaque (atheromatous plaque) Morphology of an Atheromatous Plaque - Fibrous cap – SMCs and dense collagen (overlying the lesion) - Necrotic core – lipid debris, foam cells, cholesterol crystals, dead cells - Shoulder region – active inflammation (macrophages, T cells) - Neovascularization at base Vulnerable (Unstable) Plaque - Thin fibrous cap - Large lipid core - Many inflammatory cells - Prone to rupture → thrombosis → acute coronary syndrome Progression of Atherosclerosis 1. Normal artery 2. Endothelial dysfunction 3. Fatty streak – flat yellow intimal lesion; foam cells; reversible 4. Fibrofatty plaque – raised yellow-white lesion; fibrous cap + lipid core 5. Complicated plaque – calcification, ulceration, thrombosis, hemorrhage Complications of Atherosclerosis - Myocardial infarction (coronary arteries) - Stroke (cerebral/carotid arteries) - Peripheral arterial disease (lower limbs) - Aortic aneurysm (aorta) - Mesenteric ischemia (mesenteric arteries) - Renal artery stenosis → renovascular hypertension Types of Arteriosclerosis 1. Hyaline arteriolosclerosis – Homogeneous pink hyaline thickening of arteriolar walls; seen in benign hypertension and diabetes mellitus 2. Hyperplastic arteriolosclerosis – "Onion-skin" concentric laminated thickening; seen in malignant (severe) hypertension; causes marked luminal narrowing 3. Monckeberg medial calcific sclerosis – Calcification of the media of muscular arteries; does NOT narrow lumen; not clinically significant usually; seen in elderly --- TOPIC 2: ISCHEMIC HEART DISEASE (IHD) Definition A group of conditions resulting from imbalance between myocardial oxygen supply and demand , most commonly due to coronary atherosclerosis. Causes - Coronary atherosclerosis ( 90% of cases) - Coronary vasospasm ( Prinzmetal angina ) - Thromboembolism - Coronary artery anomalies - Severe anemia - Aortic stenosis (reduced coronary perfusion) Types of IHD 1. Stable (Chronic) Angina - Fixed atherosclerotic stenosis ( 70% occlusion) - Predictable chest pain on exertion, relieved by rest or nitrates - No myocardial necrosis - Caused by demand exceeding supply 2. Unstable Angina - Part of Acute Coronary Syndrome (ACS) - Plaque rupture + partial thrombosis - Chest pain at rest or minimal exertion - Increasing frequency and severity - No myocardial necrosis ( troponin negative usually) 3. Myocardial Infarction (MI) - Part of ACS - Irreversible ischemic necrosis of myocardium - Complete occlusion of coronary artery - Troponin positive 4. Sudden Cardiac Death - Death within 1 hour of symptom onset - Usually due to fatal arrhythmia ( ventricular fibrillation ) - Most common cause: severe coronary atherosclerosis - May be first manifestation of IHD Myocardial Infarction — In Detail Types by Depth - STEMI (ST-elevation MI) — Transmural infarct ; full thickness of myocardial wall; complete occlusion - NSTEMI (Non-ST-elevation MI) — Subendocardial infarct ; inner 1/3 of wall; partial occlusion Most Commonly Affected Vessel - Left anterior descending (LAD) artery — most common (~50%); anterior wall + interventricular septum - Right coronary artery (RCA) — posterior/inferior wall - Left circumflex artery — lateral wall Pathological Timeline of MI (MUST KNOW) Time Gross Appearance Microscopic Changes --- --- --- 0–6 hours Normal (invisible) Wavy myofibers, early coagulative necrosis 6–24 hours Pale/pallor Coagulative necrosis; pyknotic nuclei; wavy fibers 1–3 days Yellow-tan softening Neutrophil infiltration (peak at 24–72h) 3–7 days Hyperemic border, yellow-soft center Macrophage infiltration ; removal of necrotic debris; highest risk of rupture 1–2 weeks Depressed, red-gray Granulation tissue formation; new capillaries; fibroblasts Weeks–months Gray-white scar Dense fibrous scar (collagen replacement) Complications of MI (MUST KNOW) - Arrhythmias — Most common cause of death in first 24 hours; ventricular fibrillation - Left ventricular failure → pulmonary edema - Cardiogenic shock — large infarct ( 40% LV) - Myocardial rupture — Day 3–7; cardiac tamponade; free wall most common - Papillary muscle rupture → acute mitral regurgitation - Interventricular septal rupture → left-to-right shunt - Ventricular aneurysm — bulging thin fibrotic wall; late complication; risk of thrombus - Pericarditis — early (fibrinous, days 2–3) or late ( Dressler syndrome , weeks later — autoimmune) - Mural thrombus → systemic emboli → stroke - Reinfarction Biochemical Markers of MI - Troponin I & T — most sensitive and specific; rises 3–6 hours, peaks 12–24h, stays elevated 7–10 days - CK-MB — rises 4–8 hours, peaks 24h, returns to normal by 72h; used to detect reinfarction - LDH — late marker; rises 24–48h, peaks 3–6 days - Myoglobin — earliest marker (1–4h) but not specific --- TOPIC 3: HYPERTENSIVE HEART DISEASE Definition Cardiac and vascular changes resulting from sustained systemic arterial hypertension (BP 140/90 mmHg). Systemic Hypertensive Heart Disease Pathological changes in the heart: - Left ventricular hypertrophy (LVH) — concentric hypertrophy; increased wall thickness; normal cavity size initially - LVH → increased oxygen dema