Explore concise notes on common heart pathologies: ischemic disease, cardiomyopathies, valvular disorders, congenital defects, and inflammatory conditions. Cove
Summary This document provides a concise overview of common heart pathologies, ranging from ischemic heart disease and myocardial infarction to various cardiomyopathies, valvular disorders, and congenital defects. It also covers infectious and inflammatory conditions like endocarditis and rheumatic heart disease, as well as diseases affecting the pericardium, aorta, and vasculature. Key diagnostic features, causes, complications, and treatments are highlighted for each condition. Key Points - Myocardial infarction has a predictable timeline of changes and complications, with arrhythmias being the leading cause of early death and rupture risks peaking at 3-5 days. - Cardiomyopathies are diverse, with dilated cardiomyopathy being the most common and hypertrophic cardiomyopathy frequently causing sudden cardiac death in young athletes. - Valvular heart disease often stems from rheumatic fever, calcification, or congenital issues, leading to distinct murmurs and complications. - Infective endocarditis is classified by pathogen and valve involvement, while non-infective forms are linked to systemic conditions like SLE or malignancy. - Congenital heart defects are categorized by shunting patterns, with VSD being the most common overall and Tetralogy of Fallot as the most common cyanotic defect. Detailed Notes 1. Ischemic Heart Disease Ischemic heart disease is primarily caused by atherosclerosis , which involves plaque rupture leading to thrombus formation and subsequent coronary occlusion. Foam cells , which are macrophages engulfing oxidized LDL, contribute to the formation of a fatty streak that progresses to a fibrous plaque . The subendocardium is the most vulnerable region to ischemia. Coronary territories: - LAD → anterior LV, anterior septum - RCA → posterior LV, SA/AV nodes - LCx → lateral LV 2. Myocardial Infarction Biomarkers: - Troponin I — rises 2–4hrs, peaks 24hrs, lasts 10 days. It is the most specific biomarker. - CK-MB — rises 4–6hrs, back to normal in 48–72hrs. This marker is useful for detecting reinfarction. - Myoglobin — first to rise (1–2hrs), but it is not specific. Timeline: Time Changes --- --- 0–4 hrs Nothing visible 4–24 hrs Coagulative necrosis, neutrophils 1–3 days Fibrinous pericarditis 3–5 days Macrophages; risk of rupture (free wall, VSD, papillary muscle) 1–2 weeks Granulation tissue 4–6 weeks Dense fibrous scar Complications: - 0–24 hrs: Arrhythmia ( VF ) — the 1 cause of early death. - 3–5 days: Free wall rupture → tamponade ; VSD rupture ; papillary muscle rupture → acute MR . - Weeks later: Dressler syndrome (autoimmune pericarditis, fever, pleuritis). - Late: Ventricular aneurysm , mural thrombus → embolism . 3. Heart Failure Left HF: Results in pulmonary congestion , manifesting as dyspnea , orthopnea , paroxysmal nocturnal dyspnea (PND) , and hemoptysis . The lung tissue often shows hemosiderin-laden macrophages (also known as heart failure cells ). Right HF: The most common cause is left HF . Clinical signs include jugular venous distention (JVD) , peripheral edema , hepatomegaly , and ascites . The liver characteristically shows a nutmeg appearance . Hypertrophy: - Pressure overload (e.g., HTN, AS) leads to concentric hypertrophy , where sarcomeres are added in parallel. - Volume overload (e.g., AR, MR) leads to eccentric hypertrophy , where sarcomeres are added in series. 4. Cardiomyopathies Dilated (DCM): This is the most common cardiomyopathy, characterized by dilation of all 4 chambers and a low ejection fraction. Causes include alcohol , Coxsackievirus B , doxorubicin , peripartum state, Chagas disease ( Trypanosoma cruzi ), and thiamine deficiency (beriberi) . Hypertrophic (HCM): An autosomal dominant condition often caused by a beta-myosin heavy chain mutation . It presents with asymmetric septal hypertrophy and myofiber disarray . HCM is the 1 cause of sudden cardiac death in young athletes. It creates a dynamic LVOT obstruction that worsens with decreased preload (e.g., standing, Valsalva maneuver). The murmur associated with HCM decreases with squatting, fluids, or leg raise. Restrictive: Characterized by stiff ventricles and diastolic dysfunction, but with a normal ejection fraction. Causes include amyloidosis (most common in the developed world), endomyocardial fibrosis (most common worldwide, particularly in tropical Africa), sarcoidosis , and hemochromatosis . 5. Valvular Disease Mitral Stenosis: The 1 cause is rheumatic heart disease . It presents with an opening snap followed by a mid-diastolic rumble at the apex. Complications include atrial fibrillation (AF) , pulmonary hypertension (PHTN) , hemoptysis , and systemic emboli . Mitral Regurgitation: Causes include mitral valve prolapse (MVP) , rheumatic fever , papillary muscle rupture post-MI , and dilated cardiomyopathy (DCM) . It produces a holosystolic murmur radiating to the axilla. Mitral Valve Prolapse: This is the most common valvular disease in young women. It is characterized by a midsystolic click followed by a late systolic murmur . It is associated with Marfan syndrome and anxiety. Aortic Stenosis: In the elderly, it is typically due to calcific degeneration . In young individuals, it is often caused by a bicuspid aortic valve . The classic SAD triad of symptoms includes Syncope , Angina , and Dyspnea . It produces a harsh systolic murmur heard at the right upper sternal border, radiating to the carotids. Aortic Regurgitation: Causes include Marfan syndrome , syphilis , aortic dissection , and rheumatic fever . It presents with an early diastolic decrescendo murmur at the left sternal border and a wide pulse pressure , leading to signs like Corrigan pulse , De Musset sign , and Quincke sign . 6. Endocarditis Infective: - Acute: Typically caused by S. aureus , leading to destruction of normal valves with a rapid course. - Subacute: Usually caused by S. viridans , affecting previously damaged valves with a slower course. - In IV drug users , the tricuspid valve is commonly affected. - Signs include fever , a new murmur , Osler nodes (painful lesions on fingers/toes), Janeway lesions (painless lesions on palms/soles), Roth spots (retinal hemorrhages), and splinter hemorrhages under the nails. Non-infective: - Libman-Sacks: Associated with SLE , affecting both sides of the mitral valve . - Marantic (NBTE - Nonbacterial Thrombotic Endocarditis): Seen in patients with malignancy or debilitating illness, involving the valve edges. - Carcinoid: Primarily affects right-sided valves because serotonin is inactivated in the lungs, preventing left-sided involvement. - Rheumatic: Involves the mitral valve and chordae tendineae. 7. Rheumatic Heart Disease Rheumatic heart disease develops following Group A Strep pharyngitis due to an autoimmune cross-reaction via molecular mimicry . Pathognomonic findings include Aschoff bodies containing Anitschkow cells (also known as caterpillar cells). The Jones criteria (major) for diagnosis include Carditis , Polyarthritis , Chorea , Erythema marginatum , and Subcutaneous nodules . The valves affected, in order of frequency, are Mitral Aortic Tricuspid . The most common late complication is mitral stenosis . 8. Congenital Heart Disease Left-to-right shunts (acyanotic — blue later): - VSD: The most common congenital heart defect (30%), producing a holosystolic murmur . - ASD: Characterized by a fixed split S2 , with ostium secundum being the most common type. - PDA: Presents with a continuous machine-like murmur . It can be closed with indomethacin and kept open with PGE1 . Right-to-left shunts (cyanotic — blue early) — 5 T's: - Tetralogy of Fallot: Includes VSD + RVH (right ventricular hypertrophy) + overriding aorta + pulmonary stenosis . It causes a boot-shaped heart on CXR and is the most common cyanotic CHD. Treatment involves PGE1 to maintain PDA for pulmonary blood flow. - Transposition of Great Arteries: The aorta arises from the RV and the PA from the LV. It presents with an egg-on-string CXR . Treatmen