Heart Disease: Must Knows

## Summary Heart disease encompasses various conditions that impair the heart's ability to effectively pump blood. Heart failure can arise from six primary mechanisms, including pump failure (systolic or diastolic), obstruction to flow, regurgitant flow, shunted flow, conduction disorders, or rupture. Congestive Heart Failure (CHF) is defined by the heart's inability to meet metabolic demands, often due to systolic or diastolic dysfunction, and triggers compensatory mechanisms like the Frank-Starling law, neurohumoral activation, and hypertrophy. While these initially maintain output, chronic hypertrophy can be pathological and lead to increased oxygen demand and sudden cardiac death. Left-sided heart failure typically presents with pulmonary congestion (dyspnea, orthopnea) and is often caused by ischemic heart disease (IHD) or hypertension, leading to "heart failure cells" in the lungs. Right-sided heart failure, frequently secondary to left-sided failure or pulmonary hypertension (cor pulmonale), manifests as systemic venous congestion, including peripheral edema and "nutmeg liver." Ischemic Heart Disease (IHD), primarily caused by coronary atherosclerosis, represents an imbalance between myocardial oxygen supply and demand and is a leading cause of death worldwide. Its pathogenesis involves plaque formation, thrombosis following plaque disruption (often in plaques previously deemed non-critical), and vasospasm. "Vulnerable plaques" with large lipid cores and thin fibrous caps are prone to rupture, leading to acute coronary syndromes like unstable angina, acute myocardial infarction (MI), and sudden cardiac death. Stable angina, Prinzmetal angina, and chronic IHD are other clinical manifestations. Understanding these mechanisms, clinical presentations, and morphological changes is crucial for managing heart disease, which often progresses to biventricular CHF in its advanced stages. ## Key Points - **Pump failure**: Impaired cardiac output due to weak contraction (systolic) or impaired relaxation (diastolic). - **Congestive Heart Failure (CHF)**: Heart cannot generate sufficient output for metabolic needs, or only at elevated filling pressures. - **Forward failure**: Decreased cardiac output, almost always accompanied by backward failure (venous congestion). - **Concentric hypertrophy**: Sarcomeres added in parallel, caused by pressure overload (e.g., hypertension, valve stenosis). - **Eccentric/dilated hypertrophy**: Sarcomeres added in series, caused by volume overload (e.g., regurgitation, shunts). - **Heart failure cells**: Hemosiderin-laden macrophages found in the lungs, indicative of chronic left-sided CHF and pulmonary edema. - **Nutmeg liver**: Gross appearance of the liver in right-sided CHF, characterized by centrilobular congestion. - **Cor pulmonale**: Right ventricular hypertrophy and dilation due to pulmonary hypertension, an isolated right-sided pathology. - **Ischemic Heart Disease (IHD)**: Imbalance between coronary blood supply and myocardial oxygen demand, primarily due to coronary atherosclerosis. - **Critical stenosis**: >70% occlusion of a coronary artery, typically causing symptoms with exertion (stable angina). - **Vulnerable plaque**: Atherosclerotic plaque with a large lipid core, thin fibrous cap, and high macrophage load, prone to rupture. - **Acute coronary syndrome**: A spectrum of conditions including unstable angina, acute myocardial infarction, and sudden cardiac death, often initiated by plaque disruption and thrombosis. ## Detailed Notes ### OVERVIEW: 6 MECHANISMS OF HEART FAILURE 1. **Pump failure** — systolic (weak contraction) or diastolic (impaired relaxation) 2. **Obstruction to flow** — valve stenosis, hypertension, coarctation 3. **Regurgitant flow** — backward flow → volume overload 4. **Shunted flow** — abnormal chamber-to-chamber communication 5. **Conduction disorders** — arrhythmias → reduced output 6. **Rupture** — loss of circulatory continuity → exsanguination ### CONGESTIVE HEART FAILURE (CHF) **Definition:** Heart cannot generate sufficient output to meet metabolic demands — OR can only do so at elevated filling pressures **Epidemiology:** ~5 million affected in USA; >1 million hospitalizations/year; 300,000 deaths/year **Causes:** - Systolic dysfunction (most common) — ischemic heart disease, hypertension - Diastolic dysfunction — LV hypertrophy, fibrosis, amyloid, constrictive pericarditis; more common in elderly, diabetics, women; accounts for **40–60% of CHF** - High-output failure — hyperthyroidism, anemia **Key concept:** Forward failure (↓ output) is almost always accompanied by backward failure (venous congestion) #### Compensatory Mechanisms | Mechanism | Details | | :---------------- | :--------------------------------------------------------------- | | Frank-Starling | ↑ end-diastolic volume → ↑ stretch → ↑ contraction force | | Neurohumoral | Norepinephrine (↑ HR, contractility); RAAS (salt