Atherosclerosis is a sneaky process that builds up over time, narrowing arteries and starving the heart of oxygen. It's like plaque slowly clogging pipes, but in your blood vessels. This gradual damage can lead to serious heart problems if left unchecked.
Coronary artery disease is the end result of atherosclerosis in the heart's arteries. When these vital blood vessels get too narrow, the heart muscle suffers. This can cause chest pain, heart attacks, and other complications that seriously impact your health and quality of life.
Atherosclerosis and Coronary Artery Disease
Pathophysiology of atherosclerosis
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Atherosclerosis development progresses through several stages
Endothelial dysfunction damages arterial lining initiates process
Lipid accumulation in arterial walls forms fatty streaks (LDL cholesterol)
Inflammatory response recruits immune cells (macrophages, T-cells)
Smooth muscle cell proliferation creates fibrous cap over lipid core
Plaque formation narrows artery lumen reduces blood flow
Progression of atherosclerosis in coronary arteries gradually worsens over time
Narrowing of arterial lumen decreases blood flow capacity
Reduced blood flow to myocardium leads to ischemia (oxygen deprivation)
Potential plaque rupture and thrombosis causes acute coronary events (heart attack)
Effects on coronary circulation impair heart function
Decreased oxygen supply to heart muscle reduces contractility
Impaired removal of metabolic waste products (lactic acid) further damages tissue
Process of myocardial ischemia
Myocardial ischemia occurs when oxygen demand exceeds supply
Imbalance between oxygen supply and demand stresses heart muscle
Causes: atherosclerosis, coronary vasospasm, or increased myocardial workload (hypertension )
Reversible if blood flow restored quickly (within minutes)
Progression to myocardial infarction happens if ischemia persists
Prolonged ischemia leads to cell death (necrosis ) of heart muscle
Necrosis begins after 20-40 minutes of ischemia spreads from endocardium to epicardium
Infarct expansion over several hours increases damaged area
Types of myocardial infarction classified by ECG changes
ST-elevation myocardial infarction (STEMI) indicates full-thickness damage
Non-ST-elevation myocardial infarction (NSTEMI) suggests partial-thickness injury
Risk Factors, Clinical Manifestations, and Management
Risk factors for coronary disease
Modifiable risk factors can be controlled or eliminated
Hypertension damages arterial walls increases plaque formation
Dyslipidemia contributes to cholesterol buildup in arteries
Smoking reduces oxygen in blood promotes plaque formation
Diabetes mellitus accelerates atherosclerosis through multiple mechanisms
Obesity increases strain on heart elevates other risk factors
Sedentary lifestyle weakens heart muscle reduces overall cardiovascular health
Non-modifiable risk factors cannot be changed
Age increases risk as arteries naturally stiffen over time
Male gender associated with earlier onset of CAD
Family history indicates genetic predisposition
Ethnicity affects risk (higher in South Asians, African Americans)
Clinical manifestations vary in severity and duration
Angina pectoris presents as chest pain or pressure (often radiating)
Dyspnea occurs due to reduced cardiac output
Fatigue results from inadequate blood supply to muscles
Palpitations may indicate arrhythmias
Nausea common in inferior wall MIs
Diaphoresis often accompanies acute coronary events
Complications of myocardial infarction
Complications can occur acutely or develop over time
Arrhythmias disrupt normal heart rhythm (ventricular fibrillation, atrial fibrillation)
Heart failure develops when damaged heart can't pump effectively
Cardiogenic shock results from severe pump failure
Ventricular rupture rare but often fatal complication
Pericarditis inflammation of heart lining can occur days after MI
Immediate management focuses on restoring blood flow and limiting damage
Oxygen therapy improves myocardial oxygenation
Pain management reduces myocardial oxygen demand (morphine)
Antiplatelet agents prevent further clot formation (aspirin, clopidogrel)
Anticoagulation reduces risk of additional thrombosis (heparin)
Reperfusion strategies aim to restore blood flow quickly
Thrombolysis uses drugs to dissolve clots (tPA)
Percutaneous coronary intervention (PCI) mechanically opens blocked arteries
Long-term management prevents future events and promotes recovery
Medication therapy reduces risk factors and supports heart function
Beta-blockers decrease heart rate and blood pressure
ACE inhibitors improve cardiac remodeling
Statins lower cholesterol levels
Lifestyle modifications address modifiable risk factors
Cardiac rehabilitation improves functional capacity and quality of life
Regular follow-up and monitoring detect complications early