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

• 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
    1. Thrombolysis uses drugs to dissolve clots (tPA)
    2. 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