Coronary Heart Disease (CHD) Overview

Coronary Heart Disease (CHD)

• Caused by impaired coronary blood flow, often due to atherosclerosis
• Coronary circulation involves coronary arteries that arise from the coronary sinus above the aortic valve
• Left and right coronary arteries supply the heart, with the left artery supplying the left ventricle and interventricular septum

Coronary Atherosclerosis and Pathogenesis of Coronary Artery Disease

• Two types of atherosclerosis lesions:
  • Stable or fixed plaque (stable angina)
  • Unstable plaque (unstable angina; MI) that can rupture and cause thrombus formation

Stable Angina (Angina Pectoris)

• Initial manifestation of ischemic heart disease in half of CHD cases
• Precipitated by situations that increase the heart's workload (exercise, cold, stress)
• Pain is constricting, squeezing, or suffocating, and is relieved by rest or nitroglycerine
• Typically located in the pericardial or substernal area of the chest and may radiate to the left side

Variant or Vasospastic Angina

• Caused by spasms of the coronary arteries
• Occurs in the absence of visible disease
• May be caused by a hyperactive sympathetic nervous system or a defect in calcium handling in vascular smooth muscle

Acute Coronary Syndrome

• Determining the risk of acute myocardial infarction (AMI) depends on presenting characteristics, ECG variables, serum cardiac markers, and timing of presentation
• ECG changes:
  • T wave and ST segment changes occur first during myocardial ischemia or injury
  • Q wave changes appear later and persist
• Serum markers:
  • Creatine Kinase MB (CK-MB) elevates 4-8 hours after injury and declines to normal within 2-3 days
  • Myoglobin elevates within 1 hour and peaks within 4-8 hours, but is not cardiac-specific
  • Troponin elevates within 3 hours and remains elevated for 7-10 days, making it more capable of detecting infarction than CK-MB

Unstable Angina

• A state between stable angina and MI
• Results from atherosclerosis plaque disruption, platelet aggregation, and secondary hemostasis
• Pain is more severe and persistent, occurring at rest or with minimal exercise, and lasting more than 20 minutes
• ECG changes may occur, including ST-segment depression, ST-segment elevation, or T-wave inversion
• Cardiac markers:
  • CPK is not elevated
  • Troponin I or T may be slightly increased

Acute Myocardial Infarction (AMI)

• Abrupt onset of severe, crushing pain that radiates to the left arm, neck, or jaw
• Pain is prolonged and not relieved by rest or nitroglycerin
• Main pathophysiological cause of severe pain is an imbalance between oxygen supply and demand
• Two types of infarction:
  • Transmural infarcts (ST-segment elevation AMI) involve the full thickness of the ventricles
  • Subendocardial infarcts (non-ST-segment elevation AMI) involve the inner one-third to one half of the ventricles

Consequences of AMI

• Necrosis (irreversible myocardial cell death) occurs within 20-40 minutes of severe ischemia
• Reperfusion using thrombolytic agents or vascularization must occur within 15-20 minutes of the episode
• Three zones of tissue damage:
  • Area of necrosis (ECG = Q wave)
  • Area of injury (ECG = ST segment)
  • Ischemic zone (ECG = T wave inversion)

Ventricular Tachycardia (VT) and Ventricular Fibrillation (VF)

• Most dangerous arrhythmias that require DC shock