Untitled Quiz

Ischemic Heart Disease and Myocardial Infarction 1

• Learning Outcomes (Ischemic Heart Disease):

  • Define and classify ischemic heart disease (C3)
  • Describe the pathogenesis of ischemic heart disease (C2)
  • Explain the types of angina pectoris (C2)

• Learning Outcomes (Myocardial Infarction):

  • Describe the pathophysiology of myocardial infarction (subendocardial and transmural infarction, STEMI, non-STEMI) (C2)
  • Describe the clinical features of acute myocardial infarction (C2)

Anatomy of the Heart

• The right coronary artery (RCA) supplies the right atrium, right ventricle, lower part of the left ventricle, and back of the septum
• The left coronary artery (LCA) has two main branches, the left circumflex artery (LCX) and the left anterior descending artery (LAD)
• The LCX supplies the left atrium and sides/back of the left ventricle
• The LAD supplies the front and bottom of the left ventricle and front of the septum.
• Coronary veins carry deoxygenated blood back to the heart.

Phases of the Cardiac Cycle

• Atrial Systole: Atria contract, pushing blood into ventricles
• Ventricular Systole (Phase 1): Ventricles contract, closing AV valves
• Ventricular Systole (Phase 2): Semilunar valves open, blood ejected
• Ventricular Diastole (Phase 1): Semilunar valves close
• Ventricular Diastole (Phase 2): Chambers relax, blood passively fills

Ischemic Heart Disease (IHD)

• Defined as an acute or chronic form of cardiac disability due to an imbalance in myocardial blood supply (perfusion) and oxygen demand.
• Coronary artery disease (CAD) is a synonymous term for IHD
• IHD is the leading cause of death in developed countries, while incidence is lower in developing countries.
• Men are typically affected at an earlier age than women.

IHD - Aetiopathogenesis

• Coronary Atherosclerosis:
  • Most prevalent cause (90%).
  • Affecting one or more of the major coronary arteries (LAD, RCA, LCX)
  • Narrowing of coronary arteries is typically significant (75%) near the ostia, which are the origins of the arteries.
• Atherosclerosis (Superadded changes):
  • Plaque hemorrhage, fissuring, or ulceration leading to thrombus.
  • May be worsened by factors such as spasm, tachycardia, or hypercholesterolemia.
  • Coronary artery thrombosis leads to significant luminal blockage
• Non-atherosclerotic causes:
  • Vasospasm
  • Stenosis of coronary ostia from extension of syphilitic aortitis or from aortic atherosclerotic plaques.
  • Arteritis (inflammatory issues) like rheumatic arteritis, polyarteritis nodosa, thrombo-angiitis obliterans, Takayasu disease, tuberculosis.
  • Embolization from elsewhere in the body
  • Thrombotic disorders
  • Trauma, aneurysms, tumor compression

Clinical Presentations of IHD

• Angina Pectoris: Chest pain due to transient myocardial ischemia

• Myocardial infarction (MI): Sufficient ischemia causes cardiomyocyte death

• Chronic IHD with congestive heart failure: Progressive cardiac decompensation from MI

• Sudden cardiac death (SCD): Post-MI lethal arrhythmia

Angina Pectoris

• Intermittent chest pain caused by transient ischemia. Pain is worsened by increased demand and relieved by decreased demand.
• Pain often described as squeezing, pressure, fullness or tightness in the center of the chest. Often spreading to the neck, jaw, shoulder, or arm.

Stable Angina

• Most common type
• Pain triggered by exertion or stress, relieved by rest.
• Demonstrates ST depression on EKG.

Unstable Angina

• Most serious angina type
• More frequent, occurring at rest.
• Indicates impending acute MI
• Due to plaque disruption, thrombosis, or vasospasm

Prinzmetal Angina

• Pain is independent of exertion or stress.
• Likely due to coronary vasospasm.
• May respond to nitroglycerine or calcium channel blockers .

Acute Myocardial Infarction (MI)

• 10-25% of deaths are caused by MI and is characterized by coagulative necrosis of heart muscle. Occurs due to decreased blood supply to the heart. This can be due to atherosclerotic plaques or spasms.

• Causes:

  • Coronary artery disease and atherosclerosis.
  • Increased demand (e.g., hypertension, high heart rate)
  • Reduced blood volume (hypotension or shock)
  • Reduced oxygenation (e.g., pneumonia, heart failure)
  • Reduced oxygen capacity (e.g., anemia, carbon monoxide poisoning)

• Clinical Features: Severe crushing substernal chest pain that radiates (spreads) to the arm/jaw/neck. The pain may last several minutes and commonly occurs with sweating, nausea, dyspnea, and a weak pulse.

Types of MI

• Transmural MI (STEMI): Full-thickness cardiac muscle injury. Associated with ST-segment elevation and Q-wave formation on ECG.

• Subendocardial MI (NSTEMI): Limited to the inner third of the cardiac muscle wall. No ST-segment elevation but possible ST depression or T-wave inversion on ECG.

Distribution of Myocardial Infarction

• Left anterior descending artery (LAD): Anterior wall of the left ventricle, anterior interventricular septum, apex. (40-50%)
• Right coronary artery (RCA): Inferior wall of the left ventricle , right ventricle (30-40%)
• Left circumflex artery (LCX): Lateral wall of the left ventricle (20%)

MI Classification

• Anatomical region of LV involved.
• Degree of ventricular wall involved ( Full thickness/subendocardial)
• Age of MI (acute/fresh, healed/organized)

Pathogenesis of IHD and MI

• Acute changes like rupture, fissuring, or ulceration of atherosclerotic plaques.
• Expose thrombogenic components to the subendothelium.
• Can lead to acute coronary syndromes, including unstable angina, MI, and sudden cardiac death.

Factors affecting acute plaque change:

• Intrinsic factors (plaque composition)
• Extrinsic factors (stress/emotions)

Acute Coronary Syndrome

• Includes unstable angina, acute MI, and sudden cardiac death. -Caused by a plaque change