Pathophysiology PHMU 534 Lecture 7: Ischemic Heart Diseases

Pathophysiology PHMU 534 Lecture 7: Ischemic Heart Diseases

• Ischemic heart diseases (IHD) involve several closely related syndromes caused by myocardial ischemia, an imbalance between cardiac blood supply and myocardial oxygen requirements.
• IHD is the leading cause of mortality, accounting for 7 million deaths worldwide annually.
• In over 90% of cases, IHD results from reduced coronary blood flow secondary to obstructive atherosclerosis.
• Less frequent causes include increased demand (e.g., increased heart rate or hypertension), decreased blood volume (e.g., hypotension), decreased oxygenation (e.g., pneumonia), and reduced oxygen-carrying capacity (e.g., anemia).

Angina Pectoris

• Angina pectoris is characterized by intermittent chest pain caused by transient, reversible myocardial ischemia.
• The pain is a consequence of ischemia-induced release of adenosine, bradykinin, and other molecules that stimulate autonomic afferents.
• Three types of angina are recognized:
  • Typical or stable angina: episodic chest pain associated with exertion or increased demand, relieved by rest or medication (e.g., nitroglycerin). Pain is described as crushing or squeezing.
  • Prinzmetal or variant angina: occurs at rest and is caused by coronary artery spasm.
  • Unstable angina: increasingly frequent pain, precipitated by less exertion, or even occurring at rest.

Myocardial Infarction (MI)

• MI, also known as a heart attack, is necrosis of heart muscle resulting from ischemia.
• Atherosclerosis is the major underlying cause of MI. Risk factors are the same for IHD.
• MIs can occur at any age, but frequency increases with age and increasing atherosclerotic risk factors.
  • Approximately 10% of MIs occur before age 40, and 45% occur before age 65.
  • Men are at higher risk than women, although the gap narrows with age. Women tend to be protected during their reproductive years.
• MI Pathogenesis:
  • Most MIs are caused by coronary artery thrombosis following existing atherosclerosis.
  • Some MIs occur without atherosclerosis, primarily due to coronary artery spasm or embolization from a mural thrombus (e.g., in the setting of atrial fibrillation).
  • Subendocardial infarctions are often limited to the inner third of the myocardium.
  • Microscopic infarcts may occur in the setting of small vessel occlusions.

Clinical Features of MI

• The classic MI involves severe, crushing substernal chest pain radiating to neck, jaw, epigastrium, or left arm.
• In some cases (10-15%), MI presents with atypical symptoms.
• The classic signs of MI include:
  • Rapid and weak pulse
  • Diaphoresis
  • Nausea
  • Vomiting
  • Weakness
  • Light-headedness
• The classic ECG abnormalities in MI:
  • Inverted T waves
  • Deep Q waves
  • ST-segment elevation

Laboratory Evaluation of MI

• CK-MB activity rises within 2-4 hours of MI, peaks at 24-48 hours, and returns to normal within 72 hours.
• Troponins (TnI and TnT) are elevated within 2-4 hours of MI and remain elevated for a much longer period (2-3 days), and this is more specific.
• Absence of changes in CK and CK-MB levels within 2 days after the onset of chest pain strongly suggests that the diagnosis of MI is not likely.

Consequences and Complications of MI

• Contractile dysfunction: Left ventricular failure can lead to hypotension, pulmonary congestion, edema (fluid buildup in the lungs) and even cardiogenic shock.
• Right ventricular infarction: Commonly occurs with damage to >40% of the left ventricle and may lead to Right sided heart failure and venous circulatory pooling, systemic hypotension.
• Papillary muscle dysfunction: commonly ischemic, leading to poor contractile function and mitral regurgitation.
• Myocardial Rupture: rupture of the heart muscle which may be a fatal complication occurring within days of the MI, commonly left ventricle wall rupture and ventricular septal rupture.
• Arrhythmias: Significant source of morbidity and mortality (90%); often a sudden cardiac death can occur within an hour of symptom onset. This often happens with STEMIs (ST-elevation myocardial infarctions).
• Mural thrombus: A thrombus (blood clot) forming within the heart wall, potentially causing thromboembolism.
• Pericarditis: Inflammation of the pericardium (the sac around the heart) usually occurs 2-3 days post MI.
• Ventricular aneurysm: A weakened area in the heart wall that can, over time, balloon outward. Very late complication.

References

• Robbins Basic Pathology, 10th edition, by Vinay Kumar, Abul K Abbas, and Jon C. Aster. Elsevier, ISBN: 9780323353175, 2018. (Reference only)

This quiz covers the fundamentals of ischemic heart diseases (IHD), a major cause of global mortality. It explores the mechanisms of myocardial ischemia, its primary causes, and the symptoms of angina pectoris. Understand the critical aspects of how reduced coronary blood flow affects heart health.