Pathophysiology · MU Sofia

117. Ischemic heart disease - etiology, classification, pathogenesis, clinical manifestations.

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Topic 117 of 168 in the MU Sofia syllabus for Pathophysiology (Medicine, Year 3). The free AceMed note covers it in 1 section, about 306 words (2 min of reading), with 16 flashcards.

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  1. Ischemic heart disease – etiology, classification, etiology, pathogenesis, and clinical manifestations.

Ischemic heart disease – etiology, classification, etiology, pathogenesis, and clinical manifestations.

Ischemic heart disease (IHD) — also called coronary artery disease (CAD) — is a group of heart disorders caused by an imbalance between myocardial oxygen supply and demand, almost always due to coronary artery atherosclerosis, resulting in myocardial ischemia.

Etiology

Primary cause

Atherosclerosis of coronary arteries (most common).

Predisposing (risk) factors

Non- modifiable

Age.

Male sex.

Family history/ genetic predisposition.

Modifiable

Hyperlipidemia (high LDL, low HDL).

Hypertension.

Smoking.

Diabetes mellitus.

Obesity, metabolic syndrome.

Sedentary lifestyle.

Classification

  1. 1 Chronic coronary syndromes (stable)

Stable angina pectoris.

Silent (asymptomatic) ischemia.

Ischemic cardiomyopathy.

  1. 2 Acute coronary syndromes (ACS)

Unstable angina.

Non- ST- segment elevation myocardial infarction (NSTEMI).

ST- segment elevation myocardial infarction (STEMI).

Sudden cardiac death.

Pathogenesis

Atherosclerotic plaque formation

  1. Endothelial injury → lipid accumulation → foam cell formation → fatty streak.
  2. Smooth muscle migration, collagen deposition → fibrous cap → mature atheromatous plaque.

Plaque evolution and complications

Stable plaques: thick fibrous cap, small lipid core → cause stable angina (predictable effort- related pain).

Unstable/vulnerable plaques: thin fibrous cap, large lipid core → prone to rupture.

Acute plaque change

Plaque rupture or erosion → exposure of subendothelial collagen and necrotic core → platelet adhesion and activation → thrombus formation.

Thrombus consequences

Partial occlusion → unstable angina, NSTEMI.

Complete occlusion → STEMI.

Other mechanisms contributing to ischemia

Vasospasm (Prinzmetal angina).

Embolism.

Coronary microvascular dysfunction.

Clinical manifestations

Stable angina pectoris

Episodic chest pain, usually on exertion or emotional stress.

Relieved by rest or nitroglycerin.

Pain: substernal, may radiate to left arm, neck, jaw.

Unstable angina

Increased frequency, severity, or occurs at rest.

Precursor to infarction (part of ACS).

Myocardial infarction (MI)

Severe, prolonged chest pain (not relieved by rest).

Sweating, nausea, dyspnea.

Can lead to arrhythmias, heart failure, shock.

Silent ischemia

No symptoms; common in diabetics and elderly.

Ischemic cardiomyopathy

Chronic ischemia → myocardial fibrosis → heart failure symptoms ( dyspnea, fatigue).

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