Forms and Clinical Course
The disease proceeds chronically and wave-like: periods of relative stability are replaced by episodes of acute coronary insufficiency. Globally, two major groups are distinguished:
- Acute IHD. Includes angina pectoris, myocardial infarction, and sudden cardiac death. The primary sign is acute myocardial ischemia.
- Chronic IHD. Represented by cardiosclerosis.
In clinical practice since the 1990s, acute coronary syndrome (ACS) is singled out separately. This is because the first 24 hours of an infarction represent the most critical period, accounting for the vast majority of fatalities. The pathogenesis changes in stages during this time, and patient survival depends directly on the chosen treatment strategy. ACS is classified based on ECG findings (e.g., non-ST-segment elevation ACS clinically manifests as unstable angina).
Etiology and Risk Factors
The etiology of IHD completely overlaps with the causes of atherosclerosis and hypertension. If the lumen of at least one coronary artery narrows by more than 75% (critical stenosis), adequate blood flow becomes impossible even during minimal physical exertion.
Risk factors are divided into two groups based on their degree of impact:
- Tier I factors (their combination yields a 40–60% probability of myocardial infarction): hyperlipidemia (including exogenous hypercholesterolemia), arterial hypertension, smoking (increases risk by 2.2 times), physical inactivity, and male sex.
- Tier II factors (weaker impact): middle and older age, obesity, stress, metabolic disorders (gout, diabetes mellitus), selenium and magnesium deficiency, hypercalcemia, and hyperfibrinogenemia.
Pathogenesis of Acute Ischemia and the Vulnerable Plaque
The acute form develops due to a sudden disruption of coronary blood flow. The degree of myocardial damage depends on the duration of ischemia and the reperfusion factor.
The key trigger of acute IHD is the rupture of a vulnerable plaque. Contributing factors include a large lipid core, vascular spasm, and loss of structural strength in the fibrous cap.
Cap rupture has a pronounced inflammatory nature:
- Cellular infiltration: macrophages and lymphocytes penetrate the plaque tissue, transforming into foam cells.
- Cytokine storm: pro-inflammatory markers are activated (IL-1, IL-6, IL-12, TNF, CD40L).
- Enzymatic destruction: proteolytic enzymes (matrix metalloproteinases and serine proteinases) are triggered and degrade the matrix. Low-density lipoproteins (LDLs) further degrade the collagen framework.
An infectious theory of inflammation also exists (viruses, chlamydia, Helicobacter pylori), although attempts to treat Chlamydia pneumoniae with antibiotics have proven ineffective.
Clinical and Morphological Manifestations and Outcomes
Each form of IHD has its own morphological features and causes:
- Angina pectoris (Angina pectoris). Based on reversible ischemia. Causes: arterial spasm against a background of sclerosis, aortic ostium stenosis, aortic valve insufficiency, or hypertrophic cardiomyopathy. Chronic ischemia in angina leads to diffuse small-focal cardiosclerosis.
- Myocardial infarction. Acute focal ischemic necrosis. Occurs due to absolute or relative blood flow insufficiency.
- Sudden cardiac death. Most commonly triggered by stenosis of the right coronary artery, which supplies the sinus node.
- Cardiosclerosis. A regular outcome of angina pectoris or a prior myocardial infarction. A dangerous complication of post-infarction cardiosclerosis is the formation of a chronic cardiac aneurysm.