Forms and clinical course of the disease
The disease has a chronic and undulating course: periods of relative stability alternate with episodes of acute coronary insufficiency. Broadly, two major groups are distinguished:
- Acute IHD. Includes angina pectoris, myocardial infarction, and sudden cardiac death. The main sign is acute myocardial ischemia.
- Chronic IHD. Represented by cardiosclerosis.
In clinical practice since the 1990s, acute coronary syndrome (ACS) has been singled out as a distinct category. This is because the first day of an infarction is the most critical period, accounting for the vast majority of fatalities. The pathogenesis changes step-by-step during this time, and the patient's survival directly depends on the chosen treatment strategy. ACS is classified based on ECG data (e.g., ACS without ST-segment elevation clinically presents 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 with minimal physical exertion.
Risk factors are divided into two groups according to their degree of impact:
- Primary risk factors (their combination yields a 40–60% probability of infarction): hyperlipidemia (including exogenous hypercholesterolemia), arterial hypertension, smoking (increases risk by 2.2 times), physical inactivity (sedentary lifestyle), and male gender.
- Secondary risk 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 unstable plaque
The acute form develops due to a sudden disruption of coronary blood flow. The degree of heart muscle damage depends on the duration of ischemia and the reperfusion factor.
The key trigger of acute IHD is the rupture of an unstable atherosclerotic plaque (vulnerable plaques). This is promoted by a large lipid core, vascular spasm, and loss of fibrous cap strength.
Cap rupture has a pronounced inflammatory nature:
- Cellular infiltration: macrophages and lymphocytes infiltrate 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) additionally degrade the collagen framework.
There is also an infectious theory of inflammation (viruses, chlamydia, Helicobacter pylori), but attempts to treat Chlamydia pneumoniae with antibiotics proved ineffective.
Clinical and morphological manifestations and outcomes
Each form of IHD has its own morphological features and causes of occurrence:
- Angina pectoris (Angina pectoris). Based on reversible ischemia. Causes: arterial spasm against the background of sclerosis, aortic valve stenosis, aortic valve insufficiency, or hypertrophic cardiomyopathy. Chronic ischemia in angina leads to diffuse fine-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 sinoatrial node.
- Cardiosclerosis. A predictable outcome of angina pectoris or a prior infarction. A dangerous complication of post-infarction cardiosclerosis is the formation of a chronic cardiac aneurysm.
Briefly: answers to topical questions
What stages are distinguished in the morphogenesis of myocardial infarction?
Three successive stages are distinguished in the morphogenesis of myocardial infarction.
- Ischemic stage (prenecrotic) — metabolic disorders increase, energy deficit forms, compensatory mechanisms are activated, and the volume of the lesion is determined.
- Necrotic stage — cell death occurs.
- Organization stage (scarring) — the necrosis zone is replaced by maturing granulation tissue and then mature connective tissue with the formation of large-focal cardiosclerosis.
What types of myocardial infarction are distinguished in relation to the layers of the heart wall?
Based on the depth of the lesion (localization in the layers of the heart wall), four types of myocardial infarction are distinguished:
- Subendocardial — involvement of the subendocardial layer.
- Intramural — involvement of the middle layers of the myocardium.
- Subepicardial — involvement of the layer beneath the epicardium.
- Transmural — involvement of all myocardial layers.
What complications are characteristic of post-infarction cardiosclerosis?
Post-infarction cardiosclerosis is characterized by the development of a number of severe complications associated with the presence of scar tissue.
- Chronic cardiac aneurysm — a saccular cavity formed under blood pressure at the site of the scar (usually after a transmural infarction).
- Thromboembolic syndrome — occurs due to the presence of thrombotic masses within the aneurysm cavity.
- Cardiac tamponade — a consequence of the rupture of the chronic aneurysm wall.
- Rhythm and conduction disturbances — the scar creates potentially arrhythmogenic zones of electrical inhomogeneity.
- Chronic heart failure — develops as a result of post-infarction remodeling, left ventricular dilation, and low cardiac output.
Additionally, recurrent myocardial infarction is possible against the background of chronic IHD.
What macroscopic and microscopic changes occur in the necrotic stage of myocardial infarction?
In the necrotic stage of myocardial infarction, ischemic (white) coagulative necrosis with a hemorrhagic rim develops.
- Macroscopic changes: an irregularly shaped focus is formed, represented by merging grey-yellow areas (white ischemic zone). A wide demarcation zone of plethora and red-brown hemorrhages is located along the periphery of the focus.
- Microscopic changes: cells undergo coagulative necrosis, and a demarcation inflammation zone develops at the border with preserved living tissue. At the ultrastructural level, relaxed fibers predominate in the center of the focus, while contraction-altered myofibrils predominate at the periphery.
How does acute coronary syndrome differ from myocardial infarction?
Acute coronary syndrome (ACS) is a clinical form singled out for practical use; its classification is based on ECG data, and the first 24 hours of myocardial infarction are a critical period that determines treatment tactics. Myocardial infarction is acute focal ischemic necrosis of the heart muscle caused by absolute or relative insufficiency of coronary blood flow.
Primary risk factors are easy to remember by the acronym «H-A-M-S-P» (or equivalent): Hyperlipidemia, Arterial hypertension, Male gender, Smoking, Physical inactivity. When combined, the risk of infarction reaches 40–60%.
Class and exam questions
Why do pathological changes progress rapidly in CAD?
The heart is forced to continuously maintain systemic circulation. Reducing the load on the organ is impossible even during its severe ischemic damage.
What leads to atherosclerotic plaque rupture?
Rupture is promoted by a large lipid core, coronary artery spasm, and loss of cap strength. The latter occurs due to inflammation, cytokine storm, and enzyme-mediated collagen destruction.
What is the main cause of sudden cardiac death?
Most often this is stenosis of the right coronary artery, since it is the one that supplies blood to the sinoatrial node responsible for generating the heart rhythm.
What else to study on this topic
- Pathogenesis of myocardial infarction by hours and days
- ECG classification of acute coronary syndrome (ACS)
- Infectious theory of vascular wall injury
- Morphology of post-infarction cardiosclerosis and cardiac aneurysm
- Secondary and idiopathic cardiomyopathies
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