Pathomorphological consequences of attacks
Each episode of angina pectoris is accompanied by a temporary disruption of blood supply to a segment of the heart muscle. If such attacks recur regularly, the myocardial tissue undergoes irreversible changes. The main consequence of repeated ischemic episodes is the development of diffuse small-focal cardiosclerosis. In this condition, muscle fibers are gradually replaced by connective tissue.
It is this diffuse sclerotic process that is recognized as the morphological basis of chronic coronary heart disease. Subsequently, the progression of cardiosclerosis has its own dangerous outcomes. In particular, a chronic cardiac aneurysm—a persistent outpouching that impairs the normal contractility of the left ventricle—may form at the site of the weakened myocardial wall.
Threats of unstable angina and prognosis in CHD
Unstable angina is of particular clinical concern. Unlike the stable course, this form is associated with an extremely high risk of progressing to acute, critical conditions. The main threats of the unstable form include:
- Development of acute myocardial infarction.
- Occurrence of life-threatening arrhythmias.
- Onset of sudden cardiac death (SCD).
To assess risks in patients with coronary heart disease, clinicians rely on annual clinical statistics. The prognosis in CHD is generally as follows:
| Outcome / Complication | Annual statistics |
|---|---|
| Total mortality | 1,2–2,4% |
| Death from fatal cardiovascular complications | 0,6–1,4% |
| Non-fatal myocardial infarctions | 0,6–2,7% |
Complications of myocardial infarction: early ischemia and shock
Myocardial infarction, being the most formidable consequence of progressive ischemia, has its own spectrum of severe complications. One of the frequent unfavorable variants is early post-infarction angina and recurrent myocardial infarction.
The recurrence of ischemia is based on the following pathophysiological factors:
- Partial or complete rethrombosis of the infarct-related coronary artery.
- Stenotic lesion of other coronary arteries, aggravating overall hypoxia.
- Complications after percutaneous coronary intervention (PCI), which include thrombosis of the placed stent or coronary artery wall dissection.
- Ischemia of viable myocardium located in the peri-infarction zone. This risk increases especially in the absence of timely reperfusion therapy.
- Ischemia developing in other vascular territories.
Important clinical nuance: when recurrent chest pain occurs, it should be carefully differentiated from the pain syndrome in pericarditis.
The most severe hemodynamic complication is cardiogenic shock. As a rule, it occurs with extensive myocardial necrosis developing against the background of multiple stenotic lesions of the coronary arteries.
Hemodynamic, rhythmic, and structural complications
In addition to cardiogenic shock, the course of myocardial infarction is often complicated by other hemodynamic and rhythm disturbances. These include the progression of acute and chronic heart failure, as well as various arrhythmias. Of particular danger are disturbances of atrioventricular (AV) conduction, manifesting as blocks of varying severity.
Classical complications of myocardial infarction also include severe structural and inflammatory changes:
- Ventricular wall rupture, which is inevitably accompanied by blood leakage into the pericardial cavity and cardiac tamponade.
- Rupture of the interventricular septum, leading to a left-to-right shunt.
- Papillary muscle rupture, resulting in acute mitral regurgitation.
- Formation of an acute cardiac aneurysm. Mural thrombosis is possible within its cavity, making the aneurysm a dangerous source of systemic thromboembolism.
- Inflammatory lesions: fibrinous (epistenocarditic) pericarditis and autoimmune Dressler syndrome.
A natural outcome of the organization of the necrosis focus is the formation of post-infarction cardiosclerosis, against which a chronic cardiac aneurysm may also develop.
To recall the classical complications of myocardial infarction, divide them into 3 groups: Structural (ruptures, papillary muscle detachment, aneurysms), Hemodynamic/Electrical (shock, heart failure, blocks), and Inflammatory (epistenocarditic pericarditis, Dressler syndrome).
Class and exam questions
What do repeated attacks of angina pectoris lead to?
Regular episodes of ischemia lead to the development of diffuse small-focal cardiosclerosis, which is the morphological basis of chronic CHD. Subsequently, cardiosclerosis can lead to the formation of a chronic cardiac aneurysm.
What is the main danger of unstable angina?
The unstable form of the disease carries an extremely high risk of developing acute myocardial infarction, life-threatening rhythm disturbances, and sudden cardiac death.
What causes early post-infarction angina?
Its cause may be partial or complete arterial rethrombosis, ischemia of viable myocardium in the peri-infarction zone, stenosis of other coronary vessels, as well as iatrogenic complications after PCI (stent thrombosis or arterial dissection).
What typically precipitates cardiogenic shock?
Cardiogenic shock typically manifests in extensive myocardial infarction accompanied by multiple coronary artery lesions.
What else to study on this topic
- Immediate causes of acute myocardial ischemia
- Sudden cardiac death (SCD): clinical and morphological characteristics
- Classification of myocardial infarction
- Biological pattern of necrosis development in the myocardium
- Differential diagnosis of pain in angina pectoris and pericarditis
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