Coronary complications

Ischemic cascade and cell death

After coronary artery blood flow is blocked, a strict chronological sequence of disorders is triggered, known as the ischemic cascade (The Ischaemic Cascade):

1. Metabolic starvation: a sharp drop in ATP and phosphocreatine levels.
2. Impaired relaxation of muscle fibers (diastolic dysfunction).
3. Suppression of contractility (systolic dysfunction).
4. Local wall motion abnormalities in the affected ventricle.
5. Appearance of specific ECG changes.
6. Onset of anginal chest pain.

Time is critical. If blood flow is restored within 20–30 minutes, functional changes are reversible. If ischemia lasts longer, cardiomyocytes die irreversibly, and myocardial infarction develops.

Myocardial remodeling and healing

Immediately after the catastrophic event, the process of remodeling (Remodelling) is triggered, altering ventricular shape, size, and function for many months.

• Early phase: characterized by severe tissue edema, hemorrhages, and an acute inflammatory response. The necrotic zone stretches, and the heart wall weakens. It is during this period that the risk of early ventricular rupture or acute aneurysm formation is extremely high.
• Healing phase: dead tissue is gradually replaced by a dense, collagen-rich fibrous scar. The myocardial wall becomes thinned at this site.

To compensate for the loss of the scar's contractile function and maintain stroke volume, the unaffected myocardium begins to dilate. This compensatory dilation frequently leads to the development of severe dilated ischemic cardiomyopathy.

Specific myocardial conditions

Under conditions of inadequate perfusion, the heart muscle may enter specific protective and pathological states:

• Stunned myocardium (Stunned myocardium). Occurs after brief ischemia (up to 15 minutes) during unstable angina or vasospasm. Infarction does not develop, but cardiomyocyte function remains depressed even after full restoration of blood flow.
• Hibernating myocardium (Hibernating myocardium). Adaptation to prolonged moderate ischemia. Cells sharply reduce metabolism (both aerobic and anaerobic) to minimize energy consumption and survive. Function is depressed, but if perfusion is restored, it will return to normal, although this sometimes takes over a year.

Acute left ventricular failure

Extensive damage frequently provokes pulmonary congestion, leading to acute left ventricular failure.

• Symptoms: the leading signs are severe dyspnea and orthopnea (the patient must sit upright). Paroxysms of nocturnal cardiac asthma with suffocation and cough are characteristic.
• Objective findings: tachypnea, moist rales in the lungs, and fluid accumulation in the pleural cavity (hydrothorax).

The pathophysiological basis is pulmonary edema. Upon transition to the alveolar stage, breathing becomes bubbling, pink frothy sputum is released, the skin becomes cold, clammy, and cyanotic, and a gallop rhythm is auscultated over the heart. The extreme form of such complications is cardiogenic shock, in which the pumping function drops so drastically that hypotension develops. The preshock stage (preshock) is distinguished, where risks are immense but overt clinical signs of shock are not yet present. The combination of pulmonary edema, hypotension, and arrhythmias requires emergency resuscitation.

Class and exam questions

What else to study on this topic

• Pathogenesis of collagen-rich fibrous scar formation during healing
• Mechanisms of compensatory dilation and development of ischemic cardiomyopathy
• Criteria for the preshock stage and hemodynamic instability
• Differential diagnosis of hibernating myocardium and scar tissue changes
• Pathophysiology of cardiac asthma and the interstitial stage of pulmonary edema

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.