Etiology and pathogenesis
The fundamental basis for the development of an infarction is coronary atherosclerosis. The direct cause in 95–97% of situations is thrombosis. The mechanism is as follows: the fibrous cap of the atherosclerotic plaque ruptures, the lipid core comes into contact with blood, which triggers the activation of platelets and the coagulation cascade. As a result, a thrombus forms, blocking the vessel lumen.
Less commonly, necrosis can be caused by prolonged arterial spasm, embolism, vascular wall dissection, or congenital anomalies. Increased oxygen demand due to stress or physical exertion plays only a secondary role compared to vessel occlusion.
Clinical presentation
The most frequent manifestation is pain (status anginosus).
Key features of a typical anginal attack during myocardial infarction:
- Nature of pain: pressing, squeezing, "stabbing".
- Localization: retrosternal.
- Duration: more than 15–30 minutes (sometimes lasting hours).
- Response to medications: no effect from nitroglycerin, often not relieved even by narcotic analgesics.
In addition to the classic pain presentation, historically two other syndromes are distinguished (Obraztsov-Strazhesko classification): cardiogenic shock (vascular collapse with cyanosis) and heart failure (presenting as pulmonary edema). A painless form is also possible, which is more common in the elderly, diabetic patients, and patients with chronic heart failure.
Laboratory diagnostics
Biochemical markers are used to confirm necrosis. Currently, highly specific indicators are relied upon, while older ones (AST, ALT, LDH) are discarded due to their low specificity.
- Troponins (I and T): The earliest and most sensitive proteins specific to the heart. They begin to rise in 3–12 hours, peak at 12–48 hours, and remain in the blood for 5 to 14 days.
- CK-MB fraction: More specific for the myocardium than total CK. Rises in 3–6 hours, peaks by the end of the first day, and normalizes on days 3–4.
- Myoglobin: Rises early, but is not specific to the heart muscle.
Classification and ECG diagnostics
The modern approach divides infarctions into two groups, which directly affects treatment tactics (for example, the administration of thrombolytics).
- Q-wave myocardial infarction (transmural / large-focal):
- Necrosis penetrates the entire thickness of the wall.
- A pathological (broad and deep) Q wave appears on the ECG, and the R wave decreases.
- It has a clear staging: hyperacute (monophasic curve), acute (appearance of Q), subacute (ST on the isoline, inverted T), and scar stage.
- Non-Q-wave myocardial infarction (small-focal / intramural):
- Necrosis does not involve the entire wall.
- The QRS complex does not change (no pathological Q).
- The main ECG sign is ST-segment changes and the formation of a negative T wave.
- Assessment of clinical presentation and blood enzymes is mandatory for the diagnosis, as an isolated negative T wave is nonspecific.
Briefly: answers to topical questions
What atypical clinical forms of myocardial infarction exist?
Depending on the predominance of atypical symptoms, the following atypical clinical forms of myocardial infarction exist:
- Asthmatic variant — the clinical picture resembles a bronchial asthma attack or acute left ventricular failure.
- Abdominal variant (gastralgic form) — gastrointestinal symptoms predominate (paroxysmal upper abdominal pain, vomiting, diarrhea).
- Arrhythmic variant — cardiac rhythm disturbances predominate in the clinical picture.
- Cerebrovascular variant (cerebral form) — neurological symptoms come to the foreground.
- Pauci-symptomatic form (painless) — characterized by the complete absence of pain syndrome.
- Peripheral form — mentioned in the classification along with other atypical manifestations.
Which ECG leads reflect changes in the anterior wall of the left ventricle?
Changes in anterior wall involvement are reflected in the following ECG leads:
- Anterior wall and septum — leads V1–V3.
- Anterior wall + lateral wall ("extensive anterior") — leads I, aVL, and V1–V6.
Class and exam questions
Why do heart attacks happen more often in the morning?
In the morning hours (from 6:00 AM to 12:00 PM), a physiological increase in sympathetic nervous system activity occurs, which increases the risk of myocardial infarction.
What is the reciprocity phenomenon on the ECG?
These are mirror changes in leads reflecting the wall opposite to the necrosis zone. If ST elevation is recorded in "direct" leads, ST depression is recorded in reciprocal leads.
Does a normal ECG rule out the presence of a myocardial infarction?
No. A normal ECG at the time of recording does not rule out necrosis, especially in the early stages or when localized in "silent" zones.
What else to study on this topic
- Topical diagnosis of infarction (determining the affected wall via ECG leads)
- Post-infarction myocardial remodeling and its consequences
- Pathogenesis and triad of signs of cardiogenic shock
- Rhythm and conduction disturbances in myocardial infarction
- Application of ECG mapping and myocardial scintigraphy in complex cases
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