ECG Scar

From Ischemia to Scar: Morphogenesis

Scar formation is preceded by acute coronary artery disease (CAD)—a mismatch between myocardial oxygen demand and supply. In 90–97% of cases, the cause is stenosing atherosclerosis (with critical lumen narrowing greater than 75%) accompanied by thrombosis, and less commonly, arterial spasm or dissection. Risk factors include hyperlipidemia, smoking, arterial hypertension, as well as diabetes mellitus, which increases the risk of developing the pathology by 2 to 4 times.

Macroscopically, the myocardial area turns pale, its turgor decreases, and stasis, narrowing of the plasma flow zone, and aggregation of formed blood elements occur in the microvasculature. At the ultrastructural level, the irreversibility of damage is confirmed when the number of relaxed muscle fibers in the center of the lesion reaches 60%.

The morphogenesis of myocardial infarction goes through three strict stages:

1. Ischemic Stage (up to 18–24 hours) — mitochondrial swelling and glycogen depletion.
2. Necrotic Stage (up to 1–2 weeks) — tissue breakdown, formation of a yellow-gray coagulation necrosis with a hemorrhagic border, karyolysis, and neutrophil infiltration.
3. Organization Stage (2–6 weeks) — the necrosis zone is gradually replaced by granulation tissue, which transforms into a dense scar. Large-focal cardiosclerosis develops.

Representation of Necrosis and Scar on ECG

Characteristic changes on the electrocardiogram are part of the classical diagnostic triad of myocardial necrosis (along with signs of aseptic inflammation and enzymemia—elevated creatine kinase, AST, and ALT). However, the ECG picture directly depends on the form of acute coronary syndrome (ACS):

• ST-segment elevation ACS (STEMI): a persistent ST-segment elevation lasting more than 20 minutes (in two or more contiguous leads) or a new left bundle branch block is recorded on the ECG. The outcome is a transmural myocardial infarction, which traditionally leaves a deep scar.
• Non-ST-segment elevation ACS (NSTEMI): if cardiac troponins are elevated (T/I above the 99th percentile), a subendocardial or small-focal infarction is diagnosed. On the ECG, such a scar subsequently forms without a Q wave.

It is important to understand that ECG changes occur at the very late stages of the "ischemic cascade". Routine exercise ECG testing (Exercise ECG test) has low sensitivity (about 60%) and moderate specificity (80%). A normal test result does not exclude the presence of CAD, especially in low-risk populations (e.g., women).

Alternatives to ECG: Radionuclide Diagnostics

Since ECG is not always able to accurately identify the zone of cardiosclerosis, radionuclide diagnostics—SPECT (SPECT) and PET (PET)—has become the cornerstone of perfusion assessment. These methods work "higher up" in the ischemic cascade and allow for risk stratification of major adverse cardiac events.

The principle of the method involves the administration of radiopharmaceuticals (e.g., thallium-201 or technetium-99m sestamibi) at rest and during stress testing. In areas with impaired blood supply, radiotracer uptake decreases, forming a "defect":

• Reversible defects (Reversible defects) — appear only under stress, but are absent at rest. They indicate hemodynamically significant stenosis and viable yet ischemia-suffering myocardium.
• Fixed defects (Fixed defects) — present both under stress and at rest. These reliably reflect a post-infarction scar (myocardial scarring).

The size of such a defect closely corresponds to the myocardial volume supplied by the affected artery, and the degree of uptake reduction correlates with the severity of stenosis.

Clinical Case: When Symptoms are Absent

Sometimes scar formation and severe ischemia are completely asymptomatic. As a clinical example, consider a 49-year-old patient with type 1 diabetes mellitus. He completely lacks anginal chest pain (silent ischemia).

However, SPECT reveals an extensive reversible perfusion defect in the lateral wall of the left ventricle (ischemia volume — 19%). Additional stress MRI with late gadolinium enhancement shows an already formed partial infarction of both papillary muscles. Coronary angiography confirms severe two-vessel disease: critical stenosis (up to 80%) of the circumflex artery and the left anterior descending artery. In such cases, despite the absence of complaints and a nonspecific ECG picture, the patient requires emergency surgical treatment—coronary artery bypass grafting (CABG).

Class and exam questions

What else to study on this topic

• Pathogenesis of atherosclerotic plaque rupture and cellular mechanisms of necrosis
• Ultrastructural dynamics of ischemia: myofibril contracture and relaxation
• Laboratory markers of resorption-necrotic syndrome (CK, AST, ALT)
• Classification of acute heart failure in myocardial infarction (Killip classes)
• Stress MRI and CT coronary angiography: novel hybrid imaging modalities

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