The ventricular myocardium consists of cardiomyocytes, terminally differentiated striated muscle cells connected by intercalated discs with gap junctions allowing electrical synchrony. The LV wall is approximately 9-11 mm thick (vs RV 3-5 mm) to generate systemic pressures. Cardiomyocytes have limited regenerative capacity; myocardial infarction replaces functional myocardium with fibrous scar.
| Location | Middle layer of the ventricular walls, between the epicardium and the endocardium |
|---|---|
| Parts |
|
| Nerve Supply | Sympathetic cardiac nerves (increase force); Vagus nerves (mainly affect rate) |
| Blood Supply | Left anterior descending, circumflex and right coronary arteries |
| Venous drainage |
|
Contracts in a twisting squeeze to eject blood into the pulmonary trunk and aorta, then relaxes to refill. Loss of it in a heart attack is replaced by scar, reducing pumping power.
Myocardial infarction destroys cardiomyocytes in the territory of the occluded coronary artery, producing wall motion abnormality detectable by echocardiography (hypokinesis, akinesis, dyskinesis). Heart failure from cardiomyopathy involves global myocardial dysfunction with reduced ejection fraction (HFrEF, EF less than 40%) or preserved ejection fraction with diastolic dysfunction (HFpEF). Cardiac MRI provides tissue characterisation with late gadolinium enhancement identifying infarct scar, myocarditis, and cardiomyopathy patterns. Left ventricular hypertrophy from hypertension or HOCM increases wall thickness with potential outflow obstruction.
STEMI occlusion of the LAD produces anterior wall akinesis and septal hypokinesis on echocardiography as cardiomyocytes in the LAD territory undergo irreversible ischaemic injury; primary PCI restores flow within 90 minutes of symptom onset salvages the threatened myocardium at the ischaemic periphery, limiting infarct size and preserving ejection fraction.
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