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.
| Origin | Cardiac muscle fibres form a continuous spiral arrangement anchored at the fibrous skeleton (four cardiac valvular rings, the right and left fibrous trigones); ventricular fibres are oriented in oblique layers that convert to a wringing-twisting motion during systole |
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| Insertion | The fibrous cardiac skeleton (annuli fibrosi) at the atrioventricular junction; ventricular trabecular muscle (papillary muscles, trabeculae carneae) attach to the ventricular walls and to the mitral and tricuspid valve leaflets via chordae tendineae |
| Nerve Supply | Sympathetic (cardiac accelerator nerves from T1-T4 via cardiac plexus) — increase heart rate and contractility; Parasympathetic (vagus CN X cardiac branches) — decrease heart rate; Intrinsic cardiac conduction system (SAN, AVN, His-Purkinje) |
| Blood Supply | Left ventricular: left anterior descending (anterior wall, septum, apex) and left circumflex (lateral wall); Right ventricular: right coronary artery |
| Actions | Systolic contraction of the ventricular myocardium ejects blood into the pulmonary (RV) and systemic (LV) circulations; the LV generates approximately 5 times the pressure of the RV; myocardial contractility is regulated by preload, afterload, and inotropic state (Frank-Starling mechanism) |
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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.
