Myocardium
Myocardium
Also known as: heart muscle, cardiac muscle layer
The myocardium is the thick middle layer of the heart wall. It is made of cardiac muscle cells that contract together to pump blood, and it is thickest in the left ventricle.
Overview
Cells and coupling. The myocardium is made of branched, striated cardiomyocytes, each with one or two central nuclei. The cells are joined end to end by intercalated discs. Desmosomes and fasciae adherentes in the discs hold the cells together mechanically. Gap junctions (mainly connexin 43) couple them electrically. As a result, each pair of chambers contracts as a single functional unit (a syncytium).
Metabolism. Cardiomyocytes are packed with mitochondria (about one-third of cell volume) and contain myoglobin. They depend almost entirely on aerobic metabolism, using fatty acids, glucose and lactate as fuel.
Architecture. The fibres wind around the ventricles in helical layers. Ventricular systole therefore combines shortening, wall thickening and a wringing twist (torsion). The left ventricular wall is 8–12 mm thick, the right ventricular wall 3–5 mm and the atrial walls only about 2 mm.
Repair. Adult cardiomyocytes renew very slowly, about 1% per year in young adults and less with age. Infarcted myocardium therefore heals with a fibrous scar rather than new muscle.
- Location
Between the epicardium (outside) and the endocardium (inside). It forms the bulk of the walls of all four chambers.
Anatomy
- Arterial supply
Branches of the coronary arteries penetrate from the epicardial surface. The subendocardium is perfused last and is compressed during systole, so it is the layer most vulnerable to ischaemia.
- Histology
Striated, branched cells about 10–20 µm wide and 50–100 µm long, with central nuclei. Intercalated discs appear as dark transverse lines. T-tubules lie at the Z-lines and form diads with the sarcoplasmic reticulum. There is roughly one capillary per myocyte. Atrial myocytes also contain granules of atrial natriuretic peptide.
Function
- Generates the contractile force that ejects blood.
- Conducts electrical impulses from cell to cell through gap junctions.
- Contains the specialised conducting myocytes of the nodal tissue and His–Purkinje system.
- Secretes natriuretic peptides: atrial myocytes release ANP and stretched ventricular myocytes release BNP.
- Physiology
Excitation–contraction coupling. The action potential opens L-type Ca²⁺ channels. The Ca²⁺ that enters triggers a much larger release of Ca²⁺ from the sarcoplasmic reticulum through ryanodine receptors (RyR2), a process called Ca²⁺-induced Ca²⁺ release. This Ca²⁺ binds troponin C and allows cross-bridges to cycle.
Relaxation. Ca²⁺ is pumped back into the sarcoplasmic reticulum by SERCA2a, which is regulated by phospholamban. Some Ca²⁺ is also extruded from the cell by the Na⁺/Ca²⁺ exchanger.
Grading force. Unlike skeletal muscle, the heart cannot recruit extra motor units. Instead, force is graded by the amount of Ca²⁺ available (inotropy) and by sarcomere length (the Frank–Starling mechanism). The long refractory period prevents tetanic contraction.
Clinical significance
Ventricular hypertrophy
Concentric hypertrophy follows chronic pressure overload, as in hypertension or aortic stenosis. The wall thickens as sarcomeres are added in parallel. Eccentric hypertrophy follows volume overload, as in regurgitant valve disease. The chamber dilates as sarcomeres are added in series.
Cardiomyopathies
Hypertrophic cardiomyopathy is caused by mutations in sarcomere genes and is inherited as an autosomal dominant trait. It is a leading cause of sudden cardiac death in young athletes.
Dilated cardiomyopathy can be genetic or caused by alcohol, viral myocarditis, pregnancy (peripartum) or anthracyclines.
Restrictive cardiomyopathy is exemplified by cardiac amyloidosis.
Myocardial infarction
Ischaemic necrosis begins in the subendocardium and can extend through the full thickness of the wall (transmural infarction). Troponins I and T leak from dying myocytes and are the diagnostic biomarkers. The scar that forms does not contract.
Test yourself
Left ventricular myocardium receives most of its coronary blood flow during:
- Atrial systole
- Isovolumetric contraction
- Rapid ejection
- Diastole
Answer: Diastole
During systole the contracting myocardium squeezes the intramural vessels shut, especially in the subendocardium. Most left ventricular perfusion therefore happens in diastole, driven by the recoiling aorta. Tachycardia shortens diastole and so reduces coronary perfusion time.
Compiled from standard anatomy and physiology references — see the Cardiovascular System sources. For education only; not medical advice.