Cardiac muscle

Structure

Cardiomyocytes are about 100 µm long and 10–20 µm thick and usually have one, occasionally two central oval nuclei. At the nuclear poles is a myofibril-free, pale zone (perinuclear halo) containing mitochondria, Golgi apparatus and lipofuscin. The cells branch in a Y-shape and are joined end to end by intercalated discs – step-like lines across the fibre containing adherens junctions, desmosomes and gap junctions. Between the cells lies loose connective tissue with a very dense capillary network.

Function

Cardiac muscle contracts rhythmically, involuntarily and without fatigue. Excitation arises in the sinoatrial node and spreads from cell to cell via the gap junctions of the intercalated discs – the myocardium works as a functional syncytium. The high energy demand is met by abundant mitochondria and dense capillary supply. Adult cardiomyocytes hardly divide; lost tissue is replaced by scar tissue.

Microscopy tips

Look for a longitudinally cut area. Watch for one nucleus per cell in the middle of the fibre, often with a pale halo at both poles, and for branching fibres. In H&E, intercalated discs can only be guessed at high magnification as fine darker transverse lines; with iron haematoxylin they stand out clearly. In cross-section, the nuclei lie centrally in roundish, irregular profiles. Differential diagnosis: skeletal muscle has peripheral nuclei and unbranched fibres; smooth muscle lacks striation and has spindle-shaped cells.

Clinical relevance

In myocardial infarction, cardiomyocytes die and are replaced within weeks by collagen-rich scar tissue. Under chronic pressure overload (e.g. hypertension), the myocardium responds with hypertrophy: the cells thicken and their nuclei become large and plump. In hypertrophy the number of capillaries does not increase to the same extent, so the myocardium becomes more vulnerable to oxygen shortage. Histologically, an infarct is dated by cell necrosis, neutrophil infiltration, granulation tissue and finally scar.

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