THE CONTEXT
Myocardial contraction depends on connections between myocytes, the organisation of sarcomeres and calcium-triggered interactions between actin and myosin.
Myocytes and intercellular connections
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Myocytes are approximately 50–100 μm long and branch and interdigitate with adjacent cells.
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Intercalated discs permit electrical conduction through gap junctions and mechanical conduction through the fascia adherens.
Sarcomere and contractile proteins
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The sarcomere is the basic contractile unit and is approximately 2 μm long. Alignment with adjacent myofibrils produces the striated appearance associated with Z-lines.
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Actin filaments attach at right angles to Z-lines and interdigitate with thicker, parallel myosin filaments.
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Actin–myosin cross-links contain myofibrillar adenosine triphosphatase (ATPase), which breaks down adenosine triphosphate (ATP) to supply energy for contraction.
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Two actin chains form a helix. Tropomyosin lies in its grooves, and a troponin complex is attached to every seventh actin molecule.
Calcium, contractile force and ventricular output
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During the action potential plateau, calcium enters the cell and is mobilised from the sarcoplasmic reticulum.
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Calcium binds to troponin and precipitates contraction through sarcomere shortening as actin and myosin interdigitate.
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Calcium influx through slow calcium channels regulates the force of contraction, or inotropic state.
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The extent of sarcomere shortening determines ventricular stroke volume. Powerful inotropic drugs or marked exercise produce maximal shortening.
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Cardiac enlargement in heart failure results from slippage of myofibrils and adjacent cells rather than lengthening of sarcomeres.