The cellular basis of myocardial contraction Myocardial cells contain bundles of parallel myofibrils. Each myofibril is made up of a series of sarcomeres A sarcomere is bound by two transverse Z lines, to each of which is attached a perpendicular filament of the protein actin. The actin filaments from each of the two Z bands overlap with thicker parallel protein filaments known as myosin. Actin and myosin filaments are attached to each other by cross-bridges that contain ATPase.
During cardiac contraction the length of the actin and myosin mono filaments does not change. Rather, the actin filaments slide between the myosin filaments when a high-energy bond of ATP is split by ATPase. Magnesium ions are required to facilitate this reaction. To supply the ATP, the myocyte (which cannot stop for a rest) has an extraordinarily high mitochondrial density (35% of the cell volume). Calcium ions initiate contraction by inactivating another protein called troponin C, which ordinarily inhibits the actin-myosin interaction. Calcium is made available during the plateau phase (phase 2) of the action potential by calcium ions entering the cell and by being mobilized in mass from the sarcoplasmic reticulum. The force of cardiac muscle contraction (‘inotropic state’) is thus regulated by the influx of calcium ions into the cell through slow calcium channels.
Starling’s law of the heart
The contractile function of an isolated strip of cardiac tissue can be described by the relationship between the velocity of muscle contraction, the load that may be moved by the contracting muscle, and the extent to which the muscle is stretched before contracting. As with all other types of muscle, the velocity of contraction of myocardial tissue is reduced by increasing the load against which the tissue must contract. However, in the nonfailing heart, prestretching of cardiac muscle improves the relationship between the force and velocity of contraction.
This phenomenon was described in the intact heart as an increase of stroke volume (ventricular performance) with an enlargement of the diastolic volume (pre-load), and is known as ‘Starling’s law of the heart’ or the ‘Frank- Starling relationship’. It has been transcribed into more clinically relevant indices. Thus, stroke work (aortic pressure x stroke volume) is increased as ventricular enddiastolic volume is raised. Alternatively, within certain limits, cardiac output rises as pulmonary capillary wedge pressure increases. This clinical relationship is described by the ventricular function curve, which also shows the effect of sympathetic stimulation).