The arterial supply of the heart is built from the right and left coronary arteries, which arise from the aorta.
The cardiac muscle is composed by specialized cells: cardiac myocytes. Kumar et al. (2005) describe five major components in the myocytes: cell membrane (sarcolemma) and T-tubules; sarcoplasmic reticulum; contractile elements; mitochondria; and nucleus. The sarcolemma and T-tubules enable impulse conductions, and the sarcoplasmic reticulum is a calcium reservoir needed for contraction. Mitochondria are crucial components, since they are involved in cardiac contraction by providing a constant supply of ATP to the sarcomeres. Mitochondria are abundant in cardiac tissue, constituting 20% to 40% of cellular volume in energy-demanding zones (Marin-Garcia 2005).
Cardiac muscle is composed of sarcomeres, which are the contractile units with an arrangement of thin and thick myofilaments. The myocytes are composed of many parallel myofilaments arrays of sarcomeres in series, which are responsible for the striated appearance (Kumar 2005). Thin filaments are composed of various proteins named actin, tropomyosin, and troponin. Myosin is the thick filament, and possesses the cross-bridges that can attach to the actin. Au (2004) has described the various components of the sarcomere in great detail. Since cross-bridges possess ATPase activity, contraction may be explained as a continuous cycling of cross-bridges. Moreover, cardiac muscle fibers are joined together by junctional complexes called intercalated discs (Dunn 2004), so that the action potential is spread.
The role of Calcium
Calcium (Ca2+) regulates mechanical contractions and Vandenboom et al. (2005) have shown that "cross-bridge attachment increases thin filament activation dynamically and that this increase is proportional to the level of activation first established by Ca2+"; during membrane depolarization, a small amount of Ca2+ enters through specialized channels, and the influx triggers calcium release of the sarcoplasmic reticulum. Intracellular calcium binds to troponin C, which induces activation of the myofilaments and muscle contraction. Relaxation is initiated by dissociation of Ca2+ from troponin C, followed by its reuptake into the sarcoplasmic reticulum and removal through sodium/calcium exchangers (Chakraborti et al. 2007).
Structure and Function
Ventricular muscle contracts during systole and relaxes during diastole. The sarcomere length and sliding mechanism has been described by various researchers (Pollack et al 2005). The Frank-Starling mechanism depicts the relationship between structural components of the heart and its function: shorter sarcomeres have considerable overlap of actin and myosin filaments, reducing its contractile force, whereas longer lengths enhance contractility. In a normal heart, moderate dilation increases the subsequent force of contraction. With progressive dilation, however, there is a point at which effective overlap of filaments is reduced, and the force of contraction is reduced (Kumar 2005). The clinical consequences of