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左室肥大与高血压，解说词：
Following sustained hypertension the heart develops concentric hypertrophy that is characterized by thickening of the intraventricular septum and the free wall of the left ventricle. This hypertrophic process is initially adaptive, in that it enables the heart to maintain normal pump performance in the face of the increased afterload that is imposed by an elevated blood pressure. However, this hypertrophic process leads to a series of maladaptive changes that occur in the extracellular matrix, as well as in the cardiac myocytes themselves. As shown, there is an increase in the fibrillar collagen network that surrounds the individual cardiac myocytes. This increase in fibrillar collagen prevents the heart from contracting and relaxing normally.
In addition to the non-cellular problems in the myocardium, there are a number of problems that arise within the hypertrophied cardiac myocytes themselves. The most notable of these abnormalities involves the process of excitation contraction coupling.
One of the best characterized abnormalities of excitation contraction coupling relates to the decrease in the amount of calcium that is released from the sarcoplasmic reticulum of the hypertrophied cardiac myocyte. The mechanism that is responsible for the decreased release of calcium from the sarcoplasmic reticulum is complex and is thought to involve decreased release of calcium by the ryanodine receptor and decreased uptake of calcium from the cytosol by the calcium pump of the sarcoplasmic reticulum. This decrease in calcium results in a decrease in the extent of sarcomere shortening causing myocyte dysfunction.
In the preceding sequence we have reviewed some of the abnormalities of excitation contraction coupling in the hypertrophied heart. As shown in the lower panel, these abnormalities in excitation contraction coupling translate into a decreased activation of the actin and myosin cross-bridges that are believed to set the stage for the transition from concentric hypertrophy to dilated cardiomyopathy.
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