The American journal of medicine
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Left ventricular hypertrophy is both a target organ response to hypertensive vascular disease as well as a factor that might be responsible for other cardiovascular events. Recent work confirms that the increased cardiac mass associated with hypertension results as a structural adaptation to the increased afterload imposed on the heart. Initially there is a transient period of hyperfunction that is followed by the sustained structural adaptative period of stable hyperfunction. ⋯ These include: the pressor mechanisms per se; the age, sex, and race of the patient; and coexisting diseases. Some of these factors may account in part for the regression of cardiac mass with antihypertensive therapy. However, until we understand more clearly those factors that transduce the physical stimulus for hypertrophy into biochemical events, we shall neither understand completely the development of this structural adaptation of the heart nor its regression with treatment.
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The left ventricle adapts to an increased afterload such as that produced by arterial hypertension with concentric left ventricular hypertrophy. However, this adaptive process can be modified by a variety of physiologic and pathophysiologic states. Progressive aging, black race, and perhaps disorders with an increased sympathetic outflow seem to accelerate left ventricular hypertrophy. ⋯ Left ventricular hypertrophy has been shown to increase ventricular ectopic impulse generation and to put patients at a high risk of sudden death. Moreover, the increase in myocardial mass lowers coronary reserve and enhances cardiac oxygen requirements. Thus, the presence of left ventricular hypertrophy has to be considered as an ominous sign rather than as a benign adaptive process.
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The purpose of this study was to examine the incidence and implications of false-negative exercise electrocardiographic results among 216 consecutive patients with angiographically documented coronary artery disease (50 percent diameter narrowing or greater of one or more vessels). Exercise electrocardiography gave negative (false-negative) results in 23 patients and positive (true-positive) results in 102 patients, and were nondiagnostic in the rest. Exercise thallium-201 imaging was performed in 88 patients. ⋯ Angina during exercise was less frequent in patients with false-negative results (p less than 0.01). Abnormal exercise thallium-201 images were seen in 15 of 20 patients (75 percent) with false-negative results and in 56 of 68 patients (82 percent) with true-positive results (p = NS). It is concluded that (1) false-negative exercise electrocardiographic results are infrequent (10 percent) among patients with coronary artery disease and are associated with less extensive coronary artery disease; (2) the frequency of Q-wave infarction and left ventricular asynergy is the same in patients with false-negative results as in patients with true-positive exercise electrocardiographic results; (3) exercise thallium images can identify 75 percent of patients with coronary disease and false-negative results of exercise electrocardiography.