Cardiac Responses to Increased Afterload: State‐of‐the‐Art Review
Cardiac Responses to Increased Afterload: State‐of‐the‐Art Review
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DOI：
10.1161/01.hyp.4.3.8
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发表时间：
1982-05
期刊：
影响因子：
8.3
通讯作者：
R. Tarazi;M. N. Levy
中科院分区：
文献类型：
--
作者：
R. Tarazi;M. N. Levy
B EFORE the advent of effective antihypcrtensive therapy, heart failure was the most common cause of death from hypertension. Today, hypertension remains the most common cause of left ventricular (LV) hypertrophy in adults*• and the most common precursor of congestive heart failure.• It has usually been assumed that the link between increased arterial pressure and cardiac dysfunction was straightforward, a mechanical proposition between an increased load and an overworked pump. As happens so often, the relationship proved much more complex. It has been proven that the heart does not respond similarly to all types of overload, that cardiac hypertrophy is not a homogenous entity,*' and that arterial pressure is not linearly related to cardiac dysfunction in all types or at all stages of hypertension." Pressure overload evokes cardiac responses that are different from volume overload or intense exercise.* n Whether all types of pressure overload evoke the same type of cardiac responses is one of the questions we address, as is the closely related question of whether all types of hypertension are associated with the same pattern of cardiac hypertrophy. The proposition that hypertension is not a single or homogeneous disease is universally accepted in discussions of the genesis and mechanisms of the rise in arterial pressure; it has not usually been advanced in the analysis of its cardiac consequences. This discussion is not only of theoretical value; its clinical implications may lead to a fundamental reevaluation of our therapeutic aims and guidelines. The recent observations of significant cardiac hypertrophy in borderline hypertension* u showed that structural myocardial changes are not limited to advanced stages of the disease, and that cardiac prob-
