The heart contributes to the maintenance of hypertension by generating an increased arterial pressure. At the same time, the increased left ventricular wall tension leads to striking structural, biochemical, and physiological changes in the myocardium. As hypertrophy develops because of RNA-mediated protein synthesis, the increased myocardial mass helps to maintain left ventricular stroke volume, but dilatation of the left ventricle and eventually frank congestive heart failure may supervene. Heart failure may be attributed not only to the primary functional changes in the hypertrophied myocardium but to the interaction of a number of factors that further increase resistance to left ventricular ejection, increase venous return to the heart, or secondarily alter myocardial function. The interaction of coronary artery disease with hypertension is particularly important in the pathophysiology of so-called hypertensive heart failure.
|Original language||English (US)|
|Number of pages||11|
|Journal||Archives of Internal Medicine|
|State||Published - Jun 1974|