Factors involved in the pathogenesis of hypertensive cardiovascular hypertrophy. A review

All tissues can rapidly adapt their structural design whenever prolonged changes of load/activity occur within the limits characteristic of each tissue. This structural adaptation, however, is modified by various genetic and trophic influences. When antihypertensive therapy is considered in the hypertensive patient, such changes are usually well established and the cardiovascular system is structurally adapted to maintain a higher pressure than normal. Increased blood pressure and afterload cannot solely explain the development of cardiac hypertrophy. Permissive actions from the sympathetic nervous system and the circulating angiotensin II are likely, but conflicting results still exist. There is evidence for a functional renin-angiotensin system in the heart, which may be involved in the genesis of left ventricular hypertrophy. Also, a soluble factor in the hypertrophied myocardium that stimulates protein synthesis may play a key role in modulation of myocardial structure during development or regression of myocardial hypertrophy in hypertension. Hypertrophy of both the large and smaller arterial vessels has been shown to follow the same general pattern of development and regression as in the heart. The vascular hypertrophy (predominantly of the media in the arterioles) can be considered as the ultimate structural factor behind the progression of hypertension independent of the initiating factor. A vicious circle with the increased resistance as the key factor can be identified. There are at least 3 possible initiating factors: a small rise in arterial pressure, an abnormal or reinforced response to pressure, or trophic/mitogenic stimuli acting directly on the vascular smooth muscle cell. The ultimate goal in the treatment of high blood pressure is to reduce hypertension-related morbidity and mortality. Normalisation of structural cardiovascular changes is also important and easier to evaluate in the individual. Understanding of the pathogenesis of structural adaptation may help in the selection of the best treatment.