Hypertensive heart disease can be defined as response of the heart to the after load imposed on the left ventricle by the progressively increasing arterial pressure and peripheral vascular resistance. Other than left ventricular hypertrophy other cardiac manifestations of hypertension include congestive heart failure, cardiac dysrhythmias and ischaemic heart disease. Although risk of atherosclerotic coronary heart disease is related to the systolic and diastolic pressure, most clinical trials have not found a relation between antihypertensive therapy and reduced incidence of myocardial infarction. This observation is explained by multi factorial nature of both hypertensive and coronary heart disease, age of patient, experimental design and metabolic effects of antihypertensive agents1. Some have suggested the possibility of harmful effect if diastolic pressure is reduced too much2. Relation between the height of arterial pressure and left ventricular hypertrophy has been repoted3-6. Consequences of hypertensive heart disease and obstructive coronary disease are difficult to distinguish, former involves increased myocardial oxygen demand associated with comparatively reduced coronary blood for hypertrophied left ventricle and associated micro vascular disease, later results in reduced myocardial blood supply due to occlusive atherosclerotic epicardial arterial disease. Atherosclerotic arterial disease has its own natural progression, but hypertension facilitates this process. The heart maintains its chamber size in proportion to its workload and to body weight, growth and maturation7. The type of cardiac overload determines the pattern of hypertrophy. Volume overload produces increased ventrical cavity volume on proportion to mass called “eccentric hypertrophy"8, whereas pressure overload produces increased left ventricular mass out of proportion to volume known as “concentric hypertrophy” 8. Physiologic hypertrophy refers to increased left ventricular mass in athletes, but very few studies have assessed whether exercise induced hypertrophy is physiologic or pathologic9. Hypertension has been reported as the most common precursor of the coronary heart failure10,11. Although concentric left ventricular hypertrophy maintains systolic function at a near normal level, left ventricular relaxation is impaired with long standing pressure overload reflecting reduced distensibility of the left ventricle. The clinical recognition of cardiac involvement in hypertension depends upon non-invasive methods that detect hypertrophy or abnormal left ventricular function. The most widely used clinical classification of the severity of hypertension is based on the level of systolic and diastolic pressure27, which are risk factors for left ventricular hypertrophy. On physical examination forceful and sustained apical impulse with a fourth heart sound suggests hypertrophy, an unsustained apical impulse with a faster heart rate indicates hyperdynamic circulation, lateral displacement of apical impulse shows left ventricular dialatation and presence of third heart sound along with it suggest congestive heart failure15-17. ECG the standard method of recognizing left ventricular hypertrophy and staging hypertensive heart, is recommended for every hypertensive patient. Although ECG detects only a minority of instances of left ventricular hypertrophy identified by echocardiography but despite the relative insensitivity of this method the development or reversal of ECG changes of left ventricular hypertrophy has been a strong predictor of patients outcome28,29. Definite electrocardiographic evidence of hypertrophy provides proof of target organ demage-amendate for blood pressure control - portends a poorer prognosis. Echocardiography provides good information about the structural changes in hypertensive heart disease30-32 like posterior wall and inter ventricular septal thickness and size of left ventricular chamber. Abnormality of shape and wall motion can be detected by two-dimensional echocardiography33. Exercise electrocardiography and newer imaging methods are being used to work out true deficits in myocardial perfusion due to hypertensive arteriolar disease34,35. Positive exercise tests are common in hypertensive patients without obstructive epicardial coronary artery disease. Nuclear magnatic resonance imaging or CT scan with proper cardiac-cycle gating, provides high quality representation of cardiac size, geometry and function36-38, but these techniques are currently too expensive as compared with echocardiography, so can only be used in very selected cases. Complications of hypertensive heart includes cardiac hypertrophy, which is an adaptive benefit but confers substantial risk on the patient due to myocardial ischaemia and increased minimal vascular resistance5,6,11. Greater susceptibility to leathal dysrhythmias and ectopic ventricular activity is also a risk factor for sudden death39. Development of cardiac failure, in which diastolic dysfunction precedes systolic dysfunction during long procession of hypertensive heart disease to cardiac failure. Main therapeutic concerning coversing left ventricular hypertrophy is the need to prevent its development in the first place. This requires a commitment to the early treatment of hypertension before hypertrophy develops. Almost all antihypertensive agents, when used for long enough periods will reduce left ventricular mass, but not all agents in some class of drugs have the same effect on cardiac mass40. Only certain drugs reduce mass within a period of weeks. Short term therapy with diuretics and direct acting smooth muscle vasodilators such as hydralazine will not reduce left ventricular mass, whereas short term therapy for four to eight weeks with beta adrenergic receptor blockers, centrally acting adrenolytic drugs such as methyldopa, angiotensive converting enzyme inhibitors and calcium channel blockers will reduce left ventricular mass rapidly. These findings suggest that the reversal of left ventricular hypertrophy after short term therapy is unclear, but they may include inhibition of adrenergic or renin-angiotensin system, changes in intracellular calcium and induction or inhibition of humoral substances, growth factors or proto oncogenes20,23,24,41,42. It is still too early to identify which forms of therapy are best. In this regard it will be important to learn whether the reversal of left ventricular hypertrophy with specific antihypertensive agents increases survival or not?
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