Regression of LVH or improved prognosis (or both): what is the question?

Abstract

Left ventricular hypertrophy (LVH) can be regarded as an example of the evolution of cardiovascular disease en route to a bad outcome. Whilst LVH can also be regarded as an adaptive or compensatory response of the heart to increased blood pressure (BP) it is associated with many complications, such as sudden death, arrhythmias (including atrial fibrillation and ventricular arrhythmias), myocardial infarction, congestive heart failure and stroke. Of note, the frequency and severity of these complications are closer related to the degree of LVH than the level of the arterial pressure. Therefore, the effectiveness of anti-hypertensive treatment should not simply aim to reduce BP, but should also focus on the regression of hypertension-induced structural changes in the cardiovascular system, particularly LVH.Nevertheless, there is more to LVH than simply the elevation of BP. Other determinants of the development of LVH include hereditary and demographic factors such as age, gender, obesity, exogenous factors like dietary salt intake and alcohol, and neurohumoral factors such as the activity of the reninangiotensin-aldosterone system, the sympathetic system, insulin, parathyroid and other hormones. 1-2As hypertensive cardiovascular disease progresses, four pathophysiologic mechanisms are postulated to relate LVH with increased cardiovascular morbidity and mortality: 1 (i) impaired diastolic filling (reduction of early diastolic filling); (ii) myocardial ischaemia (impairment of coronary reserve); (iii) ventricular arrhythmias (which have been implicated in sudden death); and (iv) impaired myocardial contractility (resulting in dilatation of left ventricle and congestive heart failure).Given the large impact of LVH on hypertensive morbidity and mortality, it is not surprising that there have been more than 1000 clinical and experimental studies in both animals and humans in the literature on the issue of LVH regression. The main

Hypertension, left ventricular hypertrophy, and sudden death

“…However, LVH can also be regarded as a compensatory mechanism in response to the elevated pressure load on the heart. When the heart's workload is increased, it has the capacity to change its shape and mass [1]. In hypertension, it does so by increasing its contractile units, as well as the proliferation of fibroblasts and deposition of collagen, thus forming the basis for the development of LVH.…”