Left Ventricular Hypertrophy

Abstract

Left ventricular hypertrophy (LVH) can be detected by electrocardiography or, with greater sensitivity, by echocardiography. Its prevalence increases with age, probably due to greater disease diffusion rather than aging itself. LVH is not only a consequence of disease, but also an independent contributor to morbidity and mortality, both in young and aged populations. Attempts have been made to reduce left ventricular (LV) mass by pharmacological and other means. LVH regression is possible in young and old hypertensive patients by some but not all hypotensive drugs. The effect on LV mass seems largely independent of blood pressure reduction. Whether LV mass control should be sought beyond the treatment of the underlying disease is still debated. Preliminary data indicate prognostic benefits associated with LVH regression, but studies on the elderly are scanty. LVH is a common and ominous finding in old people. In hypertension it can be reversed by drug therapy, with apparent functional improvement. Further studies are needed to verify the long term consequence of LV mass reduction in this age group.

Circulating Total Extracellular Vesicles Cargo Are Associated with Age-Related Oxidative Stress and Susceptibility to Cardiovascular Diseases: Exploratory Results from Microarray Data

“…Interestingly, cardiac hypertrophy signaling was the top canonical pathway impacted by differentially expressed miRNAs in circulating total EVPs from aged rats. Even in healthy individuals without any cardiovascular disease, the prevalence of left ventricular hypertrophy is increased with age-independent of any predictable risk factors [34][35][36]-and thus, cardiac hypertrophy is considered a hallmark of cardiac aging [35]. Previous data have described several miRNAs in cardiac tissue associated with cardiomyocyte hypertrophic signaling, both in human and rodent models of hypertrophic cardiomyopathy-including miR-214 [37], miR-199a [38], and let-7 [39].…”