Hypertension-Mediated Left Ventricular Hypertrophy: From Hemodynamic Load to Myocardial Disease

Abstract

Background: Left ventricular hypertrophy due to hypertension (LVH) is one of the most important cardiac manifestations of chronic hypertension and is strongly associated with heart failure, atrial fibrillation, stroke, and death. While traditionally thought of as an adaptive response to an increase in afterload, recent advances in the understanding of LVH suggest that this condition is a composite myocardial phenotype resulting from several processes, including fibrosis, impaired microvascular function, activation of the neuro-hormonal axis (e.g., catecholamines, renin-angiotensin-aldosterone systems), metabolic stress, as well as co-morbidity of cardiorenal syndrome. Objectives: The purpose of this literature review is to provide an organized clinical approach to the epidemiology, pathophysiology, phenotyping, diagnostic evaluation/prognosis, and current treatment of hypertensive left ventricular hypertrophy, specifically, left ventricular hypertrophy. Methodology: This review draws on global guidelines for hypertension, cardiac imaging, major longitudinally studied cohorts, randomized control studies for antihypertensive treatments, and select existing reviews/meta-analyses pertaining to hypertensive heart disease/reverse remodeling. Main Findings: Current evidence shows that hypertensive LVH is a continuum that spans all stages, from an early concentric remodeling phase to a diffuse fibrosis phase, and has all of the following end-points: atrial dysfunction, arrhythmias, heart failure, and death. The ECG provides prognostic information but has limited predictive value; echocardiography is the primary method of assessing the patient's geometry and how the patient functions with their condition, while cardiac MRI is useful for providing information when the phenotype is atypical, presents with severe symptoms, or when the diagnosis is not known. The primary focus of treatment (ie, reversing LVH) continues to be controlled blood pressure (BP) combined with weight, kidney dysfunction, and Obstructive Sleep Apnea. Conclusion: LVH should be seen as a target organ damage that can be modified rather than as a static imaging diagnosis. In other words, LVH should lead to precise phenotyping (BP), broader cardiometabolic assessments, and treatments directed not just towards lowering BP, but precluding future progression to heart failure and arrhythmia.