RESUMO
PURPOSE OF REVIEW: The purpose of this review is to answer the question whether left ventricular hypertrophy (LVH) could be considered a therapeutic target in patients with hypertension. To fulfill this purpose, we briefly outline different methods of measuring LVH, then discuss the current evidence and unresolved controversies regarding the relationships among LVH, blood pressure (BP), and cardiovascular disease (CVD) outcomes. RECENT FINDINGS: The methods and criteria used for defining LVH in clinical studies lack consistency and are inherently different. Electrocardiogram (ECG) has been the most common method, but some studies used echocardiography, and recently, the cardiac magnetic resonance imaging was used by some studies as well. Regardless of the method, studies have shown that higher BP is a risk factor for LVH, regression of LVH is possible by successful BP lowering, and LVH is associated with CVD outcomes. Nevertheless, recent trials revealed that although intensive BP lowering (systolic BP target of < 120 mm of Hg) resulted in lower rates of developing new ECG-LVH and higher rates of regression of existing LVH, the benefit of intensive BP lowering on the risk of CV events was not meaningfully influenced by its favorable effect on ECG-LVH. These findings raise several critical questions about the mechanistic links between hypertension treatment, LVH regression, and reduction in CV events. Given these questions and findings, LVH improvement cannot yet be considered a reliable surrogate outcome measure for use in the context of hypertensive heart disease. LVH is a modifiable risk factor related to systolic BP and regression of LVH may reduce subsequent CV events. However, LVH may not be the "holy grail" in regard to therapeutic targets in hypertensive heart disease, but it could be considered one of the markers in the successful management of hypertension.