The many faces of arterial hypertension in hypertrophic cardiomyopathy and its phenocopies: bystander, consequence, modifier

Arterial hypertension is the most prevalent cardiovascular (CV) risk factor worldwide, and a major preventable cause of CV, cerebrovascular and renal disease [1]. Arterial hypertension causes progressive myocardial remodeling, mainly characterized by left ventricular hypertrophy (LVH), which, once developed, strongly associates with adverse CV outcomes [2, 3]. At the molecular level, multiple alterations may be found in hypertensive hearts, including fbrosis, microvascular coronary circulation impairment, imbalance in the arterial-ventricular coupling and derangement of energetic mechanisms [2, 3]. As all these abnormalities may contribute to myocardial remodeling, it is now believed that LVH in arterial hypertension is not solely the result of an overload (haemodynamic) condition