Pathophysiological factors that link hypertension with acute coronary syndromes. A complex interplay of genetic predisposition, abnormal vasoreactivity, and vessel wall shear stress coupled with neurohormonal activation triggers endothelial dysfunction, vessel wall remodeling, and development of atherosclerotic lesions. Coronary plaque rupture in the setting of a hypercoagulant state eventually leads to an ACS. ACE, angiotensin‐converting enzyme; ACS, acute coronary syndrome; Ang II, angiotensin II; BKB2, bradykinin B2; KCNMA1, Ca++‐dependent potassium channel alpha1 subunit; LVH, left ventricular hypertrophy; NO, nitric oxide