It is time to recognize that the quality, not quantity, of myocardium in hypertensive heart disease is responsible for adverse cardiovascular events. Experimental and clinical available data indicate that myocardial fibrosis due to the exaggerated accumulation of collagen type I and type III fibers predisposes to an enhanced risk of diastolic and/or systolic ventricular dysfunction, symptomatic heart failure, ischemic heart disease, and arrhythmias in patients with hypertensive heart disease. Thus, management of these patients must not only focus on detection and regression of left ventricular hypertrophy. Far more sensible are interventions aimed to detect and target hypertensive myocardial fibrosis. The available data on the use of biochemical and/or imaging methodologies to address excessive accumulation of collagen fibers in the myocardium of hypertensive patients are promising. On the other hand, preliminary data suggest that the goal of reducing myocardial fibrosis is achievable in patients with hypertensive heart disease treated with specific antihypertensive agents. Collectively, these findings set the stage for larger trials where-in noninvasive measures and reparative strategies of myocardial fibrosis to prevent heart failure could prove useful.