Arterial hypertension leads to both structural and functional changes of the heart. Hypertensive heart disease (HHD) is characterized by complex changes in myocardial structure (e.g., enhanced cardiomyocyte growth, excessive cardiomyocyte apoptosis, accumulation of interstitial and perivascular collagen fibers, disruption of endomysial and perimysial collagen network) that cause the remodeling of the myocardium. In the 1970s, hypertrophic growth of cardiomyocytes is compensatory to reduce wall stress on the ventricular wall imposed by pressure overload. Recent data from animal studies suggest that inhibition of ventricular hypertrophy was not associated with ventricular dilatation or reduced wall motion despite elevated wall stress. The genetic complexity (gene-gene and/or gene-environment interactions) may modulate left ventricular mass and transcriptional regulators are participated in pathologic myocardial growth. Many hormones and cytokines lead to a profibrotic and inflammatory environment. Excess of ventricular collagen in hypertensive patients is the result of both increased collagen synthesis by fibroblasts and stimulated myofibroblasts, and unchanged or decreased collagen degradation by matrix metalloproteinase. Several biochemical markers of myocardial remodeling will prove to be useful. The development of noninvasive methods like echoreflectivity, cardiac magnetic resonance imaging, speckle tracking echocardiography, and cardiac molecular imaging would enable broader application. Meta-analysis showed that there was a significant difference among medication classes in decreasing left ventricular mass.