Left ventricular hypertrophy (LVH) is a structural remodeling of the heart developing as a response to volume and/or pressure overload. Previous studies have shown that hypertension is not an independent factor in the development of LVH and occurrence does not depend on the length and severity of hypertension, but the role played by other comorbidities such as triglycerides, age, gender, genetics, insulin resistance, obesity, physical inactivity, increased salt intake and chronic stress. LVH develops through three phases: adaptive, compensatory, and pathological phase. Contractile dysfunction is reversible in the first two phases and irreversible in the third. According to the Framingham study, LVH develops in 15-20% of patients with mild arterial hypertension, and in 50% of patients with severe hypertension. The pathophysiology of LVH includes hypertrophy of cardiomyocytes, interstitial and perivascular fibrosis, coronary microangiopathy and macroangiopathy. Individuals with LVH have 2-4 times higher risk of having adverse CV events compared to patients without LVH.