Hypertensive cardiomyopathy is the cardiac structural and functional consequence of chronic systemic hypertension. Sustained pressure overload on the left ventricle triggers compensatory left ventricular hypertrophy (LVH) — the myocardium thickens to normalize wall stress according to the Law of Laplace (wall stress = pressure × radius / 2 × wall thickness). Initially, concentric LVH (wall thickening without chamber dilation) is adaptive, maintaining cardiac output. However, prolonged hypertrophy leads to pathological remodeling: myocyte hypertrophy, interstitial fibrosis, impaired coronary microvascular blood flow (supply-demand mismatch), and diastolic dysfunction (stiff, non-compliant ventricle that resists filling). Diastolic heart failure (HFpEF) is the most common cardiac consequence of chronic HTN. As disease progresses, the ventricle may dilate (eccentric hypertrophy), systolic function declines, and systolic heart failure (HFrEF) develops. LVH is also an independent risk factor for arrhythmias (atrial fibrillation from left atrial dilation, ventricular arrhythmias from myocardial fibrosis), sudden cardiac death, stroke, and coronary artery disease. ECG findings include increased voltage (Sokolow-Lyon criteria: S in V1 + R in V5 or V6 ≥35 mm), left axis deviation, and LV strain pattern (ST depression and T-wave inversion...