Abstract

Atrial cardiopathy, encompassing chamber enlargement, wall structural changes, electrical remodeling, functional impairment, and prothrombotic predisposition,1–3 may be detected in individuals in the general population, including those with normotension and hypertension. Beyond volume or pressure overload related to valvular heart disease, various factors may be associated with atrial cardiopathy.1–3 In normotensive subjects, aging, obesity, diabetes, systemic inflammation, obstructive sleep apnea, and undiagnosed ventricular dysfunction could contribute to atrial cardiopathy.1–3 In hypertensive patients, in addition to the same factors reported above, specific features related to hypertension per se, such as sympathetic nervous activation, renin–angiotensin–aldosterone system activation, left ventricular structural changes, and left ventricular diastolic and/or systolic dysfunction leading to increased end-diastolic pressure and atrial stretching predispose to atrial cardiopathy.1–4 It has been reported that atrial cardiopathy increases the risk of stroke, even in the absence of atrial fibrillation, and increases the risk of atrial fibrillation which further increases the risk of thromboembolism, stroke, and mortality.5–8

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