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Atrial fibrillation (AF) is the most common chronic cardiac arrhythmia and a major public health problem, leading to high rates of morbidity and mortality. The most prevalent cause of AF in the western world is hypertensive heart disease. Blood pressure increase leads to hemodynamic modifications which usually have direct effects on left ventricular and atrial structure and function. The renin-angiotensin-aldosterone system (RAAS) plays an important role in regulating blood volume and systemic vascular resistance. Furthermore, recent studies showed that RAAS plays a key role in left atrial and ventricle structural and functional remodeling. Experimental studies and clinical trials have shown that angiotensin-II converting enzyme (ACE) inhibitors and angiotensin-II receptor blockers are effective in preventing atrial fibrillation in patients with arterial hypertension or several forms of heart disease. In our study, we showed that ramipril is effective in preventing AF relapses in patients with lone AF (LAF: i.e AF in the absence of clinical and echocardiographic evidence of cardiovascular, pulmonary, or endocrine disease), independently of any sizeable effect on cardiac echocardiographic anatomy when compared with baseline data. In this paper, we briefly discuss: 1) the role of ACE inhibitor ramipril in preventing AF relapses in LAF patients; 2) the underlying mechanisms by which it can potentially act; 3) the possibility of considering the occurrence of LAF as a marker of subclinical organ damage in subjects with blood pressure values in the 130 to 139 mm Hg range, that is in the pre-hypertension classification according to the JNC-7 Report, of high normal blood pressure levels according to the 2007 ESC/ESH guidelines.