Left ventricular hypertrophy (LVH) detected by ECG has been shown to be associated with a higher prevalence of ventricular arrhythmias in members of the general population, in a case-control series of hypertensive patients and in never-treated hypertensive patients. In-keeping with this, it has been observed that hypertension-induced LVH increases the risk of sudden cardiac death. Furthermore, a consistent bulk of data suggests antihypertensive therapy targeted at regression or prevention of electrocardiographic LVH may reduce the incidence of arrhythmias. In this regard, recent clinical trials showed that antihypertensive therapy may delay or prevent the occurrence of cardiac arrhythmias and sudden cardiac death in patients with hypertension. Porthan et al. hypothesized that an antihypertensive therapy might also rapidly affect ventricular repolarization and sought to investigate the short-term electrophysiological effects of four common antihypertensive drugs, represented by an angiotensin II receptor blocker (losartan), a beta-blocker (bisoprolol), a calcium channel blocker (amlodipine) and a thiazide diuretic (hydrochlorothiazide) in hypertensive men. Porthan et al. showed that losartan and bisoprolol favorably affected ventricular repolarization, with beneficial effects on ECG parameters of ventricular repolarization duration and heterogeneity. On the contrary, hydrochlorothiazide significantly increased repolarization heterogeneity, while amlodipine administration did not affect ECG repolarization measures. Thus, the observed findings suggest an intriguing hypothesis on the possible role of antihypertensive therapy in favouring or preventing cardiac arrhythmias.