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ObjectivesThe aim of the present study was to verify whether angiotensin-II converting enzyme (ACE) inhibition is also effective in preventing relapses of lone atrial fibrillation (LAF), that is, in the absence of hypertension and/or heart disease.BackgroundSeveral studies have shown that ACE inhibitors are effective in preventing atrial fibrillation (AF) relapses in patients with arterial hypertension or several forms of heart disease, that is, in the presence of clinical conditions that are recognized as causing a higher risk of atrial arrhythmias.MethodsSixty-two patients admitted to the emergency department of our institution for a first-ever episode of LAF were enrolled in the study after excluding the presence of cardiac or extracardiac conditions known to be associated with an increased risk of AF, by medical history, physical examination, complete echocardiographic study, and the evaluation of blood pressure, thyroid function, urinary catecholamines, serum electrolytes, blood glucose, red blood cell count, and arterial blood gases. After cardioversion to sinus rhythm by intravenous propafenone, patients were randomized to either ramipril 5 mg/day (n = 31) or placebo (n = 31). Holter monitoring and clinical examination were performed every 3 months.ResultsAfter a 3-year follow-up, AF relapses were observed in 3 patients treated with ramipril and in 10 patients allocated to placebo (p < 0.03, Kaplan-Meier, log-rank test). During follow-up, none of the patients developed arterial hypertension or other cardiac or extracardiac condition known to be associated with increased risk of AF, that is, in all patients the diagnosis of LAF was confirmed.ConclusionsRamipril is effective in preventing relapses of LAF.

Background: Failure to achieve good blood pressure (BP) control is probably the most important reason for high rates of morbidity and mortality in patients with hypertension. Combination therapy has been shown to increase the percentage of patients in whom BP control is achieved. One combination is a calcium channel blocker (CCB) and an angiotensin-converting enzyme inhibitor (ACE-I). Objective: The aim of this study was to assess the effects of the fixed combination of the CCB manidipine and the ACE-I delapril in the treatment of hypertensive patients already given monotherapy with either component but with poor results (ie, insufficient BP control or adverse events [AEs]). Methods: In this Phase III, multicenter, open-label, clinical trial, patients with mild to moderate hypertension were assigned to 1 of 2 groups. Group 1 comprised patients whose diastolic BP (DBP) was >90 mm Hg or who experienced AEs with manidipine 20 mg once daily. Group 2 comprised patients who had a DBP >90 mm Hg or who experienced AEs with delapril 30 mg BID. In both groups, patients aged

Background: The angiotensin II (AII) receptor antagonists are effective agents for the treatment of mild to moderate hypertension. Agents within this drug class differ with respect to their pharmacologic and pharmacokinetic properties, which may translate into differences in antihypertensive effect. Objective: The purpose of this study was to compare the antihypertensive efficacy of the AII receptor antagonists losartan, valsartan, and telmisartan using 24-hour ambulatory blood pressure monitoring (ABPM). Methods: Outpatients aged 40 to 60 years with mild to moderate hypertension (sitting diastolic blood pressure [DBP] ≥95 mm Hg and ≤115 mm Hg) were enrolled. After a 4-week placebo washout period, patients were randomized to receive losartan 50 mg, valsartan 80 mg, telmisartan 40 mg, or placebo once daily for 4 weeks according to a 4-period crossover design. Each treatment period was separated by a 2-week placebo washout period. Every 2 weeks, 24-hour ABPM was performed. To assess the homogeneity of blood pressure (BP) control, the trough-to-peak (T/P) ratio and the smoothness index (SI) for systolic blood pressure (SBP) and DBP were calculated. Results: After 2 and 4 weeks of treatment, all 3 agents produced significant reductions in 24-hour, daytime, and nighttime SBP and DBP, compared with placebo ( P P P 50%. The SI for SBP and DBP was significantly higher with valsartan than with losartan and telmisartan both at 2 weeks ( P P P P Conclusions: In the present study, treatment with valsartan resulted in an earlier, greater, and smoother antihypertensive effect compared with treatment with losartan or telmisartan; this differential effect was likely due to differences in the pharmacologic properties of these agents. Analysis of SI revealed a qualitative difference in the antihypertensive action of telmisartan at the beginning of treatment.

Background: Ankle edema is one of the most common side effects of antihypertensive treatment with calcium channel blockers (CCBs). The incidence of edema is higher with dihydropyridines than with verapamil or diltiazem. Objective: The aim of this study was to compare the effect of antihypertensive treatment with the new CCB lercanidipine versus nifedipine gastrointestinal therapeutic system (GITS) on ankle-foot volume (AFV) and on pretibial subcutaneous tissue pressure (PSTP), considered objective measures of CCB-induced ankle edema. Methods: Patients with mild to moderate hypertension (diastolic >90 mm Hg and Results: Sixty patients (34 men and 26 women) aged 36 to 70 years were enrolled. Lercanidipine and nifedipine GITS produced similar reductions in systolic and diastolic BP (lercanidipine, −18.7/11.8 mm Hg; nifedipine GITS, −18.8/11.5 mm Hg; P P 2 O) compared with nifedipine GITS (AFV, 284.2 mL; PSTP, 1.8 cm H 2 O). In both treatment groups, correlation analysis showed an inverse relationship, although to a different degree, between AFV and PSTP changes, but not between absolute values of AFV and PSTP during treatment. AFV increase was greater and PSTP increase was lower with increasing age, which suggests a role for age in the type of tissue response to a stimulus for edema formation. No relationship was found between AFV and PSTP changes and BP reduction. Conclusions: These data suggest that lercanidipine produces significantly less increases in AFV and PSTP, 2 objective measures of edema formation, than nifedipine GITS.

The aim of this study was to assess the effects of adding losartan to lisinopril on 24-hour blood pressure (BP) values and on the reninangiotensin system (RAS) in patients with hypertension whose condition was not controlled by lisinopril monotherapy. We studied 52 patients with essential hypertension (27 men, 25 women; mean age, 56 ± 6 years) with sitting diastolic blood pressure (DBF) > 90 mm Hg after 4 weeks of monotherapy with lisinopril 10 mg once daily. The patients were randomly allocated to receive either losartan 50 mg once daily in addition to lisinopril 10 mg once daily or a double dose of lisinopril (20 mg once daily) for 4 weeks, according to a doublemasked, crossover design. At the end of each treatment period, casual BP and heart rate were measured, noninvasive 24-hour ambulatory blood pressure monitoring was performed, and a blood sample was obtained to measure plasma renin activity (PRA) and angiotensin (Ang) I and II levels. The combined administration of losartan 50 mg and lisinopril 10 mg produced a greater reduction in both ambulatory and casual systolic BP and DBP values compared with lisinopril 20 mg. The additive BP-lowering effect of the combination therapy occurred during both the 24-hour period and the single daytime and nighttime subperiods, without interfering with the normal circadian BP pattern. Furthermore, the losartanlisinopril combination increased PRA and Ang I more than lisinopril 20 mg and decreased the losartan-induced peak value of Ang II. Results of this study suggest that the addition of losartan to lisinopril therapy was more effective in decreasing BP and increasing PRA and Ang I than doubling the lisinopril dose; therefore, a more complete RAS blockade might improve BP control in patients with hypertension.

The aim of this prospective, randomized, open-label, masked, endpoint, crossover study was to compare the antihypertensive efficacy of valsartan with that of losartan—angiotensin II (Ang II) receptor antagonists with different pharmacologic profiles—in patients with mild-to-moderate essential hypertension. After an initial 2-week placebo washout period, 40 patients (24 men and 16 women, aged 39 to 58 years) were assigned randomly to receive valsartan 80 mg or losartan 50 mg once daily for 4 weeks. After an intermediate 2-week placebo washout period, patients were switched to the alternative regimen for an additional 4 weeks. After the initial placebo washout period and every 2 weeks thereafter, 24-hour ambulatory blood pressure monitoring (ABPM) was performed using a noninvasive device, and casual blood pressure (BP) and heart rate were measured. Both losartan and valsartan had a clear-cut antihypertensive effect. However, valsartan showed significantly better antihypertensive efficacy compared with that of losartan, as demonstrated by (1) the 24-hour, daytime, and nighttime ABPM values, which were significantly lower ( P

Prostaglandins (PGs) are thought to play a role in the genesis of cough induced by angiotensin-converting enzyme (ACE) inhibitors, whereas inhibition of PG synthesis can reduce or abolish the incidence of this side effect. Experimental and clinical data suggest that nifedipine, a dihydropyridine calcium channel blocker, can inhibit PG synthesis. Therefore, the aim of the present study was to determine whether treatment with amlodipine would also reduce cough induced by an ACE inhibitor and to compare the efficacy of amlodipine with that of indomethacin, a known inhibitor of PG synthesis. Thirty-three patients with hypertension who developed cough during chronic benazepril therapy were allocated randomly to receive slow-release nifedipine gastrointestinal therapeutic system (GITS) 30 mg once daily, amlodipine 5 mg once daily, indomethacin 50 mg twice daily, or placebo twice daily for 2 weeks. This was according to a double-masked, double-dummy, crossover, Latin square design. At the end of each phase, cough was assessed by means of a self-administered questionnaire with an ordinal 10-point visual analogue scale for rating daily cough intensity and frequency. Indomethacin eliminated or markedly reduced cough induced by the ACE inhibitor, whereas nifedipine GITS and amlodipine reduced it to a lesser degree. These findings suggest that PGs play a role in cough caused by ACE inhibitors and that a dihydropyridine calcium channel blocker can reduce the occurrence of this side effect.

The effect of sustained-release (SR) diltiazem 300 mg on 24-hour ambulatory blood pressure (BP), heart rate (HR), and left ventricular mass was evaluated in 35 elderly patients aged 75 to 84 years with mild-to-moderate essential hypertension, defined as sitting systolic blood pressure (SBP) >160 mm Hg and diastolic blood pressure (DBP) >90 mm Hg but