Objective: There is considerable knowledge of the incidence of torsades de pointes (TdP) during the administration of amiodarone The aim of our study was to determine the incidence of TdP during the loading phase of intravenous administration of amiodarone, intended to reverse paroxysmal atrial fibrillation (PAF) to sinus rhythm (SR), and to test the hypothesis that their prevalence is greater among women than men, as reported earlier. We also sought to determine factors predisposing to the occurrence of TpD, such as atrium size and hyperglycemia. Methods: We evaluated 189 patients (M = 107, F = 82, mean age = 56 ± 19 years), who were admitted for PAF, and for whom amiodarone was selected as the first-choice drug for PAF reversion. During the first 24 h of the loading phase (300 mg rapid i.v. administration within 20 min and 1,500 mg i.v. for 24 h) we recorded all ventricular arrhythmias. All patients were on anticoagulant treatment and all of them were evaluated for corrected QT (QTc), as well as additional risk factors (atrial size, serum glucose, hypopotassemia, hypomagnesemia, severe bradycardia). Patients with heart failure, hypertrophic obstructive cardiomyopathy, a history of coronary artery disease or ventricular tachycardia, as well as those treated with drugs prolonging the QT interval, were excluded from the study. Results: 108 patients (57.1%) experienced successful conversion of PAF into SR on amiodarone. Five patients (2.6%), all female, mean age 53.0 ± 1.2 years, developed TpD. All episodes occurred at the end of the loading phase (21–24 h) of amiodarone administration. None of them had hypopotassemia, hypomagnesemia, or bradycardia (HR <55 bpm). Two of the TpD patients had elevated glucose levels, and all of them had prolonged QTc immediately prior to the TpD. Conclusion: We confirm that women are at increased risk of developing TpD during the administration of amiodarone. TpD develop towards the end of the intravenous loading phase; the electrocardiographic changes should be closely monitored towards the end of the loading phase. The presence of diabetes mellitus or temporal hyperglycemia and prolonged QTc seems to be predicting factors for TpD during i.v. amiodarone administration.

Aldosterone injected i.m. decreased the release of renomedullary PGEs and the index (urinary Na/K ratio) in conscious normotensive intact and adrenalectomized rats. Coadministration of spironolactone increased the release of PGEs as well as the index (urinary Na/K ratio). The effect of spironolactone was partly inhibited by aspirin injected in a ratio 5:1 (aspirin:spironolactone), and effect which could be reversed by the infusion of a synthetic prostaglandin (PGA2) in a subhypotensive dose.

The effect of cilazapril (CLZ) treatment on serum lipids and fibrinogen was studied in 114 hypertensive patients for 18 weeks. Blood pressure, heart rate, lipid profile and fibrinogen were measured before and at the end of the study in all patients. Satisfactory blood pressure control was seen in 68% of the patients (group A) after 4 weeks of treatment with 5 mg CLZ monotherapy, while a single dose of chlorthalidone, 25 mg daily, was added to the therapeutic regimen of the remaining 32% of patients (group B) to achieve blood pressure control. We conclude that CLZ has a slight beneficial effect on the lipid profile and a significantly beneficial effect on fibrinogen, but its combination with a diuretic reverses this beneficial effect.

Urinary prostaglandins (PGEs and PGFs), sodium and potassium were measured in 17 essentially hypertensive patients. Significant positive correlations were found between a) PGEs secreted in 24 h and sodium excreted in 24 h, b) the ratio PGEs/UnaV before and PGEs/UnaV after volume expansion and c) the ration Na/K and urinary PGEs. It was suggested that renal PGEs, potent natriuretic and diuretic substances, play an important homeostatic role in the extracellular fluid regulation, and consequently in long-term control of the arterial blood pressure.