Vasovagal syncope: a prospective, randomized, crossover evaluation of the effect of propranolol, nadolol and placebo on syncope recurrence and patients’ well-being

AbstractObjectivesWe sought to assess the relative therapeutic efficacy of propranolol, nadolol and placebo in recurrent vasovagal syncope (VVS).BackgroundCentral and peripheral mechanisms have been implicated in the pathogenesis of VVS. Propranolol, nadolol and placebo have different sites of action on central and/or peripheral mechanisms. It has not yet been clarified whether one of the aforementioned treatments is more efficient than the others in reducing clinical episodes and exerting a beneficial effect on patients’ well-being.MethodsWe studied 30 consecutive patients with recurrent VVS and a positive head-up tilt test. All were serially and randomly assigned to propranolol, nadolol or placebo. Therapy with each drug lasted three months. On the day of drug crossover, patients reported the total number of syncopal and presyncopal attacks during the previous period. They also gave a general assessment of their quality of life, taking into account: 1) symptom recurrence; 2) drug side effects; and 3) their personal well-being during therapy (scale 0 to 4: 0 = very bad/discontinuation; 1 = bad; 2 = good; 3 = very good; 4 = excellent). At the end of the nine-month follow-up period, they reported whether they preferred a specific treatment over the others.ResultsSpontaneous syncopal and presyncopal episode recurrence during each three-month follow-up period was reduced by all drugs tested (analysis of variance [ANOVA]: chi-square = 67.4, p < 0.0001 for syncopal attacks; chi-square = 60.1, p < 0.0001 for presyncopal attacks) No differences were observed in the recurrence of syncope and presyncope among the three drugs. All drugs improved the patients’ well-being (ANOVA: chi-square = 61.9, p < 0.0001).ConclusionsPropranolol, nadolol and placebo are equally effective treatments in VVS, as demonstrated by a reduction in the recurrence of syncope and presyncope, as well as an improvement in the patients’ well-being

Neurocardiogenic mechanisms of unexplained syncope in idiopathic dilated cardiomyopathy

Syncope in patients with advanced heart failure is a sign of poor prognosis. The cause of syncope in patients with dilated cardiomyopathy (DC) is not fully recognized and may remain elusive even after standardized evaluation. The purpose of the present study was to examine the implication of neurally mediated mechanisms in the pathophysiology of syncopal episodes in patients with DC. Twenty-six patients (21 men, 5 women; mean age 59 +/- 2 years, range 38 to 79) with DC and left ventricular ejection fractions &lt;= 40% were included in the study. Thirteen patients with unexplained syncope or presyncope and a control group of 13 patients without unexplained syncope underwent head-up tilt tests with clomipramine challenge. The 2 groups were matched with regard to age, gender, and left ventricular ejection fractions, and there were no major differences in terms of medication. Heart rate variability analysis, and plethysmography of forearm flow were performed during the tilt tests. Blood samples were also drawn for catecholamine measurements. In the group with histories of unexplained syncope, the head-up tilt test results were positive in 11 patients (84.6%). Sympathetic and parasympathetic heart rate indexes were markedly stimulated, while catecholamine concentrations and blood flow changes indicated sympathetic withdrawal during tilting. In the control group, the head-up tilt test results were negative in 12 patients (92.3%). In conclusion, neurally mediated mechanisms seem to be implicated in the pathophysiology of syncope in patients with DC and should therefore be considered in the differential diagnosis of syncopal episodes of unexplained origin. (c) 2007 Elsevier Inc. All rights reserved