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Michele Brignole

Publications and source records attributed to Michele Brignole.

9 recordsLinked to original sources
PubMed2003

Mechanism of syncope in patients with positive adenosine triphosphate tests.

OBJECTIVES: We prospectively evaluated the mechanism of syncope in patients with positive adenosine triphosphate (ATP) tests (defined as the induction of atrioventricular [AV] block with a ventricular pause >/=6 s after an intravenous bolus of 20 mg ATP). BACKGROUND: Patients with unexplained syncope tend to have more positive ATP tests results than those without syncope. METHODS: An implantable loop recorder (ILR) was inserted in 36 ATP-positive patients (69 +/- 10 years; 22 women; median of 6 syncopal episodes); 15 of them also had a positive response to tilt testing. RESULTS: During the follow-up of 18 +/- 9 months, 18 patients (50%) had syncopal recurrence and 16 (44%) had an electrocardiographically documented episode: AV block (n = 3: paroxysmal in 2 and permanent in 1), AV block followed by sinus arrest (n = 1), sinus arrest (n = 5), sinus bradycardia <40 beats/min (n = 2), normal sinus rhythm (n = 2), sinus tachycardia (n = 1), rapid atrial fibrillation (n = 1), and ectopic atrial tachycardia (n = 1). Bradycardia was documented in a total of 11 cases (69%), and a long ventricular pause (4 to 29 s) was present in eight cases (50%). All three patients with ILR-documented AV block had previously had a negative tilt test, whereas seven of eight with ILR-documented sinus bradycardia or sinus arrest had previously had a positive tilt test. CONCLUSIONS: In patients with adenosine-sensitive syncope, the mechanism of syncope is heterogeneous, although bradycardia is the most frequent finding. Adenosine triphosphate-induced AV block predicts AV block as the mechanism of spontaneous syncope in only a few tilt-negative patients.

Adenosine Triphosphate↗
PubMed2003

Randomized clinical trials of neurally mediated syncope.

Evidence for therapy of neurally mediated syncope is generally weak. Many drugs have been used for the treatment of vasovagal syncope (beta-blockers, disopyramide, scopolamine, clonidine, theophylline, fludrocortisone, ephedrine, dihydroergotamine, etilefrine, midodrine, clonidine, serotonin reuptake inhibitors, enalapril). In general, although the results have been satisfactory in uncontrolled trials or short-term controlled trials, the majority of long-term placebo-controlled prospective trials have not been able to show a benefit of the active drug over placebo. Only two well-designed double-blind placebo-controlled randomized trials have been performed-one for etilefrine and the other for atenolol-and both were unable to show a superiority of the active drug versus placebo. Four randomized clinical trials of pacing therapy-three positive and one negative-have been performed in patients affected by vasovagal syncope. The relationship between carotid sinus hypersensitivity and spontaneous, otherwise unexplained, syncope has been demonstrated. Cardiac pacing appears to be beneficial in carotid sinus syndrome; its efficacy has been demonstrated by two randomized controlled trials and confirmed by several pre-post comparative studies, one controlled trial, and one prospective observational study. There is evidence and general agreement that cardiac pacing is useful in patients with cardioinhibitory or mixed carotid sinus syndrome. Usefulness of the treatment is less well established and divergence of opinion exists with regard to cardiac pacing in patients with cardioinhibitory vasovagal syncope. The evidence fails to support the efficacy of beta-blocking drugs. As yet there are insufficient data to support the use of any other pharmacologic therapy for vasovagal syncope.

Adrenergic alpha-Antagonists↗
PubMed2002

Isometric arm counter-pressure maneuvers to abort impending vasovagal syncope.

OBJECTIVES: We hypothesized that isometric arm exercises were able to increase blood pressure (BP) during the phase of impending vasovagal syncope and allow the patient to avoid losing consciousness. BACKGROUND: Hypotension is always present during the prodromal phase of vasovagal syncope. METHODS: We evaluated the effect of handgrip (HG) and arm-tensing in 19 patients affected by tilt-induced vasovagal syncope. The study consisted of an acute single-blind, placebo-controlled, randomized, cross-over tilt-table efficacy study and a clinical follow-up feasibility study. RESULTS: In the acute tilt study, HG was administered for 2 min, starting at the time of onset of symptoms of impending syncope. In the active arm, HG caused an increase in systolic blood pressure (SBP) from 92 +/- 10 mm Hg to 105 +/- 38 mm Hg, whereas in the placebo arm SBP decreased from 91 +/- 11 mm Hg to 73 +/- 21 mm Hg (p = 0.008). Heart rate behavior was similar in the two arms. In the active arm, 63% of patients became asymptomatic, versus 11% in the control arm (p = 0.02); conversely, only 5% of patients developed syncope, versus 47% in the control arm (p = 0.01). The patients were trained to self-administer arm-tensing treatment as soon as symptoms of impending syncope occurred. During 9 +/- 3 months of follow-up, the treatment was actually performed in 95/97 episodes of impending syncope (98%) and was successful in 94/95 (99%). No patients suffered injury or other adverse morbidity related to the relapses. CONCLUSIONS: Isometric arm contraction is able to abort impending vasovagal syncope by increasing systemic BP. Arm counter-pressure maneuvers can be proposed as a new, feasible, safe, and well accepted first-line treatment for vasovagal syncope.

Adolescent↗
PubMed2002

Mechanism of syncope in patients with heart disease and negative electrophysiologic test.

BACKGROUND: In patients with syncope and structural heart disease, syncope is suspected to be attributable to a primary cardiac arrhythmia, but little is known of its mechanism when electrophysiologic study is unremarkable. METHODS AND RESULTS: We applied an implantable loop recorder in 35 patients with overt heart disease at risk of ventricular arrhythmia, because these were patients with previous myocardial infarction or cardiomyopathy with depressed ejection fraction or nonsustained ventricular tachycardia in whom an electrophysiologic study was unremarkable. During a follow-up of 3 to 15 months, syncope recurred in 6 patients (17%) after a mean of 6+/-5 months; in 3 patients, the mechanism of syncope was bradycardia with long pauses (sudden-onset AV block in 2 cases and sinus arrest in 1 case); in 1 patient, there was stable sinus tachycardia; and in 2 patients, who had chronic atrial fibrillation, there was an increase in ventricular rate. A total of 23 episodes of presyncope were documented in 8 patients (23%): no rhythm variation or mild tachycardia in 12 cases, paroxysmal atrial fibrillation or atrial tachycardia in 10 cases, and sustained ventricular tachycardia in 1 case. No patient died during the study period nor suffered from injury attributable to syncopal relapse. CONCLUSIONS: The patients with unexplained syncope, structural heart disease, and negative electrophysiologic study had a favorable medium-term outcome with no case of death and a low recurrence rate of syncope without related injury. The mechanism of syncope was heterogeneous, and ventricular tachyarrhythmia was unlikely.

Aged↗
PubMed2002

Sick sinus syndrome.

Sinus-node dysfunction is common in the elderly and, in most cases, does not cause any symptoms. Despite the high number of laboratory investigations, most diagnoses of sinus-node dysfunction are made by 12-lead electrocardiography, which shows severe sinus bradycardia, sinus arrest, or sinoatrial block. Continuous electrocardiographic monitoring, exercise testing, and electrophysiologic investigations (including pharmacologic interventions to cause complete autonomic blockade) are sometimes useful in detecting transient or latent sinus-node abnormalities. The term sick sinus syndrome should be reserved for patients with symptomatic sinus-node dysfunction. Sick sinus syndrome has a protean presentation with variable degrees of clinical severity. Symptoms are often intermittent, changeable, and unpredictable. Because these symptoms can be observed in several other diseases, none are specific to sick sinus syndrome. Owing to the nonspecific nature of its symptoms, sick sinus syndrome can be diagnosed only when clear electrocardiographic signs corroborate symptoms. In the absence of a demonstrable link between signs and symptoms, a diagnosis can be presumed only when signs of severe sinus dysfunction are present and when every other possible cause of symptoms has been excluded carefully. Sinus-node dysfunction frequently is associated with diseases of the autonomic nervous system, and autonomic reflexes play a major role in the genesis of syncope. Survival does not seem to be affected by sick sinus syndrome. Atrioventricular block, chronic atrial fibrillation, and systemic embolism are major pathologic conditions that affect the outcome of the syndrome. Treatment should be aimed at controlling morbidity and relieving symptoms. Cardiac pacing is the most powerful therapy; physiologic pacing (atrial or dual-chamber) has been shown definitively to be superior to ventricular pacing.

Aged↗