Permanent Cardiac Pacing Versus Medical Treatment for the Prevention of Recurrent Vasovagal Syncope

Ammirati, Fabrizio; Colivicchi, Furio; Santini, Massimo

doi:10.1161/hc2601.091708

Cited by 268 publications

(111 citation statements)

References 27 publications

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“…5 On the other hand, pharmacologic therapy was shown to be disappointing in subjects with vasodepressive (VD) syncope, providing only a poor reduction of the recurrence of clinical events. 6,7 Recent studies have focused on mechanisms of the peripheral circulatory regulation in subjects affected by NMS.…”

Section: Introductionmentioning

confidence: 99%

An Increased Endothelial‐Independent Vasodilation Is the Hallmark of the Neurally Mediated Syncope

Santini¹,

Capria

Brusca³

et al. 2011

Clinical Cardiology

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Background: The neurally mediated syncope (NMS) is sustained by complex cardiac and vascular reflexes, acting on and amplified by central autonomic loops, resulting in bradycardia and hypotension. Hypothesis: Our aim was to assess whether the pathophysiology of NMS is also related to an abnormal peripheral vasoreactivity. Methods: We evaluated by ultrasound the flow-mediated vasodilation (FMD) and the nitrate-mediated dilation (NMD) in 17 patients with NMS, induced by drug-free tilt test in 6 subjects and by nitrate-potentiated tilt test in the other 11 cases; the syncope was classified as vasodepressive (VD) in 8 cases, cardioinhibitory (CI) in 7, and mixed in 2. Results: The FMD was not different from controls (10.2 ± 4.5 vs 11.4 ± 3.9, P = ns), with normal recovery times; the NMD was greater in fainting subjects than in controls (26.7 ± 7.3 vs 19.0 ± 3.6, P < 0.05), with higher values in VD than in CI syncope (31.1 ± 7.0 vs 23.1 ± 5.0, P = ns); compared to controls, subjects with NMS showed normal recovery times after FMD but longer recovery times after nitrate administration (13.0 ± 5.6 vs 6.3 ± 0.7 minutes, P < 0.05). Conclusions:The evaluation of endothelial function supports evidence that NMS is characterized by a marked and sustained endothelial-independent vasodilation, in the presence of a normal FMD; vascular hyperreactivity in response to nitrate administration is particularly overt in vasodepressive syncope and can explain the high rate of responses to nitrate administration during tilt test.

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Section: Introductionmentioning

confidence: 99%

An Increased Endothelial‐Independent Vasodilation Is the Hallmark of the Neurally Mediated Syncope

Santini¹,

Capria

Brusca³

et al. 2011

Clinical Cardiology

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“…En todos los estudios de estimulación cardiaca en pacientes vasovagales positivos a la basculación, se usó la estimulación cardiaca bicameral (con una función de respuesta en frecuencia que, ante una disminución rápida del ritmo cardiaco, el marcapasos instauraba estimulación cardiaca DDD rápida), pero no se comparó con la estimulación cardiaca bicameral convencional [20][21][22][23][24] .…”

Section: Selección Del Modo De Estimulación Cardiacaunclassified

“…La eficacia de la estimulación cardiaca se estudió en cinco ensayos clínicos multicéntricos aleatorizados [20][21][22][23][24] ; tres estudios sin enmascaramiento dieron resultados positivos y dos estudios con enmascaramiento dieron resultados negativos [21][22][23][24] . En los estudios aleatorizados y abiertos SYDIT y VASIS-PM 20,24 , se seleccionó a los pacientes por la respuesta cardioinhibitoria positiva (sobre todo asistólica) durante la prueba de basculación.…”

Section: Síncope Vasovagal Inducido Por Basculación (Recomendaciones unclassified

“…En los estudios aleatorizados y abiertos SYDIT y VASIS-PM 20,24 , se seleccionó a los pacientes por la respuesta cardioinhibitoria positiva (sobre todo asistólica) durante la prueba de basculación. La recurrencia del síncope a los 2 años en el grupo con marcapasos fue del 7% en SYDIT y el 6% en VASIS-PM.…”

Section: Síncope Vasovagal Inducido Por Basculación (Recomendaciones unclassified

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2013 ESC Guidelines on Cardiac Pacing and Cardiac Resynchronization Therapy

Brignole

Auricchio

Barón-Esquivias

et al. 2014

Revista Española de Cardiología (English Edition)

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“…Two trials showed that patients with tilt-positive cardioinhibitory syncope benefited from pacing. 34,35 However, the control groups did not get a device and placebo effect could not be excluded. In a subsequent trial, patients with pacemakers were randomized to the device being "on" or "off", and pacing therapy did not reduce NCS incidence.…”

Section: Workup For Syncopementioning

confidence: 99%

Evaluation and Management of Syncope

Bindra

Marchlinski

Lin

2008

Clinical medicine. Circulatory, respiratory and pulmonary medic

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Context Syncope is a commonly encountered by primary care physicians and cardiologists. Etiology is frequently not apparent, and patients may undergo unnecessary tests. Treatment must be tailored to the likely etiology. Complexities of diagnosis and treatment often warrant referral to a specialist. Objective To highlight the evolving recommendations for managing syncope in a clinically and cost effective manner. Evidence Acquisition An electronic literature search was undertaken of the Medline database from January 1996 to April 2006, using the Medical Subject Heading syncope, defibrillators, pacemakers, echocardiogram, cardiomyopathy, long QT syndrome, Arrhythmogenic right ventricular dysplasia, and Brugada syndrome. Abstracts and titles were reviewed to identify English-language trials. Bibliographies from the references as well as scientific statements from the Heart Rhythm Society, American Heart Association, and American College of Cardiology were reviewed. Evidence Synthesis A methodical approach to syncope can improve diagnosis, limit testing, and identify patients at risk of fatal outcome. A thorough history, physical exam and electrocardiogram are critical to the initial diagnosis. Presence of heart disease determines the extent of work-up and treatment. A trans-thoracic echocardiogram should be performed in patients with an unclear diagnosis and a positive cardiac history or an abnormal ECG. Ventricular arrhythmias are the most common cause of syncope in patients with structural heart disease. Patients with an ejection fraction less than 30 percent should receive an implantable defibrillator with few exceptions. An electrophysiology study may assist risk stratification in syncopal patients with borderline ventricular function. In patients without structural heart disease, the presence of a well defined arrhythmia syndrome consistent with a genetically determined risk of sudden death must be sought. The 12-lead electrocardiogram, family history and clinical presentation will identify most high-risk patients. Patients without structural heart disease can often be managed conservatively with well defined strategies for preventing neurocardiogenic syncope. Conclusions Managing syncope requires a methodical approach. An understanding of the limitations of the diagnostic tools and treatments is important. Lethal causes of syncope make it imperative to recognize the appropriate timing of referring patients to specialists.

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Permanent Cardiac Pacing Versus Medical Treatment for the Prevention of Recurrent Vasovagal Syncope

Cited by 268 publications

References 27 publications

An Increased Endothelial‐Independent Vasodilation Is the Hallmark of the Neurally Mediated Syncope

An Increased Endothelial‐Independent Vasodilation Is the Hallmark of the Neurally Mediated Syncope

2013 ESC Guidelines on Cardiac Pacing and Cardiac Resynchronization Therapy

Evaluation and Management of Syncope

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