Recurrent Symptoms after Ventricular Pacing in Unexplained Syncope

Fitzpatrick, Adam P.; Travill, Christopher; Vardas, Panos; Hubbard, W N; Wood, Angus; Ingram, A.; Sutton, Richard

doi:10.1111/j.1540-8159.1990.tb02078.x

Cited by 41 publications

(11 citation statements)

References 15 publications

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“…[17][18][19] There is also evidence that neurally-mediated syncope is a much greater clinical problem than is generally recognised. 20 21 A recent major European study of dual chamber pacing in patients with ''tilt positive'' cardioinhibitory syncope demonstrated that this treatment approach offers long term protection from recurrent syncope, but patient selection for pacing therapy remains challenging as even in untreated patients the burden of recurrence is low.…”

Section: Pacing For Neurally-mediated Syncopementioning

confidence: 99%

Basics of cardiac pacing: selection and mode choice

Morgan¹

2005

Heart

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T herapeutic cardiac stimulation has been in clinical practice for many decades.1 During the evolution of the therapy, pacing generators have shrunk in size, increased in longevity, and increased in device complexity. They offer rhythm and disease state diagnostics, with various algorithms designed to offer timing of delivery of pacing impulse and more recently diagnostics indicative of pathophysiology. Pacing leads have also reduced in size and improved in durability. Pacing electrode configurations have enhanced sensing capability and stability of long term pacing function.With the potential for a range of biosensors that could be incorporated in pacemaker devices to further the potential for pathophysiological monitoring, cardiac pacing has achieved an extraordinary maturity in the armoury of cardiac treatments. However, it has taken much longer for there to be large scale clinical trials on the therapeutic efficacy of devices, long term patient well being, and the impact of right ventricular pacing on left ventricular function. INDICATIONS AND MODE CHOICE cThese are summarised in published European and North American guidelines.2 3 There are three electrophysiological conditions (sinus node disease, atrioventricular (AV) node disease, and neurally-mediated (cardio-inhibitory) syncope) which may cause either prognostically or symptomatically significant bradycardia, and this review focuses only on these. These conditions may be treated by single chamber ventricular sensing/pacing, dual chamber sensing/pacing or (if AV nodal function is normal) single chamber atrial sensing/pacing.The choice of appropriate pacing modality to treat these electrophysiological abnormalities is governed by our understanding of the morbidity that attends the conditions themselves, the influence of pacing on that morbidity, and a further morbidity that may attend the chosen pacing mode. To understand this complex interaction we need to look to the evidence base that reports efficacy and complications of pacing therapy in varying patient populations with differing electrophysiological and cardiac disease. STUDY BACKGROUNDSThis article focuses on six major studies which have investigated the relative benefits and disadvantages of dual and single chamber pacing 4-8 and on a single major investigation of vasovagal syndrome. 9 Many studies have investigated the effect of different pacing modalities in specific electrophysiological disease conditions. Others have investigated the pacing modality on a generality of bradycardia syndromes. These different approaches complicate the understanding of the relative merits of pacing modality choice.There are three physiological mechanisms contributing to generation of increased cardiac output with exercise: myocardial contractility, AV synchrony, and heart rate. It is the latter that is the most effective in generating an increased cardiac output. Pacing per se is unable to influence contractility (although it is arguable that the benefits of resynchronisation pacing is a manifestation of improved...

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Section: Pacing For Neurally-mediated Syncopementioning

confidence: 99%

Basics of cardiac pacing: selection and mode choice

Morgan¹

2005

Heart

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“…VVI (ventricular demand-inhibited) pacing has been unsuccessful in preventing symptoms. The loss of atrioventricular (AV) synchrony actually potentiates the hypotension [2,3]. AAI (atrial demand-inhibited) pacing would not be adequate due to the possibility of AV block or asystole during a vasovagal episode.…”

Section: Vasovagal Syncopementioning

confidence: 99%

Emerging indications for permanent pacing

Wolbrette

Naccarelli

2000

Curr Cardiol Rep

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New indications for pacing are being investigated in the areas of vasovagal syncope, hypertrophic obstructive cardiomyopathy, dilated cardiomyopathy, and atrial fibrillation. It is hoped that pacing will offer an alternative therapy to patients who are refractory to medical therapy. Although pacing for vasovagal syncope continues to be controversial, it appears that a highly symptomatic group with a predominately cardioinhibitory component can benefit. Current data indicate that dual-chamber pacing should not be considered therapeutically equal to septal myectomy in patients with hypertrophic obstructive cardiomyopathy, but may be considered in those more than 65 years of age, or in others who are not good surgical candidates. Biventricular or left ventricular pacing appears promising in heart failure patients and may be combined with implantable cardioverter-defibrillator therapy. Lead technology for coronary vein placement needs further improvement. Dual-site atrial pacing appears to help prevent recurrences of atrial fibrillation and may become a useful adjunct to drug, ablative, and implantable cardioverter-defibrillator therapies.

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“…In susceptible patients, hyperactivated C receptors can produce, via the tractus nucleus solitarius, a sudden withdrawal of sympathetic tone with enhanced parasympathetic activity, resulting in severe peripheral vasodilation (hypotension) and bradycardia leading to syncope. [3][4][5][14][15][16][17][18][19][20]31,32 These factors usually function by increasing the catecholamine discharge 18 and further enhancing inotropism. 14 In fact, most patients show a marked increase in heart rate and a low frequency/high frequency ratio that reflects sympathetic activity in heart rate variability immediately before vasovagal syncope during HUT testing.…”

Section: Discussionmentioning

confidence: 99%