Vasovagal reactions may occur after orthotopic heart transplantation

Fitzpatrick, Adam P.; Banner, N.R.; Cheng, Alfred B.; Yacoub, Magdi H.; Sutton, Richard

doi:10.1016/0735-1097(93)90235-s

Cited by 203 publications

(54 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Experiments in animals have demonstrated that despite bilateral vagotomy or total cardiac denervation, sympathetic nerve activity falls (in a manner reminiscent of neurally mediated syncope) during hypotensive hemorrhage (11). In humans, neurally mediated hypotension and bradycardia with preceding sympathetic withdrawal have been similarly observed in patients with intact and with denervated ventricles (i.e., heart transplant patients) (12,13). Furthermore, others, using echocardiographic measurements of left atrial and ventricular chamber size and determinations of stroke volume, found no evidence of excessive cardiac emptying before the onset of syncope in susceptible patients (14).…”

Section: Introductionmentioning

confidence: 99%

Yohimbine in neurally mediated syncope. Pathophysiological implications.

Mosqueda‐Garcia

Fernandez-Violante²,

Tank³

et al. 1998

J. Clin. Invest.

View full text Add to dashboard Cite

In this study, we evaluated if increased sympathetic stimulation is an essential requirement for the development of neurally mediated syncope (NMS) by manipulating overall sympathetic outflow in subjects susceptible to tilt-induced syncope.Eight previously characterized patients with recurrent NMS (five females and three males; 34 Ϯ 2 yr) were recruited from the Vanderbilt Syncope Unit and eight age-matched controls underwent initial administration of clonidine (CLO) or yohimbine (YHO). This was done, prospectively, to determine doses of these agents that would increase or decrease plasma norepinephrine levels by Ն 30%. On a different day, in all subjects we determined intraarterial blood pressure, EKG and muscle sympathetic nerve activity (MSNA) both supine and during upright tilt. After this, subjects randomly received either CLO or YHO, and 3 h later another tilt was performed. After 1 wk, a similar procedure with the other drug was performed.During the two basal tilts, all the control subjects completed the study, whereas all the NMS patients developed syncope. Reduction in sympathetic tone by CLO resulted in a decreased tolerance to tilt in three out of eight controls and in all the NMS patients. In contrast, YHO not only increased basal plasma NorEpi levels and MSNA, but also prevented syncope in seven out of eight patients.In a selected population of patients, increased sympathetic activity is not a prerequisite for the development of syncope. Yohimbine-induced enhancement of sympathetic tone in patients with NMS improves orthostatic tolerance and raises the possibility that this drug may be a useful agent in the treatment of NMS. ( J. Clin. Invest. 1998. 102: 1824-1830.)

show abstract

Section: Introductionmentioning

confidence: 99%

Yohimbine in neurally mediated syncope. Pathophysiological implications.

Mosqueda‐Garcia

Fernandez-Violante²,

Tank³

et al. 1998

J. Clin. Invest.

View full text Add to dashboard Cite

show abstract

“…1 Furthermore, low-pressure cardiopulmonary baroreceptors have been hypothesized to be more sensitive to orthostatic stress in habitual fainters. 26 Finally, the occurrence of vasoinhibitory fainting in patients with heart transplants 27,28 further suggests the existence of mechanisms different from the activation of vagal ventricular receptors. Among them, Dickinson 29 proposed the anomalous activation of venoatrial stretch receptors as a possible trigger of the sequence of events occurring in vasovagal fainting.…”

Section: Progressive Sympathetic Activationmentioning

confidence: 99%

Cardiac Autonomic Patterns Preceding Occasional Vasovagal Reactions in Healthy Humans

et al. 1998

View full text Add to dashboard Cite

Background-The wide range of clinical presentation of orthostatic vasovagal syncope suggests different underlying changes in the cardiac autonomic modulation. Methods and Results-To evaluate the beat-by-beat modifications in the neural control of heart period preceding a syncopal event, we studied RR interval variability in 22 healthy subjects who experienced fainting for the first time during a 90°head-up tilt and in 22 control subjects by means of time-variant power spectral analysis. Sympathetic and vagal modulations to the sinoatrial node were assessed by the normalized power of the low-frequency (LF, Ϸ0.1-Hz) and high-frequency (HF, Ϸ0.25-Hz) oscillatory components of RR variability. When the patients were supine, no differences were observed in the hemodynamic and spectral parameters of the 2 groups. During the tilt procedure, RR, LF NU , and HF NU (NUϭnormalized units) values were relatively stable in control subjects. During early tilt (T 1 ), subjects with syncope had reduced RR intervals compared with control subjects. In 13 subjects with syncope, RR decreased while LF NU and LF/HF increased in the last minute of tilt before syncope (T 2 ). Conversely, in the remaining 9 fainters, LF NU and LF/HF decreased from T 1 to T 2 and HF NU increased slightly. Conclusions-Two different patterns may be recognized in the cardiac autonomic changes preceding an occasional vasovagal event, namely, one characterized by a progressive increase of the marker of cardiac sympathetic modulation up to the onset of syncope, the other by a sympathetic inhibition with an impending vagal predominance. The recognition of different pathophysiological mechanisms in fainters may have important therapeutic implications.

show abstract

“…14 Furthermore, the occurrence of vasovagal reaction in subjects after orthotopic heart transplantation provides strong evidence that mechanisms other than the Bezold-Jarisch reflex are involved in the pathogenesis of vasovagal syncope. 15,16 Different humoral factors also seem to play a role, including epinephrine and a possible relative lack of norepinephrine, 17 a decrease of vasopressin and endothelin in plasma, 18,19 increased endorphin levels, 20,21 and possibly nitric oxide and serotonin. 22 However, the contributions of these neurohumoral factors are still controversial.…”

mentioning

confidence: 99%

Dysfunctional Baroreflex Regulation of Sympathetic Nerve Activity in Patients With Vasovagal Syncope

Béchir¹,

Binggeli²,

Corti³

et al. 2003

Circulation

View full text Add to dashboard Cite

Background— The interplay of resting muscle sympathetic nerve activity (MSA) and the baroreceptor reflex in patients with vasovagal syncope remains elusive. Hence, the aim of the present study was to investigate MSA, baroreceptor sensitivity, heart rate, and blood pressure under resting conditions and during orthostatic stress in patients with a history of vasovagal syncope. Methods and Results— MSA was measured using microneurography at rest and during lower body negative pressure (LBNP) to mimic orthostatic stress in patients with a history of vasovagal syncope (n=10) and in age-matched healthy controls (n=8). Heart rate and blood pressure were simultaneously recorded. Cardiac baroreceptor sensitivity was calculated with the spectral technique (α coefficient). Resting MSA in the patients with syncope was significantly increased as compared with controls (42.4±2.3 versus 26.5±3.6 bursts/min, P =0.001), whereas activation of MSA during orthostatic stress in the patient group was significantly blunted (5.1±1.6 versus 15.2±2.1 bursts/min at LBNP −50 mm Hg, P =0.002). In the patients with syncope, cardiac baroreceptor sensitivity was significantly reduced under supine resting conditions (8.5±0.7 versus 13.0±1.1 ms/mm Hg, P =0.001), as well as under orthostatic stress (7.3±0.7 versus 13.4±1.5 ms/mm Hg, P =0.003). Conclusions— This study shows that in patients with vasovagal syncope, resting MSA is increased and baroreflex regulation during orthostatic stress is blunted, thus leading to impaired MSA adaptation. These results provide new insights into mechanisms of vasovagal syncope and suggest that pharmacological modulation of baroreceptor sensitivity may represent a promising treatment of neuromediated syncope.

show abstract

Vasovagal reactions may occur after orthotopic heart transplantation

Abstract: Vagal efferent reinnervation can occur after orthotopic heart transplantation in humans. However, the absence of such reinnervation in some patients with vasovagal responses to tilt calls into question the role of left ventricular receptors in inducing the vasovagal reaction.

Cited by 203 publications

References 29 publications

Yohimbine in neurally mediated syncope. Pathophysiological implications.

Yohimbine in neurally mediated syncope. Pathophysiological implications.

Cardiac Autonomic Patterns Preceding Occasional Vasovagal Reactions in Healthy Humans

Dysfunctional Baroreflex Regulation of Sympathetic Nerve Activity in Patients With Vasovagal Syncope

Contact Info

Product

Resources

About