Recurrent Syncope in a Patient After Myocardial Infarction

Credner, Susanne; Lehmann, Ralf; Grubb, Blair P.; Hohnloser, Stefan H.; Klingenheben, Thomas

doi:10.1046/j.1460-9592.2003.t01-1-00161.x

Cited by 1 publication

(3 citation statements)

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“…Symptoms of parasympathetic activation, such as vagally induced bradycardia, sweating, and nausea are usually absent in patients with parasympathetic dysfunction that present with a sudden onset of postural syncope [23][24][25][26]. In the present study, complete cardiac vagal blockade did not disturb the baroreflex control of arterial blood pressure during HUT.…”

Section: Discussionmentioning

confidence: 50%

“…Orthostatic hypotension and its more life-threatening clinical sequel of postural syncope are prevalent in elderly populations [23,24], patients with diabetic autonomic neuropathy [25], and patients with cardiac disease [26]. Each of these populations exhibits parasympathetic dysfunction, which is consistent with altered arterial baroreflex control of the heart [27][28][29][30][31].…”

Section: Discussionmentioning

confidence: 99%

“…Their mean age was 27 years (range [21][22][23][24][25][26][27][28][29][30][31][32][33][34][35][36], height 183 cm (168-198), and weight 77 kg (57-97). All subjects provided written informed consent, which conformed to the Declaration of Helsinki and was approved by the Ethics Committee of Copenhagen (KF 01-369/97).…”

Section: Methodsmentioning

confidence: 99%

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Carotid-Cardiac Baroreflex Function Does Not Influence Blood Pressure Regulation during Head-Up Tilt in Humans

et al. 2006

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Abstract:The influence of the carotid-cardiac baroreflex on blood pressure regulation was evaluated during supine rest and 40° head-up tilt (HUT) in 9 healthy young subjects with and without full cardiac vagal blockade. The carotid baroreflex responsiveness, or maximal gain (G MAX ), was assessed from the beatto-beat changes in heart rate (HR) and mean arterial pressure (MAP) by the variable neck pressure and suction technique ranging in pressure from +40 to -80 Torr, with and without glycopyrrolate (12.0 ± 1.0 µg/kg body weight; mean ± SE). In the supine position, glycopyrrolate increased the HR to 91 ± 3 bpm, from 54 ± 3; MAP to 89 ± 2 mmHg, from 76 ± 2; and cardiac output to 6.8 ± 0.3 l·min -1 , from 4.9 ± 0.3 (P < 0.05). The G MAX of the carotid baroreflex control of HR was reduced to -0.06 ± 0.01 bpm·mmHg -1 , from -0.30 ± 0.02 (P < 0.05) with no significant effect on the G MAX of the carotid baroreflex control of MAP. During HUT the carotid baroreflex control of MAP was unchanged, though the G MAX of the carotid baroreflex control of HR was increased (P < 0.05). During HUT, central blood volume, assessed by electrical thoracic admittance, and total vascular conductance were decreased with and without glycopyrrolate. Furthermore, glycopyrrolate reduced G MAX of the carotid baroreflex control of HR during HUT (P < 0.05) with no significant effect on G MAX of the carotid baroreflex control of MAP. These data suggest that during supine rest and HUT-induced decreases in central blood volume, the carotid baroreflex control of HR is mediated primarily via parasympathetic activity. Furthermore, the maintenance of arterial blood pressure during postural stress is primarily mediated by arterial and cardiopulmonary reflex regulation of sympathetic activity and its effects on the systemic vasculature.Key words: arterial blood pressure, baroreflex, central blood volume, heart rate.The balance between the contribution of the carotid-cardiac and the carotid-vasomotor reflex arms to the carotid baroreflex (CBR) responses to changes in arterial pressure is altered during upright seating compared to the supine position [1]. This change in balance identified that the major adjustment to changes in posture primarily involved the carotid-vasomotor arm of the reflex [1]. This finding confirmed earlier work involving reflex adjustments to reductions in central blood volume (CBV) induced by lower body negative pressure (LBNP) [2]. Furthermore, in average healthy and fit young adults the maximal gains (G MAX ) of the carotid-cardiac and the carotid-vasomotor arms of the CBR were augmented during decreases in CBV [3,4] induced by head-up tilt (HUT) or LBNP [5,6].However, patients who exhibit parasympathetic dysfunction during an orthostatic challenge also exhibit decreased vasomotor responsiveness [7][8][9], indicating that a dysfunction of the carotid-vasomotor arm may be the underlying mechanism of the postural syncope despite the parasympathetic dysfunction. These findings raise the question of whether parasympathetic dysfunctio...

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Section: Discussionmentioning

confidence: 50%