Characterization of subcutaneous microvascular blood flow during tilt table-induced neurally mediated syncope.

OBJECTIVES: This study aimed to characterize subcutaneous blood flow changes during neurally mediated syncope and to determine whether microvasculature oscillation (vasomotion) is characteristically altered in conjunction with syncopal events. BACKGROUND: Marked pallor is commonly associated with neurally mediated syncope. However, little attention has been paid to the evaluation of subcutaneous blood flow and vasomotion in this setting. METHODS: This study utilized laser Doppler flowmetry to assess changes in subcutaneous microvascular blood flow during head-up tilt table testing in 13 patients with syncope and 6 control subjects. Blood flow and vasomotion frequency were measured continuously before, during and after completion of 80 degrees head-up tilt testing (< or = 25-min duration). RESULTS: Among the 13 patients with syncope, tilt testing reproduced syncopal symptoms in 9 (tilt-positive group) but not in 4 (tilt-negative group). None of the six control subjects developed symptoms during testing. Baseline mean subcutaneous blood flow did not differ significantly among the three groups. However, during upright tilt, blood flow gradually diminished in the tilt-positive group, reaching a nadir of 0.8 +/- 0.33 ml/min per 100 g of tissue (mean +/- SD), but remained relatively constant in the tilt-negative group and control subjects. The difference in mean blood flow response to tilt was statistically significant when the tilt-positive group was compared with either the tilt-negative group or control subjects (p < 0.001). Similarly, baseline blood flow oscillation frequency did not differ significantly in the three subgroups (tilt-positive group 0.2 +/- 0.11 Hz; tilt-negative group 0.2 +/- 0.02 Hz; control subjects 0.2 +/- 0.11 Hz). Subsequently, during tilt testing only the tilt-positive group exhibited increased oscillation frequency; oscillation frequency remained essentially constant throughout the tilt test in the tilt-negative group and control subjects (p < 0.001, tilt-positive group vs. either the tilt-negative group or control subjects). CONCLUSIONS: These findings document an expected diminution of subcutaneous blood flow in association with neurally mediated syncope and indicate that characteristic changes in microvasculature oscillation frequency occur in conjunction with syncopal symptoms. To the extent that microvasculature vasomotion is influenced by neural control, the changes in vasomotion frequency are consistent with relative diminution of peripheral sympathetic neural influence during neurally mediated syncopal episodes.

Cardiac asystole: a manifestation of neurally mediated hypotension-bradycardia.

It has been proposed that prolonged cardiac asystole mimicking an episode of sudden cardiac death may occur as a manifestation of neurally mediated hypotension-bradycardia syndrome. To assess this possibility, electrocardiographic and hemodynamic findings during upright tilt testing were evaluated in six survivors of suspected asystolic sudden cardiac arrest with normal conventional electrophysiologic evaluation (Group I). These observations were compared with findings in two control groups: six patients with syncope but without evident asystole and with normal conventional electrophysiologic evaluation but demonstrable neurally mediated hypotension-bradycardia (Group II), and six patients with syncope in whom conventional electrophysiologic evaluation provided a presumptive diagnosis (Group III). Patients in all three groups ranged in age from 16 to 59 years. During head-up tilt testing (either alone or with isoproterenol infusion), patients in both Groups I and II developed syncope in less than or equal to 5 min, whereas patients in Group III remained asymptomatic. Patients in Groups I and II exhibited a similar tilt-induced decrease in mean arterial pressure (-46 +/- 9 and -40 +/- 9 mm Hg, respectively, p = NS) and heart rate (-44 +/- 28 and -49 +/- 12 beats/min, respectively, p = NS). In contrast, patients in Group III manifested only a moderate decrease in mean arterial pressure (-14 +/- 5 mm Hg) and had an increase in heart rate (+14 +/- 8 beats/min). Both mean arterial pressure and heart rate changes in Group I and Group II patients differed significantly (p less than 0.001) from values in Group III patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Usefulness of combined propranolol and verapamil for evaluation of surgical ablation of accessory atrioventricular connections in patients without structural heart disease.

Successful surgical ablation of atrioventricular (AV) accessory connections may be confirmed during postoperative electrophysiologic testing by the absence of accessory connection conduction in both the anterograde and retrograde directions. Whereas the former may be readily apparent by examination of the surface electrocardiogram during sinus rhythm or atrial pacing, assessment of the latter may be complicated by the frequent presence of enhanced retrograde AV nodal conduction in the postoperative period. Consequently, availability of interventions that selectively affect AV nodal conduction and refractoriness without concomitant effects on accessory connections may be helpful for assessing the success of the surgical procedure. In this study the effects of combined propranolol and verapamil administration on electrophysiologic properties of the AV node and the accessory AV connection were assessed both pre- and postoperatively in 17 patients (12 men and 5 women, mean age 33 years) undergoing surgical ablation of accessory connections. Preoperatively, electrophysiologic characteristics of all but 1 of the accessory AV connections were unaffected by propranolol and verapamil administration. Postoperatively, on the other hand, propranolol and verapamil significantly prolonged both the retrograde AV node effective refractory period (baseline: 272 +/- 34 ms vs after drugs: 384 +/- 70 ms [p less than 0.0001]) and the shortest cycle length maintaining 1:1 ventriculoatrial conduction (baseline: 357 +/- 99 ms vs after drugs: 485 +/- 64 ms [p less than 0.0001]). Late postoperative electrophysiologic evaluation (7 +/- 3 weeks) revealed no evidence of residual accessory AV connection conduction, and all patients remain asymptomatic at 21 +/- 10 months follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)

Usefulness of disopyramide for prevention of upright tilt-induced hypotension-bradycardia.

Susceptibility to transient hypotension-bradycardia of neurally mediated origin has been attributed in part to accentuated afferent neural traffic arising from cardiopulmonary mechanoreceptors, and consequently, may be diminished by agents with anticholinergic and negative inotropic effects, such as disopyramide phosphate. This study assessed electrocardiographic and hemodynamic responses to upright tilt testing (alone or during isoproterenol infusion) before and after disopyramide therapy in 10 patients (age range 16 to 74 years) with recurrent syncopal episodes of neurally mediated origin. Untreated, syncope occurred at less than or equal to 7 minutes of tilt alone (6 patients) or tilt plus isoproterenol at less than or equal to 3 micrograms/min (4 patients) and was associated with hypotension (mean arterial pressure, 40 +/- 16 mm Hg vs baseline 76 +/- 10 mm Hg, p less than 0.001) and inappropriate heart rate slowing (mean heart rate, 59 +/- 39 beats/min vs baseline 88 +/- 18 beats/min, p less than 0.005). After oral disopyramide 150 mg 3 times daily (mean plasma level, 3.0 +/- 0.64 micrograms/ml), all patients tolerated 10 minutes of both tilt and tilt plus isoproterenol (maximum dose, 3 micrograms/min) without symptoms, hypotension (mean arterial pressure; tilt 1 min, 79 +/- 7 mm Hg vs tilt 10 min, 77 +/- 8 mm Hg, difference not significant) or bradycardia (mean heart rate; tilt 1 min, 81 +/- 12 beats/min vs tilt 10 min, 83 +/- 11 beats/min, difference not significant). Furthermore, during subsequent 20 +/- 5 months of disopyramide therapy, all but 1 patient remain asymptomatic. Thus, oral disopyramide may be effective for preventing inducible and spontaneous neurally mediated syncope.

Cardiac electrophysiologic and hemodynamic correlates of neurally mediated syncope.

This study assessed the temporal relation of RR interval, AH interval and systemic blood pressure changes during induced symptomatic bradycardia-hypotension episodes in 14 patients with recurrent syncope suspected of being neurally mediated. Upright tilt with isoproterenol reproduced symptoms in 9 of 14 patients (positive response) and was negative in 5 of 14 (negative response). Isoproterenol alone shortened supine RR intervals in all patients. With tilt, however, isoproterenol prolonged RR intervals in those with positive results (supine 519 +/- 124 ms vs tilt 845 +/- 212 ms, p less than 0.005) while further shortening RR intervals among negative responders (supine 436 +/- 90 ms vs tilt 377 +/- 82 ms, p less than 0.05). Similarly, tilt with isoproterenol prolonged AH intervals in patients with positive responses despite RR prolongation, while shortening AH in negative responders. Additionally, with combined tilt and isoproterenol, systemic arterial pressure decreased significantly in patients with positive responses (systolic 99 +/- 13 vs 57 +/- 13 mm Hg, p less than 0.001, diastolic 62 +/- 17 vs 28 +/- 9 mm Hg, p less than 0.001) but not in patients with negative responses. Further, onset of hypotension (42 +/- 14 seconds after tilt) preceded onset of RR interval prolongation (52 +/- 23 seconds after tilt). Syncope (142 +/- 72 seconds after tilt) coincided closely with nadir of systemic pressure (136 +/- 74 seconds) and both tended to precede maximum RR prolongation (152 +/- 87 seconds). Thus, the bradycardia and hypotension associated with neurally mediated syncope exhibit characteristic but distinctly different time courses, with arterial pressure changes developing earlier and coinciding more closely with symptom development.

An office-based exercise protocol for predicting chronotropic response of activity-triggered, rate-variable pacemakers.

Activity-triggered, rate-variable pacing systems offer a wide range of pacemaker patients the benefits of an appropriate paced chronotropic response. However, optimizing settings for these devices often entails treadmill exercise testing. To assess simpler procedures for predicting appropriate settings, pacing rates of "strapped-on" and implanted Activitrax pacemakers were evaluated during arm exercise, walk-in-place exercise and treadmill exercise (0% slope at 1.5, 2.0 and 3.0 mph). For exercise of similar duration, steady-state pacing rates of implanted devices during arm and walk-in-place exercise were lower than those achieved during treadmill exercise. Linear regression analysis resulted in the slope of these relations most closely approaching 1.0 for arm exercise at "low" activity threshold, while walk-in-place tended to result in slopes approaching 1.0 at all activity thresholds. Similarly, although strapped-on devices underestimated rates obtained with implanted devices, differences fell within a narrow range (-6 to -14%). Thus, in patients with implanted or strapped-on Activitrax pacemakers, relatively simple exercise procedures suitable for office or clinic environment may be useful to provide an estimate of pacing rates during physical activity, and may thereby facilitate selection of appropriate programmable settings.

Sensor-triggered, rate-variable cardiac pacing. Current technologies and clinical implications.

Conventional implantable dual-chamber cardiac pacemakers adjust heart rate and maintain normal atrial and ventricular contraction by tracking "native" atrial electrical activity and pacing the ventricles after a predetermined programmable atrioventricular delay. However, in patients with symptomatic bradyarrhythmias, optimal function of "atrial-tracking" devices may be limited by concomitant sinoatrial disease. Provision of chronotropic response during physical exertion or emotional stress may be achieved by using physiologic sensors to alter pacing rate independently of atrial activity. Additional systems using sensor technologies are being developed. Future pacing systems will have dual-chamber pacing capability and may use several sensors coupled synergistically in order to take advantage of particular strengths of each. Physiologic sensor technology may be of diagnostic value in both antitachycardia devices and implantable cardioverter and defibrillator systems.