Failure of Reflex Venoconstriction During Exercise in Patients With Vasovagal Syncope
Background In this study, we tested two hypotheses. First, we tested the hypothesis that reflex constriction of the venous capacitance beds in patients with vasovagal syncope is impaired during both subhypotensive lower-body negative pressure. Second, we proposed that splenic venoconstriction may be impaired during exercise in patients with vasovagal syncope.
Methods and Results We evaluated 25 patients with vasovagal syncope (age, 45.0±15.9 years; 12 men, 13 women) and 24 control subjects (age, 41.3±13.7 years; 16 men, 8 women). A nuclear technique was used to assess changes in forearm venous tone during lower-body negative pressure and in splenic venous volume during cycle exercise. Changes in forearm vascular resistance (FVR) during cycle exercise were assessed with a strain-gauge plethysmography technique. The percentage reduction in unstressed forearm vascular volume during lower-body negative pressure was similar in patients and control subjects (9.0±8.0% versus 9.7±5.9%, P=NS). During exercise, splenic venous volume decreased less in patients than in control subjects (15.8±21.7% versus 42.6±12.6%, P<.0001). FVR decreased by 2±32% in patients but increased 108±90% in control subjects (P<.0001). There was no relation between percentage change in splenic volume and percentage change in FVR during exercise in either patients or control subjects (r=−.06, P=NS and r=−.18, P=NS, respectively).
Conclusions Patients with vasovagal syncope exhibit a failure of the normal increase in tone in the splenic capacitance bed and in forearm resistance vessels during dynamic exercise. Forearm venous tone increases normally during lower-body negative pressure.
Vasovagal syncope is a common disorder. Common precipitants include prolonged standing, emotion, and pain. Activation of left ventricular mechanoreceptors,1 especially in the setting of an underfilled hypercontractile ventricle, has been proposed as a mechanism of the vasovagal response.2 Stimulation of these receptors leads to reflex bradycardia and hypotension.3 4 Sneddon et al5 demonstrated impaired immediate vasoconstrictor responses during head-up tilt in patients with recurrent neurally mediated syncope, long before the onset of overt vasovagal syncope, which suggests an abnormality in cardiopulmonary baroreceptor reflex arc. Recent animal6 and clinical7 evidence calls the central role of this mechanism into question, at least in some patients. It was proposed recently that activation of other cardiopulmonary mechanoreceptors in the atria or great veins may be responsible for vasovagal syncope.8 The observation of a greater reduction in left ventricular volumes and increases in ejection fraction during tilt table testing in patients with vasovagal syncope than in control subjects also has been considered support for the concept that the vasovagal response may be related to a sudden reduction in cardiac volume.9 10 11 This might be explained by a failure or overriding of normal reflex venoconstriction in response to postural stress. Alternatively, the exaggerated decrease in cardiac volume may be a consequence of the vasovagal reaction (caused by the greater decrease in systemic vascular resistance) rather than its cause.
We previously demonstrated that patients with vasovagal syncope exhibit impaired constriction or paradoxical vasodilation instead of the normal reflex vasoconstrictor response of resistance vessels in nonactive muscle during exercise.12 In another report, we suggested that exercise syncope in some patients with normal hearts may be a variant of vasovagal syncope.13 This raises the possibility that patients with vasovagal syncope may have an exaggerated reflex response from cardiopulmonary mechanoreceptors during exercise, overriding the normal baroreflex vasoconstrictor mechanisms and leading to vasodilation. Dynamic leg exercise in normal subjects is associated with both a marked reduction in splanchnic venous capacitance14 and vasoconstriction of resistance vessels in nonexercising muscle.15 The latter helps to maintain or augment stroke volume in the face of the reduced diastolic filling time that accompanies exercise sinus tachycardia, thereby compensating for the diversion of blood volume to exercising muscles.
We tested two hypotheses in this study. First, we proposed that forearm venoconstriction may be impaired during application of subhypotensive lower-body negative pressure (LBNP) in patients with vasovagal syncope (ie, at a level of LBNP insufficient to induce an overt vasovagal response). Impaired venoconstriction might lead to the small hypercontractile ventricle proposed as the mechanism of the vasovagal response. We assessed this by plotting the forearm volume-pressure relation before and during LBNP to characterize the venous response. This method allows assessment of changes in venous tone. If the volume-pressure coordinates fall on a different curve during LBNP, an intrinsic change in forearm venous properties is implied (active venous response), whereas movement along the same volume-pressure curve represents no change in these intrinsic venous properties (passive venous response). Second, we proposed that splenic venoconstriction may be impaired during exercise in patients with vasovagal syncope and that this is associated with the impaired reflex increase in tone in resistance vessels that we previously described in patients with vasovagal syncope.12 13
Sixty-eight patients were referred to the Royal Brisbane (Australia) Hospital Syncope Clinic between January 1993 and November 1994 for assessment of syncope. A diagnosis of vasovagal syncope was established in 35 patients on the basis of a typical history, negative cardiovascular and neurological examinations, normal echocardiography, a negative EEG and cardiac electrophysiological study (where appropriate), and a positive head-up tilt test without isoproterenol (45 minutes at 60° tilt). Patients who were not in sinus rhythm were excluded. Of these 35 patients, 25 (12 men, 13 women; age, 20 to 70 years [mean age, 45.0 years]) satisfied the above entry criteria and consented to be included in the study. Twenty-four normal subjects (16 men, 8 women; age, 21 to 70 years [mean age, 41.3 years]) from the Gastroenterology Department endoscopy database with no previous cardiac history or current symptoms, normal cardiovascular examination, normal ECG and echocardiogram, and a negative tilt test were enrolled as control subjects.
The investigations were performed at the Royal Brisbane Hospital with the approval of the hospital ethics committee. Informed consent was obtained from all patients and control subjects. Each subject was studied on 3 consecutive days at 8 am after fasting since midnight. No control subjects were on vasoactive medications. Of the patients with vasovagal syncope, 3 had been taking vasoactive medications before enrollment in the study (atenolol 50 mg daily in 1, metoprolol 50 mg twice daily in 1, and sotalol 80 mg twice daily in 1). All vasoactive medications were withdrawn for at least five half-lives before the study. The radionuclide scintigraphic studies were performed on day 1, and assessment of exercise forearm vascular responses during dynamic leg exercise was done on day 2.
Red Cell Labeling
Red cells were labeled with 99mTc pertechnetate by a modified in vivo technique. A cannula was inserted into an antecubital vein of the left arm. Ten minutes after intravenous injection of ≈1.7 mg of stannous pyrophosphate, 5 mL blood was drawn into a heparinized syringe and incubated for 20 minutes with 925 MBq (25 mCi) of 99mTc pertechnetate before reinjection.
Assessment of Changes in Forearm Venous Tone During Application of Subhypotensive LBNP
The subjects lay in a specially constructed LBNP bed and were allowed to rest for 20 minutes. The laboratory was quiet and maintained at a constant temperature of 22°C to 24°C. Venous tone was assessed in the forearm with a standard radionuclide volume-pressure technique.16 In brief, a sphygmomanometer cuff was placed around the upper arm. The forearm was comfortably positioned and restrained on the face of a wide-field-of-view gamma camera (Siemens Orbiter ZLC) interfaced to a dedicated computer system (Max Delta, Siemens) and equipped with a low-energy general-purpose parallel-hole collimator. The region of interest extended from the elbow to the wrist. The static image of the forearm was recorded at 0, 10, 20, and 30 mm Hg venous occluding pressure, beginning at 0 mm Hg and increasing stepwise at 90-second intervals. The counts in the region of interest were acquired in the final 30 seconds of each interval. Repeated studies were performed during application of 20 mm Hg LBNP (insufficient to induce systemic hypotension).
The count rate in this region of interest obtained with no occluding pressure or LBNP was arbitrarily taken to represent 100% forearm blood volume. All subsequent readings were expressed as a percentage of this value. Measures of scintigraphic vascular volumes (in percent units) at occluding cuff pressures of 0, 10, 20, and 30 mm Hg were used to construct venous volume-pressure plots after correction for physical decay.
Changes in Splenic Blood Volume During Erect Cycle Exercise
One hour later, the patient was seated on an erect cycle ergometer in a quiet room maintained at a constant room temperature of 22°C to 24°C. Imaging of the spleen was acquired on a small-field-of-view gamma camera (GE 300A, GE Medical Systems) fitted with a low-energy, general-purpose, parallel-hole collimator and interfaced to a dedicated microcomputer (Max Delta, Siemens). The detector was adjusted for the posterior view with best imaging of the spleen. A 3-minute resting acquisition was performed. Before exercise, a 5-mL blood sample was drawn for subsequent analysis of radioactive counts per 1 mL. The subjects then began exercise at a 25-W workload, increasing by 25-W increments every 4 minutes until the patient was limited by symptoms. Splenic counts were acquired continuously in 30-second epochs, systolic pressure was measured by palpation at rest at the middle of each stage of exercise and at peak exercise, and the ECG was recorded continuously. In the final minute of exercise, another 5-mL blood sample was drawn for subsequent analysis of radioactive counts per 1 mL. Exercise was terminated because of patient fatigue or breathlessness.
Assessment of Changes in Right Atrial Pressure During Erect Cycle Exercise
To explore the possibility that an attenuated reduction in splenic counts may reflect a shift caused by increased pressure along the same venous volume-pressure relation rather than a failure to appropriately increase venous tone, we measured right atrial pressure during maximal erect cycle exercise in 5 patients with vasovagal syncope who exhibited abnormal splenic venous responses in the initial test and in 5 healthy approximately age-matched controls. A central venous long line was inserted through the right antecubital fossa. Pressures were measured with a Baxter transducer referenced to atmosphere at the midchest level and recorded with an Acq Knowledge data acquisition system (Biopac Systems) and an Apple Macintosh IIci microcomputer.
Exercise Forearm Vascular Responses
Subjects were studied in a quiet environment at a constant room temperature of 22°C to 24°C. Forearm blood flow was measured with a standard mercury-in-Silastic strain-gauge plethysmography technique (Hokanson).17 Patients were positioned semierect (at 70° to the horizontal) on a cycle ergometer. The right forearm was elevated to allow free venous drainage. A pneumatic collecting cuff was placed around the upper arm; a second cuff was placed around the wrist and inflated for the duration of the recordings to suprasystolic pressure to exclude hand circulation from the measurements. Measurements of forearm blood flow were obtained by inflating the collecting cuff to 40 mm Hg to prevent venous return. Thus, the rate of increase of forearm girth was proportional to forearm blood flow. The cuff was inflated for 10 seconds and then deflated for 10 seconds. This was repeated three times, and the forearm flow was calculated from the mean of the three slopes. The volume variations of the limb segment were measured by means of the electrical resistance variations of the mercury-filled strain gauge. The volume output from the strain gauge was measured with a high-gain preamplifier and recorded with surface ECG data by an Apple Macintosh IIci computer and an Acq Knowledge multichannel data acquisition system. Blood pressure was measured in the opposite limb with a mercury sphygmomanometer. After measurements were made with patients at rest, patients performed symptom-limited semierect cycle exercise, beginning at 25 W and increasing by 25 W every 3 minutes. Forearm blood flow was measured during the final minute of each stage of exercise. Forearm vascular resistance (FVR), expressed in resistance units, was calculated as the quotient of the mean arterial pressure (in millimeters of mercury) and forearm blood flow (milliliter per minute per 100 mL).
Forearm Venous Tone During LBNP
At 0 and −20 mm Hg LBNP, forearm counts were assessed at each venous occlusion pressure to give paired venous volume-pressure plots for each patient. Linear regressions were performed on each set of data points to determine whether a linear model described the data. A linear model was accepted if r>.8. We then determined whether the slopes of the two lines in each data set were different (ie, to determine whether the lines were parallel or not) using an established method for testing the difference between two independent regressions.18
Unstressed venous volume was defined as the intercept on the volume axis. Changes in unstressed volume reflect changes in venous tone.
Splenic Counts During Erect Cycle Exercise
A region of interest was drawn around the spleen, and counts were measured within this region of interest. Resting and peak exercise crude counts were corrected for the counts per gram in the blood samples taken at rest and at peak exercise to assess changes in splenic volume.
Data are expressed as mean±SD. Statistical analysis was performed with paired and unpaired t tests, the χ2 test, and linear regression as appropriate. A value of P<.05 was considered significant.
Of the patients, 12 were men and 13 were women 20 to 70 years of age (mean, 45.0 years). The control group consisted of 16 men and 8 women 21 to 70 years of age (mean, 41.3 years) (statistically similar in age to the patient group). On specific inquiry, 5 patients but no control subjects recalled a history of exercise syncope or presyncope. Of these patients, 3 had previously demonstrated exercise-induced hypotension during erect treadmill exercise according to standard criteria.19 The patients had suffered 9.4±8.1 episodes of syncope in the past, whereas no control subjects had any previous episodes of syncope.
Forearm Venous Responses During LBNP
Two volume-pressure plots were performed for each subject, one with the patient resting and one with −20 mm Hg LBNP applied. Linear regressions were performed on each plot, and r values were .87 to .99 (mean, .96±.03). Therefore, a linear model was adopted. All control subjects and 24 of the 25 patients showed a downward shift in the forearm volume-pressure relation during LBNP. One patient showed a paradoxical upward shift in the volume-pressure relation during LBNP (ie, her unstressed forearm vascular volume increased by 15% during −20 mm Hg LBNP). Although volume-pressure plots varied in slope (compliance) between individuals, within individuals there was little change in slope between control and LBNP states. Thus, shifts induced by LBNP were parallel. To confirm this, we used a standard method18 to test whether the slopes of each set of paired data were different and found that they were not (P=NS).
All patients and control subjects completed the LBNP study without complications. As Table 1⇓ shows, heart rate and systolic pressure in the two groups were similar at rest and at −20 mm Hg LBNP. In no subject was systolic pressure during LBNP >10 mm Hg lower than at rest.
The percentage change in forearm counts at −20 mm Hg compared with rest was similar in patients and control subjects. Linear regression yielded the equations V=Detected Activity (cps)=647+5.90×Before and V=Detected Activity (cps)=593+5.90×During −20 mm Hg LBNP in patients with vasovagal syncope (P<.0001). In normal subjects, linear regression yielded the equations V=Detected Activity (cps)=609+5.90×Before and V=Detected Activity (cps)=543+5.90×During −20 mm Hg LBNP (P<.0001). The percentage decrease in unstressed forearm vascular volume during application of LBNP was similar in patients and control subjects (9.0±8.0% versus 9.7±5.9%, P=NS). Fig 1⇓ is an example of volume-pressure plots both at rest and during −20 mm Hg LBNP from 1 patient.
Splenic Volumes During Erect Cycle Exercise Testing
The erect cycle exercise test was completed without complication in all patients and control subjects. As Table 2⇓ shows, heart rate and systolic pressure were similar at rest in patients and control subjects. At peak exercise, heart rate was similar in the two groups, whereas systolic pressure was markedly lower in patients versus control subjects (165±23 versus 191±12 mm Hg, P=.001). Two patients developed presyncope during erect cycle exercise associated with documented exercise-induced hypotension. Both had previously given a history of syncope or presyncope on exercise.
As Table 2⇑ and Fig 2⇓ show, the patients exhibited an attenuated reduction in corrected splenic counts during exercise compared with control subjects (−15.8±21.7% versus −42.6±12.6%, P<.0001). Three patients exhibited an increase in counts during exercise, a response not seen in any control subjects. An abnormal exercise splenic venous response was defined as an increase in counts during exercise or a decrease of ≤30% (ie, 1 SD below the mean of the control group). On this basis, only 5 patients exhibited a normal response.
Right Atrial Pressure Measurements
The attenuated fall in splenic venous volume during exercise in patients might reflect either impaired venoconstriction or a movement along the same venous pressure-volume relation resulting from an increase in splenic venous pressure during exercise in patients. To assess the latter possibility, 5 patients who exhibited abnormalities of splenic venous volume change on the initial test (−25.2%, −12.9%, −10.9%, 7.9%, and 28.4%) underwent another upright cycle exercise test with measurement of right atrial pressure at rest and during the same maximal workload as in the initial test and were compared with 5 of the control subjects studied at rest and at peak exercise. During exercise, right atrial pressure fell by 2 to 7 mm Hg (mean, 4.3 mm Hg) in the patients; in the control subjects, right atrial pressure changed by −4 to 2 mm Hg (mean, 0 mm Hg; P=.05). This implies that the attenuated reduction in splenic venous volume during exercise in patients reflects a failure to increase venous tone.
Measurement of Forearm Blood Flow During Semierect Exercise Testing
Semierect exercise was completed without complication in all patients. As Table 3⇓ shows, heart rates at rest and at peak exercise were similar in the two groups, although mean blood pressure tended to be slightly lower at peak exercise in patients versus control subjects (116±18 versus 127±17 mm Hg, P=.1). FVR was similar at rest in patients and control subjects but decreased by 2±32% in patients and increased by 108±90% in control subjects during exercise (P<.0001). FVR fell during exercise in 16 of the 25 patients, a response seen in only 1 control subject.
Relation Between Exercise Splenic Venous Volume and Changes in Exercise Forearm Venous Responses
For both the patient and control groups, the percentage change in splenic venous volume was not related to the percentage change in FVR (r=−.06, P=NS and r=−.18, P=NS, respectively).
The important new finding of this study is that patients with vasovagal syncope exhibit a normal increase in forearm venous tone during subhypotensive LBNP but markedly impaired reductions in splenic venous volume (and in 3 patients, paradoxical increases in splenic venous volume) during exercise. Assessment of right atrial pressure in a subset suggests that the latter reflects a failure to increase splenic venous tone on exercise. There was also a failure of constriction of resistance vessels in nonactive muscles, but the percentage changes in splenic volumes and FVR were unrelated.
Is the Vasovagal Response Caused by a Failure of Reflex Venoconstriction?
Almquist and coworkers2 proposed that vasovagal syncope is a consequence of left ventricular mechanoreceptor activation in the setting of an underfilled hypercontractile ventricle. Hemorrhage experiments in conscious rabbits were initially thought to support this concept. With progressive hemorrhage, there is initial tachycardia and increased renal sympathetic nerve activity (phase 1), but when blood volume decreases by ≈30% and cardiac output by 50% in this model, renal sympathetic nerve activity and heart rate both decrease (phase 2), a phenomenon analogous to the vasovagal response.6 This phase can be blocked by intrapericardial procaine,20 leading to the suggestion that left ventricular mechanoreceptor activation is solely responsible. However, a recent report demonstrated that vagotomy does not always completely abolish phase 2, although the onset is delayed.6 Similarly, vasovagal responses have been reported during aggressive tilt table protocols in cardiac transplant recipients in whom there is cardiac vagal deafferentation.7 Thus, left ventricular mechanoreceptor activation probably is not the sole mechanism of the vasovagal response. Dickinson8 recently suggested that collapse firing of cardiopulmonary receptors at the junction of the atria and the great veins may be responsible. It seems likely on balance that firing of one or more groups of cardiopulmonary mechanoreceptors may be at least partly responsible for the vasovagal response. The observation of greater decreases in left ventricular end-diastolic volume and greater increases in ejection fraction during tilt testing in patients with vasovagal syncope compared with control subjects is consistent with an exaggerated decrease in cardiac volume as the mechanism,9 10 11 perhaps because of abnormal local left ventricular wall stresses.21 This leads to the hypothesis that a failure of appropriate reflex venoconstriction during postural stress may result in an exaggerated decrease in cardiac volume, the enhanced epinephrine response, which has been demonstrated in patients with vasovagal syncope,22 and finally paradoxical cardiopulmonary mechanoreceptor activation. One group previously showed that patients who become syncopal on head-up tilt have greater increases in calf venous volume during tilt testing and less variability in the venous volume during the tilted period.23 Another group demonstrated impaired forearm venoconstrictor responses during mental arithmetic stress,24 lending support to this concept.
In this study, we evaluated whether forearm venous tone increased normally during application of minor (subhypotensive) LBNP. Forearm venoconstriction was similar in patients and control subjects, although the observation of paradoxical venodilation during subhypotensive LBNP in 1 patient warrants further investigation in a large series and may suggest occasional individuals in whom a primary failure of venoconstriction during LBNP might occur. We demonstrated previously that during subhypotensive LBNP, impaired forearm constriction or paradoxical vasodilation of resistance vessels is present,25 implying that although hypotension has not developed, the vasovagal reaction may have already begun. The patient population for this earlier study had considerable overlap with the population in the present study. Similarly, Sneddon et al5 demonstrated impaired constriction of forearm resistance vessels after only 2 minutes of head-up tilt in patients with vasovagal syncope. Conversely, it must be noted that this group demonstrated exaggerated constriction of forearm resistance vessels during minor subhypotensive LBNP in patients with vasovagal syncope.26 Nevertheless, given the fact that our patient populations in the venous and resistance vessel studies are largely the same, it is reasonable to conclude that normal forearm venoconstriction is occurring at a stage when impaired constriction or dilation of resistance vessels is present. This makes it unlikely that a failure of venoconstriction during central volume unloading is the initial trigger for the vasovagal reaction. Despite this, venodilation may be an important contributory mechanism in other situations. As Manyari and Sheldon24 demonstrated, forearm venoconstriction is impaired during mental arithmetic stress. Similarly, a loss of venous tone is likely to occur with the onset of the vasovagal reaction and may then lead to a vicious circle of left ventricular volume reduction and hence aggravation of the vasovagal response.
Splenic Venous Capacitance During Exercise
We previously reported that exercise syncope in patients with normal hearts may be a variant of vasovagal syncope.13 Furthermore, we recently demonstrated that patients with vasovagal syncope exhibit impaired constriction or paradoxical dilation of forearm vessels during dynamic leg exercise.12 This suggests that reflex vascular control mechanisms may be abnormal during exercise in patients with vasovagal syncope. In this study, we tested the hypothesis that there is failure of reflex splenic venoconstriction during exercise in patients with vasovagal syncope. In normal subjects, there is a marked reduction in splanchnic and splenic venous capacitance during exercise.14 This may be an important mechanism of augmenting stroke volume in the face of a reduced diastolic filling time associated with sinus tachycardia. Our data suggest that there is a markedly attenuated reduction in splenic venous volume (and in 3 patients, a paradoxical increase) during exercise compared with control subjects. Simultaneous measurement of right atrial pressure during exercise in a subset of patients and control subjects suggests that this represents a failure of active venoconstriction rather than passive venous volume changes.
Mark et al27 28 proposed that the abnormal vasodilator response seen in forearm resistance vessels during dynamic leg exercise in patients with aortic stenosis may be due to exaggerated left ventricular mechanoreceptor activation. Our observation of abnormal forearm resistance vasodilatation during exercise in patients with vasovagal syncope may have a similar basis, as may our previous observations about ischemic heart disease29 and hypertrophic cardiomyopathy.30 31 The mechanism of splenic and splanchnic venoconstriction during exercise is unclear. It may also be a consequence of exaggerated left ventricular mechanoreceptor activation, but this is speculative. Cardiac distension decreases venous tone presumably by activation of left ventricular mechanoreceptors.32 33 34 Stimulation of chemosensitive left ventricular receptors by intracoronary prostacyclin decreases intestinal venous tone.35 The recent observation of a marked decrease in splanchnic venous tone during phase 2 in the animal hemorrhage model described above is consistent with venodilation as a consequence of the vasovagal phenomenon36 but does not necessarily prove that it is due to left ventricular mechanoreceptor activation.
The lack of a relation between changes in splenic venous volume and FVR during exercise in both patients and control subjects, while not inconsistent with ventricular mechanoreceptor activation as the mechanism of the failure of venoconstriction in patients, may imply that the control mechanisms for the venous capacitance and resistance vessels during exercise are not identical. Given the known differences in hemodynamics in normal subjects and patients with cardiac disease during exercise in the supine versus erect position, the difference in exercise protocols (semierect cycle for the FVR studies versus erect cycle for the venous studies) dictates some caution in this conclusion.37 38 However, we have demonstrated that in normal subjects, the change in FVR is similar during semierect (70° to horizontal) versus supine exercise.39 The difference in forearm vascular response during supine cycle exercise at 70° to horizontal and erect cycle exercise is likely to be less than the difference between semierect and supine exercise.
Although this study demonstrates forearm venoconstriction to be normal during application of subhypotensive LBNP in patients with vasovagal syncope, we cannot exclude a failure of venoconstriction in the quantitatively more important splanchnic and splenic venous beds. Imaging of splenic venous volume in the LBNP bed proved technically impossible, and intubation of the splenic vein to assess venous pressure-volume relations rather than volume alone was not ethically feasible.
One of the primary problems with this investigation is the different exercise protocols used to assess changes in splenic venous volume and changes in FVR. It was technically not possible to assess splenic venous volume on the semierect cycle because the spleen is best imaged posteriorly and the semierect cycle interferes with that imaging. Conversely, forearm vascular responses could not be obtained with any accuracy during erect cycle exercise because increased movement artifact in this position renders the traces unreadable. The exercise stages were also of slightly different lengths (4 versus 3 minutes). While conceding this limitation, as outlined earlier, we believe there is still some validity to comparing vascular responses during the two forms of exercise.
There is a failure of reflex constriction or paradoxical dilation of both resistance and venous capacitance vessels during exercise in patients with vasovagal syncope, and this may lead to exercise-induced hypotension in some patients. The mechanism of this abnormality of reflex vascular control during exercise remains speculative. Reflex venoconstriction during subhypotensive LBNP was normal.
This work was supported in part by grants from the NH&MRC of Australia (project grant number 665 941193, scholarship number 948220).
- Received August 1, 1995.
- Revision received September 27, 1995.
- Accepted October 1, 1995.
- Copyright © 1996 by American Heart Association
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