(Circulation. 2000;101:777.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
Left Ventricular Geometry and Function Preceding Neurally Mediated Syncope
From the Department of Medicine, Division of Cardiology, The New York Hospital-Cornell Medical Center, New York, NY.
Correspondence to Bruce B. Lerman, MD, Division of Cardiology, The New York Hospital-Cornell Medical Center, 525 East 68th Street, Starr Pavilion, 4th floor, New York, NY 10021.
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Abstract |
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Background—Neurally mediated syncope has been associated with increased left ventricular (LV) fractional shortening (FS) during tilt testing, which is consistent with the hypothesis that the stimulation of LV mechanoreceptors leads to reflex hypotension and/or bradycardia. However, FS does not represent true LV contractility because of its dependence on afterload and preload.
Methods and Results—To elucidate the role of increased contractility in the mediation of neurally mediated syncope, we compared echocardiographic measures of LV performance corrected for end-systolic stress (ESS) in 21 patients (13 women and 8 men) with unexplained syncope who had either positive (n=10) or negative (n=11) responses to a tilt-table test. Two-dimensional echocardiographic LV imaging was performed at baseline and during the initial 5 minutes of upright tilt. In the supine position, both groups had similar LV end-diastolic volume indexes, stroke volumes, FS, circumferential ESS, and afterload-independent measures of LV performance (stress-corrected midwall and FS). However, after 5 minutes of upright tilt, patients who subsequently had a positive test had a lower stroke volume, lower stress-corrected midwall shortening, and endocardial FS. The tilt-positive group also had a greater fall in ESS and FS early during upright tilt.
Conclusions—Reduced ESS, LV volume, and chamber function during initial upright tilt are associated with a subsequent positive tilt response in patients with unexplained syncope. These data suggest that if paradoxic activation of LV mechanoreceptors has a role in mediating neurally mediated syncope, it is not triggered by LV hypercontractility or increased systolic wall stress during the initial period of upright tilt.
Key Words: echocardiography • syncope • tilt-table test • ventricular function
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Introduction |
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Loss of consciousness due to neurally mediated syncope is generally attributed to the activation of left ventricular (LV) mechanoreceptors that mediate the Bezold-Jarisch reflex.1 2 This reflex may be triggered by venous pooling, sympathetic nervous system activation, and/or hypercontractility of a relatively unloaded left ventricle. Support for the involvement of LV mechanoreceptors in human neurally mediated syncope is based on reports of increased LV fractional shortening (FS) and decreased LV volume during tilt testing in patients with a positive response.3 4 However, the force imposed on the LV wall and on the mechanoreceptors contained therein is more directly assessed by LV wall stress than by systolic fiber shortening, which does not directly measure contractility due to its dependence on preload and afterload.
To gain insight into the role of increased myocardial contractility in the mechanism of neurally mediated syncope, this study was designed to evaluate LV end-systolic stress (ESS), midwall shortening, segmental fiber shortening, and wall thickening before and during the imposition of orthostatic stress during tilt-table testing in patients with unexplained syncope. These and other indices were calculated to provide more direct measures of myocardial function and load than are provided by chamber performance alone.5
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Methods |
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Patient Selection
Patients referred to the Cardiac Electrophysiologic Laboratory at The New York Hospital–Cornell Medical Center for tilt-table testing as part of their evaluation of unexplained syncope or presyncope were eligible for inclusion in this study. Reasons for exclusion from the study included a poor echocardiographic window or the presence of known cardiac structural abnormalities such as aortic stenosis, hypertrophic cardiomyopathy, or LV wall motion abnormalities. A total of 21 patients with unexplained syncope, 8 men and 13 women, who had a mean age of 43 years (range, 18 to 91 years) were enrolled in the study. All subjects had a normal baseline echocardiogram. No patient had any clinical contraindication to the use of isoproterenol.
Tilt-Table
Test Protocol
All patients were studied after a 4-hour fast. After informed
consent was obtained, patients were positioned supine on the tilt
table, and an intravenous catheter was inserted into a
peripheral arm vein. Continuous electrocardiographic
monitoring was initiated, and an external cardiac pacing unit (Zoll
Cardiac Pacing Unit, ZMI Medical Corporation) was connected to
the patient for emergency antibradycardia pacing. Noninvasive blood
pressure (Dinamap, Critikon) was recorded at 1-minute intervals
throughout the protocol. Blood pressure measurements were also obtained
with a manual blood pressure cuff to verify any decrease in blood
pressure detected by the automatic cuff or when warranted by clinical
symptoms.
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After a 15-minute supine control phase (stage I), patients were tilted upright at 60o (stage II). Upright tilt was maintained for 30 minutes. If a positive response (see definition below) occurred during upright tilt, patients were returned to the supine position, and the protocol was terminated. If stage II was completed without a positive response, patients were returned to the supine position, and an isoproterenol infusion was started at a rate of 1 µg/min (stage III). The infusion rate was increased over 5 minutes to produce a 20% increment in the resting (supine) heart rate (maximum isoproterenol infusion rate was 5 µg/min). After titration of isoproterenol, patients were again tilted upright (stage IV) for 15 minutes. If a positive response occurred, patients were returned to the supine position, and the protocol was terminated. Completion of the full duration of upright tilt in both stages II and IV without a positive response constituted a negative tilt-table test. A positive response (with or without concomitant isoproterenol) was defined as either a sudden loss of consciousness or the development of presyncope in association with an abrupt fall in systolic blood pressure to <80 mm Hg and reproduction of the patient’s clinical symptoms.
Echocardiography
Echocardiographic examinations were performed in
a standard fashion using a 2.0- or 2.5-MHz transducer (HP Sono 2500,
Hewlett-Packard). Two-dimensional echocardiographic
images of the LV were recorded at baseline and during the initial 5
minutes of upright tilt before symptoms developed (stage II), a time
period chosen to ensure that early tilt findings were predictive,
rather than a consequence of, the neurally mediated reflex (images for
analysis in most patients were obtained during minutes 3 to 5).
The patients were imaged in a lateral decubitus position in both the
supine and upright positions. The parasternal long-axis and short-axis
and apical views were recorded on videotape. LV measurements were
made in the parasternal long- and short-axis views at the level of the
papillary muscle tips using an off-line reading station
(Digisonics, Inc).
Three measurements from different cardiac cycles within 10 consecutive
beats of each other were made and then averaged. Septal and posterior
wall thickness and LV chamber dimensions were measured according to the
conventions of the American Society of
Echocardiography.6 To verify the
stability of the LV imaging plane used for LV measurements between
supine and upright tilts, the cross-sectional area of the LV
myocardium was calculated from LV wall thicknesses and
internal dimensions at end-diastole and end-systole using
the method of Ditchey et al.7 The cross-sectional areas at
baseline (13.0±2.8 cm2) and during tilt
(13.2±3.2 cm2; P=0.69) were virtually
identical. To assess LV systolic function, endocardial FS was
calculated as follows8 :
 | (1) |
Midwall shortening was calculated by taking into account the epicardial
migration of the midwall during systole using a model similar to that
commonly used to calculate LV mass9 (see Appendix). Stroke
volume was estimated using the Teichholz correction of the cube
formula10 (which was validated in the symmetrically
contracting LV),11 12 and it was used to calculate cardiac
output and peripheral resistance. Myocardial afterload was
assessed by meridional ESS (mESS)13 and circumferential
ESS (cESS), which were calculated at the midwall at the level of the LV
minor axis using the method of Gaasch et al14 (see
Appendix). Equations derived from normal subjects were used to predict
expected endocardial and midwall FS for observed cESS15 as
follows:
 | (2) |
 | (3) |
) multiplied by 100. Stress-corrected midwall
shortening5 was calculated as the ratio between observed
midwall shortening and midwall shortening predicted from cESS (equation 3) multiplied by 100. To assess segmental LV wall function, 2D short-axis images at the level of the papillary muscles were analyzed using a commercially available review station with additional custom software. Briefly, endocardial and epicardial interfaces were traced in end-diastolic and end-systolic frames, and the computer program converted these primary data into measures of total, inner-shell, and outer-shell wall areas; mean wall thickness and systolic thickening; endocardial, midwall, and epicardial circumferential fiber shortening; and ESS in each of six 60° sectors around the center of the left ventricle. In the present study, systolic wall thickening in the segments corresponding to the anterior and inferior septum, anterior wall, anterolateral wall, posterolateral wall, and inferior wall were used as measures of segmental myocardial performance. All echocardiograms were interpreted by 2 investigators blinded to the results of the tilt-table response.
Statistical Analysis
Data are expressed as mean±SD. The independent samples
t test was used to compare patient groups with and without
positive tilt-table responses. A 2-tailed P<0.05 was
considered significant.
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Results |
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Patient Characteristics
A total of 37 patients were enrolled in this study; 16 were eliminated from further analysis due to a suboptimal echocardiographic window. The study group, therefore, comprised 21 patients, all of whom had a normal baseline ECG. No patient had structural heart disease, but 2 patients had mitral valve prolapse. Ten patients had a positive tilt test (7 women and 3 men aged 46±20 years), and 11 patients had a negative tilt test (6 women and 5 men aged 40±21 years; both P=NS). Among the 10 positive responders, 6 patients developed syncope during passive (drug-free) tilt (stage II), and 4 developed syncope during the isoproterenol infusion phase (stage IV). In patients who developed a positive response during stage II of the tilt-table testing, the average time to syncope was 22 minutes (range, 6 to 30 minutes). In all patients, the echocardiographic measurements were performed before the development of a clinically evident neurally mediated response.
Hemodynamic Findings
No differences existed in baseline supine blood pressures between
patients with negative and positive tilt tests (Table 1). Patients with a positive tilt
response had a higher mean baseline heart rate than those with a
negative test (77±17 versus 62±12 beats/min; P=0.03).
During upright tilt, no differences between patient groups existed with
respect to systolic, diastolic, or mean blood
pressures during the period in which the
echocardiographic images were analyzed. The
mean systolic blood pressure remained unchanged during the
initial 5 minutes of upright tilt in both the tilt-negative and
tilt-positive groups. As was the case at baseline, the positive group
had a higher average heart rate during the initial period of upright
tilt than did the negative group (82 versus 68 beats/min;
P=0.04). However, no differences existed between the 2
groups with respect to the change in heart rate related to position
(supine to upright; mean increase, 6±7 versus 5±12 beats/min,
respectively, in the positive and negative groups).
Echocardiographic Data
During the supine baseline period, patients with negative and
positive tilts did not differ in end-diastolic LV volumes,
end-systolic volumes, stroke volumes, endocardial FS, or
midwall shortening (Table 2). In
addition, the 2 groups had similar mESS, cESS, stress-corrected
endocardial FS, and midwall shortening (Figure 1). However, after 5 minutes of tilt, the
positive-tilt group had lower mean LV end-diastolic volume
indexes, stroke volumes, and stress-corrected endocardial FS and
midwall shortening (all P<0.05). As shown in Table 3, during the initial period of tilt, no
differences existed between positive and negative responders with
respect to change in FS, midwall shortening, or ejection fraction.
However, patients who subsequently developed a positive tilt had a
significantly greater fall in mESS (P=0.03), cESS
(P=0.02), stress-corrected FS (P=0.006), and
stress-corrected midwall shortening (P=0.02) (Figure 2). In addition, a greater reduction in
end-diastolic volume index (P=0.02) occurred in
patients with positive tilts, and the cardiac index fell significantly
during initial tilt in the positive group, but not in patients with
negative tilts (P=0.02) (Table 3).
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0.03). C and D, Similar findings are also seen
in stress-corrected FS and midwall shortening (MWS)
(P
No differences in segmental LV wall thickness in diastole
and systole or in percent thickening existed between the groups at
baseline (Table 4). However, during the
initial upright tilt, the percent thickening of the
inferior wall was less in the group with a positive tilt
response than in the group with a negative response
(P=0.05). No differences existed in percent thickening in
the other LV segments between the groups.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
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This study found that a marked decrease occurred in LV end-systolic wall stress and stress-corrected FS during the early phase of upright tilt in patients with neurally mediated syncope. Similarly, compared with those who do not develop syncope, cESS (myocardial afterload) and stress-corrected midwall shortening (myocardial contractility) fell significantly in patients with a positive tilt test. These hemodynamic findings occurred well before the onset of syncope, which suggests that these early changes predict a subsequent positive tilt response.
The present study also confirms that a greater decrease in LV end-diastolic volume occurs during upright tilt in patients who develop neurally mediated syncope than in those who do not3 4 16 17 and that these patients have a lower percent thickening of the inferior wall, where the greatest density of C-fibers are thought to be located.18 Despite data suggesting that the activation of LV mechanoreceptors correlates linearly with LV end-diastolic pressure19 and that enhanced contractility may have a synergistic (but not independent) effect on receptor discharge, it has also been shown that acute hemorrhage (unloading of the left ventricle) triggers a paradoxical increase in mechanoreceptor activation. Therefore, one cannot disregard the possibility that the lower end-diastolic volume observed in the tilt-positive patients may have had a role in activating LV mechanoreceptors and triggering reflex bradycardia and hypotension. It is also important to recognize that LV wall stress may not necessarily be synonymous with or linearly related to mechanical deformation of LV mechanoreceptors. To that end, the response or sensitivity of LV mechanoreceptors at a given level of mechanical stress may vary among patients and, therefore, although our data show that increased LV wall stress is not responsible for triggering neurally medially syncope during tilt, we have not excluded the potentially important role of LV mechanoreceptor activation through other means in mediating this process. Nevertheless, the presence of neurally mediated syncope in patients with functionally denervated hearts after orthotopic cardiac transplant also strongly suggests that mechanisms independent of LV mechanoreceptor stimulation may be operative in some patients.20
Consistent with recent evidence showing that sympathetic responses in subjects with neurally mediated syncope are heterogeneous,21 22 LV contractility did not increase with orthostasis in patients with a positive-tilt response. These patients have impaired arterial baroreceptor reflex sensitivity, which results in a diminished sympathetic response to orthostatic stress,21 22 impaired splenic venoconstriction during exercise,23 and blunted cardiopulmonary (low-pressure) baroreceptor responses during tilt or lower body negative pressure that results in paradoxical arterial vasodilatation.24 25 Other studies also showed that these patients may have a blunted increase in muscle sympathetic nerve activity compared with control subjects on initial tilt, which is followed by a progressive decrease in sympathetic nerve activity.21
Study Limitations
Inadequate echocardiographic windows limited the
number of patients available for analysis. Accurate
analysis of segmental wall thickening and wall stress requires
"perfect" on-axis parasternal views, which are especially difficult
to obtain in the upright position. However, our data showing the
stability of the echocardiographic cross-sectional area
between supine and tilt recordings indicates that a stable
imaging plane can be maintained, despite a change in body position.
Another limitation is that patients with positive tilts were not
homogenous with respect to the requirement of isoproterenol for
induction. It is also important to note that although this study was
designed to detect initial hemodynamic changes during
upright tilt that would predict a subsequent positive tilt response, it
is possible that increases in wall stress or
contractility might occur more proximate to the
syncopal event during tilt at a time when
echocardiographic recordings were not obtained.
However, in the 1 patient who had echocardiographic
recordings in proximity to the time (within 2 minutes) of
syncope, a decrease in systolic wall stress and chamber
function was also observed. Other researchers also showed that
characteristic hemodynamic changes (decrease in forearm
resistance) in patients with neurally mediated syncope occur within 2
minutes of upright tilt, well before the onset of
syncope.25 Finally, in 2 patients (1 tilt-positive and 1
tilt-negative), echocardiographic data were
analyzed at several intervals during upright tilt (at 1-minute
intervals up to 5 and 10 minutes, respectively). These data showed that
a persistent reduction of LV chamber size occurred during sequential
upright tilt recordings.
Implications
The results of this study add further support to the notion that
neurally mediated syncope may be a manifestation of a final common
efferent pathway with multiple potential afferent inputs. Contrary to
the assumptions implicit in the mechanoreceptor hypothesis of neurally
mediated syncope, patients in this study with a positive tilt response
showed reduced ESS and LV volume, with diminished chamber function
during the first 5 minutes of upright tilt. The results of this study
make it unlikely that LV hypercontractility is a
universal trigger for the activation of LV mechanoreceptors in the
pathogenesis of neurally mediated syncope.
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Acknowledgments |
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This work was supported in part by grants from the National Heart, Lung, and Blood Institute (RO1 HL56139), the Michael Wolk Heart Foundation, and the Rosenfeld Heart Foundation.
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Appendix 1 |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
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cESS was calculated using the following formula13 (see Figure 3
): SBPx(LVIDs/2)2x(1+{[(LVIDs/2)
 | (4) |
mESS was calculated using the mean cuff systolic blood pressure
during the initial 5 minutes of each phase of the tilt-table test using
the following validated formula (abbreviations as in equation 4):
 | (5) |
 | (6) |
 | (7) |
On the basis of equation 6, the systolic thickness of the inner
shell can be calculated, which allows the computation of midwall
shortening as follows:
 | (8) |
Received May 5, 1999; revision received September 19, 1999; accepted September 29, 1999.
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References |
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TopAbstractIntroductionMethodsResultsDiscussionAppendix 1References |
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1. Abboud FM. Neurocardiogenic syncope. N Engl J Med. 1993;328:1117–1120.
2. Mark AL. The Bezold-Jarisch reflex revisited: clinical implications of inhibitory reflexes originating in the heart. J Am Coll Cardiol. 1983;1:90–102.[Abstract]
3. Shalev Y, Gal R, Tchou PJ, Anderson AJ, Avitall B, Akhtar M, Jazayeri M. Echocardiographic demonstration of decreased left ventricular dimensions and vigorous myocardial contraction during syncope induced by head-up tilt. J Am Coll Cardiol. 1991;18:746–751.[Abstract]
4. Fitzpatrick A, Williams T, Ahmed R, Lightman S, Bloom SR, Sutton R. Echocardiographic and endocrine changes during vasovagal syncope induced by prolonged head-up tilt. Eur J CPE. 1992;2:121–128.
5.
Devereux RB, de Simone G, Pickering TG, Schwartz JE,
Roman MJ. Relations of left ventricular midwall function to
cardiovascular risk factors and arterial
structure and function. Hypertension. 1998;31:929–936.
6.
Sahn DJ, DeMaria A, Kisslo J, Weyman A. The committee
on M-mode standardization of the American Society of
Echocardiography: recommendations regarding
quantitation in M-mode echocardiography: results of
a survey of echocardiographic measurements.
Circulation. 1978;58:1072–1083.
7. Ditchey RV, Schuler G, Peterson KL. Reliability of echocardiographic and electrocardiographic parameters in assessing serial changes in left ventricular mass. Am J Med. 1981;70:1042–1050.[Medline] [Order article via Infotrieve]
8.
Gutgesell HP, Paquet M, Duff DF, McNamara DG.
Evaluation of left ventricular size and function by
echocardiography: results in normal children.
Circulation. 1977;56:457–462.
9.
Shimizu G, Hirota Y, Kita Y, Kawamura K, Saito T,
Gaasch WH. Left ventricular midwall mechanics in systemic
arterial hypertension: myocardial function is depressed in
pressure-overload hypertrophy. Circulation. 1991;83:1676–1684.
10. Teichholz LE, Kreulen T, Herman MV, Gorlin R. Problems in echocardiographic-angiographic correlations in the presence or absence of asynergy. Am J Cardiol. 1976;37:7–11.[Medline] [Order article via Infotrieve]
11.
Asanoi H, Sasayama S, Kameyama T.
Ventriculoarterial coupling in normal and failing heart in
humans. Circ Res. 1989;65:83–93.
12. Devereux RB, Roman MJ, Paranicas M, O’Grady MS, Wood EP, Howard BV, Welty TK, Lee ET, Fabsitz RR. Relations of Doppler stroke volume and its components to left ventricular stroke volume in normotensive and hypertensive American Indians: the Strong Heart Study. Am J Hypertens. 1997;10:619–628.[Medline] [Order article via Infotrieve]
13.
Reichek N, Wilson J, St John Sutton M, Plappert TA,
Goldberg S, Hirshfeld JW. Noninvasive determination of left
ventricular end-systolic stress: validation of the
method and initial application. Circulation. 1982;65:99–109.
14.
Gaasch WH, Battle WE, Oboler AA, Banas JS, Levine HJ.
Left ventricular stress and compliance in man with special
reference to normalized ventricular function curves.
Circulation. 1972;45:746–762.
15. de Simone G, Devereux RB, Roman MJ, Ganau A, Saba PS, Alderman MH, Laragh JH. Assessment of left ventricular function by the midwall FS/end-systolic stress relation in human hypertension. J Am Coll Cardiol. 1994;23:1444–1451.[Abstract]
16. Yamanouchi Y, Jaalouk S, Shehadeh AA, Jaeger F, Goren H, Fouad-Tarazi FM. Changes in left ventricular volume during head-up tilt in patients with vasovagal syncope: an echocardiographic study. Am Heart J. 1996;131:73–80.[Medline] [Order article via Infotrieve]
17. Mizumaki K, Fujiki A, Tani M, Shimono M, Hayashi H, Inoue H. Left ventricular dimensions and autonomic balance during head-up tilt differ between patients with isoproterenol-dependent and isoproterenol-independent neurally-mediated syncope. J Am Coll Cardiol. 1995;26:164–173.[Abstract]
18.
Thames MD, Klopfenstien HS, Abboud FM, Mark AL, Walker
JL. Preferential distribution of inhibitory cardiac
receptors with vagal afferents to the inferoposterior wall of the dog.
Circ Res. 1978;43:512–519.
19. Gupta BN, Thames MD. Behavior of left ventricular mechanoreceptors with myelinated and unmyelinated afferent vagal fibers in cats. Circ Res. 52;1983:291–301.
20. Scherrer U, Vissing S, Morgan BJ, Hanson P, Victor RG. Vasovagal syncope after infusion of a vasodilator in a heart-transplant recipient. N Engl J Med. 1990;322:602–604.[Medline] [Order article via Infotrieve]
21. Mosqueda-Garcia R, Furlan R, Fernandez-Violante R, Desai T, Snell M, Jarai Z, Ananthram V, Robertson RM, Robertson D. Sympathetic and baroreceptor reflex function in neurally-mediated syncope evoked by tilt. J Clin Invest. 1997;99:2736–2744.[Medline] [Order article via Infotrieve]
22.
Morillo CA, Eckberg DL, Ellenbogen KA, Beightol LA,
Hoag JB, Tahvanainen KU, Kuusela TA, Diedrich AM. Vagal and
sympathetic mechanisms in patients with orthostatic
vasovagal syncope. Circulation. 1997;96:2509–2513.
23. Sneddon JF, Counihan PJ, Bashir Y, Haywood GA, Ward DE, Camm AJ. Impaired immediate vasoconstrictor responses in patients with recurrent neurally-mediated syncope. Am J Cardiol. 1993;71:72–76.[Medline] [Order article via Infotrieve]
24.
Thomson HL, Atherton JH, Khafagi FA, Frenneaux MP.
Failure of reflex venoconstricton during exercise in patients with
vasovagal syncope. Circulation. 1996;93:953–959.
25.
Thomson HL, Wright K, Frenneaux M. Baroreflex
sensitivity in patients with vasovagal syncope. Circulation. 1997;95:395–400.
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