CLINICAL STUDIES
False positive head-up tilt:
Hemodynamic and neurohumoral profile
Fabio M. Leonelli, MD, FACC*  ,
Ke Wang, MD* ,
Joyce M. Evans, MS ,
Abhijit R. Patwardhan, PhD ,
Michael G. Ziegler, MD  ,
Andrea Natale, MD* ,
Charles S. Kim, BSE ,
Kathleen Rajikovich, RN* and
Charles F. Knapp, PhD
* Department of Cardiology, University of Kentucky, Lexington, Kentucky, USA
Center for Biomedical Engineering, University of Kentucky, Lexington, Kentucky, USA
Department of Medicine, University of Kentucky, Lexington, Kentucky, USA
University of San Diego, San Diego, California, USA
Manuscript received July 24, 1998;
revised manuscript received July 8, 1999,
accepted September 10, 1999.
Reprint requests and correspondence: Dr. Fabio Leonelli, 740 South Limestone Street, Room L543, KY Clinic, University of Kentucky, Lexington, Kentucky 40536-0084
OBJECTIVES
This study examined differences in mechanisms of head-up tilt (HUT)-induced syncope between normal controls and patients with neurocardiogenic syncope.
BACKGROUND
A variable proportion of normal individuals experience syncope during HUT. Differences in the mechanisms of HUT-mediated syncope between this group and patients with neurocardiogenic syncope have not been elucidated.
METHODS
A 30-min 80° HUT was performed in eight HUT-negative volunteers (Group I), eight HUT-positive volunteers (Group II) and 15 patients with neurocardiogenic syncope. Heart rate and blood pressure (BP) were monitored continuously. Epinephrine and norepinephrine plasma levels, as well as left ventricular dimensions and contractility determined by echocardiography, were measured at baseline and at regular intervals during the test.
RESULTS
The main findings of this study were the following: 1) All parameters were similar at baseline in the three groups; and 2) During tilt: a) the time to syncope was shorter in Group III than in group II (9.5 ± 3 vs. 17 ± 3 min p < 0.05); b) there was an immediate, persisting drop in mean BP in Group III; c) the decrease rate of left ventricular end-diastolic dimensions was greater in Group III than in Group II or Group I (–1.76 ± 0.42 vs. –0.87 ± 0.35 and –0.67 ± 0.29 mm/min, respectively, p < 0.05); d) the left ventricular shortening fraction was greater in Group III than in the other two groups (39 ± 1 vs. 34 ± 1 and 32 ± 1%, respectively, p < 0.05); and e) although the norepinephrine level remained comparable among the groups, there was a significantly higher peak epinephrine level in Group III than in Group II and Group I (112.3 ± 34 vs. 77.6 ± 10 and 65 ± 12 pg/ml, p < 0.05).
CONCLUSIONS
Mechanisms of syncope during HUT appeared to be different in normal volunteers and patients with neurocardiogenic syncope. In the latter, there was evidence of an impaired vascular resistance response from the beginning of the orthostatic challenge. Furthermore, in the patients there was more rapid peripheral blood pooling, as indicated by the echocardiographic measurements of left ventricular end-diastolic changes, leading to more precocious symptoms. In syncopal patients, the higher level of plasma epinephrine probably mediated the increased cardiac contractility and possibly contributed to the impaired vasoconstrictive response.
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Abbreviations and Acronyms
| | BP | = blood pressure | | ECG | = electrocardiogram | | HR | = heart rate | | HUT | = head-up tilt | | LVEDD | = left ventricular end-diastolic dimension | | LVESD | = left ventricular end-systolic dimension | | SF | = shortening fraction |
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