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Left ventricular size, blood volume, and baroreflex control of heart period in healthy humans susceptible to syncope
Author(s) -
Okazaki Kazunobu,
Fu Qi,
Shook Robin,
Shibata Shigeki,
Hastings Jeff,
Conner Colin,
Palmer M Dean,
Ogoh Shigehiko,
Levine Benjamin D
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.lb14-a
Subject(s) - baroreflex , supine position , medicine , orthostatic intolerance , cardiology , orthostatic vital signs , circulatory system , stroke volume , hemodynamics , presyncope , anesthesia , heart rate , blood pressure
We tested the hypothesis that individuals who develop syncope have a smaller left ventricular (LV) size and blood volume (BV) and therefore reduced stroke volume (SV) and impaired baroreflex circulatory control. METHODS In 22 healthy young subjects who had no history of syncope, LV size (MRI) and BV (Evans blue or CO rebreathing) were determined; beat‐to‐beat SBP (Finapres), RRI, and HR were recorded and cardiac output (Qc, C 2 H 2 rebreathing) and SV (Qc/HR) were measured while supine and during 60°head‐up tilt (HUT) for 45 min or until pre‐syncope; dynamic arterial baroreflex gain was calculated by using cross spectral analysis. RESULTS Ten subjects (3 M, 7 F) developed pre‐syncope at 26±12 (SD) min of HUT (low tolerance, LT), while 12 subjects (7 M, 5 F) completed the HUT (high tolerance, HT). LV mass was smaller in the LT than in the HT (66±13 vs 80±14 g/m 2 , P = 0.03), while there were no significant differences in LVEDV (67±9 vs 71±10 ml/m 2 , P = 0.40), BV (70±6 vs 75±12 ml/kg, P = 0.28), hemodynamics, dynamic baroreflex gain, or the ability of the baroreflex to modify systemic flow (HRxSV) between the groups while supine or during HUT. CONCLUSION Individuals susceptible to syncope have a smaller LV mass with preserved BV and baroreflex circulatory control while supine and during acute orthostatic challenge. We speculate that these subjects have impaired diastolic function during prolonged orthostatic stress which may contribute to orthostatic intolerance. Funded by NIH K23 and GCRC grant.