False positive head-up tilt: Hemodynamic and neurohumoral profile

OBJECTIVES This study examined differences in mechanisms of head-up tilt (H UT)-induced syncope between normal controls and patients with neurocardioge nic syncope. BACKGROUND A variable proportion of normal individuals experience syncope d uring HUT. Differences in the mechanisms of HUT-mediated syncope between th is group and patients with neurocardiogenic syncope have not been elucidate d. METHODS A 30-min 80 degrees HUT was performed in eight HUT-negative volunte ers (Group I), eight HUT-positive volunteers (Group II) and 15 patients wit h neurocardiogenic syncope. Heart rate and blood pressure (BP) were monitor ed continuously. Epinephrine and norepinephrine plasma levels, as well as l eft 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 paramete rs 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. 1 7 +/- 3 min p < 0.05); b) there was an immediate, persisting drop in mean B P in Group III; c) the decrease rate of left ventricular end-diastolic dime nsions was greater in Group III than in Group TI 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 t he 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 Grou p 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 no rmal volunteers and patients with neurocardiogenic syncope. In the latter, there was evidence of an impaired vascular resistance response from the beg inning 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 pr ecocious symptoms. In syncopal patients, the higher level of plasma epineph rine probably mediated the increased cardiac contractility and possibly con tributed to the impaired vasoconstrictive response. (C) 1999 by the America n College of Cardiology.