RT Journal Article
SR Electronic
T1 Effect of parasympathetic impairment on the haemodynamic response to handgrip in Chagas's heart disease.
JF British Heart Journal
JO Heart
FD BMJ Publishing Group Ltd and British Cardiovascular Society
SP 204
OP 210
DO 10.1136/hrt.55.2.204
VO 55
IS 2
A1 Marin-Neto, J A
A1 Maciel, B C
A1 Gallo Júnior, L
A1 Junqueira Júnior, L F
A1 Amorim, D S
YR 1986
UL http://heart.bmj.com/content/55/2/204.abstract
AB Haemodynamic responses to sustained isometric exercise (handgrip at 30% of maximum voluntary capacity) were studied in 10 patients with Chagas's cardiopathy without previous or current heart failure. Five of the patients (group 1) had profound impairment of parasympathetic control of heart rate. They had no tachycardia in response to intravenous administration of atropine and no bradycardia during phase IV of the Valsalva manoeuvre. The other five (group 2) showed normal vagal regulation of heart rate, as judged by chronotropic responses to these tests. The heart rate change (mean (SD] elicited by the handgrip test was significantly lower in group 1 (from 93.0 (14.1) to 95.0 (16.7) beats/min) than in group 2 (from 78.2 (15.8) to 92.8 (18.1) beats/min). Pressor responses to handgrip were of similar magnitude (from 91.6 (7.8) to 109.0 (8.0) mm Hg in group 1 and from 88.6 (11.9) to 106.8 (20.9) mm Hg in group 2). In both groups no significant change in stroke index was detected during handgrip. Cardiac index increased during handgrip from 4.0 (1.2) to 4.8 (1.3) 1/min/m2 in group 2, but there was no significant change in group 1 (from 4.9 (0.7) to 4.8 (1.1) 1/min/m2). Changes in calculated systemic vascular resistance were significantly higher in group 1 (from 934 (175) to 1176 (383) dyn s cm-5) than in group 2 (from 1109 (404) to 1112 (424). This study shows that parasympathetic impairment adversely influences the haemodynamic pattern of response to isometric exercise in patients with Chagas's heart disease. In such conditions, the pressor response to handgrip is predominantly mediated by an increase in systemic vascular resistance rather than an increase in cardiac output.