Postprandial and orthostatic cardiovascular changes after acute stroke.

OBJECTIVE

Large falls in blood pressure after meals have been demonstrated in fit and frail elderly subjects; these changes may be associated with an increased incidence of stroke. Postprandial falls in BP may be particularly deleterious after acute stroke, when normal baroreflex mechanisms and cerebral autoregulation are already impaired, resulting in stroke progression. Therefore, the postprandial hemodynamic responses to orthostasis were examined in nine acute stroke subjects and eight age-, sex-, and blood pressure-matched control subjects after an oral energy load.

METHODS

All subjects were studied on two occasions in a randomized, double-blind, crossover trial after administration of either oral glucose (1 g/kg body wt) or equivalent isovolumic, isosmotic xylose (0.83 g/kg). Measurements of blood pressure, pulse rate, and forearm blood flow were recorded for 30 minutes preprandially and 90 minutes postprandially. Hemodynamic responses to 60 degrees tilt, along with plasma glucose and insulin changes, were measured at baseline and at 30-minute intervals postprandially.

RESULTS

Supine mean arterial and diastolic blood pressures fell significantly after glucose but not xylose ingestion in control subjects (P < .03) but not stroke subjects, whereas supine pulse rate increased in stroke subjects (P < .04) only. No significant changes in forearm vascular resistance were recorded in either control or stroke subjects. After tilt, stroke subjects showed a fall in mean arterial pressure compared with control subjects preprandially (P = .03) and at 30 (P < .005) and 90 (P < .03) minutes postprandially, although no differences were observed between the xylose and glucose phases. Orthostatic tolerance was maintained in control subjects throughout both phases of the study. Pulse rate increased significantly to tilt at all time intervals in both groups, although there were no significant changes in forearm vascular resistance.

CONCLUSIONS

Acute stroke subjects are not at significantly greater risk of blood pressure falls in response to an oral energy load than age-, sex-, and blood pressure-matched control subjects. Unlike control subjects, the stroke group had an increased pulse-rate postprandially, which could result in a compensatory rise in cardiac output as a result of increased sympathetic nervous system activity in the poststroke period. Although orthostatic blood pressure control is impaired after acute stroke, these changes are unaffected by meals.