Impact of ischemic heart disease and cardiac rehabilitation on cerebrovascular compliance

We aimed to determine the influence of ischemic heart disease (IHD) and cardiac rehabilitation (CR) on cerebrovascular compliance index (Ci). Eleven (one female) patients with IHD (mean[SD]: 61[11] yr, 29[4] kg/m(2)) underwent 6 mo of CR, which consisted of >= 3 sessions/wk of aerobic and resistance training (20-60 min each). Ten (three female) similarly aged controls (CON) were tested at baseline as a comparator group. Middle cerebral artery velocity (MCAv) and mean arterial pressure were monitored continuously using transcranial Doppler ultrasound and finger photoplethysmography, respectively, during a rapid sit-to-stand maneuver. A Windkessel model was used to estimate cerebrovascular Ci every five cardiac cycles for a duration of 30 s. Cerebrovascular resistance was calculated as the quotient of MAP and MCAv. Two-way ANOVAs were used to determine whether cerebrovascular variables differ during postural transitions between groups and after CR. Baseline MCAv was higher in CON versus IHD (P = 0.014) and a time x group interaction was observed (P = 0.045) where MCAv decreased more in CON after standing. Compared with the precondition, CR had no effect on MCAv (condition P = 0.950) but a main effect of time indicated that MCAv decreased from the seated position in both conditions (time P = 0.013). Baseline cerebrovascular Ci was greater in IHD versus CON (P = 0.049) and the peak cerebrovascular Ci during the transition to standing was significantly higher in IHD compared with CON (interaction P = 0.047). CR did not affect cerebrovascular compliance (P = 0.452) and no time-by-condition interaction upon standing was present (P = 0.174). Baseline cerebrovascular Ci is higher in IHD at baseline compared with CON, but 6 mo of CR did not modify the transient increase in cerebrovascular Ci during sit-to-stand maneuvers.NEW & NOTEWORTHY Post-cardiac event cognitive impairment is common and exercise-based rehabilitation may be an effective intervention to mitigate cognitive decline. Microvascular damage due to high blood pressure pulsatility entering the brain is the putative mechanism of vascular dementia. Whether patients with ischemic heart disease exhibit lower cerebrovascular compliance, and if cardiac rehabilitation can improve cerebrovascular compliance is unknown. We observed that patients with ischemic heart disease have paradoxically higher cerebrovascular compliance, which is not affected by cardiac rehabilitation.