The effect of hypertension on cerebrovascular carbon dioxide reactivity in atrial fibrillation patients

Atrial fibrillation (AF) and hypertension (HTN) are both associated with impaired cerebrovascular carbon dioxide reactivity (CVRCO2), an indicator of cerebral vasodilatory reserve. We hypothesised that CVRCO2 would be lower in patients with both AF and HTN (AF + HTN) compared to normotensive AF patients, due to an additive effect of AF and HTN on CVRCO2. Forty AF (68 +/- 9 years) and fifty-seven AF + HTN (68 +/- 8 years) patients underwent transcranial Doppler ultrasound measurement of middle cerebral artery blood velocity (MCA V-m) during stepped increases and decreases in end-tidal carbon dioxide (PETCO2). A cerebrovascular conductance index (CVCi) was calculated as the ratio of MCA V-m and mean arterial pressure (MAP). CVRCO2 was determined from the linear slope for MCA V-m and MCA CVCi vs PETCO2. Baseline MAP was higher in AF + HTN than AF (107 +/- 9 vs. 98 +/- 9 mmHg, respectively; p < 0.001), while MCA V-m was not different (AF + HTN:49.6 [44.1-69.0]; AF:51.7 [45.2-63.3] cm.s(-1); p = 0.075), and CVCi was lower in AF + HTN (0.46 [0.42-0.57] vs. 0.54 [0.44-0.63] cm.s(-1).mmHg(-1); p < 0.001). MCA V-m CVRCO2 was not different (AF + HTN: 1.70 [1.47-2.19]; AF 1.74 [1.54-2.52] cm/s/mmHg(-2); p = 0.221), while CVCi CVRCO2 was 13% lower in AF + HTN (0.013 +/- 0.004 vs 0.015 +/- 0.005 cm.s(-1).mmHg(-1); p = 0.047). Our results demonstrate blunted cerebral vasodilatory reserve (determined as MCA CVCi CVRCO2) in AF + HTN compared to AF alone. This may implicate HTN as a driver of further cerebrovascular dysfunction in AF that may be important for the development of AF-related cerebrovascular events and downstream cognitive decline.