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 (CVR), an indicator of cerebral vasodilatory reserve. We hypothesised that CVR 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 CVR. 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) during stepped increases and decreases in end-tidal carbon dioxide (PCO). A cerebrovascular conductance index (CVCi) was calculated as the ratio of MCA V and mean arterial pressure (MAP). CVR was determined from the linear slope for MCA V and MCA CVCi vs PCO. Baseline MAP was higher in AF + HTN than AF (107 ± 9 vs. 98 ± 9 mmHg, respectively; p < 0.001), while MCA V was not different (AF + HTN:49.6 [44.1-69.0]; AF:51.7 [45.2-63.3] cm.s; 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.mmHg; p < 0.001). MCA V CVR was not different (AF + HTN: 1.70 [1.47-2.19]; AF 1.74 [1.54-2.52] cm/s/mmHg; p = 0.221), while CVCi CVR was 13% lower in AF + HTN (0.013 ± 0.004 vs 0.015 ± 0.005 cm.s.mmHg; p = 0.047). Our results demonstrate blunted cerebral vasodilatory reserve (determined as MCA CVCi CVR) 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. We demonstrated reduced cerebrovascular CO responsiveness in atrial fibrillation with hypertension (AF+HTN) vs. atrial fibrillation (AF). Furthermore, AF per se (as opposed to normal sinus rhythm) predicts reduced cerebrovascular CO responsiveness. Our findings suggest additional cerebrovascular dysfunction in AF+HTN vs. AF.