Rapid Changes in Cerebrovascular Compliance During Vasovagal Syncope

Abstract

Background: The rapid reduction in arterial blood pressure (ABP) during vasovagal syncope (VVS) is associated with a characteristic decline in diastolic cerebral blood velocity (CBV) and maintained systolic CBV as measured by transcranial Doppler. This increased pulsatility was originally considered to be indicative of a “dysfunctional” increase in cerebrovascular resistance (CVR). Conversely, it may be due to increased cerebrovascular compliance (Ci) that partially attenuates the cerebral effects of rapid hypotension. We tested the hypothesis that Ci supports CBV during pre-syncope in VVS. Method: Finger ABP and right middle cerebral artery blood velocity (MCAv) were recorded from 15 otherwise healthy patients (n = 11 female, 40 ± 16 years, 24.9 ± 4.0 kg/m2) at rest and during head-up tilt (80°, 5 to 28 min). Individual ABP and CBV waveforms of every second heartbeat during VVS were input into a modified Windkessel model to calculate Ci and CVR. MCAv pulsatility was determined as pulse amplitude (systolic MCAv-diastolic MCAv) and Pulsatility Index (Pi; pulse amplitude/mean MCAv). Linear mixed models assessed the contribution of Ci to changes in CBV and Pi. Within-subject mediation analysis investigated the possibility of Ci mediating the relation between blood pressure (i.e., mean ABP and pulse pressure, PP) and cerebrovascular pulsatility. Results: Diastolic and systolic ABP decreased progressively during presyncope, resulting in a nadir reduction of mean ABP of Δ24 ± 9 mmHg at end-tilt (all p ≤ 0.04 vs mid-tilt). Mean MCAv decreased by 22 ± 12% prior to end-tilt (p < 0.01 vs mid-tilt). CVR decreased progressively for 10s prior to end-tilt (p ≤ 0.04 vs mid-tilt). Pi increased significantly, with peak increases occurring at 4 s prior to end-tilt (77 ± 50%, p < 0.01 vs mid-tilt). The increase in Ci (307 ± 223%, p < 0.01 vs mid-tilt) significantly contributed to changes in MCAv (χ2 =10.6, p < 0.01) and Pi (χ2 = 4.9, p = 0.03). Correlations of PP and ABP with Pi were not significant. However, PP was related to MCAv pulse amplitude (total effect: b = 1.57) and Ci ( b = -0.01, both p < 0.01). Ci partially mediated (indirect effect: b = -0.78, p < 0.01) the direct relation between PP and MCAv pulse amplitude ( b = 0.79, p = 0.01). Conclusion: These data provide evidence that Ci attenuates the fall in CBV under conditions of falling PP. Cerebrovascular regulation in VVS appears to be functioning as in healthy populations. However, this regulation is not suffcient to preserve flow in the presence of such extreme and rapid reductions in ABP. USRI — Western University, Natural Sciences and Engineering Research Council of Canada (NSERC, Grant No. RGPIN-2018-06255). This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.