Abstract
Background and PurposeIncreased cerebral arterial pulsatility is associated with cerebral small vessel disease, recurrent stroke and dementia despite best medical treatment. However, no study has identified rates and determinants of progression of arterial stiffness and pulsatility.MethodsIn consecutive patients within 6 weeks of TIA or non-disabling stroke (Oxford Vascular Study), arterial stiffness (PWV) and aortic systolic (aoSBP), diastolic (aoDBP) and pulse pressures (aoPP) were measured by applanation tonometry (Sphygmocor), whilst middle cerebral artery peak (MCA-PSV) and trough (MCA-EDV) flow velocity and Gosling’s pulsatility index (MCA-PI) were measured by transcranial ultrasound (TCD, DWL DopplerBox). Repeat assessments were performed at the 5 year follow-up visit after intensive medical treatment and agreement determined by intraclass correlation coefficients (ICC). Rates of progression and their determinants, stratified by age and sex, were determined by mixed-effect linear models, adjusted for age, sex and cardiovascular risk factors.ResultsIn 188 surviving, eligible patients with repeat assessments after a median of 5.8 years. PWV, aoPP and MCA-PI were highly reproducible (ICC 0.71,0.59 and 0.65 respectively), with progression of PWV (2.4%, p<0.0001) and aoPP (3.5%, p<0.0001) but not significantly for MCA-PI overall (0.93, p=0.22). However, PWV increased at a faster rate with increasing age (0.009m/s/yr/yr, p<0.0001), whilst aoPP and MCA-PI increased significantly above the age of 55 (aoPP p<0.0001, MCA-PI p=0.009). Higher aortic SBP and DBP predicted a greater rate of progression of PWV and aoPP, but not MCA-PI, although current MCA-PI was particularly strongly associated with concurrent aoPP (p<0.001).ConclusionsArterial pulsatility and aortic stiffness progressed significantly after 55 years of age despite best medical treatment. Progression of stiffness and aortic pulse pressure was determined by high blood pressure, but MCA-PI predominantly reflected current aortic pulse pressure. Treatments targetting cerebral pulsatility may need to principally target aortic stiffness and pulse pressure to have the potential to prevent cerebral small vessel disease.
Highlights
AND PURPOSE: Increased cerebral arterial pulsatility is associated with cerebral small vessel disease, recurrent stroke, and dementia despite the best medical treatment
pulse wave velocity (PWV), aortic pulse pressures (aoPP), and middle cerebral artery (MCA)-pulsatility index (PI) were highly reproducible, with progression of PWV (2.4%; P
PWV increased at a faster rate with increasing age (0.009 m/s per y/y; P
Summary
In consecutive patients within 6 weeks of transient ischemic attack or nondisabling stroke (OXVASC [Oxford Vascular Study]), arterial stiffness (pulse wave velocity [PWV]) and aortic systolic, aortic diastolic, and aortic pulse pressures (aoPP) were measured by applanation tonometry (Sphygmocor), while middle cerebral artery (MCA) peak (MCA-PSV) and trough (MCAEDV) flow velocity and Gosling pulsatility index (PI; MCA-PI) were measured by transcranial ultrasound (transcranial Doppler, DWL Doppler Box). Consecutive, consenting patients with transient ischemic attack or minor stroke were recruited between September 2010 and September 2019, as part of the Phenotyped Cohort of OXVASC (Oxford Vascular Study).[14,15] Participants were recruited at the OXVASC daily emergency assessment clinic, following a referral from primary care or after attendance at the Emergency Department, usually within 24 hours. The OXVASC population consists of >92 000 individuals registered with about 100 primary care physicians in Oxfordshire, United Kingdom.[16] All consenting patients underwent a standardized medical history and examination, ECG, blood tests, and a stroke protocol magnetic resonance imaging brain and contrastenhanced MRA (or computed tomography brain and carotid Doppler ultrasound or computed tomography angiogram), an echocardiogram, and 5 day ambulatory cardiac monitor. Medication is prescribed according to guidelines, most commonly with dual antiplatelets (aspirin and clopidogrel) for 1 month and monotherapy thereafter, high-dose statins (atorvastatin, 80 mg), and a combination of perindopril and indapamide, with the addition of amlodipine and other agents as required to reach a target of
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