Increased Cerebral Arterial Pulsatility in Patients With Leukoaraiosis

Abstract

Background and Purpose-Arterial stiffening reduces damping of the arterial waveform and hence increases pulsatility of cerebral blood flow, potentially damaging small vessels. In the absence of previous studies in patients with recent transient ischemic attack or stroke, we determined the associations between leukoaraiosis and aortic and middle cerebral artery stiffness and pulsatility. Methods-Patients were recruited from the Oxford Vascular Study within 6 weeks of a transient ischemic attack or minor stroke. Leukoaraiosis was categorized on MRI by 2 independent observers with the Fazekas and age-related white matter change scales. Middle cerebral artery (MCA) stiffness (transit time) and pulsatility (Gosling's index: MCA-PI) were measured with transcranial ultrasound and aortic pulse wave velocity and aortic systolic, diastolic, and pulse pressure with applanation tonometry (Sphygmocor). Results-In 100 patients, MCA-PI was significantly greater in patients with leukoaraiosis (0.91 versus 0.73, PϽ0.0001).Severity of leukoaraiosis was associated with MCA-PI and aortic pulse wave velocity (Fazekas: 2 ϭ0.39, MCA-PI Pϭ0.01, aortic pulse wave velocity Pϭ0.06; age-related white matter change: 2 ϭ0.38, MCA-PI Pϭ0.015; aortic pulse wave velocity Pϭ0.026) for periventricular and deep white matter lesions independent of aortic systolic blood pressure, diastolic blood pressure, and pulse pressure and MCA transit time with MCA-PI independent of age. In a multivariate model (r 2 ϭ0.68, PϽ0.0001), MCA-PI was independently associated with aortic pulse wave velocity (Pϭ0.016) and aortic pulse pressure (PϽ0.0001) and inversely associated with aortic diastolic blood pressure (PϽ0.0001) and MCA transit time (Pϭ0.001). Conclusions-MCA pulsatility was the strongest physiological correlate of leukoaraiosis, independent of age, and was dependent on aortic diastolic blood pressure and pulse pressure and aortic and MCA stiffness, supporting the hypothesis that large artery stiffening results in increased arterial pulsatility with transmission to the cerebral small vessels resulting in leukoaraiosis. (Stroke. 2012;43:2631-2636.)Key Words: arterial stiffness Ⅲ cerebral pulsatility Ⅲ etiology Ⅲ leukoaraiosis Ⅲ white matter disease P revention of premature leukoaraiosis by treating the underlying causes in middle age may reduce the risk of stroke 1 and dementia 2 and other consequences of cerebral small vessel disease, 3,4 but the etiology is not yet fully understood. The relative importance of hemodynamic factors as opposed to a primary microangiopathy 5 in the development of leukoaraiosis is unclear and associations with age, hypertension, and diabetes are consistent with both processes. 6 Previous studies have suggested a relationship between increased middle cerebral artery (MCA) pulsatility measured by transcranial Doppler ultrasound and leukoaraiosis or lacunar infarction in patients with hypertension 7 and diabetes, 8 although not necessarily independent of age. However, increased cerebral pulsatility has often been interpreted as a...

Cerebral Hemodynamics in Normal Aging: Central Artery Stiffness, Wave Reflection, and Pressure Pulsatility

“…6 Such increase in central pulse pressure would be transmitted into the high flow, low resistance organs such as the brain and the kidney. [28][29][30] In support of this, our data showed that age-related increase in CBF pulsatility was accompanied by the concurrent elevations in carotid pulse pressure. Moreover, carotid pulse pressure was an independent predictor of CBF pulsatility.…”

“…While limited by a small sample, our observations are, at least in part, consistent with the findings by Webb et al who reported the associations of WMH with higher CBF pulsatility and lower diastolic blood pressure in patients within 6 weeks of a transient ischemic attack or minor stroke. 28 The present study further extends clinical implications of this study by showing that falling diastolic CBF and elevations in CBF pulsatility are related to the severity of cerebral small vessel disease in normal subjects without a history of transient ischemic attack and stroke. Therefore, these findings suggest that prevention and treatment of central arterial aging may attenuate the detrimental hemodynamic impact of increases in pressure and CBF pulsatility on cerebral circulation and lower the risks of CVD and cognitive impairment.…”

“…Notably, steeper changes in CBF pulsatility occurred after middle age, which also correspond accelerated changes in central hemodynamics during the similar age (Supplementary Figure S3). 27 In addition to the greater total volume of CBF in women which has been reported in the literature, 22,28 women showed lower diastolic CBF compared with men. Sex-related difference in diastolic CBF was further explained by the difference in central hemodynamics (i.e., carotid pulse pressure and arterial wave reflection).…”

Relationship Between the Ambulatory Arterial Stiffness Index and the Lower Limit of Cerebral Autoregulation During Cardiac Surgery

“…Thus, central PP and pressure pulsatility are increased. In fact Webb et al33 reported that greater MCA pulsatility was independently associated with higher aortic PP. It is therefore conceivable that increased pressure pulsatility may trigger microvascular remodeling that limits CBF because the remodeled microvascular lumen area is reduced even when maximally vasodilated 30.…”

Central Hemodynamics and Target Organ Damage in Hypertension

“…The fact that the PWV is an indicator of lacunar infarction and white matter lesions (Hashimoto et al 2008a;Henskens et al 2008;Mitchell et al 2011;Wohlfahrt et al 2014) can be considered evidence that aortic stiffening underlies these associations between the increased central pressure and cerebral microvascular damage. In addition, a recent study has found an independent association between the cerebral blood flow pulsatility and white matter lesions (Webb et al 2012), suggesting that the flow as well as pressure pulsations are responsible for microvascular damage in the brain (Hirata et al 2006;Adji et al 2011;Mitchell et al 2011), as in the kidney.…”