Abstract TP472: The Interplay Between Subclinical Micro- and Macro-Vascular Disease in Asymptomatic Individuals

Abstract

Introduction: Pathophysiological changes within large arteries, among many other factors, are considered to contribute to cerebral small vessel disease. Craniocervical sonography is a valuable tool in this regard to evaluate various physiological metrics of extra- and intra-cranial large arteries. Herein, we tried to evaluate the interplay between markers of small vessel disease, and internal carotid (ICA) and middle cerebral artery (MCA) pulsatility, carotid distensibility and intima media thickness (IMT). Methods: We prospectively evaluated a total of 278 subjects without any prior history of stroke using transcranial and cervical Doppler ultrasound, and magnetic resonance imaging. Pulsatility index was determined by Gosling’s index from bilateral MCA’s and ICA’s. We also measured carotid distensibility and IMT (by AutoIMT TM ) from both carotids and calculated their mean values. The relationship of all these sonographic metrics with imaging markers of chronic small vessel disease [lacunes, microbleeds, perivascular spaces (PVS), white matter hyperintensities (WMH)] were evaluated in multivariate models where age and cardiovascular risk factors were included as additional covariates. Results: The study population consisted of 108 males and 170 females with a mean±SD age of 64±9 years. In bivariate analyses, higher carotid IMT, higher MCA and ICA pulsatility indices, and lower carotid distensibility were significantly associated with high burden of WMH (Fazekas score of ≥2), basal ganglia PVS (PVS score ≥2) and presence of lacunes, but not with microbleeds or centrum semiovale PVS. In multivariate models, each 0.1 mm change in IMT increased the odds of severe WHM by 1.4 (95%CI 1.0-1.9), severe basal ganglia PVS by 1.4 (1.0-1.8) and lacunes by 1.6 (1.0-2.6), while no significant association remained for pulsatility index or distensibility. Conclusion: Our analyses highlight that IMT, is not only a subclinical marker of atherosclerosis, but also emerges as a factor intimately related with cerebral small vessel disease. These findings raise the possibility that IMT and cerebral small vessel disease might together reflect downstream events that culminate in vascular disease involving the large and small vessels of the brain.