Abstract MP13: Evaluation Of The Effect Of Low Grade Inflammation And Hypertension On The Development Of White Matter Lesions

Abstract

Introduction: The risk of degenerative disease development is closely linked to persistent and continuous systemic inflammation. Although relationships between chronic low-grade inflammation (LGI) measurements and the progression of cardiovascular diseases are becoming established, the burden of the cardio-pathology and LGI on the central nervous system has not been fully investigated. Specifically, there is limited data on how hypertension (HTN) and related LGI impact white matter lesion (WML) pathogenesis. Methods: We examined 448 subjects with a mean age of 69.3 ± 7.4 years, with 62% of the cohort being women (n=276), and 45% having hypertension (n=200). Components of the LGI score included white blood cell count, albumin levels, platelet counts, and granulocyte/lymphocyte ratio, modified after. Larger LGI scores represented an increase in measured LGI intensity at that time point. MR images were obtained on a 3T system using fluid attenuation inversion recovery (FLAIR) sequence. WML burden was ascertained using Fazekas scale, done separately for both deep WML and periventricular WML. Summated score of greater than or equal to 4 was considered high overall WML burden. Results: It was found that subjects with hypertension had significantly higher LGI score when compared to subjects without hypertension after accounting for sex and BMI (F=4.8, p=0.03). Using logistic regression. we found that LGI score was related to higher WML burden (p=0.047) within the entire cohort. However, further analyses have shown that this finding was driven by the normotensive group, in which the relationship between higher WML burden and respective LGI score was significant (p=0.007). This was not the case among hypertensive subjects. Conclusion: It is clear from the data presented that a relationship between LGI and hypertension exists, confirming that inflammation is an underlying process in cardiovascular pathogenesis. However, LGI scores were related to WML in only normotensive cohorts. We offer that the effects of chronic HTN (related to higher inflammatory score itself ) overshadow the effect of LGI among hypertensive subjects. It is worth emphasizing that even in subjects without HTN white matter damage is related to LGI