(555.1) Middle Cerebral Artery Pulsatility Index is Elevated in Chronic Kidney Disease

Poster Board Number: E61

Touré Jones (Emory University School of Medicine, Atlanta Veterans Affairs Medical Center), Justin Sprick (Emory University School of Medicine, Atlanta Veterans Affairs Medical Center), Dana DaCosta (Emory University School of Medicine, Atlanta Veterans Affairs Medical Center), Jeanie Park (Emory University School of Medicine, Atlanta Veterans Affairs Medical Center)

Introduction: CKD patients exhibit an increased risk of cerebrovascular disease such as stroke, transient ischemic attacks, and cerebral small vessel disease. One mechanism that may contribute to this risk is increased cerebrovascular stiffness and augmented pulsatility of blood flow into the cerebral microcirculation. Middle cerebral artery pulsatility index (MCA PI) provides an indirect measure of cerebrovascular stiffness and can be measured with transcranial Doppler (TCD) ultrasonography. Prior work suggests that MCA PI is elevated in CKD patients following stroke, but it remains unclear if MCA PI is elevated in CKD patients without a history of cerebrovascular disease. Moreover, whether MCA PI correlates with central (aortic) arterial stiffness in CKD remains unknown. We hypothesized that MCA PI would be elevated in CKD patients stages III-IV compared to controls without CKD matched for age, race, sex, diabetes and hypertension. Furthermore, we hypothesized that MCA PI would correlate with central arterial stiffness and estimated glomerular filtration rate (eGFR) in CKD.

Methods: 13 CKD participants stages III-IV (mean eGFR=38±3 ml/min/1.73m2) and 10 controls without CKD (age=60±2y) underwent measurement of middle cerebral artery blood velocity via TCD during 5 minutes of seated rest. MCA PI was averaged over the 5 minute period and calculated as MCA PI = (peak systolic blood velocity – diastolic blood velocity)/(mean blood velocity). In CKD, central arterial stiffness was measured via carotid-femoral pulse wave velocity (cfPWV) after 5 minutes of supine rest. MCA PI was compared between CKD vs CON via 2-tailed, independent sample T-tests and the relationships between MCA PI, cfPWV, and eGFR CKD were examined via linear regression.

Results: MCA PI was elevated in CKD compared to CON (0.91±0.06 vs 0.73±.04, P=0.04) and was associated with cfPWV (R=0.72, P=0.01). However, we observed no relationship between MCA PI and eGFR in CKD (P=0.83).

Discussion: In support of our hypothesis, MCA was elevated in CKD compared to controls and was associated with central arterial stiffness. These findings suggest that cerebrovascular stiffness is elevated in CKD patients without a history of cerebrovascular disease, and that MCA PI correlates with central arterial stiffness in CKD. Increases in cerebrovascular stiffness and subsequent flow pulsatility may comprise one mechanism of cerebrovascular disease risk in CKD. Future work should clarify the relationship between MCA PI and severity of renal disease in a larger cohort, and examine the prognostic value of MCA PI as a predictor of future cerebrovascular disease burden in CKD.

This work was supported by National Institutes of Health (NIH) Grant R01 HL135183; VA Merit I01CX001065, the Department of Veterans Affairs, Veterans Health Administration, Office of Research and Development, Decatur, Georgia, grant program number NHLBI; 1 R25 HL115473-01).