Does vascular stiffness predict white matter hyperintensity burden in ischemic heart disease with preserved ejection fraction?

Autor: Balestrini CS; Schulich School of Medicine and Dentistry, Western University, London, Ontario, Canada., Al-Khazraji BK; Department of Kinesiology, McMaster University, Hamilton, Ontario, Canada., Suskin N; Cardiac Rehabilitation and Secondary Prevention Program of Saint Joseph's Health Care London, London, Ontario, Canada.; Division of Cardiology, Department of Medicine, and Program of Experimental Medicine, Western University, London, Ontario, Canada., Shoemaker JK; School of Kinesiology, Western University, London, Ontario, Canada.; Department of Physiology and Pharmacology, Western University, London, Ontario, Canada.
Jazyk: angličtina
Zdroj: American journal of physiology. Heart and circulatory physiology [Am J Physiol Heart Circ Physiol] 2020 Jun 01; Vol. 318 (6), pp. H1401-H1409. Date of Electronic Publication: 2020 May 01.
DOI: 10.1152/ajpheart.00057.2020
Abstrakt: The survival rate of patients with ischemic heart disease (IHD) is increasing. However, survivors experience increased risk for neurological complications. The mechanisms for this increased risk are unknown. We tested the hypothesis that patients with IHD have greater carotid and cerebrovascular stiffness, and these indexes predict white matter small vessel disease. Fifty participants (age, 40-78 yr), 30 with IHD with preserved ejection fraction and 20 healthy age-matched controls, were studied using ultrasound imaging of the common carotid artery (CCA) and middle cerebral artery (MCA), as well as magnetic resonance imaging (T1, T2-FLAIR), to measure white matter lesion volume (WMLv). Carotid β-stiffness provided the primary measure of peripheral vascular stiffness. Carotid-cerebral pulse wave transit time (ccPWTT) provided a marker of cerebrovascular stiffness. Pulsatility index (PI) and resistive index (RI) of the MCA were calculated as measures of downstream cerebrovascular resistance. When compared with controls, patients with IHD exhibited greater β-stiffness [8.5 ± 3.3 vs. 6.8 ± 2.2 arbitrary units (AU); P = 0.04], MCA PI (1.1 ± 0.20 vs. 0.98 ± 0.18 AU; P = 0.02), and MCA RI (0.66 ± 0.06 vs. 0.62 ± 0.07 AU; P = 0.04). There was no difference in WMLv between IHD and control groups (0.95 ± 1.2 vs. 0.86 ± 1.4 mL; P = 0.81). In pooled patient data, WMLv correlated with both β-stiffness ( R = 0.34, P = 0.02) and cerebrovascular ccPWTT ( R = -0.43, P = 0.02); however, β-stiffness and ccPWTT were not associated ( P = 0.13). In multivariate analysis, WMLv remained independently associated with ccPWTT ( P = 0.02) and carotid β-stiffness ( P = 0.04). Patients with IHD expressed greater β-stiffness and cerebral microvascular resistance. However, IHD did not increase risk of WMLv or cerebrovascular stiffness. Nonetheless, pooled data indicate that both carotid and cerebrovascular stiffness are independently associated with WMLv. NEW & NOTEWORTHY This study found that patients with ischemic heart disease (IHD) with preserved ejection fraction and normal blood pressures exhibit greater carotid β-stiffness, as well as middle cerebral artery pulsatility and resistive indexes, than controls. White matter lesion volume (WMLv) was not different between vascular pathology groups. Cerebrovascular pulse wave transit time (ccPWTT) and carotid β-stiffness independently associate with WMLv in pooled participant data, suggesting that regardless of heart disease history, ccPWTT and β-stiffness are associated with structural white matter damage.
Databáze: MEDLINE