Endothelial dysfunction a risk factor for early-onset cryptogenic ischaemic stroke

18 Jul 2021
Endothelial dysfunction a risk factor for early-onset cryptogenic ischaemic stroke

Endothelial dysfunction appears to independently contribute to an increased risk of developing early-onset cryptogenic ischaemic stroke (CIS) in men and individuals approaching middle age, a study reports.

The study included 136 consecutive adult patients (median age 41 years, 44 percent female) with a recent CIS and 136 matched stroke‐free individuals (controls). Researchers used an EndoPAT 2000 device to measure endothelial function, which was grouped into tertiles of natural logarithm of reactive hyperaemia index (lower values indicated dysfunction).

Compared with controls, patients tended to have a lower level of education, to be smokers and obese, and have a lower diet score. Patient used antihypertensive treatments before stroke more frequently (11.0 percent vs 7.4 percent) but used statins less frequently (2.9 percent vs 7.4 percent). At baseline, patients had lower low-density lipoprotein cholesterol (LDL‐C), high-density lipoprotein cholesterol (HDL‐C), glycated albumin (GA), and total cholesterol/HDL‐C ratio compared with controls.

Patients in the lowest tertile of natural logarithm of reactive hyperaemia index were more likely to be men and obese, have a history of dyslipidaemia, have a lower diet score, and lower HDL-C. Multivariable conditional logistic regression analysis revealed no association between endothelial function and CIS in the entire cohort.

However, in sex‐ and age‐specific analyses, endothelial dysfunction increased the odds of CIS by more than threefold in men (lowest vs highest natural logarithm of reactive hyperaemia index tertile: adjusted odds ratio [aOR], 3.50, 95 percent confidence interval [CI], 1.22–10.07) and in patients aged ≥41 years (aOR, 5.78, 95 percent CI, 1.52–21.95). These associations persisted despite replacing dyslipidaemia with the total cholesterol/HDL-C ratio.

More studies are needed to examine whether targeting secondary prevention on endothelial dysfunction may improve long‐term outcomes in the present population.

J Am Heart Assoc 2021;doi:10.1161/JAHA.121.020838