Anatomical vertebral artery hypoplasia and insufficiency impairs dynamic blood flow regulation.

Abstract

Recent studies have suggested that vertebral artery (VA) hypoplasia is a predisposing factor for posterior cerebral stroke. We examined whether anatomical vertebrobasilar ischemia, i.e., unilateral VA hypoplasia and insufficiency, impairs dynamic blood flow regulation. Twenty-eight female subjects were divided into three groups by defined criteria: (i) unilateral VA hypoplasia (n = 8), (ii) VA insufficiency (n = 6), and (iii) control (n = 14). Hypoplastic VA criterion was VA blood flow of 40 ml min(-1) , whereas VA insufficiency criterion was net (left + right) VA blood flow of 100 ml min(-1) or less. We evaluated left, right, and net VA blood flows by ultrasonography during hypercapnia, normocapnia, and hypocapnia to evaluate VA CO2 reactivity. The unilateral VA hypoplasia group showed lower CO2 reactivity at hypoplastic VA than at non-hypoplastic VA (2.65 ± 0.58 versus 3.00 ± 0.48% per mmHg, P = 0.027) and net VA CO2 reactivity was preserved (Unilateral VA hypoplasia, 2.95 ± 0.48 versus Control, 2.93 ± 0.42% per mmHg, P = 0.992). However, the VA insufficiency group showed a lower net VA CO2 reactivity compared to the control (2.29 ± 0.55 versus 2.93 ± 0.42% per mmHg, P = 0.032) and the unilateral VA hypoplasia (P = 0.046). VA hypoplasia reduced CO2 reactivity, although non-hypoplastic VA may compensate this regulatory limitation. In subjects with VA insufficiency, lowered CO2 reactivity at the both VA could not preserve normal net VA CO2 reactivity. These findings provide a possible physiological mechanism for the increased risk of posterior cerebral stroke in subjects with VA hypoplasia and insufficiency.