Patients with pulmonary arterial hypertension (PAH) may have an impaired cerebral pressure-flow relationship, resulting in passively transmitted blood pressure changes to the brain, according to a study published in the Journal of the American Heart Association.
Researchers performed a prospective study of 11 patients with idiopathic and heritable PAH, with New York Heart Association functional classes 2 and 3, and matched them for age, sex, body weight, and height with 11 healthy sedentary individuals. Results were recorded during 2 visits separated by at least 48 hours. The following tests were assessed and analyzed in both groups: resting mean flow velocity in the middle cerebral artery (MCAvmean), cerebral pressure-flow relationship, cerebrovascular reactivity to CO2, and central chemoreflex.
“Cerebrovascular reactivity to CO2 was reduced (P =.03), whereas central chemoreceptor sensitivity was increased in PAH (P <.01), the latter correlating with increased resting ventilation (R2=0.47; P <.05) and the exercise ventilation/CO2 production slope (VE=VCO2 slope; R2=0.62; P <.05) during exercise for patients,” the authors wrote.
Patients with PAH demonstrated limited exercise-induced increases in MCAvmean overall. In addition, impaired cerebral oxygen delivery and oxygenation was affected by reduced MCAvmean (both P <.05), with oxygenation correlating with exercise capacity in patients with PAH (R2=0.52; P =.01).
The investigators concluded that presyncope symptoms and syncope in patients with PAH could be caused by impaired pressure-flow relationships, and therefore therapies that lower blood pressure in patients with PAH should be used cautiously, as brain perfusion is very sensitive to blood pressure changes. Further, exercise intolerance may be caused by premature central fatigue, secondary to exercise-induced cerebral hypoxia.
Malenfant S, Brassard P, Paquette M, et al. Compromised cerebrovascular regulation and cerebral oxygenation in pulmonary arterial hypertension [published online on October 12, 2017]. J Am Heart Assoc. doi: 10.1161/JAHA.117.006126