Compromised Cerebrovascular Regulation and Cerebral Oxygenation in Pulmonary Arterial Hypertension

Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

Steeve Provencher¹  Valérie Nadeau¹  Simon Malenfant¹  Sébastien Bonnet¹  Olivier Le Blanc²  Sébastien Simard²  Myriam Paquette²  Audrey Chouinard²  Patrice Brassard²  Philip D. Allan³  Yu‐Chieh Tzeng³ 

[1] Pulmonary Hypertension and Vascular Biology Research Group, Université Laval, Quebec City, Canada;Quebec Heart and Lung Institute Research Center, Université Laval, Quebec City, Canada;Wellington Medical Technology Group, Center for Translational Physiology, University of Otago, Wellington, New Zealand;

关键词: central chemoreceptor sensitivity;    cerebral ischemia;    cerebral oxygenation;    cerebrovascular reactivity to CO2;    exercise physiology;   

DOI  :  10.1161/JAHA.117.006126

来源: DOAJ

【 摘 要 】

BackgroundFunctional cerebrovascular regulatory mechanisms are important for maintaining constant cerebral blood flow and oxygen supply in heathy individuals and are altered in heart failure. We aim to examine whether pulmonary arterial hypertension (PAH) is associated with abnormal cerebrovascular regulation and lower cerebral oxygenation and their physiological and clinical consequences. Methods and ResultsResting mean flow velocity in the middle cerebral artery mean flow velocity in the middle cerebral artery (MCAvmean); transcranial Doppler), cerebral pressure‐flow relationship (assessed at rest and during squat‐stand maneuvers; analyzed using transfer function analysis), cerebrovascular reactivity to CO2, and central chemoreflex were assessed in 11 patients with PAH and 11 matched healthy controls. Both groups also completed an incremental ramp exercise protocol until exhaustion, during which MCAvmean, mean arterial pressure, cardiac output (photoplethysmography), end‐tidal partial pressure of CO2, and cerebral oxygenation (near‐infrared spectroscopy) were measured. Patients were characterized by a significant decrease in resting MCAvmean (P<0.01) and higher transfer function gain at rest and during squat‐stand maneuvers (both P<0.05). Cerebrovascular reactivity to CO2 was reduced (P=0.03), whereas central chemoreceptor sensitivity was increased in PAH (P<0.01), the latter correlating with increased resting ventilation (R2=0.47; P<0.05) and the exercise ventilation/CO2 production slope (V˙E/V˙CO2 slope; R2=0.62; P<0.05) during exercise for patients. Exercise‐induced increases in MCAvmean were limited in PAH (P<0.05). Reduced MCAvmean contributed to impaired cerebral oxygen delivery and oxygenation (both P<0.05), the latter correlating with exercise capacity in patients with PAH (R2=0.52; P=0.01). ConclusionsThese findings provide comprehensive evidence for physiologically and clinically relevant impairments in cerebral hemodynamic regulation and oxygenation in PAH.

【 授权许可】

Unknown