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Vasodilator response varied in patients with idiopathic PAH
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Patients with idiopathic pulmonary arterial hypertension who responded to an acute vasodilator challenge had fewer baseline hemodynamic abnormalities compared with nonresponders, according to a research letter published in Annals of Internal Medicine.
“Despite sharing the baseline hemodynamic profile of [idiopathic] PAH, responders and nonresponders represent different vascular phenotypes and perhaps different diseases,” David Langleben, MD, from McGill University, Montreal, and colleagues wrote.
Langleben and colleagues hypothesized that nonresponders would be unable to recruit substantial capillary surface area during an acute vasodilator challenge, and that increased pulmonary vascular resistance observed in responders would be based on vascular tone.
The researchers performed an acute vasodilator challenge on 14 patients with idiopathic PAH who had not received idiopathic PAH-specific therapy and did not have evidence of intracardiac shunting based on echocardiography.
They performed standardized right heart catheterization on each patient and inserted a femoral artery sheath. After 30 minutes, baseline hemodynamic measurements were taken, followed by assessment of metabolic activity of pulmonary capillary, endothelium-bound (PCEB)-ACE.
An acute vasodilator challenge was performed using IV epoprostenol (Flolan, GlaxoSmithKline). The researchers then measured PCEB-ACE metabolic activity and hemodynamics at peak epoprostenol dose. They calculated functional capillary surface area and normalized it to body surface area.
In the 12 nonresponders, mean pulmonary arterial pressure did not change with vasodilator challenge, cardiac output increased and pulmonary vascular resistance decreased, but in the two responders, mean pulmonary arterial pressure and pulmonary vascular resistance decreased and cardiac output increased.
Mean percentage of single-pass, transpulmonary metabolism and hydrolysis of 3H-benzoyl-Phe-Ala-Pro decreased in nonresponders (P<.001) but was unchanged in responders, according to the researchers.
Nonresponders had a low functional capillary surface area at baseline, which did not increase at peak vasodilator dose, but the responders had higher functional capillary surface area at baseline, which increased markedly at peak vasodilator dose, the researchers wrote.
“The decrease in the percentage of single-pass, transpulmonary metabolism and hydrolysis in nonresponders suggests that the increased blood flow passes through the remaining patent and already maximally recruited vascular tree,” Langleben and colleagues wrote. “The absence of a reduction in percentage of single-pass, transpulmonary metabolism and hydrolysis suggests that [responders] accommodate the increased cardiac output by true microvascular recruitment and not distension … this group can achieve normal levels of lung perfusion.”
Disclosure: The study was supported by the William and Ida Pencer Family Foundation, the Dimitrios Banousis Foundation, the Bank of Montreal Center for the Study of Heart Disease in Women and the Jewish General Hospital Annual Walk for Pulmonary Hypertension. The researchers report no relevant financial disclosures.
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