Background. Pulmonary hypertension (PH) frequently complicates heart failure. In some patients, pulmonary vessels undergo reactive changes due to the chronic elevation of the left ventricular pressure, resulting in severe pulmonary hypertension and increased transpulmonary gradient (TPG). There is evidence that nitric oxide (NO) synthesized by the respiratory epithelium plays a role in the regulation of pulmonary artery pressure. Aims and objectives. To evaluate whether exhaled NO has a role in reactive PH Methods. Seven patients with reactive PH (rPH) were compared to 14 patients with passive PH (pPH) and to 15 control patients without PH. All the patients underwent heart catheterization, lung function tests and exhaled NO (FENO), assessed at multiple flow-rates. Alveolar NO and bronchial NO flux (J‘awNO) were calculated using the slope–intercept model. Results Patients with PHr had significantly lower FEV1/VC% ratio, lung diffusion (TLCO) and J‘awNO. J‘awNO was closely inversely related to TPG (r=0.385, p=0.032). Conclusion. It is still unknown why some patients develop severe and/or fixed PH with the same degree of elevated left-sided filling pressure. Our findings suggest that decreased bronchial NO flux and lung diffusing capacity may contribute to reactive PH.
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