Open AccessHaemodynamic effects and potential clinical implications of inhaled nitric oxide during right heart catheterization in heart transplant candidates
Author(s) -
Strong Christopher,
Raposo Luís,
Castro Mariana,
Madeira Sérgio,
Tralhão António,
Ventosa António,
Rebocho Maria José,
Almeida Manuel,
Aguiar Carlos,
Neves José Pedro,
Mendes Miguel
Publication year - 2020
Publication title -
esc heart failure
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.787
H-Index - 25
ISSN - 2055-5822
DOI - 10.1002/ehf2.12639
Subject(s) - medicine , vascular resistance , cardiology , pulmonary artery , heart failure , pulmonary hypertension , heart transplantation , cardiac catheterization , hemodynamics , ejection fraction , transplantation , cardiac output , population , anesthesia , environmental health
Aims Right heart catheterization (RHC) is indicated in all candidates for heart transplantation (HT). An acute vasodilator challenge is recommended for those with pulmonary hypertension (PH) to assess its reversibility. The effects of inhaled nitric oxide (iNO) on pulmonary and systemic haemodynamics have been reported only in small series. Our purpose was to describe the response to iNO in a larger population and its potential clinical implications. Methods and results From 210 RHC procedures performed between 2010 and 2019, vasodilator challenge with iNO was used in 108 patients, of which 66 had advanced heart failure undergoing assessment for HT (55±11 years old; 74.2% male gender; 43.9% ischaemic cardiomyopathy; left ventricular ejection fraction 28.4 ± 11,4%; and peak VO2 12.1 ± 3.0 mL/kg/min). iNO was administered through a tight‐fitting facial mask regardless of baseline pulmonary pressures. Clinical endpoints (all‐cause mortality and acute right heart failure) were assessed according to baseline haemodynamic findings over the available follow‐up period. There were no side effects from iNO administration. Typical response consisted of a reduction in pulmonary vascular resistance, consequent to an increase in left ventricular filling pressures, no significant change in mean pulmonary artery pressure (resulting in a lower mean transpulmonary gradient) and a mild increase in cardiac ouput. Pulmonary arterial compliance increased significantly, whereas systemic vascular resistance was only mildly affected. In five cases (7.6%), pulmonary vascular resistance increased paradoxically. All‐cause mortality and post‐HT right heart failure events were overall low and similar in patients without PH or reversible PH. Conclusions Vasodilator challenge with iNO is safe in advanced heart failure patients undergoing RHC prior to HT listing. It produces a reasonably predictable haemodynamic response, which occurs predominantly at the pulmonary circulation level. Clinical implications of iNO‐induced reversibility may be relevant, but further systematic validation is warranted in larger cohorts.