Objectives To determine the prevalence and factors associated with persistent pulmonary hypertension (PH) following transcatheter aortic valve replacement (TAVR) and its relationship with long-term mortality.
Methods Consecutive patients who underwent TAVR from July 2011 through January 2016 were studied. The prevalence of baseline PH (mean pulmonary artery pressure ≥25 mm Hg on right heart catheterisation) and the prevalence and the predictors of persistent≥moderate PH (pulmonary artery systolic pressure (PASP)>45 mm Hg on 1 month post-TAVR transthoracic Doppler echocardiography) were collected. Cox models quantified the effect of persistent PH on subsequent mortality while adjusting for confounders.
Results Of the 407 TAVR patients, 273 (67%) had PH at baseline. Of these, 102 (25%) had persistent≥moderate PH. Mortality at 2 years in patients with no baseline PH versus those with PH improvement (follow-up PASP≤45 mm Hg) versus those with persistent≥moderate PH was 15.4%, 16.6% and 31.3%, respectively (p=0.049). After adjusting for Society of Thoracic Surgeons Predicted Risk of Mortality and baseline right ventricular function (using tricuspid annular plane systolic excursion), persistent≥moderate PH remained associated with all-cause mortality (HR=1.82, 95% CI 1.06 to 3.12, p=0.03). Baseline characteristics associated with increased likelihood of persistent≥moderate PH were ≥moderate tricuspid regurgitation, ≥moderate mitral regurgitation, atrial fibrillation/flutter, early (E) to late (A) ventricular filling velocities (E/A ratio) and left atrial volume index.
Conclusions Persistency of even moderate or greater PH at 1 month post-TAVR is common and associated with higher all-cause mortality.
- pulmonary vascular disease
- transcatheter valve interventions
- aortic stenosis
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Contributors AM, IA, JSL, TGG, JTS and JLC: designed the study, data extraction, wrote and revised the manuscript. JX and WH: data extraction. MSS and ADA: designed the study, performed the analysis, wrote and revised the manuscript. SYC, WEK, FWC, MEH, DEK and FN: designed the study, reviewed the manuscript.
Funding This work was supported by the National Institutes of Health (HL096834, HL124021 to SYC) and the American Heart Association (14GRNT19600012 to SYC).
Competing interests JLC and TGG received investigator-initiated grant support from Medtronic. None of the other coauthors have any conflict of interest relevant to the content of this manuscript.
Ethics approval IRB-University of Pittsburgh.
Provenance and peer review Not commissioned; externally peer reviewed.
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