Abstract

<h3>Purpose</h3> To evaluate the effects of treating patients with pulmonary arterial hypertension (PAH) with parenteral prostacyclin (IV/SC PGI<sub>2</sub>) therapy on echocardiographic parameters. <h3>Methods</h3> We retrospectively assessed echocardiograms of patients diagnosed with PAH by right heart catherization between 2007 and 2020. Patients were included if they had group 1 PAH with a baseline echocardiogram performed 0 - 12 months prior to starting PGI<sub>2</sub> therapy and follow up echocardiogram performed 3 - 18 months post therapy. Comparison between the two studies was done using paired Student t-tests or Wilcoxon signed rank tests, and categorical variables were reported as percentages. <h3>Results</h3> Out of 166 patients with PAH, 122 met study criteria. Mean age was 47 ± 13, 79% were female and IPAH/HPAH (52%) and CTD-PAH (32%) were the most common diagnoses. At baseline, severe right heart abnormalities were seen. Mean RVSP was 83 ± 21, and most patients had a moderately (33%) or severely (43%) dilated RA and a moderately (32%) or severely (40%) dilated RV. Echocardiogram was performed a mean 202 ± 105 days after IV/SC PGI2 therapy was initiated. Significant improvement in most echocardiographic parameters was seen, as shown in table 1. This included improvements in RVSP, RV size, RV function and tricuspid regurgitation severity. Of note, individuals with severely diminished RV function went down from 40% to 23% (p < 0.001), and patients with a severely dilated RV decreased from 55% to 23% (p < 0.001). Notably, however, there was no significant change in RA size, and while only 34% patients had a pericardial effusion at baseline, this increased to 44% (p = 0.047) at follow-up. In addition to the RV changes, LA size (p = 0.024) and LV diastolic diameter (p < 0.001) both increased. <h3>Conclusion</h3> Given the significant changes in key echocardiographic variables after prostacyclin therapy and the non-invasive nature of these studies, echocardiograms may be useful in monitoring patient responses to prostacyclin therapies.

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