Improved Outcomes WithSodium-glucose Cotransporter 2 InhibitorsIn Pulmonary Arterial Hypertension

Purpose Sodium-glucose Cotransporter 2 Inhibitors (SGLT2i) have been found to decrease risk of cardiovascular death, heart failure hospitalizations, and worsening heart failure in heart failure with reduced and preserved ejection fraction, irrespective of diabetic status. Currently, investigations into the use of SGLT2i in pulmonary arterial hypertension (PAH) are limited. Methods A single center retrospective study was conducted on twenty-eight (N=28) patients diagnosed with PAH who were initiated on SGLT2i for other diagnoses. The primary analysis involved paired comparative tests per subject of conventional non-invasive cardiovascular indices measured prior to initiation of SGLT2i therapy and following at least three months of continued therapy. At these time periods, our included patients were clinically compensated and on stable PAH therapies. Comparisons were made using paired t-test and Wilcoxon Signed Rank test where appropriate. All tests were two-tailed and a p-value of <0.05 was considered statistically significant. The individual variables for pre- and post- test results with normal distributions had their means and standard deviations reported. Results A summary of the primary analysis is presented in Table 1. Conclusion Our analysis shows promise in further thought and studies regarding SGLT2i use in PAH patients. As we cannot determine causation from our retrospective analysis, future prospective studies would be needed prior to routine use of SGLT2i in this patient population. Sodium-glucose Cotransporter 2 Inhibitors (SGLT2i) have been found to decrease risk of cardiovascular death, heart failure hospitalizations, and worsening heart failure in heart failure with reduced and preserved ejection fraction, irrespective of diabetic status. Currently, investigations into the use of SGLT2i in pulmonary arterial hypertension (PAH) are limited. A single center retrospective study was conducted on twenty-eight (N=28) patients diagnosed with PAH who were initiated on SGLT2i for other diagnoses. The primary analysis involved paired comparative tests per subject of conventional non-invasive cardiovascular indices measured prior to initiation of SGLT2i therapy and following at least three months of continued therapy. At these time periods, our included patients were clinically compensated and on stable PAH therapies. Comparisons were made using paired t-test and Wilcoxon Signed Rank test where appropriate. All tests were two-tailed and a p-value of <0.05 was considered statistically significant. The individual variables for pre- and post- test results with normal distributions had their means and standard deviations reported. A summary of the primary analysis is presented in Table 1. Our analysis shows promise in further thought and studies regarding SGLT2i use in PAH patients. As we cannot determine causation from our retrospective analysis, future prospective studies would be needed prior to routine use of SGLT2i in this patient population.