Abstract

<h3>Purpose</h3> One of the most concerning issues immediately post-heart transplant (HTx) is the development of primary graft dysfunction (PGD) and/or vasoplegia. It has been suggested that patients on angiotensin-converting enzyme inhibitors (ACEi) are at risk for the development of PGD and vasoplegia due to activation of the kallikrein pathways which can activate bradykinin (vasodilator). It is not known whether ACEi with low systolic blood pressure (SBP) prior to HTx is associated with the development of PGD and vasoplegia. We sought to answer this question in our large, single center patient population. <h3>Methods</h3> Between 2017 and 2020, we assessed 189 patients awaiting HTx treated with ACEi (n=19) who had SBP less than 100 mmHg at the time of HTx and those patients without ACEi (n=170) but also with SBP less than 100 mmHg. Endpoints included the development of PGD (ISHLT grading scale) and vasoplegia (defined as requiring more than 2 vasoconstricting drugs with SBP still < 90 mmHg). A control group (n=176) of patients with SBP > 100mmHg was included for comparison. <h3>Results</h3> Patients treated with ACEi and with low SBP at the time of HTx appear to have significantly increased risk of PGD and vasoplegia development post-HTx. However, their 30-day and 1-year survival was no different compared to those patients not on ACEi (with low SBP) and those with normal blood pressure. (See table.) <h3>Conclusion</h3> ACEi and lower SBP at the time of heart transplantation may be a significant risk factor for the development of PGD and vasoplegia. Stopping ACEi prior to heart transplant may be warranted but requires further study.

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