Search

Hemodynamic compromise rejection (HCR) after heart transplantation (HTx) historically is seen in approx. 5% of our HTx patients (pts). HCR is a form of severe rejection, defined as pulmonary capillary wedge ≥15, cardiac index ≤2.0, and requirement of inotropic support. In the current era of tacrolimus, mycophenolate mofetil, and corticosteroids, incidence of HCR has not been firmly established. Further, it is not known whether treatment for these pts affects outcomes and whether there are significant sequelae in terms of cardiac dysfunction, reduced survival, or development of cardiac allograft vasculopathy (CAV). We sought to answer these questions in a review of our large single center. Between 2010 and 2017, we assessed 20 HTx pts who developed HCR. Pts who developed primary graft dysfunction immediately post-HTx were excluded. Treatment at the time of HCR was characterized as well as the long-term sequelae of HCR. Long-term sequelae included 5-year survival, freedom from cardiac dysfunction (defined as LVEF ≤40% by echo), and development of CAV. Type of rejection was also characterized. These pts were compared to a contemporaneous case-control of pts (3:1) matched for age, gender, time from HTx and era who did not develop HCR. The incidence of HCR over this study period was 3.0%. Pts developed HCR at an average of 576 ± 385 days post-Htx and majority were treated with combinations of high dose steroids, ATG, plasmapheresis, and IVIg. HCR pts compared to controls had significantly lower survival at 5 years after HTx and a significantly lower 5-year freedom from cardiac dysfunction and freedom from CAV. At biopsy, 40% had acute cellular rejection, 5% had antibody-mediated rejection, 5% had mixed rejection and 50% had no rejection (biopsy-negative rejection). See table. In the current era, pts with HCR after HTx continue to have significant morbidity and mortality following an HCR event. These pts require intensive follow-up and a search for a more effective treatment. [ABSTRACT FROM AUTHOR]

In heart transplantation, donor-to-recipient (D-R) size matching has been done by height and weight. Recently, predicted heart mass (PHM) has been found to be more clinically useful to predict outcome. Using PHM, under-sizing a donor heart for a larger recipient with high pulmonary artery pressures leads to increased mortality. It has recently been noted in the ISHLT registry that there may be increased risk in placing an oversized donor heart using weight into a smaller recipient. This clinical outcome has not been established using PHM. We sought to address this question in our large, single center experience using PHM. Between January 2010 and June 2020, we assessed 588 D-R heart matches. We used PHM to assess outcome differences when the donor hearts were oversized. We divided the D-R ratio by PHM into two categories: Normal (N: 90-110%, n=524), and markedly oversized (MO: greater than 140%, n=64). Outcomes included 1-year survival, freedom from 1-year rejection (acute cellular rejection [ACR], antibody-mediated rejection [AMR]), freedom from cardiac allograft vasculopathy (CAV: stenosis ≥30%), freedom from cardiac dysfunction (LVEF ≤40%), and freedom from non-fatal major adverse cardiac events (NF-MACE: myocardial infarction, new congestive heart failure, percutaneous coronary intervention, implantable cardioverter defibrillator/pacemaker implant, stroke). MO (n=64) compared to N (n=524) using PHM showed no difference in 1-year survival, freedom from ACR, freedom from CAV, freedom from NF-MACE, and freedom from cardiac dysfunction. There was a significantly lower freedom from 1-year AMR in the MO group due to more female recipients (sensitized due to previous pregnancies) in this group (71% MO group vs 20% N group). Markedly oversized donor to recipient matching using PHM does not result in poor outcomes after heart transplantation. This has potential to expand the donor pool, particularly for smaller patients. [ABSTRACT FROM AUTHOR]