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Background Despite the limited donor pool, current guidelines recommend against the use of hearts from donors that abuse alcohol. Study aim To explore the effect of donor alcohol abuse (AA) on cardiac allograft arrhythmias, function, and outcomes in heart transplant (HTx) recipients. Methods Overall, 370 HTx recipients transplanted between 2005 and 2016 were divided into two groups: (1) the AA donor group (AD, n=58), and (2) the non-AA donor group (NAD, n=312). The median follow-up was 4.0 (25%-75% IQR 1.8-5.8) years. Results Recipients in the AD group had a slower heart rate (HR, 86±13 vs. 93±13, p=0.004) and an increased incidence of early atrial fibrillation [17 (30%) vs. 34 (11%), p=0.003]. Echocardiographic left ventricular mass was higher in AA donors (171.7±66.7 vs. 151.6±54.7, p=0.02). This difference became even more prominent 1 year following HTx (185±43 vs. 166±42, p=0.007). E/E’ was higher in the AD group (9.5±3.9 vs. 8.4±2.9, p=0.04) and a larger number of AD recipients had a ventilatory equivalent for VCO 2 >34 (50% vs. 31%, p=0.04) on cardiopulmonary stress test. There was no significant difference in rejection, cardiac allograft vasculopathy (CAV), or survival between the groups. Conclusions Our data suggest that donor AA is associated with an increased incidence of post-HTx atrial fibrillation and impaired cardiac allograft diastolic function. Therefore, although the incidence of rejection, CAV, and intermediate-term survival were not affected, hearts from donors that abuse alcohol should be used with caution.

Background Sinus tachycardia (ST) is common after heart transplantation (HTx). The aim of the study was to evaluate the effect of Diltiazem treatment during the first year after HTx on heart rate (HR), cardiac allograft function and exercise capacity. Methods From the total cohort, 25 HTx recipients started Diltiazem treatment 4±2 weeks after HTx and continued it for at least 1 year (Diltiazem group). Each study case was matched to a control. All patients underwent hemodynamic assessment and cardiopulmonary exercise test (CPET) at one year after HTx. Results HR decreased in the Diltiazem group from 99±11 bpm to 94±7 bpm (p=0.03) and did not change in the controls (98±11 bpm vs. 100±13 bpm, p=0.14). The difference between the groups at 1 year after HTx was significant (p=0.04). In the Diltiazem group left ventricular (LV) stroke volume and ejection fraction increased (48 ± 16 vs. 55± 17 ml, p=0.02, and 60% ± 10% vs. 62% ± 12% p=0.03 respectively) but did not differ from controls. E/E’ decreased (10.7 ± 2.7 vs. 7.3 ± 1.9, p=0.003) while cardiac index was higher (3.5 ± 0.8 vs. 3.1 ± 0.5; p=0.05) in the Diltiazem group at 1 year follow up. The absolute peak VO2 (21 ± 4 vs. 18 ± 6 ml/kg/min; p=0.05) and normalized peak VO2 (73% ± 17% vs. 58% ± 14%; p=0.004) were significantly higher in the Diltiazem group. Conclusions This study showed that Diltiazem treatment reduces ST, may improve cardiac allograft function and exercise tolerance during the first year after HTx. This article is protected by copyright. All rights reserved.

BACKGROUND Sinus tachycardia often presents in heart transplantation (HTx) recipients, but data on its effect on exercise performance are limited. METHODS Based on mean heart rate (HR) value 3 months after HTx, 181 patients transplanted from 2006 to 2015 at University of Nebraska Medical Center were divided into two groups: (i) HR