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Abstracts
multivariate regression models, PVD was associated with substantially longer hospital ( ⫽ 26 ⫾ 6.2, p ⬍ .001) and ICU LOS ( ⫽ 21 ⫾ 3.8, p ⬍ .001) while controlling for other preoperative risk factors. Conclusions: Pre-existing moderate PVD is associated with worse survival and longer LOS in cardiac transplant recipients. Prospective studies may elucidate distinct exclusion criteria for these patients. 343 INHALED NITRIC OXIDE AS RESCUE THERAPY FOR RIGHT VENTRICULAR INSUFFICIENCY AFTER ORTHOTOPIC HEART TRANSPLANTATION S. Datta,1 A. Machaal,1 J. Thekkudan,1 R. Sivaprakasan,1 A.K. Deiraniya,1 N. Yonan,1 1Transplant Unit, Wythenshawe Hospital, Manchester, Lanchershire, United Kingdom Statement of Purpose: Primary graft failure from right ventricular (RV) insufficiency remains a serious cause of early death following heart transplantation (HTx). It is difficult to predict threshold haemodynamic parameters beyond which RV failure is certain to occur. Inhaled Nitric Oxide (iNO) is a potent pulmonary vasodilator that may decrease pulmonary pressure and improve RV function. This study evaluates the efficacy of iNO therapy in recipients with RV failure after HTx. Statement of Procedures: Since 1998, twenty-five patients (23 male, 2 female; age 47 ⫹- 11 years) with early RV failure following HTx were treated with iNO. Therapy comprised of iNO commensing at 30-40 ppm, supported by inotropes and vasopressors in addition to intra-aortic balloon pump in ten and RVAD in two recipients. Haemodynamic parameters were monitored before starting iNO, during iNO administration and after iNO discontinuation at 2, 6, 12 and 24 hours respectively. Statement of Results: Central venous pressure (CVP), mean pulmonary artery pressure (MPAP), pulmonary capillary wedge pressure (PCWP) and transpulmonary gradient (TPG) began to fall at two hrs following iNO administration. Right heart haemodynamics remained stable at six, 12 and 24 hrs and this was statistically significant (p ⬍ 0.004). INO was weaned at 3-5ppm/2hours. Discontinuation led to mild increase in CVP, MPAP, PCWP and TPG at two hours (p ⬍ 0.24) after which haemodynamics remained stable at six, 12 and 24 hours. There was no change in systemic haemodynamics or gaseous exchange. Total duration of iNO was 21 to 260 hours. One recipient died of multiorgan failure. 19 (76%) recipients were extubated within 24-48 hours after iNO discontinuation. Conclusion: A high index of suspicion for RV failure is warranted in HTx recipients who are haemodynamically compromised during the early post-operative period. In our study iNO was successfully used to treat RV failure. It was easy to wean and had no side effects. In combination with other modalities of treatment, iNO appears to be a promising therapeutic adjuvant. 344 PRIMARY GRAFT FAILURE (PGF) IN CARDIAC TRANSPLANTATION (OHT) OVER AN 8 YEAR PERIOD: THE RELATIONSHIP BETWEEN DONOR AND RECIPIENT FACTORS P. Anagnostopoulos,1 C. Savopoulou,1 L. Shears,1 J. Ristich,1 A. Patel,1 R. Kormos,1 1Department of Cardiothoracic Surgery, University of Pittsburgh, Pittsburgh, PA Background: PGF accounts for up to 45% of early (30 day) mortality after OHT. Our goal was to identify recipient and donor factors predisposing to PGF. Methods: Of 311 consecutive patients undergoing OHT between 01/01/1994 and 10/31/2002, donor records were available for 286 (92%). Patients with PGF developed ventricular dysfunction (not due
The Journal of Heart and Lung Transplantation February 2004
to hyperacute rejection or technical problems) that required extraordinary doses of inotropic agents or post-transplant mechanical circulatory assistance (intra-aortic balloon pump(IABP), ECMO or a ventricular assist device (VAD)). Results: Twenty nine patients (10%) developed PGF which had a thirty-day mortality of 70% compared to 2% in those without. Patients with PGF were older (58 years vs 52 years, p ⬍ 0.02), and had longer ischemia time (247 vs 191 min, p ⬍ 0.001) compared to those without PGF. The incidence of PGF was 14% in ischemic cardiomyopaths vs 6% in patients with other diagnoses (p ⬍ 0.03). Patients needing mechanical support (IABP and/or VAD support) pre-OHT had an incidence of PGF of 15% vs 4% in those on inotropes or no support (p ⬍ 0.02). PGF occurred in 24% of patients with the PRA-DTT ⬎⫽10% vs 8% if the PRA was ⬍10% (p ⬍ 0.02. Male recipients of a female donor heart had a higher incidence of PGF(p ⬍ 0.02). Conclusions: The development of PGF is a serious complication of cardiac transplantation that is influenced by specific recipient and donor characteristics. These variables may be even more critical in patients on mechanical support as a bridge to OHT.
345 IMPACT OF LATE POST-TRANSPLANT ACUTE CARDIAC REJECTIONS ON GRAFT FUNCTION AND DEVELOPMENT OF CORONARY ARTERIOPATHY M. Dandel,1 C. Knosalla,1 R. Meyer,1 H. Lehmkuhl,1 R. Hetzer,1 1 Cardiothoracic and Vascular Surgery, Deutsches Herzzentrum Berlin, Berlin, Berlin, Germany The impact of late acute cardiac rejections (ARs) on long-term graft function and development of transplant coronary arteriopathy (TxCA) is controversial. We investigated the potential links between late ARs and both left ventricular (LV) dysfunction and development of TxCA. Methods: Patients with ⬎2 years of survival after heart transplantation (HTx) performed between 6/1986-6/2000 were analyzed to evaluate the prevalence and severity of late ARs and also the potential relationship between late ARs and development or progression of TxCA. Results: A total of 59 biopsy-proven late ARs, accompanied by relevant LV dysfunction revealed by tissue Doppler (TD) wall motion analysis, were diagnosed in 36 (4.9%) of the evaluated patients. Of the 59 functionally severe late ARs only 9 (15.3%) were cellular ARs ⱖ3A. The other 47 (84.7%) were mild cellular ARs grade 1A or 1B accompanied all by intense vascular reaction and 20 of them were evidently severe vascular ARs. LV dysfunction was completely reversible in only 2 (5.6%) of the 36 patients, whereas 12 (33.3%) died due to AR-related graft failure. In other 22 patients LV function remained at least moderately altered and shortly ( ⬍6 weeks) after AR, sudden cardiac death occured in 5 patients. In 12 patients without TxCA during their first functionally relevant late AR, control angiography revealed relevant TxCA lesions already 2.3 ⫾ 1.2 years later. Of 17 patients who died during or ealy after a late AR, 10 had also angiographic TxCA that developed in 9 of them after the 2nd post-HTx year. The mean number of late ARs/year/patient was higher in those who developed angiographic TxCA after the 2nd post-HTx year than in those without TxCA at that time (p ⬍ .01). Conclusions: Late ARs are an important cause of late acute and chronic allograft dysfunction. Our data suggest that late ARs also contribute to the development of TxCA after the 2nd post-HTx year. The severity of late ARs is rarely related to the ISHLT grading system and for prognostic evaluation or therapeutic decisions, both functional data and additional diagnosis of humoral (vascular) AR are helpful.