Introduction: ASCT offers a chance of prolonged remission and even cure in different oncohematological diseases. Pre transplant impairment of cardiac function is usually referred as a cause of increased morbility and mortality in these patients. In Blood 2006, Vol 108, abst. # 2982 our group reported the findings in patients with previous cardiopathy undergoing ASCT, detecting no differences in the short-term outcome of this population compared with non cardiac affected pts.
Objective: Analyze the long term outcome in ASCT pts. who underwent the procedure with a previous cardiac disease.
Patient and Methods: Between 1991–2008, 364 pts. received an ASCT at our BMT unit. During the pretransplant evaluation 14/364 pts. (3.8%) were diagnosed with an impairment of the cardiac condition: Dilated left ventricle > 55 mm. and/or abnormal systolic function with ejection fraction < 55%:11/14pts; ischemic cardiopathy including wall motion abnormalities 3/14pts, and moderate to severe valvulopathy 1/14 pts. 3/14 pts died early because of relapse and were not included in this study. Pts population at follow up: mean age 50,1 years (r 28–68), female 45%. Diagnoses: Non Hodgkin lymphoma 6/11, multiple myeloma 2/11, amyloidosis 1/11, acute myeloblastic leukemia 1/11, and Hodgkin disease 1/11. Conditioning chemotherapy regimens included BEAM (5/11), Melphalan (3/11), BuCy (1/11) and CVB (2/11). In the pre ASCT evaluation 7/11 pts showed cardiopathy probably related to previous ASCT chemotherapy toxicity, 2/11 ischemic disease, 1/11 cardiac amyloidosis and 1/11 valvulopathy with the following echocardiographic findings: 5/11 showed dilated left ventricle; 9/11 impaired left ventricle systolic function and segmentary wall motion abnormalities in 2/11. Patient evaluation procedure included: clinical evaluation according to the New York Heart Association (NYHA) functional classification system (FCS), electrocardiography and bidimensional echocardiography. Post ASCT pts were referred to the cardiologist and enalapril treatment was recommended.
Results: The post ASCT median time of follow-up was 30 months (r 7–41 months). At the moment of the study evaluation 5/11 patients have relapsed of their haematological disease. 6/11 changed the FCS compared to the pre ASCT evaluation; 3/11 showed improvement and 3/11 worsened the FCS. 5/11 did not show any difference. Echocardiography analysis reported 4 patients with a better condition (reduction of left ventricle enlargement in 1 and increased contractility in 3 cases including one pt with cardiac amyloidosis) and 3 pts worsened their echocardiographic findings showing a severe dysfunction of the ejection fraction in 2 pts. and a more dilated left ventricle in one case. Only one patient presented a major cardiac event in the form of an acute myocardial infarction. He also required a permanent pacemaker. 4/11 pts were not under enalapril treatment as it was recommended. No pt died due to cardiac events.
Conclusions: We did not observed cardiac associated mortality in the group of pts with mild or moderate cardiac dysfunction in a follow up of 30 months post-ASCT. Pre ASCT cardiac dysfunction as described above does not preclude the procedure. ASCT seems not to worsen the natural course of the cardiac disease. Further clinical studies are needed to support our findings.
Disclosures: No relevant conflicts of interest to declare.