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Factors associated with the development of persistently depressed cardiac output during the first year after cardiac transplantation
Author(s) -
Glazier James J.,
Mullen G. Martin,
Johnson Maryl R.,
Heroux Alain L.,
Kao Walter G.,
Koch Dorothea,
Khatib Yazan,
Fisher Susan G.,
Costanzo Maria Rosa
Publication year - 1994
Publication title -
clinical cardiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.263
H-Index - 72
eISSN - 1932-8737
pISSN - 0160-9289
DOI - 10.1002/clc.4960170906
Subject(s) - medicine , transplantation , cardiac index , heart transplantation , perioperative , cardiac output , hemodynamics , cardiac surgery , cardiology , surgery
The purpose of this study was to determine factors associated with the development of a persistently depressed cardiac output during the first year after cardiac transplantation. With this aim in mind, the records of 133 consecutive patients undergoing orthotopic cardiac transplantation and surviving for ≥1 year after transplantation were reviewed. For each patient, the mean cardiac index for each of the 3‐month periods, 0‐3, 4‐6, 7‐9, and 10‐12 months after transplantation was calculated. of the 133 patients, 19 (14%) had a mean cardiac index < 2.41/min/m 2 during ≥3 of these 3‐month periods. The pre‐ and post‐transplantation clinical, immunologic, and hemodynamic data of these 19 patients (study group) were compared with the remaining 114 patients (control group). Compared with the control group, the patients in the study group were older (56±5 vs. 46±15 years; p = 0.0001), more frequently had ischemic heart disease as the original diagnosis (58 vs. 37%; p < 0.05), had a lower preoperative cardiac index (1.91 ± 0.53 vs. 2.71 ± 1.0 1/min/m 2 ; p = 0.0001), more frequently did not receive perioperative anti‐T cell therapy (47 vs. 25%; p=0.046), and had a greater median number of infections during the first year after transplantation (5 vs. 3; p = 0.027). However, only one factor—a low preoperative cardiac index—emerged as an independent predictor of the development of a persistently depressed cardiac index during the first year after transplantation. Of note, mean systemic vascular resistance was higher in the study group than in the control group at every 3‐month period following cardiac transplantation. One possible although largely speculative explanation of the latter observation is that heart transplantation does not entirely reverse the neurohumoral abnormalities of chronic heart failure. Furthermore, this persistently elevated systemic vascular resistance may impact negatively on long‐term allograft function.

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