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Ann Thorac Surg 1999;68:629-630
© 1999 The Society of Thoracic Surgeons
a Department of Cardiovascular Surgery, Union Hospital, Fuzhou, 350001, Peoples Republic of China
To the Editor
In a recent issue, De Paulis and colleagues demonstrated that cardiac troponin I (CTn I) level in circulating blood is not affected by reinfusion of shed blood after coronary artery bypass grafting (CABG), and therefore CTn I will be a useful marker for the diagnosis of perioperative myocardial infarction [1]. But they could not specifically elucidate whether or not this specific and sensitive marker for myocardial damage is influenced by reinfusion of shed blood in redo CABG. I was very interested in elucidating that mainly because of two reasons: first, the autotransfusion practice is more appealing in the setting of reoperation because dissection of dense mediastinal adhesions increases the risk of postoperative bleeding [2]; and second, adhesions obscure the cardiac anatomy and complicate perimyocardial injury when surgeons free the heart from the mediastinum and pericardium [2]. From a theoretical point of view, those damaged perimyocardium may locally release CTn I into the pericardial cavity and therefore shed mediastinal blood if a redo operation should contain a higher CTn I level than that in the primary one. When the shed blood containing a higher CTn I level is reinfused, the CTn I level in circulating blood would be affected.
Therefore, I made the two following observations in order to demonstrate this: (1) whether or not the CTn I level in circulating blood in a redo CABG is affected by autotransfusion of shed mediastinal blood; and (2) whether or not shed mediastinal blood contains a higher CTn I level in redo cardiac operation than that in the primary one. CTn I levels in circulating blood were obtained from 48 consecutive patients undergoing redo CABG at the time of preoperative, immediately after admission to the surgical intensive care unit, 16 hours postoperatively, and on the 2nd and 4th postoperative days. All patients received intraoperative myocardial protection with moderate body hypothermia, cold blood potassium cardioplegia, and topical ice slush. Shed mediastinal blood was collected in a reinfusion system (Pleur-evac; Deknatal, Fall River, MA). Patients with more than 400 mL of shed blood within the first 4 hours after chest closure underwent reinfusion of the shed blood. The collected shed blood was reinfused through a standard blood filter without any special management. There were 2 patients with early postoperative myocardial infarction and 1 patient with low cardiac output syndrome. Those 3 patients were excluded from the observation. In the remaining 45 patients, 19 underwent reinfusion of shed blood (group 1), while the other 26 patients did not (group 2). CTn I data were compared with a Mann-Whitney U test because CTn I is not distributed normally [3], while other data were analyzed by analysis of variance or students t test. Differences were considered significant at a probability level less than 0.05.
There were no significant differences in age, sex, cardiac ejection fraction, cardiopulmonary bypass and aortic cross-clamp time, minimum body temperature, and number of grafts between two groups. The circulating blood CTn I levels averaged 0.0265 ± 0.0503, 0.6408 ± 0.4288, 1.6977 ± 1.2844, 1.5605 ± 0.5776, and 0.5776 ± 0.5587 µg/L in group 1, and 0.0218 ± 0.0283, 0.05161 ± 0.7547, 1.6536 ± 2.1875, 1.0873 ± 1.1204, and 0.3286 ± 0.4094 µg/L in group 2 at the time of preoperative, immediately after admission to the surgical intensive care unit, 16 hours postoperatively, and 2nd and 4th postoperative days, respectively. There were no significant differences between the two groups at all time points.
In the second observation, I measured CTn I levels in shed mediastinal blood of 15 consecutive patients accepting redo valve replacement (11 cases) or redo CABG (4 cases) (group 3) and 15 randomly selected patients undergoing primary valve replacement (11 cases) or primary CABG (4 cases) (group 4). Shed blood samples were collected 4 hours after chest closure. CTn I data were compared with a Wilcoxin nonparametric test while other data were analyzed as that in the first observation.
There were no significant differences in age, sex, cardiac ejection fraction, cardiopulmonary bypass time, and aortic cross-clamp time between the two groups, but duration of intervention in group 3 (273.4 ± 44.4 minutes) was longer than that in group 4 (203.5 ± 38.3 minutes). The shed blood CTn I levels were not significantly different between the two groups (1.4091 ± 1.5093 µg/L in group 3 and 1.2329 ± 1.1710 µg/L in group 4).
The present results of those two observations indicate: (1) CTn I levels in circulating blood are not affected by reinfusion of shed mediastinal blood in redo CABG; and (2) dissection of dense adhesions between the heart and its surrounding tissues does not significantly induce perimyocardium to liberate CTn I into shed mediastinal blood; that is, perimyocardial damage caused by dissection of adhesions in redo open heart operation using modern surgical techniques is limited.
References
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