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Excerpt
With great interest, we read the recent study by Lecharny et al. (1). However, we feel that several issues raised by the authors may need further discussion.
The authors found a mild increase up to 2.0 ng/mL in plasma procalcitonin (PCT) concentrations in their prospective analysis of plasma PCT concentrations of ten patients undergoing cardiopulmonary bypass (CPB) for open heart surgery. This is in accordance with previous studies, as the authors stated (1). Furthermore, the authors performed a retrospective analysis of plasma samples in 23 matched patients with high troponin I concentrations (63.7 ± 47.5 ng/mL) indicative of perioperative myocardial infarction (PMI) 20 hrs after cardiac surgery and in 25 patients with troponin I concentrations of <5.0 ng/mL (2.1 ± 0.7). In the first group, Lecharny et al. detected a pronounced elevation of PCT concentrations, but only two of the control group of 25 patients showed PCT concentrations >4 ng/mL. Eighteen of 23 (78.3%) patients with marked hypertroponinemia needed inotropic support in the early phase after CPB, compared with ten of 25 (40%) patients with moderate hypertroponinemia. Five patients in the PMI group died during hospitalization compared witho two in the control group, and again PCT concentrations were significantly higher in these patients. The authors concluded that elevations of PCT concentrations are associated with PMI.
However, we doubt whether the increase of PCT can be explained simply by a diagnosis of PMI based on elevated concentrations of troponin I. As the authors mentioned in their Methods, the diagnosis of PMI was “confirmed by electrocardiogram and echocardiograpy,” but there is no information concerning the extent of myocardial damage, that is, whether it was a transmural or only a non-Q-wave infarction or whether the patients developed cardiogenic shock. Because 22% of the patients with PMI did not need inotropic support, we believe that PMI was not a serious event, indicating the higher mortality rate in these patients.
We performed daily PCT measurements in 691 consecutive patients undergoing CPB in open heart surgery (2). Patients were followed for up to 30 days. PCT significantly increased at day 1 postoperatively compared with baseline values (0.25 ± 1.65 vs. 6.49 ± 22.0 ng/mL, p < .005). However, in 55.1% of patients, PCT was <1.0 ng/mL. In 12.8% of coronary artery bypass graft patients, PCT was increased to >5.0 ng/mL, compared with 39% in valve patients and 35% of patients with aortic surgery. An elevated PCT concentration >1.0–5.0 ng/mL at day 1 was predictive of increased in-hospital mortality rates (p < .03 vs. 1.0 ng/mL), with an additional accuracy when concentrations <5.0 ng/mL were measured (p < .002 vs. 1.0 ng/mL). Whereas the increase in PCT at day 1 after surgery was not associated with myocardial infarction, the amount of vasopressor support administered for low systemic vascular resistance immediately after CBP correlated with a postoperative increase in PCT concentrations, with a trend to higher PCT concentrations in nonsurvivors. Additionally, PCT was significantly higher in patients with a CPB time of >80 mins in coronary artery bypass graft procedures and >100 mins in valve procedures. In 51 patients needing an intra-aortic ballon pump for postcardiotomy heart failure, the increase in PCT concentrations was more pronounced than in surviving patients without intra-aortic ballon pump insertion (p < .001).
In summary, we believe that the increase of PCT concentrations found by the authors may be attributable to the inflammatory response after the extracorporeal circuit or to intestinal malperfusion with consecutive translocation of bacteria or endotoxins rather than to myocardial infarction itself.
