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Electronic Letters to:
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Electronic letters published:
![[Read eLetter]](/icons/misc/sectionDOWN.gif){kind=icon}
Biological Markers of Left Ventricular Dysfunction in Septic Shock
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Christian Wiedermann, Professor of Medicine Dept. Medicine, Univ. Innsbruck, Austria
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christian.wiedermann{at}uibk.ac.at Christian Wiedermann
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Ver Elst et al. (1) suggest that in septic shock, myocardial cell injury as measured by increased plasma levels of cardiac troponins is a marker of left ventricular dysfunction which occurs more often in severely ill older patients with underlying cardiovascular disease. In a total of 46 patients with early fully resuscitated septic shock, troponin- positivity was associated with reduced survival. The extent to which myocardial damage was a cause or a consequence of left ventricular dysfunction, however, remains unknown. Comparison of biochemical markers of sepsis [procalcitonin (PCT) and C- reactive protein (CRP)] in patients that were either troponin-positive or troponin-negative revealed that statistically PCT and CRP did not differ in the two groups. Peak CRP levels (interquartile range) in troponin I- positive and troponin I-negative patients were 245 (159 – 346) mg/L and 284 (243 – 361) µg/L, respectively, suggesting comparable severity of sepsis. PCT levels were 19.5 (2.8 – 45.5) µg/L in troponin I-positive and 5.3 (1.3 – 23.2) µg/L in troponin I-negative patients; this difference was not statistically significant probably because the sample size could be too small given the wide range of levels. Myocardial tissue injury causes changes of plasma levels of acute phase reactants (2) and may have contributed to the observed divergence of PCT and CRP levels between the two troponin groups (1). We have recently monitored in a prospective study of consecutive cases with acute myocardial infarction plasma levels of PCT, CRP and interleukin-6 (IL-6). The study was performed in the emergency room and a 14-bed coronary and medical intensive care unit of a university hospital. Fourty four patients (15 women and 29 men; median age 64.4 years, range 24 to 78) with acute myocardial infarction were included in the study 4 ± 1.3 hours after the onset of symptoms, as described (3). Plasma samples were obtained at admission, and after 3, 6, 12, 18, 24 and 48 hours. Plasma levels of PCT (Brahms Diagnostica; Berlin, Germany) and IL-6 (Medgenix Diagnostics; Fleurus, Belgium) were determined using commercially available test kits. CK-MB, leukocyte counts and CRP were measured by routine laboratory methods. The StatView software package (Abacus, Berkeley, CA) was used to calculate statistics including Spearman-Rank correlation, non-parametric multiple group comparison for dependent variables (Friedman test) and two-tailed Student t-test for paired samples. Mean plasma levels of PCT and IL-6 gradually increased from the almost normal range at admission and reached the maximum after 24 hours followed by a decline. CK-MB was increased maximally after 12 hours and leukocytes after 3 hours. Highest CRP levels were measured after 48 hours. Peak levels of PCT and IL-6 were 1.0 ± 0.35 µg/L and 110 ± 17.8 ng/L, respectively. Peak level of CK-MB and leukocytes were 83 ± 12.1 U/L and 14730 ± 4600 cells/ml, respectively, and that of CRP was 110 ± 52 mg/L. The increases of IL-6, CK-MB, CRP and leukocytes were found to be statistically significant (p-trend < 0.0001), but that of PCT was not (p-trend > 0.05). PCT levels rose in 27 of 44 patients whereas IL-6 levels increased in all 44 patients. Peak levels of PCT and IL-6 were significantly related (0.78; p < 0.0001). Maximal levels of plasma CK- MB and the maximal PCT or IL-6 levels were also significantly related (0.58, p < 0.001; and 0.59, p < 0.001; respectively). In summary, although statistically not significant, there is a clear tendency of PCT to increase with time after acute myocardial infarction, in a fashion similar to IL-6. Time-courses of IL-6 and PCT are quite similar, while for CRP and CK-MB different kinetics are found. When compared to sepsis patients, peak levels of PCT, however, remain low after myocardial infarction. Therefore, elevation of plasma PCT in troponin- positive sepsis patients most likely develops independent of myocardial damage. Recent reports show that the severity of disease measured in infection and sepsis by APACHE II is associated with levels of PCT but not with CRP (4, 5). The tendency of higher PCT levels in troponin-positive as compared to troponin-negative patients as was observed by Ver Elst (1) then suggests that troponin-positive patients had more severe sepsis. Significantly higher APACHE II scores found in these patients also support such a conclusion. If this is the case, myocardial damage may well be a cause of left ventricular dysfunction. Thomas Buratti, Manfred Herold, Franz J. Wiedermann,* Giovanni Ricevuti,+ and Christian J. Wiedermann Department of Internal Medicine, and *Department of Anesthesiology and Intensive Care Medicine, University of Innsbruck, Innsbruck, Austria; +Department of Internal Medicine, University of Pavia, Pavia, Italy. References |
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