There was no difference in coronary blood flow between patients with septic shock who developed myocardial depression and those who did not, and in no patient was net myocardial lactate production demonstrated. In addition, several animal models have shown that myocardial oxygen metabolism and high-energy phosphate levels are well-preserved during experimental septic shock., Nevertheless, it is still a matter of debate whether troponin release in patients with sepsis reflects irreversible myocardial damage or reversible myocardial depression. Whereas troponin levels are elevated for several days in patients with myocardial infarction, transient, short-lasting (ie, a few hours) increases in cardiac troponin levels in patients with unstable angina have been observed, which suggests that troponin leakage due to ischemia or other stimuli is possible even if myocardial necrosis does not occur.
Experimental evidence supporting this theory was provided by Piper and coworkers, who demonstrated reversible membranous bleb formation in rat cardiomyocytes during limited periods of hypoxia and the consecutive release of myocardial enzymes in cell supernatant. In addition, in the study by Ver Elst et al histopathologic examination revealed contraction band necrosis in only half of patients with a positive premortem troponin level, but also in one troponinnegative patient, suggesting that troponin release does not necessarily indicate myocardial cell necrosis. other
However, in many ICU patients with sepsis troponin release can still be due to preexisting flow-limiting CAD, and myocardial necrosis precipitated by sepsis-associated tachycardia and anemia. These patients cannot be differentiated from those without CAD and real sepsis-induced troponin release at bedside. With regard to this limitation, most of the studies that have been cited were hampered by the fact that the presence of an underlying CAD was not systematically sought. In the largest prospective study on the topic, we could exclude flow-limiting CAD in the majority of troponin-positive patients who had sepsis and septic shock by stress echocardiography, coronary angiography, or autopsy. Nevertheless, myocardial injury due to microvascular thrombosis could still play a role. There is a close relationship between the presence of inflammatory cytokines and a procoagulant state in patients with severe sepsis.