Iatrogenic tracheal rupture is a dangerous complication with potentially high postoperative mortality, mostly influenced by the underlying disease. Early surgical repair must be the preferred treatment.

In terminally failing human myocardium of patients receiving drug therapy, complex I depression is not caused by mtDNA damage and disturbed mitochondrial gene expression. The absence of mtDNA damage should facilitate recovery of the overloaded myocardium, if effective unloading could be achieved.

Cardiopulmonary bypass is associated with an injury that may cause pathophysiological changes in the form of systemic inflammatory response syndrome (SIRS) or multiple organ dysfunction syndrome (MODS). In the present study, we investigated the inflammatory response of patients with multiple organ dysfunctions following open-heart surgery. Plasma levels of cytokines (IL-1beta, IL-6, IL-8, IL-18) and procalcitonin (PCT) were measured on the first four postoperative days in 12 adult male patients with SIRS and two or more organ dysfunctions after myocardial revascularization (MODS group), and 15 patients without organ dysfunctions (SIRS group). All cytokines (except IL-1beta) and PCT were significantly elevated in MODS patients, with peak values at the first two postoperative days. The results of our study show a different expression of members of the IL-1 family following extracorporeal circulation. For the first time, we can document that IL-18 is involved in the inflammatory response and the initiation of the MODS following cardiopulmonary bypass. In addition to APACHE-II score, PCT, IL-8, and IL-18 may be used as parameters for the prognosis of patients with organ dysfunctions after cardiac surgery. Furthermore, it must be noted that the duration of the surgical procedure is one of the most important factors for the initiation of the inflammatory response.

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In the terminally failing human myocardium, the caspase cascade is partially activated in the presence of a consistent phenotype shift toward enhanced susceptibility to apoptosis. Although the system is still under a fragile control, the partial initiation of the apoptotic program may be of functional relevance also for the surviving cardiomyocytes.