Key result
Antioxidant therapies show limited evidence for mitigating cardiopulmonary bypass-induced myocardial inflammation and apoptosis.
Answers are grounded in this paper and cite their sources.
Cardiac surgery (CS), in particular cardiopulmonary bypass and cardioplegia, have been reported to trigger myocardial inflammation and apoptosis. This surgery-related inflammatory reaction appears to be of extreme complexity with regard to its molecular, cellular and tissue mechanisms. Both experimental and clinical studies have ascertained the role of several hormonal mediators, mitochondria, cardioplegia and extracorporeal circulation temperature, apoptosis and even genetic modulators of damage. However, the correlations between these factors in vivo and post-surgery outcome and prognosis have not yet been systematically investigated. In animal models of myocardial cardioplegia and/or ischemia-reperfusion, experimental drugs such as antioxidants have been documented to provide amelioration of post-intervention cardiac performance and reduction of apoptosis suggesting the possibility of new therapeutic strategies. However, these findings have been only partially confirmed in humans. Moreover, markers for the differential detection of early and late phases of apoptosis are subjects of intense investigations. This review will provide an overview of the major studies about the link between ischemia, myocardial inflammation and apoptosis during and after CS, with particular regard to the markers and methods for apoptosis detection.
No takes yet. Share an insight, caveat, or question.
Amédéo Anselmi (2004) conducted a review in Myocardial ischemia, inflammation, and apoptosis during cardiac surgery. Cardiac surgery (cardiopulmonary bypass and cardioplegia) was evaluated. Cardiac surgery with cardiopulmonary bypass and cardioplegia triggers complex myocardial inflammation and apoptosis, while human evidence for cardioprotective antioxidants remains limited.
Synapse has enriched 10 related papers. Consider them for comparative context: