Functional status and quality of life (QoL) in long-term survivors of cardiac arrest after cardiac surgery (original) (raw)
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Severity of illness, critical events, organ failure assessment and ICU outcome
Critical Care, 2000
Aims: To study the relationship between myocardial release of cTnI and myocardial cell death as assessed by the amount of apoptosis and necrosis after cardiac surgery. Methods: Eighteen young pigs were operated on with standardized cardiopulmonary bypass (CPB). Release of cTnI in the cardiac lymph (CL), coronary sinus (CS), and arterial blood (A) was related to postoperative myocardial cell death by both necrosis and apoptosis. Apoptotic cells were detected by a TUNEL detection kit. Necrotic cells were counted by light microscopy. Results: In all animals, cTnI was significantly released and reached peak values observed simultaneously in A (cTnI, 20.1±2.6 ng/ml) (mean ±SEM), CS (19.5±3.2 ng/ml) and CL (5202±2500 ng/ml). Percentage of total myocardial cell death was 3.1±0.5%, including 1.2±0.35% necrosis and 1.9±0.5% apoptosis. cTnI release during and after CPB did not correlate with the degree of myocardial apoptosis or necrosis. Conclusion: Cardiac operations with CPB are related to myocardial cell damage including myocardial cell death due to both necrosis and apoptosis. As the loss of cTnI is not related to the amount of cell death, our results suggest that increased cardiac myocyte membrane permeability more than cell death is responsible for intraoperative and postoperative cTnI release.
Non invasive mechanical ventilation (NINMV) in cardiac surgery
Critical Care, 2000
Aims: To study the relationship between myocardial release of cTnI and myocardial cell death as assessed by the amount of apoptosis and necrosis after cardiac surgery. Methods: Eighteen young pigs were operated on with standardized cardiopulmonary bypass (CPB). Release of cTnI in the cardiac lymph (CL), coronary sinus (CS), and arterial blood (A) was related to postoperative myocardial cell death by both necrosis and apoptosis. Apoptotic cells were detected by a TUNEL detection kit. Necrotic cells were counted by light microscopy. Results: In all animals, cTnI was significantly released and reached peak values observed simultaneously in A (cTnI, 20.1±2.6 ng/ml) (mean ±SEM), CS (19.5±3.2 ng/ml) and CL (5202±2500 ng/ml). Percentage of total myocardial cell death was 3.1±0.5%, including 1.2±0.35% necrosis and 1.9±0.5% apoptosis. cTnI release during and after CPB did not correlate with the degree of myocardial apoptosis or necrosis. Conclusion: Cardiac operations with CPB are related to myocardial cell damage including myocardial cell death due to both necrosis and apoptosis. As the loss of cTnI is not related to the amount of cell death, our results suggest that increased cardiac myocyte membrane permeability more than cell death is responsible for intraoperative and postoperative cTnI release.
Critical Care, 2000
Aims: To study the relationship between myocardial release of cTnI and myocardial cell death as assessed by the amount of apoptosis and necrosis after cardiac surgery. Methods: Eighteen young pigs were operated on with standardized cardiopulmonary bypass (CPB). Release of cTnI in the cardiac lymph (CL), coronary sinus (CS), and arterial blood (A) was related to postoperative myocardial cell death by both necrosis and apoptosis. Apoptotic cells were detected by a TUNEL detection kit. Necrotic cells were counted by light microscopy. Results: In all animals, cTnI was significantly released and reached peak values observed simultaneously in A (cTnI, 20.1±2.6 ng/ml) (mean ±SEM), CS (19.5±3.2 ng/ml) and CL (5202±2500 ng/ml). Percentage of total myocardial cell death was 3.1±0.5%, including 1.2±0.35% necrosis and 1.9±0.5% apoptosis. cTnI release during and after CPB did not correlate with the degree of myocardial apoptosis or necrosis. Conclusion: Cardiac operations with CPB are related to myocardial cell damage including myocardial cell death due to both necrosis and apoptosis. As the loss of cTnI is not related to the amount of cell death, our results suggest that increased cardiac myocyte membrane permeability more than cell death is responsible for intraoperative and postoperative cTnI release.
European Journal of Cardio-Thoracic Surgery, 2004
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. q
Mortality and outcome in different subgroups of patients admitted in an ICU
Critical Care, 2000
Aims: To study the relationship between myocardial release of cTnI and myocardial cell death as assessed by the amount of apoptosis and necrosis after cardiac surgery. Methods: Eighteen young pigs were operated on with standardized cardiopulmonary bypass (CPB). Release of cTnI in the cardiac lymph (CL), coronary sinus (CS), and arterial blood (A) was related to postoperative myocardial cell death by both necrosis and apoptosis. Apoptotic cells were detected by a TUNEL detection kit. Necrotic cells were counted by light microscopy. Results: In all animals, cTnI was significantly released and reached peak values observed simultaneously in A (cTnI, 20.1±2.6 ng/ml) (mean ±SEM), CS (19.5±3.2 ng/ml) and CL (5202±2500 ng/ml). Percentage of total myocardial cell death was 3.1±0.5%, including 1.2±0.35% necrosis and 1.9±0.5% apoptosis. cTnI release during and after CPB did not correlate with the degree of myocardial apoptosis or necrosis. Conclusion: Cardiac operations with CPB are related to myocardial cell damage including myocardial cell death due to both necrosis and apoptosis. As the loss of cTnI is not related to the amount of cell death, our results suggest that increased cardiac myocyte membrane permeability more than cell death is responsible for intraoperative and postoperative cTnI release.
Quality of life 6 and 12 months after discharge from the intensive care unit
Critical Care, 2000
Aims: To study the relationship between myocardial release of cTnI and myocardial cell death as assessed by the amount of apoptosis and necrosis after cardiac surgery. Methods: Eighteen young pigs were operated on with standardized cardiopulmonary bypass (CPB). Release of cTnI in the cardiac lymph (CL), coronary sinus (CS), and arterial blood (A) was related to postoperative myocardial cell death by both necrosis and apoptosis. Apoptotic cells were detected by a TUNEL detection kit. Necrotic cells were counted by light microscopy. Results: In all animals, cTnI was significantly released and reached peak values observed simultaneously in A (cTnI, 20.1±2.6 ng/ml) (mean ±SEM), CS (19.5±3.2 ng/ml) and CL (5202±2500 ng/ml). Percentage of total myocardial cell death was 3.1±0.5%, including 1.2±0.35% necrosis and 1.9±0.5% apoptosis. cTnI release during and after CPB did not correlate with the degree of myocardial apoptosis or necrosis. Conclusion: Cardiac operations with CPB are related to myocardial cell damage including myocardial cell death due to both necrosis and apoptosis. As the loss of cTnI is not related to the amount of cell death, our results suggest that increased cardiac myocyte membrane permeability more than cell death is responsible for intraoperative and postoperative cTnI release.