1999
DOI: 10.1213/00000539-199904000-00001
|View full text |Cite
|
Sign up to set email alerts
|

High Thoracic Epidural Anesthesia, but Not Clonidine, Attenuates the Perioperative Stress Response Via Sympatholysis and Reduces the Release of Troponin T in Patients Undergoing Coronary Artery Bypass Grafting

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1

Citation Types

3
41
1
3

Year Published

2004
2004
2019
2019

Publication Types

Select...
7
2

Relationship

0
9

Authors

Journals

citations
Cited by 188 publications
(48 citation statements)
references
References 29 publications
3
41
1
3
Order By: Relevance
“…Accordingly, it was previously reported in patients undergoing CABG that TEA is associated with a significantly smaller release of troponin T 24 hours after intensive care admission compared with that in patients not receiving TEA. 12 On the other hand, a recent meta-analysis including 1178 patients found that although TEA is associated with shorter time until tracheal intubation and decreased pulmonary complications and cardiac arrhythmias, no effect on mortality or rates of myocardial infarction could be found. 30 However, most of the studies included in this meta-analysis were small (Յ50 treated patients), and because the pooled mortality rate of the study was low, the authors concluded that more larger-scale randomized controlled trials are required to fully assess the potential benefits of TEA for the reduction of myocardial infarction and mortality after CABG.…”
Section: Discussionmentioning
confidence: 98%
See 1 more Smart Citation
“…Accordingly, it was previously reported in patients undergoing CABG that TEA is associated with a significantly smaller release of troponin T 24 hours after intensive care admission compared with that in patients not receiving TEA. 12 On the other hand, a recent meta-analysis including 1178 patients found that although TEA is associated with shorter time until tracheal intubation and decreased pulmonary complications and cardiac arrhythmias, no effect on mortality or rates of myocardial infarction could be found. 30 However, most of the studies included in this meta-analysis were small (Յ50 treated patients), and because the pooled mortality rate of the study was low, the authors concluded that more larger-scale randomized controlled trials are required to fully assess the potential benefits of TEA for the reduction of myocardial infarction and mortality after CABG.…”
Section: Discussionmentioning
confidence: 98%
“…8,9 In patients with ischemic heart disease, TEA has been evaluated as an adjunctive treatment for refractory chest pain during stable and unstable angina pectoris 10,11 and for improving postsurgical recovery after CABG. [12][13][14] On the other hand, it remains unclear to what extent these apparently beneficial effects of TEA are mediated by changes in myocardial blood flow or whether they are merely the result of improved pain relief.…”
mentioning
confidence: 99%
“…The results of this study showed that the HTEA could significantly narrow the LVEDd, increase the LVEF, and improve heart function in ICM patients, especially for those with severe ICM, those who were not suitable for PCI, and those with refractory heart failure awaiting a heart transplant. HTEA could delay ventricular remodeling in ICM patients by selectively blocking the cardiac sympathetic nerve, which could reduce the sympathetic activity in patients with heart failure, reduce the damage to the myocardium by catecholamines, expand the coronary artery (Loick et al, 1999), improve the ischemic myocardium oxygen supply, and balance and improve myocardial Table 2. Comparison of heart rate variability and QTV changes between the two groups before and after treatment.…”
Section: Discussionmentioning
confidence: 99%
“…It was also observed an improvement in ventricular contractility after ischemic episodes with morphine and fentanyl (28). Besides participating in the triggering of the cascade of ischemic preconditioning, opioids also seem to mediate the memory phase in some animal species and the opioid-induced cardioprotection appears to be modulated by the activation of cardiac receptors, independent of the action of these drugs on the central nervous system [40][41] . It has been proposed that opioid-induced cardioprotection is processed by the activation of ATP-dependent potassium channels, possibly in the mitochondrial membrane (29).…”
Section: Myocardial Protectionmentioning
confidence: 98%