Adjuvant Cardioprotection in Cardiac Surgery: Update

Wágner, Robert; Piler, Pavel; Gabbasov, Zufar; Maruyama, Junko; Maruyama, Kazuo; Ničovský, Jiří; Kružliak, Peter

doi:10.1155/2014/808096

Cited by 11 publications

(10 citation statements)

References 118 publications

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“…Acute myocardial dysfunction predominantly manifests as ischemic injury ( 12 ), and it is particularly prominent under ischemic, function-inhibitory or necrotic conditions ( 4 ). Currently, myocardial protections implemented in coronary artery bypass grafting (CABG) include improvement in myocardial perfusion and stress response, as well as alleviation of reperfusion injury.…”

Section: Discussionmentioning

confidence: 99%

Protective effect of active perfusion in porcine models of acute myocardial ischemia

Feng

Mao

Dong

et al. 2016

Molecular Medicine Reports

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Mortality rates associated with off-pump coronary artery bypass (CAB) are relatively high, as the majority of patients requiring CAB are at a high risk for cardiac events. The present study aimed to establish porcine models of acute myocardial ischemia, and evaluate the protective role of shunt and active perfusion. A total of 30 pigs were randomly assigned to five groups, as follows: i) Sham (control); ii) A1 (shunt; stenosis rate, 55%); iii) A2 (shunt; stenosis rate, 75%); iv) B1 (active perfusion; stenosis rate, 55%); and v) B2 (active perfusion; stenosis rate, 75%) groups. Aortic pressure (P0), left anterior descending coronary pressure (P1), and coronary effective perfusion pressure (P1/P0) were measured. The expression levels of tumor necrosis factor-α (TNF-α), cardiac troponin (cTnI), creatine kinase-myocardial band (CK-MB), interleukin (IL)-6, IL-10, B-cell lymphoma 2 (Bcl-2), and caspase-3 were detected using enzyme-linked immunosorbent assay or western blotting. The myocardial apoptosis rate was determined using the terminal deoxynucleotidyl transferase dUTP nick end labeling assay. Ischemia models with stenosis rates of 55 and 75% were successfully constructed following suturing of the descending artery. Compared with the control, the 55 and 75% stenosis groups demonstrated significantly decreased P1/P0, increased expression levels of TNF-α, cTnI, CK-MB, IL-6, IL-10 and caspase-3, an increased rate of myocardial apoptosis, and a decreased expression level of anti-apoptotic protein, Bcl-2. At 30 min following successful establishment of the model (ST segment elevation to 1 mm), group B demonstrated significantly increased P1/P0, decreased expression levels of TNF-α, cTnI, CK-MB, IL-6, IL-10 and caspase-3, a decreased rate of myocardial apoptosis, and an increased expression level of anti-apoptotic protein, Bcl-2. Furthermore, the current study indicated that active perfusion was more efficacious in maintaining myocardial perfusion and alleviating ischemic injury when compared with traditional shunt perfusion.

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Section: Discussionmentioning

confidence: 99%

Protective effect of active perfusion in porcine models of acute myocardial ischemia

Feng

Mao

Dong

et al. 2016

Molecular Medicine Reports

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“…Another study conducted to assess these maneuvers in adult patients undergoing aortic valve-replacement surgery confirmed their benefit 95. However, the aortic clamping and declamping maneuvers are not safe, and are associated with a high risk of thromboembolic complications 96,97. As with ischemic PreC, the possibility of maintaining the benefit of PostC with the use of anesthetic drugs, which avoid the risks of these maneuvers, has been the object of study 94.…”

Section: Ischemic and Anesthetic Postcmentioning

confidence: 99%

Cardioprotection with halogenated gases: how does it occur?

Guerrero-Orriach

Belmonte

Fernández

et al. 2017

DDDT

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Numerous studies have studied the effect of halogenated agents on the myocardium, highlighting the beneficial cardiac effect of the pharmacological mechanism (preconditioning and postconditioning) when employed before and after ischemia in patients with ischemic heart disease. Anesthetic preconditioning is related to the dose-dependent signal, while the degree of protection is related to the concentration of the administered drug and the duration of the administration itself. Triggers for postconditioning and preconditioning might have numerous pathways in common; mitochondrial protection and a decrease in inflammatory mediators could be the major biochemical elements. Several pathways have been identified, including attenuation of NFκB activation and reduced expression of TNFα, IL-1, intracellular adhesion molecules, eNOS, the hypercontraction reduction that follows reperfusion, and antiapoptotic activating kinases (Akt, ERK1/2). It appears that the preconditioning and postconditioning triggers have numerous similar paths. The key biochemical elements are protection of the mitochondria and reduction in inflammatory mediators, both of which are developed in various ways. We have studied this issue, and have published several articles on cardioprotection with halogenated gases. Our results confirm greater cardioprotection through myocardial preconditioning in patients anesthetized with sevoflurane compared with propofol, with decreasing levels of troponin and N-terminal brain natriuretic peptide prohormone. The difference between our studies and previous studies lies in the use of sedation with sevoflurane in the postoperative period. The results could be related to a prolonged effect, in addition to preconditioning and postconditioning, which could enhance the cardioprotective effect of sevoflurane in the postoperative period. With this review, we aim to clarify the importance of various mechanisms involved in preconditioning and postconditioning with halogenated gases, as supported by our studies.

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“…The inhibition of one pathway may thus be compensated for by the upregulation of the other. This may be of particular clinical significance in patients with HF who are known to have endothelial dysfunction and thus reduced or loss of NO pathway …”

Section: Clinical Effectiveness Of Activating Specific Natriuretic Pementioning

confidence: 99%

“…This may be of particular clinical significance in patients with HF who are known to have endothelial dysfunction and thus reduced or loss of NO pathway. [70][71][72][73][74][75][76]…”

Section: Clinical Effectiveness Of Activating Specific Natriuretic Pementioning

confidence: 99%

B‐type natriuretic peptide and heart failure: what can we learn from clinical trials?

Binoun-A-Egom

Andreas

Klimas

et al. 2015

Clin Exp Pharma Physio

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SUMMARYThe B-type natriuretic peptide (BNP) may favour natriuresis and diuresis, making it an ideal drug to aid in diuresing a fluid-overloaded patient with poor or worsening renal function. Several randomized clinical trials have tested the hypothesis that infusions of pharmacological doses of BNP to acute heart failure (HF) patients may enhance decongestion and preserve renal function in this clinical setting. Unfortunately, none of these has resulted in a better outcome. The current challenge for BNP research in acute HF lies in a failure of concept and reluctance to abandon a demonstrably ineffectual research model. Future success will necessitate a detailed understanding of the mechanism of action of BNP as well as a better integration of basic and clinical science.

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Adjuvant Cardioprotection in Cardiac Surgery: Update

Cited by 11 publications

References 118 publications

Protective effect of active perfusion in porcine models of acute myocardial ischemia

Protective effect of active perfusion in porcine models of acute myocardial ischemia

Cardioprotection with halogenated gases: how does it occur?

B‐type natriuretic peptide and heart failure: what can we learn from clinical trials?

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