Remote ischaemic preconditioning ameliorates sinus rhythm restoration rate through Cox maze radiofrequency procedure associated with inflammation reaction reduction

Jiang, Qin; Xiang, Bo; Wang, Haitao; Huang, Keli; Kong, Hong; Hu, Shengshou

doi:10.1007/s00395-019-0723-4

Cited by 28 publications

(27 citation statements)

References 33 publications

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“…Meanwhile, production of massive ROS is a well‐known harmful factor for heart tissue and inhibition of its production can limit mitochondrial damage and save the heart tissue (Akhnokh et al, 2016; Kastenschmidt et al, 2019). In addition, mitochondria recently have been regarded as a promising target for cardio‐protection in acute myocardial infarction (Ertracht, Malka, Atar, & Binah, 2014; Jiang et al, 2019). However, the relationship between ER stress and mitochondrial dysfunction during hypertension is still unknown (M. Cao, Long, et al, 2019; Song et al, 2019).…”

Section: Discussionmentioning

confidence: 99%

Bcl‐2‐associated athanogene 5 overexpression attenuates catecholamine‐induced vascular endothelial cell apoptosis

Zhu

Zhao

Chen

et al. 2020

Journal Cellular Physiology

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Bcl-2 associated athanogene 5 (Bag5) is a novel endoplasmic reticulum (ER) regulator. However, its role in catecholamine-induced endothelial cells damage has not been fully understood. In our study, catecholamine was used to mimic hypertensionrelated endothelial cell damage. Then, western blots, enzyme-linked immunosorbent assay, immunofluorescence, quantitative polymerase chain reaction and pathway analysis were conducted to analyze the role of Bag5 in endothelial cell damage in response to catecholamine. Our results indicated that the endothelial cell viability was impaired by catecholamine. Interestingly, Bag5 overexpression significantly reversed endothelial cell viability. Mechanistically, Bag5 overexpression inhibited ER stress, attenuated oxidative stress and repressed inflammation in catecholaminetreated endothelial cells. These beneficial effects finally contributed to endothelial cell survival under catecholamine treatment. Pathway analysis demonstrated that Bag5 was under the control of the mitogen-activated protein kinase (MAPK)-extracellular-signal-regulated kinase (ERK) signaling pathway. Reactivation of the MAPK-ERK pathway could upregulate Bag5 expression and thus promote endothelial cell survival through inhibiting oxidative stress, ER stress, and inflammation. Altogether, our results illustrate that Bag5 overexpression sustains endothelial cell survival in response to catecholamine treatment. This finding identifies Bag5 downregulation and the inactivated MAPK-ERK pathway as potential mechanisms underlying catecholamine-induced endothelial cell damage.

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Section: Discussionmentioning

confidence: 99%

Bcl‐2‐associated athanogene 5 overexpression attenuates catecholamine‐induced vascular endothelial cell apoptosis

Zhu

Zhao

Chen

et al. 2020

Journal Cellular Physiology

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“…The patients with coronary artery disease in one surgical ward from October 2017 through December 2017 were prospectively recruited and randomly assigned by computerized block randomization to receive "no-touch" (group A) or conventional (group B) SVGs harvest technique. 9) The emergency coronary bypass surgery, concomitant valve or aortic surgery, severe poor-quality SVGs, and ventricular aneurysm were excluded from the enrollment. All the included patients in this study had triple vessel disease and underwent the same procedure protocol that LIMA anastomosed to left anterior descending (LAD) artery and a sequential SVG onto the other three coronary arteries at the left side of heart with target runoff ≤2 mm.…”

Section: Methodsmentioning

confidence: 99%

Stable Hemodynamics within “No-Touch” Saphenous Vein Graft

Jiang

Yang

Sun

et al. 2020

ATCS

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Purpose: To investigate the hemodynamics characteristics of the "no-touch" saphenous vein graft (SVG) conduits by nicardipine intraluminal administration in vivo experiment. Methods: A total of 59 consecutive patients were enrolled and underwent a sequential SVG to three non-left anterior descending (LAD) targets with the average runoff ≤2 mm, 30 with "no-touch" harvest technique (group A) and 29 with conventional preparation (group B). The patients were subject to nicardipine intraluminal injection during offpump coronary artery bypass grafting (CABG) procedure. The intraoperative flow was measured with the ultrasonic transit time flow meter (TTFM), and the graft patency testified by multi-detector computed tomography (MDCT) angiography, respectively. Results: The baseline blood flow was higher in group A than that in group B (p <0.05). However, the increases in blood flow of SVG conduits in group A were lower than those in group B with 19.7 ± 5.9 vs. 35.4 ± 9.2 mL/min, 14.8 ± 5.6 vs. 23.1 ± 6.8 mL/min, 6.6 ± 2.1 vs. 11.2 ± 4.3 mL/min before the first, second, and third anastomose after nicardipine intraluminal administration, respectively (all p <0.01). Conclusions: No-touch SVGs were associated with higher baseline blood flow and less rises after nicardipine intraluminal administration during off-pump CABG procedure compared with conventional preparation. The no-touch SVGs seemed to be less spastic and well-tolerated on flow dilatation.

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“…After pooling the results of 30 trials of CABG or valve surgery, RIPC was found to reduce postoperative troponin release compared to the control arm [97]. Moreover, RIPC ameliorated sinus rhythm restoration up to 1 year after surgery and reduced postoperative markers of systemic inflammation in patients undergoing Cox maze radiofrequency ablation with concomitant mitral valve surgery [98].…”

Section: Clinical Studies Evaluating Remote Ischemic Conditioningmentioning

confidence: 99%

“…Other confounding factors that may contribute to the no effects of RIPC on cardioprotection in cardiac surgery patients include nitrates [75,98] and beta-adrenergic blocking agents [110,111,112,113,114]. However, a retrospective analysis of a randomized trial did not find any significant associations between age, gender, beta-adrenergic receptor blocking agents, angiotensin converting enzyme inhibitors, angiotensin receptor blockers, intraoperative nitroglycerine, and RIPC-induced cardioprotection during CABG [115].…”

Section: Clinical Studies Evaluating Remote Ischemic Conditioningmentioning

confidence: 99%

Perioperative Cardioprotection by Remote Ischemic Conditioning

Cho

2019

IJMS

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Remote ischemic conditioning has been investigated for cardioprotection to attenuate myocardial ischemia/reperfusion injury. In this review, we provide a comprehensive overview of the current knowledge of the signal transduction pathways of remote ischemic conditioning according to three stages: Remote stimulus from source organ; protective signal transfer through neuronal and humoral factors; and target organ response, including myocardial response and coronary vascular response. The neuronal and humoral factors interact on three levels, including stimulus, systemic, and target levels. Subsequently, we reviewed the clinical studies evaluating the cardioprotective effect of remote ischemic conditioning. While clinical studies of percutaneous coronary intervention showed relatively consistent protective effects, the majority of multicenter studies of cardiac surgery reported neutral results although there have been several promising initial trials. Failure to translate the protective effects of remote ischemic conditioning into cardiac surgery may be due to the multifactorial etiology of myocardial injury, potential confounding factors of patient age, comorbidities including diabetes, concomitant medications, and the coadministered cardioprotective general anesthetic agents. Given the complexity of signal transfer pathways and confounding factors, further studies should evaluate the multitarget strategies with optimal measures of composite outcomes.

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Remote ischaemic preconditioning ameliorates sinus rhythm restoration rate through Cox maze radiofrequency procedure associated with inflammation reaction reduction

Cited by 28 publications

References 33 publications

Bcl‐2‐associated athanogene 5 overexpression attenuates catecholamine‐induced vascular endothelial cell apoptosis

Bcl‐2‐associated athanogene 5 overexpression attenuates catecholamine‐induced vascular endothelial cell apoptosis

Stable Hemodynamics within “No-Touch” Saphenous Vein Graft

Perioperative Cardioprotection by Remote Ischemic Conditioning

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