Chaoyi Qin

Release of mitochondrial DNA correlates with peak inflammatory cytokines in patients with acute myocardial infarction.

Objective: The present study is an exploration of the dynamic changes of plasma mitochondrial deoxyribonucleic acid (mtDNA) and inflammatory level in patients with acute myocardial infarction (MI). Methods: Thirty-eight patients with acute MI and 33 control participants were included in the study. Blood samples were collected on admission, 12 hours post-percutaneous coronary intervention (PCI), 24 hours post-PCI, and 48 hours post-PCI. White blood cell (WBC) count and C-reactive protein (CRP) level were determined. Plasma was isolated from whole blood. Plasma mtDNA was measured using real-time polymerase chain reaction, and tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) were measured using enzyme-linked immunosorbent assay kits. Bivariate correlation analysis was used to find correlation between plasma mtDNA and inflammatory level on admission. Results: Plasma mtDNA was significantly higher in patients with acute MI than controls on admission (p<0.01). Plasma mtDNA decreased significantly after PCI treatment (p=0.01). WBC count, TNF-α, IL-6 and CRP showed similar pattern: elevation after onset of acute MI and contraction after PCI treatment (p<0.05). Positive correlations between plasma mtDNA and WBC count (r=0.435; p<0.001), TNF-α (r=0.538; p<0.001), IL-6 (r=0.518; p<0.001), and CRP (r=0.524; p<0.001) were identified. Conclusion: Plasma mtDNA elevated after onset of acute MI and positive correlation was observed between plasma mtDNA and inflammatory level, suggesting that mtDNA may play a key role in inflammatory responses in patients with acute MI.

Rare case of left ventricular mesenchymal hamartoma

From the Department of Cardiovascular Surgery, West China Hospital, Sichuan University, Chengdu, Sichuan, People’s Republic of China. Drs L.L. and C.Q. contributed equally to this article. Disclosures: Authors have nothing to disclose with regard to commercial support. Received for publication Feb 11, 2017; revisions received Aug 14, 2017; accepted for publication Sept 9, 2017. Address for reprints: Yingqiang Guo, MD, Department of Cardiovascular Surgery, West China Hospital, Chengdu, Sichuan, People’s Republic of China, 610041 (E-mail: guoyingqianghuaxi@163.com). J Thorac Cardiovasc Surg 2017;-:1-5 0022-5223/

Potential Mechanism of Post-Acute Aortic Dissection Inflammatory Responses: The Role of mtDNA from Activated Platelets

36.00 Copyright 2017 by The American Association for Thoracic Surgery https://doi.org/10.1016/j.jtcvs.2017.09.051

Analysis of circulatory mitochondrial DNA level after cardiac surgery with cardiopulmonary bypass and potential prognostic implications.

Background: Acute aortic dissection (AD) is a lethal cardiovascular disease with severe inflammatory complications. Considering the proinflammatory properties of plasma mitochondrial DNA (mtDNA), we postulate that plasma mtDNA from activated platelets may be responsible for post-acute AD inflammatory responses. Methods: We consecutively enrolled 68 patients with acute AD as well as matched hypertensive and healthy participants. Blood samples were collected on admission for blood routine tests, mtDNA assay, and inflammatory cytokine analysis. A computed tomography scan was used to evaluate the extent of dissections. Results: Our results demonstrate that plasma mtDNA, platelet activation, and inflammatory levels were remarkably higher in acute AD patients than in hypertensive or healthy participants. These parameters were also higher in the Stanford A group than in the Stanford B group (p < 0.05). Bivariate correlation analysis demonstrated positive associations between mtDNA and inflammatory levels (tumor necrosis factor-α: r = 0.577; interleukin-6: r = 0.632), mtDNA and platelet activation (r = 0.642), and platelet activation and the extent of dissection (r = 0.635). Conclusion: Our study suggests that acute AD-induced tunica media exposure causes platelet activation, which leads to the initiation of inflammatory responses via the release of mtDNA into the circulation. Our study provides a novel fundamental basis and a potential therapeutic target for the prevention and treatment of post-AD inflammatory responses.

Epigallocatechin gallate attenuates mitochondrial DNA-induced inflammatory damage in the development of ventilator-induced lung injury

Our research letter found that circulatory mtDNA level increased after the end of CPB and positive correlations between mtDNA and peak CRP level, peak BNP level, and peak PCT level, which revealed the prognostic role of perioperative circulatory mtDNA level in patients who underwent cardiopulmonary bypass.

Bullet incarcerated in aortic root

OBJECTIVE We aim to investigate the role of mitochondrial DNA (mtDNA), a novel endogenous pro-inflammatory cytokine, in the development of ventilator-induced lung injury (VILI). Moreover, the protective effect of epigallocatechin gallate (EGCG) on VILI through inhibiting local mtDNA release was examined. METHODS From March 2015 to March 2016, bronchoalveolar lavage fluid (BALF) from 36 patients with VILI and well-matched 36 patients without VILI after major surgery were consecutively collected. The expression levels of mtDNA and inflammatory cytokines in BALF were tested. SD rats were divided into five groups: control, low tidal volume (7 ml/kg) group, high tidal volume (HTV, 40 ml/kg) group, HTV+low dose EGCG and HTV+high dose EGCG groups. BALF were collected to examine the expression levels of mtDNA and several inflammatory cytokines and the lung tissue was harvested for pathological examinations. In addition, cyclic stretch cell culture was used and culture media was collected to analyze expressions of inflammatory cytokines. Administration of mtDNA in a rat model and in vitro cell culturing were used to confirm its pro-inflammatory properties in the development of inflammatory lung injury. RESULTS A Significant elevation of mtDNA was detected in BALF from patients with VILI (581 ± 193 vs. 311 ± 137, p < 0.05) and also in rats ventilated with HTV. EGCG could significantly inhibit HTV-induced local mtDNA release and attenuate the level of inflammatory lung injuries (reduced infiltration of local inflammatory cells, lower lung wet/dry ratio and expression levels of inflammatory cytokines). The beneficial effects of EGCG on preventing inflammatory lung injuries were in a concentration-dependent manner. Meanwhile, higher expression levels of mtDNA and inflammatory cytokines were observed in the media of cyclic stretched cell culture compared to those in the control group (p < 0.05). Furthermore, intra-tracheal administration of mtDNA in rats could lead to a marked increase of local inflammatory cytokines and subsequent inflammatory lung injuries (p < 0.05). And by adding mtDNA into the cell culture, higher level of inflammatory cytokines in the media was detected (p < 0.05). EGCG also showed preventive effects on inflammatory responses on a concentration-dependent manner (p < 0.05). CONCLUSION The increased expression level of mtDNA and subsequent inflammatory cytokines overproduction may play an important role in the development of VILI. EGCG may be a potential novel therapeutic candidate for protection against VILI by inhibiting the local release of mtDNA.

Multiple images of pacemaker-related endocarditis and superior vena cava syndrome

A 47-year-old man was admitted to our emergency department with thoracic gunshot after 11 h. He complained no dizzy, headache, or short of breath. Physical examinations showed an …

Variation of perioperative plasma mitochondrial DNA correlate with peak inflammatory cytokines caused by cardiac surgery with cardiopulmonary bypass

A 32-year-old male was referred to our institution after developing a persistent fever and symptomatic superior vena cava (SVC) obstruction following implantation of a dual-chamber cardiac pacemaker 4 years earlier due to sick sinus syndrome (Fig. 1a). The physical examination was remarkable for swelling of the face, neck, and right arm and varicosities at the surface of the skin around the upper body. Three-dimensional volume-rendered images demonstrated numerous dilated superficial veins over the right chest (Fig. 1b). Contrast enhanced computed tomography (Fig. 1c) and venography (Fig. 1d, Video 1) revealed occlusion of SVC and brachiocephalic vein. Transesophageal echocardiography (TEE) further confirmed the obstruction of SVC due to a solid mass (Fig. 1e, Video 2), part of which was located at the right atrium and prolapsed into the right ventricle during diastole (Fig. 1f, Video 3). The patient underwent surgical intervention with the aid of cardiopulmonary bypass. After opening the right atrium, a 40x40x60 mm grey-yellowish mass attached to the pacing leads was identified (Fig. 1g). The mass within the atrial chamber was then completely excised (Fig. 1h-j, Video 4), and no vegetation or thrombus was observed at the tip of the ventricular lead. A new dual-chamber pacemaker with permanent epicardial pacing leads was implanted after the removal of the infected previous pacemaker and intracardiac wires (Fig. 1k). Histopathological examinations of the mass showed a mixture of thrombotic and fibrotic tissues, and cultures yielded no growth (Fig. 1l). Multiple images of pacemaker-related endocarditis and superior vena cava syndrome