Symbiotic combination of Akkermansia muciniphila and inosine alleviates alcohol-induced liver injury by modulating gut dysbiosis and immune responses.

Background: Alcoholic liver disease (ALD) is exacerbated by disruptions in intestinal microecology and immune imbalances within the gut-liver axis. The present study assesses the therapeutic potential of combining Akkermansia muciniphila (A. muciniphila) with inosine in alleviating alcohol-induced liver injury. Methods: Male C57BL/6 mice, subjected to a Lieber-DeCarli diet with 5% alcohol for 4 weeks, served as the alcoholic liver injury model. Various analyzes, including quantitative reverse transcription polymerase chain reaction (qRT-PCR), ELISA, immunochemistry, 16S rRNA gene sequencing, and flow cytometry, were employed to evaluate liver injury parameters, intestinal barrier function, microbiota composition, and immune responses. Results: Compared to the model group, the A. muciniphila and inosine groups exhibited significantly decreased alanine aminotransferase, aspartate aminotransferase, and lipopolysaccharide (LPS) levels, reduced hepatic fat deposition and neutrophil infiltration, alleviated oxidative stress and inflammation, and increased expression of intestinal tight junction proteins (Claudin-1, Occludin, and ZO-1). These effects were further pronounced in the A. muciniphila and inosine combination group compared to individual treatments. While alcohol feeding induced intestinal dysbiosis and gut barrier disruption, the combined treatment reduced the abundance of harmful bacteria (Oscillibacter, Escherichia/Shigella, and Alistipes) induced by alcohol consumption, promoting the growth of butyrate-producing bacteria (Akkermansia, Lactobacillus, and Clostridium IV). Flow cytometry revealed that alcohol consumption reduced T regulatory (Treg) populations while increasing those of T-helper (Th) 1 and Th17, which were restored by A. muciniphila combined with inosine treatment. Moreover, A. muciniphila and inosine combination increased the expression levels of intestinal CD39, CD73, and adenosine A2A receptor (A2AR) along with enhanced proportions of CD4+CD39+Treg and CD4+CD73+Treg cells in the liver and spleen. The A2AR antagonist KW6002, blocked the beneficial effects of the A. muciniphila and inosine combination on liver injury in ALD mice. Conclusion: This study reveals that the combination of A. muciniphila and inosine holds promise for ameliorating ALD by enhancing the gut ecosystem, improving intestinal barrier function, upregulating A2AR, CD73, and CD39 expression, modulating Treg cells functionality, and regulating the imbalance of Treg/Th17/Th1 cells, and these beneficial effects are partly A2AR-dependent.

Identification of key immune-related genes associated with LPS/D-GalN-induced acute liver failure in mice based on transcriptome sequencing.

Background: The aim of this study was to identify key immune-related genes in acute liver failure (ALF) by constructing an ALF mouse model for transcriptome sequencing. Methods: The C57BL/6 mouse with ALF model was induced by lipopolysaccharide (LPS)/ D-galactosamine (D-GalN). After successful modelling, the liver tissues of all mice were obtained for transcriptome sequencing. The key immune-related genes in mice with ALF were identified by differential expression analysis, immune infiltration analysis, weighted gene co-expression network analysis (WGCNA), enrichment analysis, and protein-protein interaction (PPI) analysis. Results: An LPS/D-GalN-induced ALF mouse model was successfully constructed, and transcriptome sequencing was performed. Significant differences in the proportions of monocytes, macrophages M0, macrophages M1 and neutrophils were shown by immune infiltration analysis, and 5255 genes highly associated with these four immune cells were identified by WGCNA. These immune genes were found to be significantly enriched in the TNF signalling pathway by enrichment analysis. Finally, PPI analysis was performed on genes enriched in this pathway and three key genes (CXCL1, CXCL10 and IL1B) were screened out and revealed to be significantly upregulated in ALF. Conclusions: Key immune-related genes in ALF were identified in this study, which may provide not only potential therapeutic targets for treating ALF and improving its prognosis, but also a reliable scientific basis for the immunotherapy of the disease.

Prognostic and diagnostic accuracy of intracoronary electrocardiogram recorded during percutaneous coronary intervention: a meta-analysis.

OBJECTIVE: Intracoronary ECG (IC-ECG) recording has been shown to be sensitive and reliable for detecting myocardial viability and local myocardial ischaemia in some studies. But IC-ECG is neither widely used during percutaneous coronary intervention (PCI) nor recommended in guidelines. This up-to-date meta-analysis of published studies was conducted to evaluate the prognostic and diagnostic accuracy of IC-ECG recorded during PCI. METHODS: Relevant studies were identified by searches of MEDLINE until 19 June 2021. Observational and diagnostic studies which reported the prognostic or diagnostic accuracy of IC-ECG were included. Data were extracted independently by two authors. Summary estimates of clinical outcomes were obtained using a random effects model. Summary diagnostic accuracy was obtained by using a Bayesian bivariate random effects model. RESULTS: Of the 12 included studies, 7 studies reported the clinical outcomes (821 patients) and 6 studies reported the diagnostic accuracy (485 patients) of IC-ECG. The pooled ORs with 95% CIs of ST-segment elevation recorded by IC-ECG were 4.65 (1.69 to 12.77), 5.08 (1.10 to 23.44), 4.53 (0.79 to 25.90) and 1.83 (0.93 to 3.62) for major adverse cardiac events, myocardial infarction, cardiac death and revascularisation, respectively. The weighted mean difference were 6.49 (95% CIs 3.84 to 9.14) for ejection fraction when ST-segment resolution was recorded, and 0.86 (95% CIs -8.55 to 10.26) when ST-segment elevation was recorded. The pooled sensitivity and specificity of ST-segment elevation were 0.78 (95% credibility intervals 0.64 to 0.89) and 0.87 (95% credibility intervals 0.75 to 0.94), respectively. CONCLUSIONS: These findings provide quantitative data supporting that IC-ECG had promising diagnostic ability for local myocardial injury, and could predict clinical outcomes.

Novel variant in BRAT1 with the lethal neonatal rigidity and multifocal seizure syndrome.

BACKGROUND: Lethal neonatal rigidity and multifocal seizure syndrome (RMFSL) is caused by variants in BRAT1 (BRCA1-associated protein required for ATM activation-1). However, the molecular mechanism of RMFSL is still unclear. METHODS: An RMFSL infant was recruited and the peripheral blood samples from his trio-family were collected. The genomic DNA was extracted, and then the whole-exome sequencing was performed. The expression of BRAT1 was analyzed by Western blotting. The subcellular localization of BRAT1 and MitoSOX (mitochondrial superoxide level) was investigated by confocal microscopy. The RNA samples were obtained from transfected cells, and then the RNA sequencing was performed. RESULTS: In this study, a novel homozygous BRAT1 variant c.233G > C with amino acid change of R with P at residue 78 (R78P) was identified. This variant altered the peptide structure and subcellular localization, as well as the expression in vitro. However, R78P did not alter the ability of BRAT1 to downregulate MitoSOX in mitochondria. Meanwhile, R78P BRAT1 was positively correlated with temporal lobe epilepsy, autosomal recessive primary microcephaly, defective/absent horizontal voluntary eye movements, and neuron apoptotic process as indicated by gene set enrichment analysis (GSEA). CONCLUSIONS: The BRAT1 variant spectrum has been expanded, which will be helpful for genetic counseling. We also explored the molecular mechanism altered by R78P, which will provide a better understanding of the pathogenesis of RMFSL. IMPACT: The detailed course of an infant with lethal neonatal RMFSL was depicted. A novel disease-causing variant R78P in BRAT1 for lethal neonatal RMFSL was identified. R78P led to reduced BRAT1 expression and nuclear localization in vitro. R78P did not alter the ability of BRAT1 to downregulate MitoSOX in the mitochondria. The variant R78P in BRAT1 was positively correlated with temporal lobe epilepsy, autosomal recessive primary microcephaly, defective/absent horizontal voluntary eye movements, and neuron apoptotic process as indicated by GSEA.

Predictive value of early amplitude integrated electroencephalogram (aEEG) in sleep related problems in children with perinatal hypoxic-ischemia (HIE).

BACKGROUND: While great attention has been paid to motor and cognitive impairments in children with neonatal Hypoxic-Ischemic Encephalopathy (HIE), sleep related circadian rhythm problems, although commonly present, are often neglected. Subsequently, no early clinical indicators have been reported to correlate with sleep-related circadian dysfunction during development. METHODS: In this study, we first analyzed patterns of the amplitude integrated electroencephalogram (aEEG) in a cohort of newborns with various degrees of HIE. Next, during follow-ups, we collected information of sleep and circadian related problems in these patients and performed correlation analysis between aEEG parameters and different sleep/circadian disorders. RESULTS: A total of 101 neonates were included. Our results demonstrated that abnormal aEEG background pattern is significantly correlated with circadian rhythmic (r = 0.289, P = 0.01) and breathing issues during sleep (r = 0.237, P = 0.037). In contrast, the establishment of sleep-wake cycle (SWC) showed no correlation with sleep/circadian problems. Detailed analysis showed that summation of aEEG score, along with low base voltage (r = 0.272, P = 0.017 and r = -0.228, P = 0.048, respectively), correlates with sleep circadian problems. In contrast, background pattern (BP) score highly correlates with sleep breathing problem (r = 0.319, P = 0.004). CONCLUSION: Abnormal neonatal aEEG pattern is correlated with circadian related sleep problems. Our study thus provides novel insights into predictive values of aEEG in sleep-related circadian problems in children with HIE.

Inhibiting MicroRNA-497 Improves the Effects of Exercise Training on Myocardial Infarction.

Exercise training (ET) could improve myocardial infarction (MI), and microRNA-497 is highly associated with MI. This study aimed to investigate whether the regulation of miR-497 is involved in the positive effects of ET on MI. MI rat models induced by left anterior descending (LAD) were subjected to interval training and infarct size was observed. Blood and myocardial samples were collected from the rats for determining the expressions of miR-497. To evaluate the functions of miR-497, miR-497 agomir and antagomir were injected accordingly into grouped rats during ET, and subsequently, the expressions of apoptotic and inflammatory factors were determined. ET reduced the infarct size in MI rats and inhibited the levels of miR-497. MiR-497 agomir injection enlarged the infarct size, and reversed the shrunk infarct size induced by ET. However, miR-497 antagomir further promoted the positive effect on MI improved by ET. Chloride voltage-gated channel 3 (CLCN3) was identified as the most possible target for miR-497. Moreover, ET improving MI also involved the regulation of apoptotic and inflammatory factors. The mechanisms underlying the positive effects of ET on MI were highly associated with the regulation of miR-497.

Predictive value of serum myostatin for the severity and clinical outcome of heart failure.

BACKGROUND: The exact relationship between serum myostatin and the severity and prognosis of chronic heart failure (CHF) is unclear. In this study, we investigated the association between serum myostatin and the severity and prognosis in patients with CHF. METHODS: Two hundred and eighty-eight CHF patients and 62 healthy controls were studied. Cardiac ultrasound and serum myostatin, N-terminal pro-B-type natriuretic peptide (NT-proBNP) and other parameters were detected. CHF patients were divided into 3 groups according to tertiles of NT-proBNP or myostatin levels respectively. RESULTS: Serum myostatin levels were higher in CHF patients than in controls. New York Heart Association (NYHA) class IV patients had the highest levels of serum myostatin among the four NYHA classes. Compared with the low tertile NT-proBNP group, serum myostatin levels were significantly higher in the moderate and high tertile groups (15.47 ±â€¯4.25 vs. 14.18 ±â€¯3.69 ng/mL, p = .026; 16.28 ±â€¯5.34 vs. 14.18 ±â€¯3.69 ng/mL, p = .002). During 51-months follow-up, of 173 patients there were 36 deaths. Compared to survivors, nonsurvivors had significantly higher serum myostatin (18.11 ±â€¯4.52 vs. 14.85 ±â€¯5.11 ng/mL, p < .01). Patients in the high tertile myostatin group had lower survival rate (73.95% vs. 93.75%; p < .05) and larger number of CHF rehospitalization than those in the low tertile group. Cox regression analysis showed that serum myostatin was an independent predictor of mortality. CONCLUSIONS: Serum myostatin levels can reflect the severity of CHF and be a predictor of adverse prognosis in CHF patients.

Serum Peroxisome Proliferator-activated Receptor Gamma Coactivator-1α Related to Myocardial Energy Expenditure in Patients With Chronic Heart Failure.

BACKGROUND: Peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) plays key roles in controlling cardiac metabolism and function. Myocardial energy expenditure (MEE) can reflect myocardial energy metabolism and cardiac function. Whether the variation of PGC-1α can influence MEE levels in chronic heart failure (CHF) is unclear. Therefore, we investigated the relationship between PGC-1α and MEE. MATERIAL AND METHODS: We studied 219 patients with CHF and 66 healthy controls. MEE was measured according to echocardiographic parameters. Serum PGC-1α, N-terminal pro-B-type natriuretic peptide and other parameters were detected. Patients with CHF were divided into different groups according to the left ventricular ejection fraction (LVEF) and the tertile range of MEE. RESULTS: Serum PGC-1α was lower in the MEE 2 and 3 groups compared with controls (both P < 0.05). Patients in the MEE 2 (1.73 ± 0.83 versus 2.16 ± 0.82 ng/mL, P = 0.001) and 3 groups (1.65 ± 0.73 versus 2.16 ± 0.82 ng/mL, P < 0.001) possessed lower levels of PGC-1α than those in the MEE 1 group. Compared with high LVEF, patients with low LVEF had higher MEE (median, 167 versus 73 cal/minute, P < 0.05) and lower PGC-1α (1.71 ± 0.65 versus 1.95 ± 0.91 ng/mL, P = 0.032). Multivariate logistic regression analysis showed that MEE (OR = 0.517, 95% CI = 0.267-0.998, P = 0.049) and creatinine (OR = 2.704, 95% CI = 1.144-6.391, P = 0.023) were independently associated with increased PGC-1α. CONCLUSIONS: Serum PGC-1α was related to MEE and LVEF in patients with CHF and can reflect the degree of MEE and the systolic function of the left ventricle.

Association of ACE2 polymorphisms with susceptibility to essential hypertension and dyslipidemia in Xinjiang, China.

BACKGROUND: Cardiovascular benefits by reversing environmental risks factors for essential hypertension (EH) and dyslipidemia could be weaken by high genetic risk. We investigated possible associations between ACE2 polymorphisms and dyslipidemia in patients with EH. METHODS: Four hundred and two hypertensive patients were enrolled in an EH group and 233 normotensive individuals were enrolled as control group from the Xinjiang region of China. Fourteen ACE2 polymorphisms were genotyped by Matrix-assisted laser desorption ionization time-of-flight mass spectrometry. RESULTS: Participants carrying T allele (TT + CT) of rs2074192 (P = 0.006), rs4646155 (P = 0.030) and rs4646188 (P < 0.001), C allele (CT + CT or CC + CG) of rs4240157 (P = 0.012), rs4830542 (P = 0.020) and rs879922 (P < 0.001) and TT genotype of rs2106809 (P = 0.012) were associated with EH. Meanwhile,ACE2 SNPs also exhibited association with dyslipidemia but exhibited obvious heterogeneity. rs1978124 (TT + CT, P = 0.009), rs2106809 (TT, P = 0.045), rs233575 (CC + CT, P = 0.018), rs4646188 (CC, P = 0.011) and rs879922 (CC + CG, P = 0.003) were association with increased LDL-C (≥1.8 mmol/L). rs2106809 (CC + CT, P < 0.001), rs2285666(TT + CT, P = 0.017), rs4646142(CC + CG, P = 0.044), rs4646155(TT + CT, P < 0.001) and rs4646188(TT + CT, P = 0.033) were association with decreased HDL-C (< 1.0 mmol/L). rs2074192 (TT + CT, P = 0.012), rs4240157 (CC + CT, P = 0.027), rs4646156 (AA+AT, P = 0.007), rs4646188 (TT + CT, P = 0.005), rs4830542 (CC + CT, P = 0.047) and rs879922 (CC + CG, P = 0.001) were association with increased TC (≥5.2 mmol/L). rs2106809 (P = 0.034) and rs4646188 (P = 0.013) were associated with hypertriglyceridemia. Further, ischemic stroke was more prevalent with rs4240157 (CC + CT, P = 0.043), rs4646188 (CC + CT, P = 0.013) and rs4830542 (CC + CT, P = 0.037). In addition, rs2048683 and rs6632677 were not association with EH, dyslipidemia and ischemic stroke. CONCLUSION: The ACE2 rs4646188 variant may be a potential and optimal genetic susceptibility marker for EH, dyslipidemia and its related ischemic stroke.

[Attenuation rules and germicidal efficacy of ozoneted water].

OBJECTIVE: To determine initial concentrations of ozonated water under different temperatures, attenuation rules of ozonated water under the room temperature (25 ℃), and to inspect the effects of ozonated water under different concentrations on common microorganisms.
 Methods: The online test method and the plate cultivation method were employed to check the concentrations and killing rates on common microorganisms of ozonated water produced by HZ-2601 B Ozone Water Generating Instrument.
 Results: The initial concentrations of ozonated water at 20, 25, 30, 35, and 40 ℃ were 4.38, 4.26, 3.12, 2.76, and 1.31 mg/L, respectively. The ozonated water was rapidly attenuated at first 10 min. The concentration of ozonated water still remained at 1.06 mg/L and 0.37 mg/L at 25 and 30 ℃ after 30 min. The average killing rates for Pseudomonas aeruginosa, Escherichia coli, Staphylococcus aureus, methicillin-resistant Staphylococcus aureus, and Candida albicans in 1.0 mg/L ozonated water for 1 min were 99%, 100%, 100%, 100%, and 100%, respectively. The average killing rates of Escherichia coli, Staphylococcus aureus, methicillin-resistant Staphylococcus aureus, Pseudomonas aeruginosa, and Candida albicans in 0.3 mg/L ozonated water for 1 min were 100%, 100%, 100%, 95%, and 92%, respectively.
 Conclusion: The initial concentrations of ozonated water produced by HZ-2601 B Ozone Water Generating Instrument decrease with the increase of temperature. Ozonated water under 20-30 ℃ has good sterilization effect on common microorganisms.

[Effect of ozone on Staphylococcus aureus colonization in patients with atopic dermatitis].

OBJECTIVE: To verify the effect of ozone on Staphylococcus aureus (S. aureus) colonization in patients with atopic dermatitis (AD) and its correlation with the patient's status.
 Methods: A total of 12 patients with moderate or severe AD, aged from 6 to 65 years, were recruited from outpatient of the Third Xiangya Hospital. The treatment sides were showered with ozonated water and smeared with ozonated oil for 7 days (twice a day), while the control sides were washed with warm running water and smeared with base oil. At different time points, the severity scoring of atopic dermatitis (SCORAD) scores, sleep and pruritus scores were assessed and compared between the two sides. Meanwhile, plate cultivation was used to quantitatively detect the changes of S. aureus colonization in skin lesions.
 Results: After 7 days treatment, erythema and pimples were decreased in the treatment sides. The clear skin texture, smooth skin, improved skin lesions were also observed by dermoscopic examination. The results of reflectance confocal microscopy (RCM) demonstrated that the parakeratosis was improved, the structures were clearer, and the inflammatory cells infiltration was reduced after ozone treatment for 7 days. After ozone treatment for 3 and 7 days, the S. aureus colonization in the treatment sides decreased by (75.55±21.81)% and (97.24±2.64)% respectively. Compared to that of control sides, the percentage of S. aureus colony after ozone treatment for 7 days decreased significantly (P<0.01). After ozone treatment for 7 days, the SCORAD scores, sleep and pruritus scores were significantly decreased (all P<0.01). There was a linear correlation between the decreasing percentage of S. aureus colony and the declining percentage of SCORAD scores in AD patients.
 Conclusion: Topical ozone therapy can effectively reduce S. aureus colony in skin lesions and alleviate the severity of AD patients with moderate to severe degree.

[Topical ozone application: An innovative therapy for infantile atopic dermatitis].

OBJECTIVE: To evaluate the clinical efficacy and safety of the innovative topical ozone therapy for infantile atopic dermatitis.
 Methods: Sixty children with atopic dermatitis were divided into a treatment group and a control group. The treatment group was showered with ozonated water (3-5 times a week) and smeared with ozonated oil (twice a day), while the control group was washed with warm running water and smeared with base oil, adding moisturizer if necessary. The treatment course was 2 weeks. Efficacy and side effect were evaluated.
 Results: The skin exudation was reduced and erosion was healing after 3-5 days topical ozone therapy for infantile atopic dermatitis. The effective rates were 80.0% and 20.0% in the treatment group and control group for 1 week, and 89.6% and 30.7% for 2 weeks, respectively, with significant difference between the 2 groups (P<0. 001).
 Conclusion: Innovative treatment of infantile atopic dermatitis with topical ozone application is safe and effective, which is worth popularizing in clinic.

[Topical ozone therapy: An innovative solution to patients with herpes zoster].

OBJECTIVE: To observe the clinical efficacy and safety of topical ozone therapy for patients with herpes zoster by reflectance confocal microscopy (RCM).
 Methods: A total of 60 patients with herpes zoster were divided into a control group and an ozone treatment group (n=30). In the control group, patients took oral valacyclovir tablets or granules (0.3 g per day, three times a day) and they were subjected to local weak laser irradiation treatment plus topical 2% mupirocin ointment twice a day. In the ozone group, the treatment is same as the control group except mupirocin ointment was replaced with topical ozone treatment (hydrotherapy every day plus ozonated oil twice a day). The clinical symptoms, discoid cell and adverse reactions were observed and taken records at day 0, 3, 7 and 14. Statistical analysis was performed to compare the clinical efficacy between the 2 groups. 
 Results: On the seventh day of treatment, the discoid cells of the ozone group disappeared, and the difference between the control group and the ozone group was statistically significant (P<0.05). The difference of decreased percentage of pain scores at each time point between the 2 groups was statistically significant (P<0.05). The clinical efficacy was 100% in the ozone group and 86.7% in the control group, with significant difference between the 2 groups (P<0.05).
 Conclusion: Topical ozone therapy in patients with herpes zoster is helpful in relieving pain, shortening the course as well as improving the clinical efficacy without obvious adverse reactions. It is worth to be popularized.

The clinical experience of double-orifice tricuspid valve.

BACKGROUND AND AIM OF THE STUDY: Double-orifice tricuspid valve (DOTV) is an extremely rare congenital anomaly. By analysing the feature of its diagnosis and surgical treatment, we want to summarise the clinical experience of treating DOTV. MATERIALS AND METHODS: Review two cases of DOTV treated by us between August 2009 and December 2011. One case was diagnosed as partial atrioventricular septum defect, and the other was tetralogy of Fallot. The defects were both identified during the operation for other congenital cardiac malformations and both accessory orifices were normal. But one of them was sutured because of its possible effect in future. RESULTS: Cardiac colour Doppler echocardiogram was made at three to five days after operation and all results were normal. No operative complication or late deaths occurred. The time of follow-up were one month, three months, six months, one year and two years after operation, and all examinations were normal. CONCLUSIONS: The accessory orifice of DOTV patients has its own independent chordae tendinea and mastoid muscle. So the gap of tricuspid valve should be excluded and the classification should be amended according to it. It should be surgically treated, when there is of dysfunction with it or potential harmful effect in sequent treatment.

Altered serum creatine kinase level and cardiac function in ischemia-reperfusion injury during percutaneous coronary intervention.

BACKGROUND: Myocardial ischemia-reperfusion injury (MIRI) resulting from primary percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI) is considered harmful to the patient, but its clinical significance remains unclear. This study explored the relationship of cardiac function examined by echocardiography and serum creatine kinase (CK) and CK-MB levels with MIRI in a cohort of Chinese AMI patients. MATERIAL/METHODS: We retrospectively analysed the clinical and angiographic data in 228 AMI patients in whom the infarct-related artery (IRA) was successfully recanalized by primary PCI. Cardiac function was evaluated by use of echocardiography before discharge from hospital. RESULTS: The in-hospital mortality rate in the MIRI group was 13.4% (16/119), which was significantly higher than the 4.6% (5/109) mortality rate in the non-MIRI group (P=0.021). The median of peak serum CK level was remarkably lower in the suppression-type MIRI group than in the non-MIRI group. There were no significant differences in the peak serum CK or CK-MB levels between the irritation-type MIRI group and the non-MIRI group. The peak CK and CK-MB levels were significantly higher in the no-reflow-type MIRI group than in the non-MIRI group. Left ventricular ejection fraction in the no-reflow-type MIRI group was significantly lower than in the non-MIRI group; left ventricular end-diastolic volume was significantly higher than in the irritation-type MIRI subgroup; and left ventricular end-systolic volume was greater than that in non-MIRI group and suppression-type MIRI group. CONCLUSIONS: MIRI (especially the no-reflow type) may lead to acute hemodynamic disorders and increase the mortality rate. However, suppression- and irritation-type MIRI may imply the existence of surviving myocardium.

Determinants and prognostic implications of reperfusion injury during primary percutaneous coronary intervention in Chinese patients with acute myocardial infarction.

BACKGROUND: The poor clinical outcome in acute myocardial infarction (AMI) patients undergoing primary percutaneous coronary intervention (PCI) has been attributed to myocardial ischemia-reperfusion injury (MIRI). OBJECTIVE: This study aimed to identify the predictive factors of MIRI during PCI in Chinese AMI patients with or without ST-segment elevation. METHODS: Clinical and angiographic data of 228 patients in whom the infarct-related artery (IRA) was successfully recanalized by primary PCI were retrospectively analyzed. Multiple logistic regressions were used. RESULTS: Compared with non-MIRI group (n=109), patients with MIRI (n=119) were characterized by more inferior infarct location, shorter ischemic duration, more frequently right coronary artery as IRA, more lesion vessels, more often thrombolysis in myocardial infarction (TIMI) 0 flow in IRA prior to PCI, less preinfarction angina, and more renal insufficiency. Ischemic time

[Reperfusion arrhythmias in acute myocardial infarction do not enhance myocardial injury].

OBJECTIVE: To investigate the clinical implications of reperfusion arrhythmias during primary percutaneous coronary intervention (PCI) for patients with acute myocardial infarction (AMI). METHODS: Data from 228 AMI patients in whom the infarct-related artery (IRA) were successfully recanalized by primary PCI were retrospectively analyzed. The 228 patients were divided into 2 groups: myocardial ischemia-reperfusion injury (MIRI) group (n=119) in whom MIRI events occurred within minutes after successful recanalization of IRA, and non-MIRI group (n=109). The 119 patients in MIRI group were further divided into 3 subgroups: severe bradycardia with hypotension (brady-arrhythmia subgroup), lethal ventricular arrhythmias requiring electrical cardioversion (tachy-arrhythmia subgroup), and IRA antegrade flow less than or equal to TIMI 2 grade without angiographic evidence of abrupt closure (no-reflow subgroup). RESULTS: (1) Clinical and angiographic data: Compared with non-MIRI group, MIRI group was characterized by more inferior infarct location, shorter ischemic duration, more frequently right coronary artery as IRA, more diseased vessels, more often TIMI 0 grade of initial antegrade flow in IRA, less pre-infarction angina, more renal insufficiency, and higher in-hospital mortality (13.4% vs. 4.6%, P=0.021). (2) The peak CK level was remarkably lower in brady-arrhythmia subgroup than that in non-MIRI group (2010 IU/L vs. 2521 IU/L, P=0.039). The peak CK or CK-MB level was notably higher in no-reflow subgroup than in non-MIRI group (4573 IU/L, 338 IU/L, respectively, P=0.000). (3) Left ventricular ejection fraction in no-reflow subgroup was significantly lower than in non-MIRI group (38.7% +/- 8.3% vs. 51.2% +/- 8.1%, P=0.000), left ventricular end-diastolic volume in no-reflow subgroup was greater than that in tachy-arrhythmia subgroup [(135 +/- 32) ml vs. (105 +/- 19) ml, P=0.029]. CONCLUSION: Reperfusion arrhythmias may imply the existence of much survived myocardium and do not enhance myocardial damage, while no-reflow increases myocardial injury and induces permanent impairment of cardiac function.

[Analysis on correlative factors for occurrence of myocardial ischemia-reperfusion injury during primary percutaneous coronary intervention for acute myocardial infarction].

OBJECTIVE: To explore the risk and protective factors for the occurrence of myocardial ischemia-reperfusion injury (MIRI) during primary percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI). METHODS: Clinical and angiographic data of 228 AMI patients in whom the infarct-related arteries (IRA) were successfully revascularized by primary PCI were analyzed retrospectively. MIRI was defined if the following conditions existed after PCI: severe bradycardia with hypotension, or lethal ventricular arrhythmias requiring electrical cardioversion, or IRA antegrade flow < or = TIMI 2 grade flow without angiographic evidence of thrombus, emboli, dissection or spasm. Multivariate logistic regression was used to identify independent relative factors among 18 clinical and angiographic factors for occurrence of MIRI. RESULTS: Multivariate logistic regression analysis showed that independent risk factors for MIRI were the time intervals from AMI onset to IRA reflow < or = 6 h (P = 0.014), inferior infarction localization (P = 0.006), IRA antegrade flow prior to PCI < or = TIMI 1 grade (P = 0.028), multivessel lesions (P = 0.063) and renal insufficiency (P = 0.067). Pre-infarction angina was found to be an independent protective factor (P = 0.005). CONCLUSIONS: Short time intervals from AMI onset to IRA revascularization, inferior wall infarction location, low IRA antegrade flow prior to PCI, multivessel lesions and renal insufficiency may promote the occurrence of MIRI during primary PCI, whereas pre-infarction angina may be a cardioprotective factor attenuating MIRI.

[Effect of percutaneous coronary intervention on QT dispersion and its clinical implication in patients with acute myocardial infarction].

OBJECTIVE: To observe the effects of percutaneous coronary intervention (PCI) on QT dispersion (QTd) and explore its clinical significance in patients with acute myocardial infarction (AMI). METHODS: The electrocardiograms recorded before and one day after PCI were analyzed in 138 patients with AMI. The duration from the onset of AMI to PCI operation was less than 6 h in 72 patients and 6 to 12 h in the other patients. All the patients underwent emergency percutaneous transluminal coronary angioplasty and subsequent coronary stenting. QT intervals, QTd, and heart rate-corrected QT intervals (QTc) and QTd (QTcd) were measured and calculated. RESULTS: In both patient groups receiving PCI with delay shorter and longer than 6 h after AMI, QT and QTc after PCI were not significantly different from that before PCI, but the QTd and QTcd were remarkably decreased after PCI (all the P <0.01). Moreover, the QTd and QTcd in the patients with delay of PCI less than 6 h were significantly shorter than those in patients the with greater-than-6-hour delay (P<0.05), and the inhospital mortality was 4.2% and 7.6% in the two groups, respectively (P=0.394). CONCLUSION: Successful PCI may notably reduce QTd in the patients with AMI, whose earlier performance usually produces better effects.