Antiarrhythmic Efficacy of Neferine Assessed by Programmed Electrical Stimulation in a Canine Model of Electropharmacology

An ishemic ventricular tachyarrhythmias canine model was established in open-chest dogs subjected to programmed electrical stimulation (PES)for 5-8 days after acute myocardial infarction. The electrophysiologic effects of neferine (Nef) and procainamide (PA) were observed in this model. With routine methods of PES,ventricular tachycardia (VT)and ventricular fibrillation (VF) could be reproducibly initiated. Both drugs lengthened the QTc interval (P【0.01) and effective refractory period(ERP)of normal and ischemic ventricular myocardia (NERP and IERP) respectively (P【0.01), decreased the dispersion of ERP in ischemic myocardium and the dispersion of ERP in left ventricle (P【0.01), and increased the diastolic excitability threshold of normal and ischemic ventricular myocardia (P【0.01). The two compounds prevented the PES-induced VT or VF (Nef group P【0.01, PA group P【0.05) and ischemia-induced VF (P【0.05). The results indicated that neferine and procainamide may be effective in preventing the onset of reentrant ventricular tachyarrhythmias after myocardial ischemic damage in dogs.

Electrophysiologic-electropharmacologic Method for Evaluating the Effects of Antagonizing Ventricular Tachyarrhythmic Drugs

Objective To establish a canine model of electrophysiologic - electropharmacology as assessed by programmed electrical stimulation (PES),and to observe the electrophysiologic effects of Procainamide(PA) on normal and ischemic myocardium in case of ischemic ventricular tachyarrhythmia in this model. Methods A ishemic ventricular tachyarrhythmias canine model was established in open-chest dogs subjected to programmed electrical stimulation(PES)for 5-8 days after acute myocardial infarction. The electrophysiologic effects of procainamide were observed in this model. With routine methods of PES,ventricular tachycardia(VT) and ventricular fibrillation (VF) could be reproducibly initiated. Results Procainamide distinctly lengthened the QTc interval (P【0.01) and effective refractory period(ERP) of normal and ischemic ventricular myocardium(NERP and IERP) respectively (P【0.01), decreased the dispersion of ERP in ischemic myocardium and the dispersion of ERP in left ventricle (P【0.01), and increased the diastolic excitability threshold of normal and ischemic ventricular myocardium remarkably (P【0.01). Procainamide effectively prevented the PES-induced VT or VF (P【0.05) and ischemia-induced VF (P【0.05). Conclusion The results indicated that PES-induced VT/VF were highly reproducible and reliable, this canine model is a worthy and reliable one, procainamide may be effective in preventing the onset of VT and VF after myocardial ischemic damage, and deserves further attention as an antifibrillatory agent.

Electrophysiologic Effects of Sophoridine on a Canine Model of Ischemic Ventricular Tachyarrhythmias

A canine model of ischemic ventricular tachyarrhythmias was established in open-chest dogs subjected to programmed electrical stimulation (PES) for 5￣8 days after acute myocardial infarction. The electrophysiologic effects of sophoridine (Sop) and procainamide (PA) were observed in this canine model. With routine methods of PES, ventricular tachycardia (VT) and ventricular fibrilation (VF) could be reproducibly initiated in this model. Both drugs distinctly lengthened the QTc interval ( P <0.01) and the effective refractory period (ERP) in normal and ischemic ventricular myocardium ( P <0.01), decreased the dispersion of ERP in ischemic myocardium and the dispersion of ERP in left ventricle (P <0.05), and increased the diastolic excitability threshold of normal and ischemic ventricular myocardium remarkably ( P <0.01). Both drugs effectively prevented the PES-induced VT or VF and ischemia-induced VF ( P <0.05). The results indicated that this canine model is a good and reliable one, sophoridine and procainamide may be effective in preventing the onset of reentrant ventricular tachyarrhythmias after myocardial ischemic damage.

Optimal time for mesenchymal stem cell transplantation in rats with myocardial infarction

Background:Bone marrow mesenchymal stem cell (MSC) transplantation is a promising strategy in the treatment of myocardial infarction (MI). However, the time for transplanting cells remains controversial. The aim of this study was to find an optimal time point for cell transplantation. Methods: MSCs were isolated and cultured from Sprague-Dawley (SD) rats. MI model was set up in SD rats by permanent ligation of left anterior descending coronary artery. MSCs were directly injected into the infarct border zone at 1 h, 1 week and 2 weeks after MI, respectively. Sham-operated and MI control groups received equal volume of phosphate buffered saline (PBS). At 4 weeks after MI, cardiac function was assessed by echocardiography; vessel density was analyzed on hematoxylin-eosin stained slides by light microscopy; the apoptosis of cardiomyocytes was evaluated by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assay; the expressions of proteins were analyzed by Western blot. Results: MSC transplantation improved cardiac function, reduced the apoptosis of cardiomyocytes and increased vessel density. These benefits were more obvious in 1-week group than in 1-h and 2-week groups. There are more obvious in-creases in the ratio of bcl-2/bax and the expression of vascular endothelial growth factor (VEGF) and more obvious decreases in the expression of cleaved-caspase-3 in 1-week group than those in other two groups. Conclusion: MSC transplantation was beneficial for the recovery of cardiac function. MSC transplantation at 1 week post-MI exerted the best effects on increases of cardiac function, anti-apoptosis and angiogenesis.

Human bone marrow-derived mesenchymal stem cells transplanted into damaged rabbit heart to improve heart function

Objective: The present study was designed to test whether transplantation of human bone marrow-derived mesen- chymal stem cells (hMSCs) in New Zealand rabbits with myocardial infarction can improve heart function; and whether engrafted donor cells can survive and transdifferentiated into cardiomyocytes. Methods: Twenty milliliters bone marrow was obtained from healthy men by bone biopsy. A gradient centrifugation method was used to separate bone marrow cells (BMCs) and red blood cells. BMCs were incubated for 48 h and then washed with phosphate-buffered saline (PBS). The culture medium was changed twice a week for 28 d. Finally, hematopoietic cells were washed away to leave only MSCs. Human MSCs (hMSCs) were premarked by BrdU 72 h before the transplantation. Thirty-four New Zealand rabbits were randomly divided into myocardial infarction (MI) control group and cell treated group, which received hMSCs (MI+MSCs) through intramyocardial injection, while the control group received the same volume of PBS. Myocardial infarction was induced by ligation of the left coronary artery. Cell treated rabbits were treated with 5×106 MSCs transplanted into the infarcted region after ligation of the coronary artery for 1 h, and the control group received the same volume of PBS. Cyclosporin A (oral solution; 10 mg/kg) was provided alone, 24 h before surgery and once a day after MI for 4 weeks. Echocardiography was measured in each group before the surgery and 4 weeks after the surgery to test heart function change. The hearts were harvested for HE staining and immunohistochemical studies after MI and cell transplantation for 4 weeks. Results: Our data showed that cardiac function was significantly improved by hMSC transplan- tation in rabbit infarcted hearts 4 weeks after MI (ejection fraction: 0.695±0.038 in the cell treated group (n=12) versus 0.554±0.065 in the control group (n=13) (P<0.05). Surviving hMSCs were identified by BrdU positive spots in infarcted region and transdifferentiated into cardiomyocytes characterized with a positive cardiac phenotype: troponin I. Conclusion: Transplan- tation of hMSCs could transdifferentiate into cardiomyocytes and regenerate vascular structures, contributing to functional im- provement.

Early association of electrocardiogram alteration with infarct size and cardiac function after myocardial infarction

Objective: Myocardial infarction (MI) is the main cause of heart failure, but the relationship between the extent of MI and cardiac function has not been clearly determined. The present study was undertaken to investigate early changes in the electrocardiogram associated with infarct size and cardiac function after MI. Methods: MI was induced by ligating the left anterior descending coronary artery in rats. Electrocardiograms, echocardiographs and hemodynamic parameters were assessed and myocardial infarct size was measured from mid-transverse sections stained with Masson抯 trichrome. Results: The sum of pathological Q wave amplitudes was strongly correlated with myocardial infarct size (r = 0.920, P < 0.0001), left ventricular ejection fraction (r = -0.868, P < 0.0001) and left ventricular end diastolic pressure (r = 0.835, P < 0.0004). Furthermore, there was close relationship between MI size and cardiac function as assessed by left ventricular ejection fraction (r = -0.913, P < 0.0001) and left ventricular end diastolic pressure (r = 0.893, P < 0.0001). Conclusion: The sum of pathological Q wave amplitudes after MI can be used to estimate the extent of MI as well as cardiac function.

Correlation between growth differentiation factor-15 and collagen metabolism indicators in patients with myocardial infarction and heart failure

BackgroundGrowth differentiation factor （GDF）-15, a divergent member of the transforming growth factor beta super-family does appear to be up-regulated in response to experimental pressure overload and progression of heart failure （HF）. HF frequently develops after myocardial infarction （MI）, contributing to worse outcome. The aim of this study is to assess the correlation between GDF-15 levels and markers related to collagen turnover in different stages of HF.MethodsThe study consists of a cohort of 179 patients, including stable angina pectoris patients （AP group,n= 50）, old MI patients without HF （OMI group,n = 56）, old MI patients with HF （OMI-HF group,n= 38） and normal Control group （n = 35）. Both indicators reflecting the synthesis and degradation rates of collagen including precollagen I N-terminal peptide （PINP）, type I collagen carboxy-terminal peptide （ICTP）, precollagen III N-terminal peptide （PIIINP） and GDF-15 were measured using an enzyme-linked inmunosorbent assay.ResultsThe plasma GDF-15 level was higher in OMI-HF group （1373.4 ± 275.4 ng/L） than OMI group （1036.1 ± 248.6 ng/L）, AP group （784.6 ± 222.4 ng/L） and Control group （483.8 ± 186.4 ng/L） （P〈 0.001）. The indi-cators of collagen turnover （ICTP, PINP, PIIINP） all increased in the OMI-HF group compared with Control group （3.03 ± 1.02μg/Lvs. 2.08 ± 0.95μg/L, 22.2 ± 6.6μg/Lvs. 16.7 ± 5.1μg/L and 13.2 ± 7.9μg/Lvs. 6.4 ± 2.1μg/L, respectively;P〈 0.01）. GDF-15 positively cor-related with ICTP and PIIINP （r = 0.302,P〈 0.001 andr= 0.206,P= 0.006, respectively）. GDF-15 positively correlated to the echocardio-graphic diastolic indicators E/Em and left atrial pressure （r= 0.349 and r= 0.358, respectively;P〈 0.01）, and inversely correlated to the systolic indicators left ventricular ejection fraction and the average of peak systolic myocardial velocities （Sm） （r=-0.623 and r=-0.365, respectively;P〈 0.01）.ConclusionPlasma GDF-15 is associated with the indicators of type I and III collagen turnover.

Bone marrow mesenchymal stem cell transplantation combined with perindopril treatment attenuates infarction remodelling in a rat model of acute myocardial infarction

Objective: This study was performed to evaluate whether implantation of mesenchymal stem cell (MSC) would reduce left ventricular remodelling from the molecular mechanisms compared with angiotensin-converting enzyme inhibitors (ACEIs) perindopril into ischemic myocardium after acute myocardial infarction. Methods: Forty rats were divided into four groups: control, MSC, ACEI, MSC+ACEI groups. Bone marrow stem cell derived rat was injected immediately into a zone made ischemic by coronary artery ligation in MSC group and MSC+ACEI group. Phosphate-buffered saline (PBS) was injected into control group. Perindopril was administered p.o. to ACEI group and MSC+ACEI group. Six weeks after implantation, the rats were killed and heart sample was collected. Fibrillar collagen was observed by meliorative Masson’s trichome stain. Western Blotting was employed to evaluate the protein expression of matrix metalloproteinase (MMP)-2, matrix metalloproteinase (MMP)-9 in infarction zone. The transcriptional level of MMP2, MMP9 and tissue inhibitor of matrix metalloproteinase (TIMP)-1 in infarction area was detected by reverse transcriptase PCR (RT-PCR) analysis. Results: The fibrillar collagen area, the protein expression of MMP2, MMP9 and the transcriptional level of MMP2, MMP9 mRNA in infarction zone reduced in MSC group, ACEI group, and MSC+ACEI group. No significant difference was detected in the expression of TIMP1 mRNA among the 4 groups. Conclusion: Both MSC and ACEI could reduce infarction remodelling by altering collagen metabolism.

Epidemiology and genetics of ventricular fibrillation during acute myocardial infarction

Sudden cardiac death （SCD） from ventricular fibrillation （VF） during coronary artery disease （CAD） is a leading cause of total and cardiovascular mortality, and in more than half of SCD cases VF occurs as the first symptom of CAD. Several epidemiological studies have shown that sudden death of a family member is a risk factor for SCD and VF during acute myocardial infarction （MI）, independent of traditional risk factors including family history of MI, suggesting a genetic component in the susceptibility to VF. To prevent SCD and VF due to MI, we need a better understanding of the genetic and molecular mechanisms causing VF in this apparently healthy population. Even though new insights and technologies have become available, the genetic predisposition to VF during MI remains poorly understood. Findings from a variety of different genetic studies have failed to reach reproducibility, although several genetic variants, both common and rare variants, have been associated to either VF or SCD. For this review, we searched PubMed for potentially relevant articles, using the following MeSH-terms： ＂sudden cardiac death＂, ＂ventricular fibrillation＂, ＂out-of-hospital cardiac arrest＂, ＂myocardial infarction, myocardial ische- mia＂, ＂coronary artery disease＂, and ＂genetics＂. This review describes the epidemiology and evidence for genetic susceptibility to VF due to MI.

Granulocyte-macrophage colony stimulating factor improves cardiac function in rabbits following myocardial infarction

Objective: To investigate the therapeutic potency of recombinant human Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF) in a rabbit myocardial infarction model. Methods: A myocardial infarction was created by the ligation of the major ventricular branch of the left coronary artery in rabbits. After myocardial infarction, the animals were randomly assigned to GM-CSF treatment group, untreated groups and sham-operated group. The rabbits of the treated group were injected into GM-CSF by subcutaneous administration, 10 μg/kg/day, once a day for 5 days. The untreated and sham-operated group received a equal saline in the same manner as treated group. Six weeks later echocardiography and haemodynamic assessment were undertaken to assesse cardiac function. The size of the infarct region of the heart were also studied. Results: The untreated group exhibited significant higher left ventricle end-diastolic pressure, higher central venous pressure, and with significant lower mean blood pressure, lower peak first derivative of left ventricle pressure (dP/dt) than the sham group. Also, Rabbits in untreated group display significant systolic dysfunction shown by the decreased ejection fraction, diastolic dysfunction shown by increasing in the ratio of E wave to A wave (E/A), and display left ventricle enlargement. However, GS-CSF singnificantly prevented heart dysfunction, left ventricle enlargement, and reduced infarct size in treatment group. Conclusion: Administration GM-CSF after cardiac infarction can improve heart function. These findings indicate the technique may be a novel and simple therapeutic method for ischemic myocardium.

Effect of Chinese national holidays and weekends versus weekday admission on clinical outcomes in patients with STEMI undergoing primary PCI

Background Data regarding the influence of weekends and Chinese national holiday＇s admission on the outcomes of patients with ST-elevated myocardial infarction （STEMI） is lacking. This study sought to investigate the effect of Chinese national holidays and weekend admission on outcomes in patients with STEMI undergoing primary percutaneous coronary intervention （PPCI）. Methods Patients pre- senting with STEMI within 12 h of symptom onset who underwent PPCI were retrospectively enrolled. The primary outcome of in-hospital mortality and major adverse cardiovascular events in patients presenting Chinese national holiday＇s and weekends versus weekdays was evaluated. Results A total of 441 STEMI patients were enrolled in this study. Of these, 129 （29.3%） patients were admitted during Chinese national holidays and weekends and 312 （70.7%） during weekdays. Patients admitted during holidays and weekends were more likely to present with Killip class Ⅲ-Ⅳ. Patients admitted during holidays and weekends experienced a significantly longer door-to-baUoon time, symptom onset-to-door time as well as symptom onset-to-balloon time. The in-hospital mortality between patients presenting holidays and weekends versus weekdays was comparable. However, patients admitted during holidays and weekends have a signitieantly higher rate of in-hospital major adverse cardiovascular events. Multivariate analysis demonstrated that holidays and weekends admission was independ- ently associated with adverse outcomes. Conclusions In China, STEMI patients undergoing PPCI during national holidays and weekends have worse in-hospital outcomes compared to those admitted during weekdays. These findings suggest that continuous efforts should be undertaken to enhance the Chinese healthcare system and to ensure that comparable outcomes are achieved for all STEMI patients regardless of time of presentation.

COMPARISON OF THE EFFECTS OF LOSARTAN,ENALAPRIL AND THEIR COMBINATION IN THE PREVENTION OF LEFT VENTRICULAR REMODELING AFTER ACUTE MYOCARDIAL INFARCTION IN THE RAT

Objectives. To compare the effects of losartan, enalapril and their combination in the prevention ofleft ventricular remodeling (LVRM) after acute myocardial infarction (AMI) in the rat. Methods. AMI model was induced in female SD rats by ligating left coronary artery. Forty-eight hours after the procedure, 83 surviving rats were randomized into one of the following 4 groups: 1 ) AMI control group (n =19), 2) losartan group (n= 22, 3 mg @ kg - 1 @ d - 1 ), 3 ) enalapril group (n = 20, 1 mg @ kg - 1 @ d - 1 ), 4) losartan - enalapril combinative group (n = 22, 3 and 1 mg @ kg- 1 @ d - 1 respectively). 5 ) sham-operated group ( n =10) and 6) normal rats group (n = 10) were selected randomly to serve as non-infarction controls. Losartan and enalapril were delivered by direct gastric gavage. After 4 weeks of medical therapy, hemodynamic studies were performed in each group, then the rat hearts were fixed with 10% formalin and pathologic analysis on them was performed. Complete experimental data was obtained in 56 rats, comprising 1 ) AMI controls (n = 11 ), 2) losartan group (n = 10), 3 ) enalapril group (n = 10), 4) the combination of losartan and enalapril group (n = 11 ),5) sham - operated group (n = 6) and 6) normal controls (n=8). Results. There were no significant differences among the 4 AMI groups in MI size (41.7% ～ 43.4%, all P＞ 0.05). Compared with sham group, the left ventricular (LV) end diastolic pressure (LVEDP), volume (LVV), long and short axis length (L and D), as well as LV absolute and relative weight (LVAW and LVRW)in AMI group were all significantly increased ( P ＜0.05 ～ 0. 001 ); whereas the maximum left ventricular pressure rising and droping rates ( + dp/dt) and their corrected values by LV systolic pressure ( + dp/dt/LVSP)were significantly reduced (all P ＜0.001 ), indicating LVRM occurred and LV systolic and diastolic function impaired after AMI. Compared with AMI group , LVEDP, LVV, LVAW and LVRW were all significantly decreased (P ＜0.05～0.001 ); while + dp/dt/LVSP were significantly enhanced in all 3 treatment groups (P ＜0.05～0.001 ) except -dp/dt/LVSP in losartan group (P＞ 0. 05 ). There were no significant differences in the above indices among the 3 treatment groups (all P＞ 0.05). Conclusion. Both losartan and enalapril can prevent from LVRM after AMI in the rat and improve LV function with equivalent effects. There seems no additive effect when the 2 drugs are used in combination.

Comparison between type-2 and type-1 myocardial infarction：clinical features, treatment strategies and outcomes

Objective To assess the differences in incidence, clinical features, current treatment strategies and outcome in patients with type-2vs. type-1 acute myocardial infarction （AMI）.Methods We included 824 consecutive patients with a diagnosis of type-1 or type-2 AMI. Dur-ing index hospitalization, clinical features and treatment strategies were collected in detail. At 1-year follow-up, mortality, stroke, non-fatal myocardial infarction and major bleeding were recorded.ResultsType-1 AMI was present in 707 （86%） of the cases while 117 （14%） were classified as type-2. Patients with type-2 AMI were more frequently female and had higher co-morbidities such as diabetes, previous non-ST segment elevation acute coronary syndromes, impaired renal function, anaemia, atrial fibrillation and malignancy. However, preserved left ventricular ejection fraction and normal coronary arteries were more frequently seen, an invasive treatment was less common, and anti-platelet medications, statins and beta-blockers were less prescribed in patients with type-2 AMI. At 1-year follow-up, type-2 AMI was associated with a higher crude mortality risk （HR： 1.75, 95% CI： 1.14-2.68;P = 0.001）, but this association did not remain significant after multivariable adjustment （P = 0.785）. Furthermore, we did not find type-2 AMI to be associated with other clinical outcomes.Conclusions In this real-life population, compared with type-1, type-2 AMI were predominantly women and had more co-morbidities. Invasive treatment strategies and cardioprotective medications were less used in type-2, while the 1-year clinical outcomes were similar.

Five-year major clinical outcomes between first-generation ana second- generation drug-eluting stents in acute myocardial infarction patients underwent percutaneous coronary intervention

Background There were limited data comparing the major clinical outcomes between first-generation （1G）-drug eluting stentts （DES） and second-generation （2G）-DES in patients with acute myocardial infarction （AMI） after percutaneous coronary intervention （PCI） during very long follow-up periods. We thought to investigate the comparative efficacy and safety of 2G-DES compared with 1G-DES in AMI patients during 5-year follow-up periods. Method A total of 1016 eligible AMI patients who underwent PCI with 1G-DES [paclitaxel-, sirolimus-, 1G-zotarolimus-eluting stent （endeavor~ or endeavor sprintS）, n = 554] or 2G-DES [2G-zotarolimus （endeavor resolute~）- or everolimus-eluting stent, n = 462] were enrolled. The primary endpoint was the occurrence of major adverse cardiac events （MACE） defined as total death, non-fatal myocardial infarction （MI）, target lesion revascularization （TLR）, target vessel revascularization （TVR）, non-target vessel revascularization （Non-TVR） and the secondary endpoint was stem thrombosis （ST） at 5 years. Results Two propensity score-ma- tched （PSM） groups （232 pairs, n = 464, C-statistic = 0.802） were generated. During the 5-year follow-up period, the cumulative incidence of TLR [hazard ratio （HR）： 3.133; 95% confidence interval （CI）： 1.539-6.376; P = 0.002], TVR （HR： 3.144; 95% CI： 1.59645.192; P = 0.001） and total revascularization rate （FIR： 1.874; 95% CI： 1.086-3.140; P = 0.023） were significantly higher in 1G-DES compared with 2G-DES after PSM. However, the incidence of total death, non-fatal MI and ST were similar between the two groups. Conclusion In this single-center and all-comers registry, 2G-DES＇s superiorities for TLR, TVP, and total revascularization in AMI patients suggested during 5-year clinical follow-up periods.

Optimal timing of staged percutaneous coronary intervention in ST-segment elevation myocardial infarction patients with multivessel disease

Background Studies have shown that staged percutaneous coronary intervention （PCI） for non-culprit lesions is beneficial for prog- nosis of ST-segment elevation myocardial infarction （STEMI） patients with multivessel disease. However, the optimal timing of staged re- vascularization is still controversial. This study aimed to find the optimal timing of staged revascularization. Methods A total of 428 STEMI patients with multivessel disease who underwent primary PCI and staged PCI were included. According to the time interval between primary and staged PCI, patients were divided into three groups （〈 1 week, 1- weeks, and 2-12 weeks after primary PCI）. The primary endpoint was major adverse cardiovascular events （MACE）, a composite of all-cause death, non-fatal re-infarction, repeat revascularization, and stroke. Cox regression model was used to assess the association between staged PCI timing and risk of MACE. Results During the follow-up, 119 participants had MACEs. There was statistical difference in MACE incidence among the three groups （〈 1 week： 23.0%; 1-2 weeks： 33.0%; 2-12 weeks： 40.0%; P = 0.001）. In the multivariable adjustment model, the timing interval of staged PCI ≤ 1 week and l-2 weeks were both significantly associated with a lower risk of MACE [hazard ratio （HR）： 0.40, 95% confidence intervals （CI）： 0.24-4）.65; HR： 0.54, 95% CI： 0.3 lq3.93, respectively], mainly attributed to a lower risk of repeat revascularization （HR： 0.41, 95% CI： 0.24-0.70; HR： 0.36, 95% CI： 0.18-0.7）, compared with a strategy of 2-12 weeks later of primary PCI. Conclusions The optimal timing of staged PCI for non-culprit vessels should be within two weeks after primary PCI for STEMI patients.

Polymorphisms in the genes for coagulation factor II,V,VII in patients undergoing coronary angiography

Objective: To determine whether polymorphisms in the genes for coagulation factor II,V, VII could predispose an individual to increase risk for coronary artery disease (CAD) and/or myocardial infarction (MI) in Chinese. Methods: We screened coagulation factor II(G20210A),V(G1691A),VII (R353Q and HVR4) genotype in 374 patients undergoing coronary angiography by polymerase chain reaction and restriction fragment length polymorphism (PCR RFLP) assay. Results: The R353Q and HVR4 genotype of the factor VII distribution was in accordance with Hardy Weinberg equilibrium. The frequencies of FVII genotype or allele did not show statistically significant differences between CAD group and controls or between male and female. The frequencies of the Q allele and (RQ+QQ) genotype were significantly higher among the CAD patients without myocardial infarction (MI) history than among those with MI history ( P <0.05). However, HVR4 polymorphism was not significantly different within groups. We only find one normal control of factorII(G20210A) mutation. No coagulation factor V(G1691A) mutation was found in the CAD patients and controls. Conclusion: The factor II(G20210A),V(G1691A) mutation is absent and may not be a major genetic factor for CAD and/or MI; the Q allele of the R353Q polymorphism of the factor VII gene may be a protective genetic factor against myocardial infarction in Chinese.

Total ischemic time and outcomes for patients with ST-elevation myocardial infarction： does time of admission make a difference？

Objective To investigate whether admission time was associated with the delay of reperfusion therapy and in-hospital death in patients with ST-elevation myocardial infarction （STEMI）. Methods All patients with STEMI who were admitted to the emergency depart- ment and underwent primary percutaneous coronary intervention at Peking University People＇s Hospital between April 2012 and March 2015 were included. We examined differences in clinical characteristics, total ischemic time, and in-hospital death between patients admitted during off-hours and those admitted during regular hours. Multivariate logistic regression was used to estimate the relationship between off-hours admission and clinical outcome. Results The sample comprised 184 and 105 patients with STEMI admitted to hospital during off-hours and regular hours, respectively. Total ischemic and onset-to-door times were significantly shorter in patients admitted during off-hours than among those admitted during regular hours （all P 〈 0.05）. Door-to-balloon （DTB） time, the rate of DTB time 〈 90 min, and in-hospital death were comparable between groups. Multivariate logistic regression showed that age and creatinine level, but not off-hours admission, were associated independently with increased in-hospital death. Conclusions Off-hours admission did not result in delayed reperfusion therapy or increased in-hospital mortality in patients with STEMI. Further efforts should focus on identifying pivotal factors associated with the pre-hospital and in-hospital delay of reperfusion therapy, and implementing quality improvement initiatives for reperfusion programs.

Acute myocardial infarction in a patient with Wolff-Parkinson-White syndrome

It is known that the Wolff-Parkinson-White syndrome （WPW） may either mimic myocardial infarction （MI） or mask the ECG changes of MI. Thus, the diagnosis of MI coexisting with WPW is frequently difficult. Furthermore, patients with WPW occurring acute MI may be life threat- ening. Therefore, early recognition and correct treatment allows rapid restoration of normal sinus rhythm and may decrease morbidity and mortality.

Incremental age-related one-year MACCE after acute myocardial infarction in the drug-eluting stent era （from KAMIR-NIH registry）

Objectives To evaluate the age-related one-year major adverse cardiocerebrovascular events （MACCE） after percutaneous coronary intervention （PCI） in acute myocardial infarction （AMI）. We analyzed the association between age and one-year MACCE after AMI. Methods A total of 13,104 AMI patients from Korea Acute Myocardial Infarction Registry-National Institue of Health （KAMIR-NIH） between November 2011 and December 2015 were classified into four groups according to age （Group I, 〈 60 years, n = 4199; Group II, 60-70 years, n = 2577; Group III; 70-80 years, n = 2774; Group IV, ≥ 80 years, n = 1018）. Patients were analyzed for one-year composite of MACCE （cardiac death, myocardial infarction, target vessel revascularization, cerebrovascular events） after AMI. Results The one-year MACCE in AMI were 3.5% （Group I）, 6.3% （Group II）, 9.6% （Group III） and 17.6% （Group IV）. After adjustment for confounding para- meters, the analysis results showed that patients with AMI had incremental risk of one-year MACCE [Group II, adjusted hazard ratios （aHR） = 1.224, 95% CI： 0.965-1.525, P = 0.096; Group III, aHR = 1.316, 95% CI： 1.037-1.671, P= 0.024; Group IV, aHR = 1.975, 95% CI： 1.500-62.601, P〈 0.001） compared to Group I. Especially, cardiac death in the composite of primary end point played a major role in this effect （Group II, aHR = 1.335, 95% CI： 0.941-1.895, P= 0.106; Group III, aHR = 1.575, 95% CI： 1.122-2.210, P= 0.009; Group IV, aHR = 2.803, 95% CI： 1.937-4.054, P 〈 0.001）. Conclusions Despite advanced techniques and medications for PCI in AMI, age still exerts a powerful influence in clinical outcomes. Careful approaches, even in the modem era of developed cardiology are needed for aged-population in AMI intervention.