OBJECTIVETo observe the early reperfusion therapy status for patients with ST elevation acute myocardial infarction (STEMI) hospitalized in tertiary and secondary hospitals in Henan province.

METHODSBaseline data, early reperfusion treatment and in-hospital mortality of STEMI patients hospitalized in 17 hospitals in Henan province (8 tertiary hospitals, 9 secondary hospitals) from June 2011 to June 2012 were obtained using a uniformed questionnaire.

RESULTSOne thousand six hundred and eighty six patients were enrolled, of which 886 patients were hospitalized in tertiary hospitals and 880 patients were early hospitalized in secondary hospitals. Six hundred and fifty four patients (38.8%, 654/1 686) underwent early reperfusion therapy (543 with thrombolysis and 111 with primary percutaneous coronary intervention (PCI)). There was no difference in the proportion of early reperfusion therapy between tertiary and secondary hospitals (40.1% (355/886) vs. 37.4% (299/800), P = 0.257). The median time from symptom onset to first medical contact, door-to-needle and door-to-balloon was 132 min, 18 min and 60 min, respectively. The median time from symptom onset to first medical contact (150 min vs. 120 min, P = 0.001), door-to-needle (30 min vs. 18 min, P = 0.003) and symptom onset-to-thrombolysis (3.5 h vs. 2.7 h, P = 0.001) were significantly longer in tertiary hospitals than in secondary hospitals. No difference was found in median time of door-to-balloon, symptom onset-to-primary PCI or symptom onset-to-elected PCI between tertiary and secondary hospitals (all P > 0.05). The proportion of door-to-needle ≤ 30 min was lower in tertiary hospitals than in secondary hospitals (46.4% (84/181) vs. 62.2% (153/246), P = 0.001). However, there was no difference in the proportion of door-to-balloon ≤ 90 min between tertiary and secondary hospitals (58.8% (60/102) vs. 57.1% (4/7), P = 1.000). In-hospital mortality was also similar between tertiary and secondary hospitals (5.8% (51/886) vs. 5.5% (44/800), P = 0.820).

CONCLUSIONSEarly reperfusion rate is low, and thrombolysis is the main early reperfusion therapy in both tertiary and secondary hospitals in Henan province. Tertiary hospitals did not take advantage of their primary PCI capability. There is great room for improvement in early reperfusion therapy in tertiary and secondary hospitals.

Hospital Mortality ; Hospitals ; Humans ; Myocardial Infarction ; Myocardial Reperfusion ; Percutaneous Coronary Intervention ; Secondary Prevention ; Surveys and Questionnaires

Humans ; Myocardial Reperfusion Injury/prevention & control* ; Melatonin/therapeutic use* ; Mitochondria ; Myocardial Infarction

Writing Committee of Korean clinical practice guidelines for secondary prevention of stroke has reviewed recent randomized controlled trials of cilostazol published after the first edition of Korean clinical practice guidelines that considered evidences published before June 2007. Two clinical trials and 1 meta-analysis which compared cilostazol directly with aspirin in the prevention of stroke in patients with cerebral infarction or transient ischemic attack (TIA) were identified and included for the current guideline update. Review of findings indicates that cilostazol as compared to aspirin achieved a greater reduction of stroke as well as composite vascular events of stroke, myocardial infarction, and vascular death. For safety, cilostazol was associated with fewer major bleeding events than aspirin. Accordingly, new recommendations for cilostazol are made for prevention of stroke in the setting of noncardioembolic stroke or TIA. Changes in the guidelines necessitated by new evidences will be continuously reflected in future guidelines.
Aspirin ; Cerebral Infarction ; Hemorrhage ; Humans ; Ischemic Attack, Transient ; Myocardial Infarction ; Secondary Prevention ; Stroke ; Tetrazoles ; Writing

Background: Secondary preventive therapies play a key role in the prevention of adverse outcomes after coronary artery bypass grafting (CABG). However, medication adherence after CABG is often poor, and conventional interventions for improving adherence have limited success. With increasing penetration of smartphones, health-related smartphone applications might provide an opportunity to improve adherence. Carefully designed trials are needed to provide reliable evidence for the use of these applications in patients after CABG. Methods: The Measurement and Improvement Studies of Surgical Coronary Revascularization: Medication Adherence (MISSION-2) study is a multicenter randomized controlled trial, aiming to randomize 1000 CABG patients to the intervention or control groups in a 1:1 ratio. We developed the multifaceted, patient-centered, smartphone-based Heart Health Application to encourage medication adherence in the intervention group through a health self-management program initiated during hospital admission for CABG. The application integrated daily scheduled reminders to take the discharge medications, cardiac educational materials, a dynamic dashboard to review cardiovascular risk factors and secondary prevention targets, and weekly questionnaires with interactive feedback. The primary outcome was secondary preventive medication adherence measured by the Chinese version of the 8-item Morisky Medication Adherence Scale at 6 months after randomization. Secondary outcomes included all-cause death, cardiovascular rehospitalization, and a composite of death, myocardial infarction, stroke, and repeat revascularization. Discussion: Findings will not only provide evidence regarding the feasibility and effectiveness of the described intervention for improving adherence to CABG secondary preventive therapies but also explore a model for outpatient health self-management that could be translated to various chronic diseases and widely disseminated across resource-limited settings. Trial Registration https://clinicaltrials.gov (NCT02432469).
Coronary Artery Bypass ; methods ; Humans ; Medication Adherence ; Myocardial Infarction ; prevention & control ; Secondary Prevention ; methods ; Smartphone ; Stroke ; prevention & control

OBJECTIVETo investigate whether adiponectin plays a role in the protection of myocardium in the rat myocardial ischemia preconditioning (IPC) model.

METHODInfarct size was measured by Masson's Trichrome staining, the expression of protein and mRNA of adiponectin at 0, 6, 12 and 24 h after IPC was examined by immunohistochemistry and quantitative real time RT-PCR, plasma levels of adiponectin at above mentioned four time points after IPC were detected by ELISA in IPC and MI rats.

RESULTInfarct size was smaller in IPC than in MI rats (20% ± 2% vs. 31% ± 3%, P < 0.05). The expression of adiponectin mRNA at 6 h and 12 h after IPC was 2.2 and 2.1 times higher than in Sham rats at respective time points (P < 0.05). Immunohistochemistry staining evidenced increased adiponectin expression in the ischemic area and weak expression of adiponectin in non-ischemic area (P < 0.05). Compared to the sham group, the plasma level of adiponectin increased significantly at 0, 6 and 12 h after IPC (0 h: 7.40 ± 0.47 vs. 10.90 ± 1.74; 6 h: 8.18 ± 1.41 vs. 10.98 ± 1.74; 12 h: 6.97 ± 1.02 vs. 9.31 ± 0.96, P < 0.05).

CONCLUSIONIPC reduced infarction size, upregulated the myocardial expression of adiponectin at mRNA and protein levels, and increased plasma adiponectin concentration, suggesting that the adiponectin may play a critical role in the protective effect of IPC.

Adiponectin ; metabolism ; Animals ; Ischemic Preconditioning, Myocardial ; Male ; Myocardial Infarction ; metabolism ; prevention & control ; Myocardial Ischemia ; metabolism ; prevention & control ; Myocardium ; metabolism ; Rats ; Rats, Sprague-Dawley

BACKGROUNDThis study aimed at assessing the effect of noninvasive limb preconditioning on myocardial infarct size, and determining whether nitric oxide and neurogenic pathway play an important role in the mechanism of acute remote ischemic preconditioning (IPC).

METHODSForty Wistar rats were randomly divided into four experimental groups. In Group I, the rats underwent 30-minute occlusion of the left anterior descending coronary artery, and 120-minute reperfusion. In Group PL, the rats underwent four cycles of 5-minute occlusion and reperfusion of both hind limbs using a tourniquet before the experiment was continued as in Group I. In Group PL-N and Group PL-H, we administered L-nitro-arginine methyl ester (L-NAME) 10 mg/kg or hexamethonium chloride 20 mg/kg intravenously, 10 minutes before IPC. Infarct size as a percentage of the area at risk was determined by triphenyltetrazolium chloride staining.

RESULTSThere were no statistically significant differences in mean arterial pressure and heart rate among these groups at any time point during the experiment (P>0.05). The myocardial infarct size (IS) was decreased significantly in Group PL and Group PL-H compared with Group I, and the IS/AAR was 34.5%+/-7.6%, 35.9%+/-8.6% and 58.5%+/-8.5%, respectively (P< 0.05). The IS/AAR was 49.1%+/- 6.5% in Group PL-N, and there was no significant difference compared with Group I (P>0.05).

CONCLUSIONSNoninvasive limb IPC is effective in protecting the myocardium from ischemia reperfusion injury. Nitric oxide plays an important role in the mechanism of acute remote IPC, in which the neurogenic pathway is not involved.

Animals ; Blood Pressure ; Extremities ; blood supply ; Heart Rate ; Ischemic Preconditioning, Myocardial ; Myocardial Infarction ; prevention & control ; Myocardial Reperfusion Injury ; prevention & control ; Rats ; Rats, Wistar

Early restoration of blood flow to the ischemic myocardium not only saves myocardium but also induces reperfusion injury. While no specific therapy to reduce reperfusion injury has yet been established, recent laboratory studies have shown that G protein-coupled receptor (GPCR) agonists, insulin, and postconditioning can effectively prevent reperfusion injury in various experimental settings and animal species. The potential mechanisms underlying the cardioprotection initiated by these interventions may include activation of the reperfusion injury salvage kinase (RISK) pathway, inactivation of glycogen synthase kinase 3beta (GSK-3beta), and modulation of mitochondrial permeability transition pore (mPTP) opening. These encouraging laboratory findings may help us develop successful clinical strategies to salvage reperfused myocardium in patients with acute myocardial infarction.
Glycogen Synthase Kinase 3 ; metabolism ; Humans ; Mitochondrial Membrane Transport Proteins ; physiology ; Myocardial Infarction ; complications ; Myocardial Reperfusion Injury ; prevention & control ; Myocardium

BACKGROUND: The prediction of the absolute risk of ischemic heart disease (IHD) is commonly based on the risk prediction equations, originated from the Framingham Heart Study. METHOD: Framingham equation model was applied to participants from 2001 Korean National Health and Nutrition Examination Survey (KNHNES) to estimate the 5 year risk of IHD among Koreans ranging from 30 to 74 year-olds. The estimated risks were compared to the incidence and admission rates from two statistical reports among Koreans. Five year admission rate was estimated by the annual report from National Health Insurance Corporation (NHIC). RESULTS: The average ages (standard deviation) were 34.31(27.23) year-old for KNHNES and 48.26(12.87) year-old for Framingham population used in this study. The risk of IHD predicted by the Framingham equation model substantially exceeded the risks actually reported in Korea. Five-year predicted risks by Framingham equation model were 4.86% for men and 1.93% for women; whereas from incidence data in Korea, five-year risks for acute myocardial infarction (AMI) were for 0.47% for men and 0.18% for women. These AMI incidence was similar to the admission rate (0.34 for men and 0.15 for women) estimated by NHIC. Also, 5-year admission rate of IHD were 1.16 for men and 0.78 for women. The magnitude of risk overestimation by Framingham mode is approximately at least 150 to 320%. CONCLUSION: Korean guidelines for the management for high risk group of IHD need to develop and correct for overestimation to avoid inflation of costs in primary prevention.
Aged ; Female ; Heart ; Humans ; Incidence ; Inflation, Economic ; Korea ; Male ; Myocardial Infarction ; Myocardial Ischemia* ; National Health Programs ; Nutrition Surveys ; Primary Prevention

OBJECTIVETo evaluate the effects of antiarrhythmic peptide (AAP10) on ventricular arrhythmias in rabbits with healed myocardial infarction (OMI).

METHODSThirty rabbits were randomly divided into three groups (n = 10 each): Sham group, left thoracotomy was performed without coronary ligation; OMI group and OMI + AAP10 group, the circumflex coronaries were ligated. Three months post operation, the electrophysiological and antiarrhythmic effects of AAP10 were assessed in the arterially perfused rabbit left ventricular wedge preparation. Sham and OMI group were perfused with Tyrode's solution and OMI + AAP10 group was perfused with Tyrode's solution + AAP10 (80 nmol/L). Transmembrane action potentials were recorded simultaneously from endocardium and epicardium together with a transmural ECG by use of 2 separate intracellular floating microelectrodes. The stimulus-response-interval (SRI) of the epicardium and the incidence of ventricular tachycardia (VT) were observed. Whole heart and left ventricular weights, the left ventricular thickness at infarct border zone were measured.

RESULTSWhole heart and left ventricular weights as well as the left ventricular thickness at the infarct border zone significantly increased post infarction. VT was induced in 8 out of 10 rabbits in OMI group and in 2 out of 10 rabbits in OMI + AAP10 group (P < 0.05). SRI was also significantly shortened in OMI + AAP10 group compared to OMI group [SRI-1: (20.59 +/- 0.79) ms vs. (28.71 +/- 0.55) ms; SRI-2: (30.42 +/- 0.74) ms vs. (38.67 +/- 0.49) ms, all P < 0.01]. However, the action potential morphology and duration were similar between OMI and OMI + AAP10 groups.

CONCLUSIONThe antiarrhythmic peptide (AAP10) can increase gap junctional intercellular conductance without affecting the action potential morphology and duration and decrease the incidence of inducible ventricular tachycardia.

Animals ; Arrhythmias, Cardiac ; etiology ; prevention & control ; Male ; Myocardial Infarction ; complications ; physiopathology ; Oligopeptides ; pharmacology ; Rabbits ; Random Allocation

BACKGROUND AND OBJECTIVES: The differential benefit of statin according to the state of dyslipidemia has been sparsely investigated. We sought to address the efficacy of statin in secondary prevention of myocardial infarction (MI) according to the level of triglyceride and high density lipoprotein cholesterol (HDL-C) on admission. SUBJECTS AND METHODS: Acute MI patients (24653) were enrolled and the total patients were divided according to level of triglyceride and HDL-C on admission: group A (HDL-C≥40 mg/dL and triglyceride<150 mg/dL; n=11819), group B (HDL-C≥40 mg/dL and triglyceride≥150 mg/dL; n=3329), group C (HDL-C<40 mg/dL and triglyceride<150 mg/dL; n=6062), and group D (HDL-C<40 mg/dL & triglyceride≥150 mg/dL; n=3443). We evaluated the differential efficacy of statin according to the presence or absence of component of dyslipidemia. The primary end points were major adverse cardiac events (MACE) for 2 years. RESULTS: Statin therapy significantly reduced the risk of MACE in group A (hazard ratio=0.676; 95% confidence interval: 0.582-0.785; p<0.001). However, the efficacy of statin was not prominent in groups B, C, or D. In a propensity-matched population, the result was similar. In particular, the benefit of statin in group A was different compared with group D (interaction p=0.042) CONCLUSION: The benefit of statin in patients with MI was different according to the presence or absence of dyslipidemia. In particular, because of the insufficient benefit of statin in patients with MI and dyslipidemia, a different lipid-lowering strategy is necessary in these patients.
Cholesterol, HDL* ; Dyslipidemias ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors* ; Myocardial Infarction* ; Prognosis ; Secondary Prevention* ; Triglycerides*