OBJECTIVETo investigate (1) whether ischemic preconditioning (IPC) could protect immature rabbit hearts against ischemia-reperfusion injury and (2) the role of K(ATP) channel in the mechanism of myocardial protection. Since cardioplegia is a traditional and effective cardioprotective measure in clinic, our study is also designed to probe the compatibility between IPC and cardioplegia.

METHODSNew Zealand rabbits aged 14 - 21 days weighing 220 - 280 g were used. The animals were anesthetized and heparinized. The chest was opened and the heart was quickly removed for connection of the aorta via Langendorff's method within 30 s after excision. All hearts were perfused with Krebs-Henseleit buffer balanced with gas mixture (O(2):CO(2) = 95%:5%) at 60 cm H(2)O (perfusion pressure). IPC consisted of 5 min global ischemia plus 10 min reperfusion. Glibenclamide was used as the K(ATP) channel blocker at a concentration of 10 micro mol/L before IPC. Cardiac arrest was induced with 4 degrees C St. Thomas cardioplegic solution, at which point the heart was made globally ischemic by withholding perfusion for 45 min followed by 40 min reperfusion. Thirty immature rabbit hearts were randomly divided into four groups: CON (n = 9) was subjected to ischemia-reperfusion only; IPC (n = 9) underwent IPC and ischemia-reperfusion; Gli (n = 6) was given glibenclamide and ischemia-reperfusion; and Gli + IPC (n = 6) underwent glibenclamide, IPC and ischemia-reperfusion. Coronary flow (CF), HR, left ventricle developed pressure (LVDP), and +/- dp/dt(max) were monitored at equilibration (baseline value) and 5, 10, 20, 30 and 40 min after reperfusion. The values resulting from reperfusion were expressed as a percentage of their baseline values. Arrhythmia quantification, myocardial enzyme in the coronary effluent and myocardial energy metabolism were also determined.

RESULTSThe recovery of CF, HR, LVDP and +/- dp/dt(max) in preconditioned hearts was best among the four groups. The incidence of arrhythmia was low and less CK-MB leaked out in the IPC group. Myocardial ATP content was better preserved by IPC. Pretreatment with glibenclamide completely abolished the myocardial protection provided by IPC, but did not affect ischemia-reperfusion injury.

CONCLUSIONSWhile applying cardioplegia, IPC provides significant cardioprotective effects. Activation of K(ATP) channels is involved in the mechanism of IPC-produced cardioprotection.

Adenosine Triphosphate ; analysis ; Animals ; Creatine Kinase ; secretion ; Creatine Kinase, MB Form ; Heart Arrest, Induced ; Hemodynamics ; Ischemic Preconditioning, Myocardial ; Isoenzymes ; secretion ; Potassium Channels ; physiology ; Rabbits

Creatine Kinase, MB Form ; analysis ; Female ; Glutathione ; metabolism ; therapeutic use ; Humans ; Infant, Newborn ; Male ; Malondialdehyde ; analysis ; Myocardial Ischemia ; drug therapy ; metabolism ; Oxidation-Reduction

OBJECTIVETo investigate the incidence of rhabdomyolysis, the relationship between striated muscular injury and myocardiac injury, and the role of elevated serum creatine kinase (CK) played in screening these two complications following acute carbon monoxide poisoning (ACOP).

METHODS280 patients with ACOP from January 2001 to April 2003 were analyzed retrospectively. According to the clinical manifestations of striated muscular injury (swelling, pain or serious myasthenia), the patients were divided into two groups: the evident injury group and non-evident injury group.

RESULTSThe abnormality rate of electrocardiogram (ECG) and cardiac troponin I (CTnI) in the evident injury group (43 patients) were significantly higher than in the non-evident injury group (73.8% vs 43.4%, P < 0.001; 77.8% vs 20.9%, P < 0.001). There was a positive correlation between peak CK and MB isoenzyme (CK-MB) in both groups, respectively (r = 0.819, r = 0.795, P < 0.01). There was no correlation in the evident injury group (P > 0.05) and only negative correlation in the non-evident injury group (r = -0.298, P < 0.01) between peak CK and MB ratio (CK-MB/CK). Multiple regression analysis indicated that peak CK and CK-MB were only related with the striated muscular injury and were not affected by the indexes of the myocardial injury (ECG and CTnI); Both peak CK and CK-MB were positively correlated with the coma time before consultation in the non-evident injury group and the latter was also affected by CTnI. The incidence of positive muscular injury symptoms increased with the elevation of CK activity. There was no significant difference either in the ECG abnormality rate between the < 5 times elevated CK level subgroup and the > 5 times elevated CK level subgroup (P > 0.05), or in the CTnI positive rate between the normal CK level subgroup and the < 5 times elevated CK level subgroup (P > 0.05).

CONCLUSIONStriated muscular injury is not a rare complication of ACOP, and always accompanied by myocardial injury. The strikingly elevated serum level of CK in patients with ACOP might be more likely to indicate the striated muscle not myocardiac injury.

Acute Disease ; Adult ; Carbon Monoxide Poisoning ; complications ; Cardiomyopathies ; chemically induced ; diagnosis ; Creatine Kinase ; blood ; Creatine Kinase, MB Form ; blood ; Electrocardiography ; Female ; Humans ; Male ; Middle Aged ; Multivariate Analysis ; Muscular Diseases ; chemically induced ; diagnosis ; Regression Analysis ; Retrospective Studies ; Troponin I ; blood

OBJECTIVETo investigate the occurrence of aspirin resistance in coronary heart disease (CHD) patients and its influence on myonecrosis among patients undergoing non-emergent percutaneous coronary intervention (PCI).

METHODS256 CHD patients who have been on aspirin (100 mg/d) for at least 7 days were recruited based on aspirin responsiveness determination. All the patients were divided into two groups: aspirin-resistant group and aspirin-sensitive group. For all patients scheduled for non-emergent PCI, a loading dose of 300 mg of clopidogrel was given at least 12 h before PCI and a 75 mg maintenance dose was given every morning before and after PCI. The incidence of myonecrosis was evaluated by the levels of creatine kinase-myocardial band (CK-MB) and troponin I (TnI) before and after PCI.

RESULTSAspirin resistance was found in 67 (26.2%) patients and 189 (73.8%) patients were aspirin-sensitive. There was a significantly higher proportion of female subjects in the aspirin-resistant group. The incidence of any CK-MB elevation was 38 (56.7%) in aspirin-resistant group and 42 (22.2%) in aspirin-sensitive group (P < 0.01). The elevation of TnI was observed in 41 (61.2%) of the aspirin-resistant group and in 67 (35.4%) of the aspirin-sensitive group (P < 0.05). Multivariate analysis revealed that aspirin resistance was an independent predictor for CK-MB elevation after PCI (OR = 2.5; 95% CI 1.5 to 6.5; P < 0.05).

CONCLUSIONAspirin resistance exists in some CHD patients, which increases the risk of myonecrosis following non-emergent PCI.

Aged ; Angioplasty, Balloon, Coronary ; adverse effects ; Aspirin ; pharmacology ; therapeutic use ; Coronary Disease ; therapy ; Creatine Kinase, MB Form ; analysis ; Drug Resistance ; Female ; Humans ; Male ; Middle Aged ; Multivariate Analysis ; Myocardium ; pathology ; Necrosis ; Platelet Activation ; Platelet Aggregation ; Stents ; Troponin I ; analysis

PURPOSE: This study compared the impact of paclitaxel-coated balloons (PCB) or drug eluting stents (DES) on peri-procedural myocardial infarction (PMI) on de novo coronary lesion in stable patients. MATERIALS AND METHODS: In this observational study, we compared the incidence of PMI amongst patients with single vessel de novo coronary lesions who underwent treatment with a PCB or DES. Propensity score-matching analysis was used to assemble a cohort of patients with similar baseline characteristics. PMI was classified as myocardial infarction occurring within 48 hours after percutaneous coronary intervention with a threshold of 5 x the 99th percentile upper reference limit of normal for creatine kinase-myocardial band (CK-MB) or troponin T (TnT). RESULTS: One hundred four patients (52 receiving PCB and 52 receiving DES) were enrolled in this study. The peak mean values of CK-MB and TnT were significantly higher in the DES group. There was a significantly higher rate of PMI in the DES group (23.1% vs. 1.9%, p=0.002). Total occlusion of the side-branch occurred in two patients treated with DES, while no patients treated with PCB. In multivariable analysis, DES was the only independent predictor of PMI compared with PCB (odds ratio 42.85, 95% confidence interval: 3.44–533.87, p=0.004). CONCLUSION: Treatment with a PCB on de novo coronary lesion might be associated with a significant reduction in the risk of PMI compared to DES.
Aged ; Creatine Kinase, MB Form/analysis ; *Drug-Eluting Stents ; Female ; Humans ; Incidence ; Kaplan-Meier Estimate ; Middle Aged ; Myocardial Infarction/enzymology/epidemiology/etiology/*prevention & control ; Odds Ratio ; Paclitaxel/*therapeutic use ; Percutaneous Coronary Intervention/*adverse effects ; Propensity Score ; Time Factors ; Treatment Outcome

OBJECTIVETo study myocardial injury and inflammatory response within 7 days after interventional therapy in children with congenital heart disease (CHD).

METHODSA total of 77 children with CHD, including 12 cases of ventricular septal defect (VSD), 14 cases of atrial septal defect (ASD), 14 cases of pulmonary stenosis (PS) and 37 cases of patent ductus arteriosus (PDA), were enrolled. The levels of myocardial enzyme (AST, CK and CKMB), cardiac troponin I (cTnI) and CRP in serum were measured before operation, immediately after operation, and 6 hrs, 24 hrs, 72 hrs and 7 days after operation.

RESULTSSerum AST levels in the VSD group were significantly higher than the other CHD groups immediately after operation, and 6 hrs and 24 hrs after operation (P<0.05). There were significant differences in serum CK and CKMB levels among the four CHD groups immediately and 6 hrs after operation (P<0.05), and the highest serum CK and CKMB levels were found in the VSD group. Serum CRP levels in the PDA group were significantly higher than the other CHD groups 72 hrs and 7 days after operation (P<0.05). Compared with before operation, serum AST levels increased significantly in all four CHD groups 6 and 24 hrs after operation groups (P<0.05). Serum CK and CKMB levels increased significantly in the VSD group immediately and 6 hrs after operation (P<0.05). Serum cTnI levels increased significantly in the VSD, PDA and PS groups immediately and 6 hrs after operation (P<0.05). The PDA group showed increased CRP levels 24 hrs, 72 hrs and 7 days after operation (P<0.05).

CONCLUSIONSMinor myocardial injury can be noted within 7 days after interventional therapy in children with CHD and mainly occurs between immediately and 24 hrs after operation. The injury is more significant in VSD cases. The interventional therapy does not cause significant inflammation.

Adolescent ; C-Reactive Protein ; analysis ; Child ; Child, Preschool ; Creatine Kinase, MB Form ; blood ; Female ; Heart Defects, Congenital ; pathology ; therapy ; Humans ; Infant ; Inflammation ; etiology ; Male ; Myocardium ; pathology ; Troponin I ; blood

No abstract available.
Aged ; Carcinoma, Renal Cell/*diagnosis/surgery ; Coronary Angiography ; Creatine Kinase, MB Form/analysis/*metabolism ; Echocardiography ; Electrophoresis ; Enzyme-Linked Immunosorbent Assay ; False Positive Reactions ; Humans ; Kidney Neoplasms/*diagnosis/surgery ; Male ; Nephrectomy

Alkaloids ; pharmacology ; Animals ; Calcium ; metabolism ; Creatine Kinase ; blood ; Creatine Kinase, MB Form ; Drugs, Chinese Herbal ; pharmacology ; Female ; Ginsenosides ; pharmacology ; Injections ; Isoenzymes ; blood ; Male ; Malondialdehyde ; analysis ; Mitochondria, Heart ; drug effects ; pathology ; Myocardial Reperfusion Injury ; drug therapy ; pathology ; Myocardium ; ultrastructure ; Protective Agents ; pharmacology ; Rabbits ; Tetrahydroisoquinolines ; pharmacology