Creatine Kinase-myocardial Isoenzyme Research Articles

Effect of Yangxin Huoxue Jiedu recipe on inflammatory factors and oxidative stress on viral myocarditis in children.

This observation purposed to investigate the effect of the Yangxin Huoxue Jiedu formula on children with viral myocarditis and its effect on inflammatory factors and oxidative response. A total of 121 children with viral myocarditis were randomly divided into two groups, namely the control group (N = 60) and the traditional Chinese medicine group (N = 61). The control group was mainly treated with routine therapy, while the traditional Chinese medicine group was treated with Yangxin Huoxue Jiedu recipes based on the control group. The creatine kinase, creatine kinase myocardial isoenzyme, aspartate aminotransferase, lactic dehydrogenase, hydroxybutyrate dehydrogenase, cardiac troponin I, brain natriuretic peptide, interleukin-6, interleukin-8, and tumour necrosis factor-alpha, superoxide dismutase and malondialdehyde in viral myocarditis patients were tested to estimate the myocardial function, inflammation, and oxidative situation. After Yangxin Huoxue Jiedu treatment, 15 cases were recovered, 20 were excellent, and 21 were effective, which had a significant difference from the control group. The concentration of creatine kinase, creatine kinase myocardial isoenzyme, aspartate aminotransferase, lactic dehydrogenase, hydroxybutyrate dehydrogenase, cardiac troponin I and brain natriuretic peptide was decreased in the traditional Chinese medicine group. The levels of interleukin-6, interleukin-8, and tumour necrosis factor-alpha in the traditional Chinese medicine group were significantly lower than those in the control group. Superoxide dismutase was higher and malondialdehyde was lower than those in the control group. The use of Yangxin Huoxue Jiedu in the treatment of viral myocarditis has a definite clinical effect, which could improve myocardial function, reduce body inflammation, and promote oxidative recovery.

Alpha-lipoic Acid Protects Against Chronic Alcohol Consumption-induced Cardiac Damage by the Aldehyde Dehydrogenase 2-associated PINK/Parkin Pathway.

Chronic alcohol intake contributes to high mortality rates due to ethanol-induced cardiac hypertrophy and contractile dysfunction, which are accompanied by increased oxidative stress and disrupted mitophagy. Alpha-lipoic acid (α-LA), a well-known antioxidant, has been shown to protect against cardiac hypertrophy and inflammation. However, little is known about its role and mechanism in the treatment of alcoholic cardiomyopathy. Here, we evaluated the role of α-LA in alcohol-induced cardiac damage by feeding mice a 4.8% (v/v) alcohol diet with or without α-LA for 6 w. Our results suggested that chronic alcohol consumption increased mortality, blood alcohol concentrations, and serum aldehyde levels, but a-LA attenuated the elevations in mortality and aldehydes. Chronic alcohol intake also induced cardiac dysfunction, including enlarged left ventricles, reduced left ventricular ejection fraction, enhanced cardiomyocyte size, and increased serum levels of brain natriuretic peptide, lactate dehydrogenase, and creatine kinase myocardial isoenzyme. Moreover, alcohol intake led to the accumulation of collagen fiber and mitochondrial dysfunction, the effects of which were alleviated by α-LA. In addition, α-LA intake also prevented the increase in reactive oxygen species production and the decrease in mitochondrial number that were observed after alcohol consumption. Chronic alcohol exposure activated PINK1/Parkin-mediated mitophagy. These effects were diminished by α-LA intake by the activation of aldehyde dehydrogenase 2. Our data indicated that α-LA helps protect cardiac cells against the effects of chronic alcohol intake, likely by inhibiting PINK1/Parkin-related mitophagy through the activation of aldehyde dehydrogenase 2.

Oral Supplementation With Butyrate Improves Myocardial Ischemia/Reperfusion Injury via a Gut-Brain Neural Circuit.

Objective: Butyrate, a short-chain fatty acid (SCFA) produced by the intestinal microbiota, plays a protective role in cardiovascular diseases (CVDs), but the mechanisms involved in this process remain unelucidated. We aimed to explore the effect of butyrate on myocardial ischemia/reperfusion (I/R) injury through the gut-brain neural circuit.Methods: Rats were randomly divided into four groups: sham group (sham), I/R group (I/R), I/R+ butyrate group (butyrate), and I/R+ butyrate+ vagotomy group (vagotomy). The rats were treated with sodium butyrate for 4 weeks, and the gut-brain neural circuit was investigated by subdiaphragmatic vagotomy.Results: Butyrate treatment significantly reduced the infarct size and decreased the expression of creatine kinase (CK), creatine kinase myocardial isoenzyme (CK-MB), and lactate dehydrogenase (LDH) compared with the values found for the I/R group. In addition, the I/R-induced increases in inflammation, oxidative stress, and apoptosis were attenuated by butyrate. However, the above-mentioned protective effects were diminished by subdiaphragmatic vagotomy. The RNA sequencing results also revealed that the butyrate-induced protective changes at the cardiac transcription level were reversed by vagotomy. An analysis of the heart rate variability (HRV) and the detection of norepinephrine (NE) showed that butyrate significantly inhibited the I/R-induced autonomic imbalance, but this inhibition was not observed in the vagotomy group. Butyrate treatment also suppressed the neural activity of the paraventricular nucleus (PVN) and superior cervical ganglion (SCG), and both of these effects were lost after vagotomy.Conclusions: Butyrate treatment significantly improves myocardial I/R injury via a gut-brain neural circuit, and this cardioprotective effect is likely mediated by suppression of the sympathetic nervous system.

Vaspin Prevents Tumor Necrosis Factor-α-Induced Apoptosis in Cardiomyocytes by Promoting Autophagy.

Visceral adipose tissue-derived serine protease inhibitor (Vaspin) is an adipocytokine that has been shown to exert anti-inflammatory effects and inhibits apoptosis under diabetic conditions. This study was designed to investigate the impact of vaspin on autophagy in tumor necrosis factor (TNF)-α-induced injury in cardiomyocytes and its cardioprotective effects in the pathogenesis of diabetic cardiomyopathy (DCM). H9C2 cells were treated with TNF-α with or without vaspin in vitro. Tumor necrosis factor-α treatment inhibited autophagy and promoted apoptosis in H9C2 cells after stimulating for 24 hours. Pretreatment with vaspin significantly mitigated apoptosis induced by TNF-α partly because of augment effects of vaspin on autophagy as demonstrated by a higher ratio of LC3-II/LC3-I, higher expression of Beclin-1, and increased autophagosomes formation. Furthermore, the AKT agonist IGF-1 significantly reversed the effect of vaspin on autophagy. In vivo DCM model was also developed by treating rats with streptozotocin followed by intraperitoneal injection with vaspin. In DCM rats, upregulation of vaspin reversed cardiac dysfunction, as identified by increased left ventricular ejection fractions and fractional shortening levels, a higher Em/Am ratio, and lower levels of TNF-α, lactate dehydrogenase, creatine kinase, and creatine kinase-myocardial isoenzyme. In conclusion, vaspin attenuated the TNF-α-induced apoptosis by promoting autophagy probably through inhibiting the PI3K/AKT/mTOR pathway and further ameliorated the cardiac dysfunction in DCM rats.

Thrombolytic therapy in a patient with inferolateral myocardial infarction after carbon monoxide poisoning.

ST segment elevation myocardial infarction (STEMI) due to coronary artery occlusion caused by intracoronary thrombosis in the setting of acute carbon monoxide (CO) poisoning is a very rare presentation. We present a case of intracoronary large and mobile thrombus formation after CO poisoning. A previously healthy 50-year-old woman was referred for CO poisoning. She had chest pain after exposure to CO. Her initial mental status was preoccupied with chest pain. Her initial CO fraction was 28.1%, and initial laboratory data showed creatine kinase-myocardial isoenzyme of 134 U/L (upper limit 25 U/L) and troponin I of >50 ng/mL (upper limit 0.06 ng/mL). Electrocardiography was carried out on admission, revealing an ST segment elevation in the inferolateral leads. After initial evaluation, coronary angiography was performed and an intracoronary large mobile thrombus was seen in the proximal left anterior descending (LAD) artery with no significant stenosis. We administered tenecteplase with heparin. After the thrombolytic therapy, ST elevation in the inferolateral leads resolved. Repeat angiography was performed after 24 h; the thrombus in LAD had resolved. The patient was discharged after 5 days, with persistent Q wave in the inferior leads and mild hypokinesia of the inferoposterior wall suggesting myocardial injury. We describe intracoronary thrombus formation induced by CO poisoning. Because intracoronary thrombus can result in myocardial infarction, its consideration following CO poisoning is important. Patients with CO poisoning who have symptoms of STEMI should be carefully evaluated with serial electrocardiograms, cardiac biomarkers, and an echocardiogram. When there is evidence of acute myocardial injury, a primer in coronary angiography can determine which patients could benefit from intervention.

Evaluation of children presenting to the emergency room after electrical injury.

To evaluate children who presented to the Pediatric Emergency Department with electrical injury and to discuss the follow-up of these cases and potential precautions that can be taken. A total of 36 patients presented to the Pediatric Emergency Department with electrical injury between May 2010 and May 2013, and these cases were investigated retrospectively. The patients' age and sex, location and form of exposure to electric current, seasonal distribution, length of hospital stay, musculoskeletal and cardiovascular system complications, renal damage, and treatments were recorded. The majority of the patients were exposed to low-voltage electrical current at home. When the patients were evaluated based on the type of electric current, alanine transaminase, aspartate transaminase, creatine kinase, and creatine kinase-myocardial isoenzyme levels were found to be significantly higher among patients who were exposed to high-voltage electric current. None of the patients died, and the mean length of hospital stay was 2.50 ± 1.06 days. Electrical injuries can present with a wide variety of problems, ranging from a simple injury to life-threatening severe multiple organ injury. Even simple precautions can prevent possible morbidity and mortality. We think that the public level of knowledge and awareness should be increased.

Effect of short-term high-dose atorvastatin on systemic inflammatory response and myocardial ischemic injury in patients with unstable angina pectoris undergoing percutaneous coronary intervention

Background Percutaneous coronary intervention (PCI) could develop periprocedural myocardial infarction and inflammatory response and statins can modify inflammatory responses property. The aim of this study was to evaluate whether short-term high-dose atorvastatin therapy can reduce inflammatory response and myocardial ischemic injury elicited by PCI. Methods From March 2012 to May 2014, one hundred and sixty-five statin-naive patients with unstable angina referred for PCI at Department of Cardiology of the 306th Hospital, were enrolled and randomized to 7-day pretreatment with atorvastatin 80 mg/d as high dose group (HD group, n=56) or 20 mg/d as normal dose group (ND group, n=57) or an additional single high loading dose (80 mg) followed 6-day atorvastatin 20 mg/d as loading dose group (LD group, n=52). Plasma C-reactive protein (CRP) and interleukin-6 (IL-6) levels were determined before intervention and at 5 minutes, 24 hours, 48 hours, 72 hours, and 7 days after intervention. Creatine kinase-myocardial isoenzyme (CK-MB) and cardiac troponin I (cTnI) were measured at baseline and then 24 hours following PCI. Results Plasma CRP and IL-6 levels increased from baseline after PCI in all groups. CRP reached a maximum at 48 hours and IL-6 level reached a maximum at 24 hours after PCI. Plasma CRP levels at 24 hours after PCI were significantly lower in the HD group ((9.14±3.02) mg/L) than in the LD group ((11.06±3.06) mg/L) and ND group ((12.36±3.08) mg/L, P <0.01); this effect persisted for 72 hours. IL-6 levels at 24 hours and 48 hours showed a statistically significant decrease in the HD group ((16.19±5.39) ng/L and (14.26±4.12) ng/L, respectively)) than in the LD group ((19.26±6.34) ng/L and (16.03±4.08) ng/L, respectively, both P <0.05) and ND group ((22.24±6.98) ng/L and (17.24±4.84) ng/L, respectively). IL-6 levels at 72 hours and 7 days showed no statistically significant difference among the study groups. Although PCI caused a significant increase in CK-MB and cTnI at 24 hours after the procedure in all groups, the elevated CK-MB and cTnI values were lower in the HD group ((4.71±4.34) ng/ml and (0.086±0.081) ng/ml, respectively) than in the ND group ((7.24±6.03) ng/ml and (0.138±0.103) ng/ml, respectively, both P <0.01) and LD group ((6.80±5.53) ng/ml and (0.126±0.101) ng/ml, respectively, both P <0.01). Conclusion Short-term high-dose atorvastatin treatment before PCI significantly reduced systemic inflammatory response and myocardial ischemic injury elicited by PCI.

Ischemia-modified albumin is not better than creatine kinase-MB and cardiac troponin I in predicting a cardiac injury in nontraumatic subarachnoid hemorrhage

BackgroundThe aims were to investigate the role of serum ischemia-modified albumin (IMA), tumor necrosis factor α (TNF-α), and myeloperoxidase (MPO) and to evaluate the relationship between IMA and cardiac markers (creatine kinase myocardial isoenzyme [CK-MB] and cardiac troponin I [cTnI]) related to cardiac abnormalities in adult patients after nontraumatic subarachnoid hemorrhage (SAH). MethodsTwenty-nine patients with nontraumatic SAH admitted to the emergency department and 20 healthy adults as the control group were included in the study. Ischemia-modified albumin, TNF-α, MPO, CK-MB, cTnI, and leukocyte count (white blood cell [WBC]) in the circulation were measured on admission. ResultsIschemia-modified albumin, TNF-α, and MPO levels were higher by mean values of 11.6%, 9.5%, and 2.9%, respectively, in patients with SAH compared with control group. However, levels of these parameters were not statistically different between the groups (P > .05). However, WBC, CK-MB, and cTnI values were significantly higher in patients with SAH compared with healthy control (P < .001, P < .01, and P < .05, respectively). White blood cell and cTnI levels in the circulation were positively correlated with patients' clinical severity (r = 0.598, P = .001 and r = 0.461, P = .012, respectively). Ischemia-modified albumin has a poor diagnostic value in comparison with WBC, CK-MB, and cTnI tests to differentiate between patients after SAH and controls according to receiver operating characteristic curve. ConclusionsThe results suggest that IMA is not better than CK-MB and cTnI in predicting a cardiac injury in patients after nontraumatic SAH.

Study on the clinical efficacy of integrative medicine for 60 maternal with viral myocarditis

Objective To find out the clinical effect of integrative therapy for pregnant women with viral myocarditis(VMC).Methods The experimental group 60 VMC maternal cases were treated by integrative therapy,while the control group 43 patients were treated by simple western medicine,the efficacy of two treatments were compared,and left ventricular function,myocardial enzymes and other indicators were compared.Results Markedly effective rate of control group was 48.84％,and total effcctive rate was 72.09％ ; markedly effective rate of experimental group was 65.00％,and total effective rate was 91.67％.Markedly effective rate and total effective rate of experimental group were significantly higher(P ＜0.05).After treatment,stroke volume,ejection fraction and cardiac output index of experimental group were significantly higher than before treatment (P ＜ 0.05 ); After treatment,the indexes of experimental group and control group were significantly different ( P ＜ 0.05 ).After treatment,creatine kinase,creatine kinase myocardial isoenzyme,aspartate aminotransferase and lactate dehydrogenase index of experimental group were significantly lower than before treatment ( P ＜ 0.05 ) ; After treatment,the indicators of experirnental group were lower than control group( P ＜ 0.05 ).Conclusion This prescription is used to treat pregnant women with valid prescriptions of VMC,the clinical efficacy of integrative medicine is significant,the cardiac contractile function can he improved,and a strong application advantages is shown compared to conventional therapy with simple western medicine. Key words: TCM WM therapy; Myocarditis; Perinatai care; Therapy

Protective effect of lipid microspheres 1 on myocardial injury following elective percutaneous coronary intervention in patients with angina pectoris

Prostaglandin E1 incorporated into lipid microspheres (lipo-PGE1) is effective in the treatment of peripheral vascular disorders and diabetic neuropathy. It is unknown whether it has protective effects in patients with angina pectoris undergoing percutaneous coronary intervention (PCI). The goal of this pilot study was to investigate whether lipo-PGE1 has protective effects in patients with angina pectoris undergoing PCI. A single-blinded, randomized controlled trial was conducted in 79 patients with stable or unstable angina pectoris. The control group received standard medical therapy, and the Lipo-PGE1 group (n = 40) received 20 μg/day of lipo-PGE1 intravenously, starting at least 48 h before PCI and continuing for 5 days. Cardiac troponin T (cTnT) and creatine kinase myocardial isoenzyme (CK-MB) were measured before lipo-PGE1 infusion and at 6, 12 and 24 h after PCI. The cTnT and CK-MB concentrations were lower in the lipo-PGE1 group than in the control group at 6 h (0.15 ± 0.33 vs. 0.43 ± 0.77; 2.87 ± 3.99 vs. 5.64 ± 6.27, respectively; P < 0.05), 12 h (0.20 ± 0.48 vs. 0.54 ± 0.85; 3.58 ± 5.22 vs. 7.45 ± 9.48; P < 0.05) and 24 h (0.18 ± 0.50 vs. 0.50 ± 0.75; 3.15 ± 4.50 vs. 6.16 ± 6.83; P < 0.05). The incidence of postprocedural myocardial injury, defined as an elevation of cTnT more than 0.1 ng/ml or CK-MB more than 5.0 ng/ml, was less in the PGE1 group than in the control group (30 vs. 54%; 13 vs. 31%, respectively; P < 0.05). Lipo-PGE1 was well tolerated and there were no serious adverse events or side-effects. Lipo-PGE1 treatment appears to reduce myocardial injury following elective PCI in angina patients.

Short-term high-dose atorvastatin for periprocedural myocardial infarction prevention in patients with renal dysfunction

Short-term high-dose atorvastatin administered before percutaneous coronary intervention (PCI) reduces the rate of periprocedural myocardial infarction (pMI) in high-risk patients, such as those with acute coronary syndromes and those with elevated high-sensitivity C-reactive protein. It is unknown whether short-term high-dose administration reduces the rate of pMI in patients with chronic kidney disease. Recently, we observed that in 304 patients with estimated creatinine clearance less than 60 ml/min randomized to receive 80 mg/day of atorvastatin or placebo for 48 h before elective coronary angiography and/or angioplasty, statin administration did not reduce contrast-induced nephropathy (CIN). In this post-hoc analysis, we evaluate the pMI in the subgroup of 161 patients who underwent PCI. In all patients, creatine kinase myocardial isoenzyme (CK-MB) [upper reference limit (URL) 5 ng/ml] was assessed before and at 12 and 24 h after PCI. The pMI, defined as CK-MB elevation more than three times the URL, occurred in 27 (17%) patients. The incidence of pMI was 10.4% (of 77 patients) in the atorvastatin and 23% (of 84 patients) in the placebo group (P < 0.05). Multivariate analysis identified the pretreatment with high-dose atorvastatin as an independent predictor of reduced risk of pMI [odds ratio 0.39, 95% confidence interval 0.16-0.96, P < 0.05]. This post-hoc analysis shows that short-term high-dose atorvastatin administration reduced pMI in patients with renal dysfunction submitted to elective PCI, but without benefit regarding CIN prevention.

Novel Approaches for Preventing or Limiting Events (Naples) II Trial: Impact of a Single High Loading Dose of Atorvastatin on Periprocedural Myocardial Infarction

Atorvastatin administered at least 7 days before the percutaneous coronary intervention (PCI) reduces the rate of periprocedural myocardial infarction (MI). It is unknown whether a single, high (80 mg) loading dose of atorvastatin may reduce the rate of periprocedural MI. Periprocedural MI is a prognostically important complication of PCI. The day before the elective PCI, 668 statin-naive patients were randomly assigned to atorvastatin 80 mg (atorvastatin group; n = 338) or no statin treatment (control group; n = 330). Creatine kinase-myocardial isoenzyme (CK-MB) (upper limit of normal [ULN] 3.5 ng/ml) and cardiac troponin I (ULN 0.10 ng/ml) were assessed before and 6 and 12 h after the intervention. Periprocedural MI was defined as a CK-MB elevation >3x ULN alone or associated with chest pain or ST-segment or T-wave abnormalities. The incidence of a periprocedural MI was 9.5% in the atorvastatin group and 15.8% in the control group (odds ratio: 0.56; 95% confidence interval: 0.35 to 0.89; p = 0.014). Median CK-MB peak after PCI was 2.10 ng/ml (interquartile range 1.00 to 12.50 ng/ml) in the atorvastatin group and 3.20 ng/ml (interquartile range 1.37 to 16.07 ng/ml) in the control group (p = 0.014). The incidence of cardiac troponin I elevation >3x ULN was 26.6% in the atorvastatin group and 39.1% in the control group (odds ratio: 0.56; 95% confidence interval: 0.40 to 0.78; p < 0.001). A single, high (80 mg) loading (within 24 h) dose of atorvastatin reduces the incidence of periprocedural MI in elective PCI.

External Quality Assessment for biochemical markers of myocardial damage: an Italian experience

In 1999 the Centre of Biomedical Research (CRB) in co-operation with the Italian interdisciplinary and intersociety Working Group on Markers of Myocardial Damage proposed a national external quality assurance scheme that was granted in accordance with the UK Clinical Pathology Accreditation Standards in 2001. The scheme, which stresses the importance of educational aspects in quality assurance, was scientifically designed to ensure that it would provide an objective assessment of participants' performance and promote quality improvements to meet the needs of participants. The present paper reports on the data collected in EQA cycles conducted to evaluate improvements in the performance of participants and in related methods. The findings obtained demonstrate that during the 4-year experience the scheme provided opportunities to improve the performance of laboratories and promoted an efficient, more satisfactory approach to analytical aspects. The number of unacceptable performances decreased from 11.6% to 5.6% for troponin I, from 19.5% to 9.0% for myoglobin and from 13.2% to 4.3% for creatine kinase myocardial isoenzyme (CK-MB). During cycles in 2001 and 2002, inter-variability (coefficient of variation, CV%) data for all markers appeared satisfactory and showed a significant improvement (lower than 10%), in particular for procedures automated on Dade Behring Dimension and Beckman Access systems. However, reference values/decisional limits declared by laboratories and those suggested by the manufacturers are not comparable, even within the same diagnostic system. The findings demonstrate that participation in EQA schemes provided an opportunity for participating laboratories to continuously improve the quality of their services.

Myocardial injury and left ventricular performance after subarachnoid hemorrhage.

Electrocardiographic abnormalities and elevations of the creatine kinase myocardial isoenzyme (CK-MB) occur frequently after subarachnoid hemorrhage. In some patients, a reversible and presumably neurogenic form of left ventricular dysfunction is demonstrated by echocardiography. It is not known whether cardiac injury of this type adversely affects cardiovascular hemodynamic performance. We retrospectively studied 72 patients admitted to our neuro-ICU for aneurysmal subarachnoid hemorrhage over a 2.5-year period. We selected patients who met the following criteria: (1) CK-MB levels measured within 3 days of onset, (2) pulmonary artery catheter placed, (3) echocardiogram performed, and (4) no history of preexisting cardiac disease. Hemodynamic profiles were recorded on the day after surgery (n=67) or on the day of echocardiography (n=5) if surgery was not performed (mean, 3. 3+/-1.7 days after onset). The severity of cardiac injury was classified as none (peak CK-MB <1%, n=36), mild (peak CK-MB 1% to 2%, n=21), moderate (peak CK-MB >2%, n=6), or severe (abnormal left ventricular wall motion, n=9). Abnormal left ventricular wall motion occurred exclusively in patients with peak CK-MB levels >2% (P<0.0001), poor neurological grade (P=0.002), and female sex (P=0.02). Left ventricular stroke volume index and stroke work index were elevated above the normal range in patients with peak CK-MB levels <1% and fell progressively as the severity of cardiac injury increased, with mean values for patients with abnormal wall motion below normal (both P<0.0001 by ANOVA). Cardiac index followed a similar trend, but the effect was less pronounced (P<0.0001). Using forward stepwise multiple logistic regression, we found that thick subarachnoid clot on the admission CT scan (odds ratio, 1.9; 95% confidence interval [95% CI], 1.0 to 3.4; P=0.04) and depressed cardiac index (odds ratio, 2.1; 95% CI, 1.0 to 4.1; P=0.04) were independent predictors of symptomatic vasospasm. Myocardial enzyme release and echocardiographic wall motion abnormalities are associated with impaired left ventricular performance after subarachnoid hemorrhage. In severely affected patients, reduction of cardiac output from normally elevated levels may increase the risk of cerebral ischemia related to vasospasm.

Results of 1,454 Free Right Internal Thoracic Artery-to-Coronary Artery Grafts

After beginning our use of bilateral internal thoracic artery grafts in 1985, we found the pedicled right internal thoracic artery grafts limiting, and expanded the application of the right internal thoracic artery by elective use as a free graft. We evaluated the results of patients having a free right internal thoracic artery (FRITA)-to-coronary artery graft as part of their coronary revascularization. From 1986 to 1995, 1,454 patients had a FRITA graft. Preoperative characteristics included mean age, 58.8 years (range 29 to 84 years); non-insulin-dependent diabetes, 116 (8%); insulin-dependent diabetes, 7 (0.5%); left ventricular ejection fraction from 0.30 to 0.40, 159 (11%); left ventricular ejection fraction less than 0.30, 14 (1%); and unstable angina, 144 (9.9%). In 11 patients the FRITA was the only graft, in 1,443 a left internal thoracic graft was also used and revascularization completed with additional arterial and vein grafts. There were 3.3 +/- 1.1 distal anastomoses per patient, the aortic clamp time was 49 +/- 12 minutes, and bypass time was 69 +/- 16 minutes. The FRITA was used to reach the circumflex marginal arteries in 718 patients (49.5%), posterior descending artery in 286 (19.7%), diagonal or intermediate in 172 (11.8%), left anterior descending artery in 119 (8.1%), right coronary artery in 115 (7.9%), and left ventricular branch of right coronary artery in 44 (3%). The proximal anastomosis was directly on the aorta in 1,441, other arterial graft in 8, and vein graft in 5. Operative mortality was 13 patients (0.9%); stroke occurred in 14 patients (1%) and myocardial infarction in 19 (1.3%). The peak creatine kinase myocardial isoenzyme serum level was 20.6 +/- 13.6 IU/L. Complications included sternal infection in 18 patients (1.2%) and reoperation for hemorrhage in 23 (1.6%). Survival at 5 and 7 years, respectively, was 96% +/- 2.1% and 94% +/- 2.5%. In 71 patients with a FRITA studied at a mean of 41.5 +/- 14 months postoperatively for recurrent symptoms, 67 FRITA grafts were widely patent (94.5%), 3 displayed a string sign, and 1 was totally occluded. Use of the right internal thoracic artery as a free graft is safe and effective and allows greater flexibility in arterial coronary revascularization.

Frequency of chronic obstructive airways disease and pulmonary hypertension in patients with acute inferior myocardial infarction with or without right ventricular infarction

Objective: Factors influencing the incidence of right ventricular infarction among patients with acute inferior myocardial infarction have not yet been fully established. Chronic obstructive airways disease and right ventricular hypertrophy were suggested as possible predisposing factors but no definite evidence was shown. This study analyses the frequency of chronic obstructive airway disease and of Doppler assessed pulmonary hypertension among patients with acute inferior myocardial infarction with or without right ventricular infarction. Design and patients: Sixty consecutive patients with acute inferior myocardial infarction were prospectively enrolled into the study. Measurements: Standard 12-lead ECG with right precordial leads (V 3–6R) were recorded on admission to the Coronary Care Unit and on days 2 and 3. Doppler echocardiography was performed within 48 h after the onset of myocardial infarction and repeated 6 weeks later together with a pulmonary function test. Routine biochemical and clinical data were collected. Results: Right ventricular infarction occurred in 35% of patients with acute inferior myocardial infarction. No differences in respiratory indices of chronic obstructive airways disease or in Doppler echocardiography parameters of pulmonary hypertension were revealed among patients with and without right ventricular infarction. Peak total creatine kinase level and creatine kinase myocardial isoenzyme levels were higher in patients with right ventricular infarction than in those without (2925 ± 1321 vs. 1682 ± 1216 U l ; P < 0.001 and 207 ± 108 vs. 127 ± 102 U l ; P < 0.05, respectively). Conclusions: In the course of acute inferior myocardial infarction, the frequencies of chronic obstructive airways disease and/or pulmonary hypertension were not higher among patients with right ventricular infarction than among those without right ventricular infarction. Thus, history of chronic obstructive airways disease and/or pulmonary hypertension do not necessitate specific precautions in respect of right ventricular infarction.

Interaction and dose equivalence of salbutamol and salmeterol in patients with asthma.

To examine the pharmacological interaction of salmeterol and salbutamol and to derive an estimate of dose equivalence of salmeterol for airway and systemic effects in patients with asthma. Randomised double blind crossover study. 12 patients with mild asthma. Placebo or salmeterol 50, 100, 200 micrograms given on separate days followed two hours later by inhaled salbutamol in cumulative doses up to 3600 micrograms. Change in forced expiratory volume in one second (FEV1), heart rate, plasma potassium concentration, QTc interval, tremor amplitude, and creatine kinase myocardial isoenzyme concentration. Compared with placebo, the mean (95% confidence interval) changes in FEV1 and heart rate after salmeterol 200 micrograms were 0.61 (0.32 to 0.90) l and 7.0 (3.8 to 10.2) beats/min. Adding salbutamol caused a large increase in FEV1 after placebo (0.69 l) with progressively smaller changes after increasing doses of salmeterol (0.19 l after salmeterol 200 micrograms). Heart rate and QTc interval increased and plasma potassium concentration decreased roughly in parallel on the four study days with a suggestion of convergence at higher doses of salbutamol. Geometric mean dose equivalences for salmeterol 50 micrograms and 100 micrograms compared with salbutamol were 4.9 and 7.8 (mean 6.4) for FEV1 and ranged from 7.1 (2.9 to 17.0) to 12.6 (4.4 to 36.4) for heart rate, plasma potassium, and tremor (mean 9.5). The effect of adding salbutamol to salmeterol is largely additive. Weight for weight salmeterol may be up to 10 times more potent than salbutamol. Considering its longer duration of action salmeterol 50 micrograms twice daily could be equivalent to salbutamol in doses up to 500 micrograms four to six hourly.

Left Ventricular Wall Motion Abnormalities in Subarachnoid Hemorrhage: An Echocardiographic Study

Although electrocardiographic (ECG) abnormalities and autopsy evidence of myocardial necrosis are associated with subarachnoid hemorrhage, their relation to in vivo measures of left ventricular function in this condition has not been established. Thirteen patients with subarachnoid hemorrhage and no prior history of heart disease were studied by two-dimensional echocardiography, performed initially 10 to 48 h (mean 18) after admission and serially for less than or equal to 14 days. Serum creatine kinase (total and myocardial isoenzyme) was determined 5 times over the first 48 h; ECGs were performed daily. Neurologic state was assessed with the use of a standard grading system. Four patients (Group I) exhibited left ventricular wall motion abnormalities in one to eight segments. In two of these patients there was also left ventricular apical mural thrombus that embolized in one patient, leading to further neurologic deterioration. The initial creatine kinase myocardial isoenzyme was higher in Group I than in Group II (patients without wall motion abnormalities) (10.3 versus 2.1 U/liter, p less than 0.001), initial heart rate was higher (91 versus 61 beats/min, p less than 0.01), neurologic grade was higher (2.5 to 4.5 versus 1 to 2, p less than 0.001) and inverted T waves were more common (4 of 4 versus 1 of 9). Three of the four patients in Group I died; two of the three underwent autopsy and were found to have no significant coronary artery disease. No other patients died.(ABSTRACT TRUNCATED AT 250 WORDS)

β-blockers, plasma total creatine kinase and creatine kinase myocardial isoenzyme, and the prognosis of subarachnoid hemorrhage

Under double-blind randomized conditions the effects of early intervention with oral propranolol or a placebo were studied in 51 cases of subarachnoid hemorrhage. Eleven out of 23 patients randomly assigned to placebo had a poor outcome at 6 months, while 2 of the 28 patients randomly assigned to propranolol had a poor outcome (p < 0.001). Patients with a poor outcome on the placebo had significantly higher mean plasma total creatine kinase levels (742 IU, standard error of the mean ± 233 IU) on the fifth day after subarachnoid hemorrhage than patients with a good outcome on the placebo (108 ± 20 IU; p < 0.05). A raised plasma creatine kinase myocardial isoenzyme was associated with a particularly poor outlook in patients receiving the placebo, in contrast to those taking a β-blocker. Clinical outcome and plasma creatine kinase levels in patients taking atenolol (hydrophilic) were similar to those observed in patients receiving propranolol.

Secondary myocardial injuries.

This study identifies a subgroup of critically ill patients most likely to develop at least creatine kinase-myocardial isoenzyme (CK-MB) evidence of acute myocardial injury. This group is composed of patients with shock syndromes associated with some combination of anemia, hypoxemia, hypercarbia, acidemia, lactic acidosis, and hypotension. The mechanism of this secondary myocardial injury in shock is not clear but may be multifactorial. Certainly subgroups of patients admitted with critical illnesses may have CK-MB abnormalities usually associated with acute myocardial injury.