Peak Creatine kinase-MB Research Articles

Quantification of the effect of clopidogrel on enzymatic infarct size related to a percutaneous coronary intervention in patients with acute coronary syndromes

Using data from the CHAMPION percutaneous coronary intervention (PCI), we determined the relationship between clopidogrel started at least 5 days before PCI (maintenance of clopidogrel) and PCI-related enzymatic infarct size. Clopidogrel is recommended in patients with acute coronary syndrome (ACS) managed with PCI, but its effect on PCI-related myonecrosis in contemporary patients has not been quantified. Patients with ACS (with or without ST-segment elevation) who underwent PCI and had at least three creatine kinase-MB (CK-MB) samples after PCI were included. Enzymatic infarct size was defined as the peak CK-MB concentration indexed by its upper limit of normal. Associations between maintenance clopidogrel and enzymatic infarct size were explored using multivariable linear regression (with and without missing data imputation) and propensity score analysis using inverse probability weighting. Of 8877 patients randomized, 6327 (71.3%) were included (median age 61 years, 73% male, 13% ACS with ST-segment elevation). Of these 6327 patients, 2015 (31.8%) were on maintenance clopidogrel. After multivariable adjustment, maintenance clopidogrel was associated with a reduction in enzymatic infarct size {β=-0.63; 47% decrease in peak CK-MB [95% confidence interval (CI) 35, 56%]}. Multivariable linear regression with multiple imputations and inverse probability weighting propensity score analysis yielded similar results, with maintenance clopidogrel associated with 44% (95% CI 33, 53%) and 29% (95% CI 24, 33%) infarct size reductions. In this subgroup analysis of modern ACS patients, clopidogrel maintenance was independently associated with smaller enzymatic infarct size after PCI. These results are consistent with previous observations suggesting a benefit of clopidogrel on the procedural outcome and quantify this benefit.

Myocardial damage following cardiac surgery: comparison between single-dose Celsior cardioplegic solution and cold blood multi-dose cardioplegia

Myocardial protection during cardiac surgery can be accomplished by different cardioplegic solutions. The aim of this study was to assess myocardial damage after heart valve surgery performed with myocardial protection of a single dose of Celsior cardioplegia or with repeated cold blood cardioplegia. After the stratification of 139 valvular patients by means of matching according to cross-clamp and cardiopulmonary bypass time, 32 patients were retained for comparison (16 patients received Celsior and 16 patients received cold blood cardioplegia). Creatine kinase-MB (CK-MB) and cardiac troponin I (cTnI) release were evaluated until six days after the operation. Pre-operative characteristics were similar in both groups. In the Celsior group, CK-MB and cTnI values were significantly higher from the first up to the sixth post-operative day. Peak cTnI values were 19.4 ± 13.4 and 9.7 ± 7 ng/mL (p=0.01) in the Celsior and the Cold Blood group, respectively. Peak CK-MB values were 79.6 ± 58.8 and 45.9 ± 20.6 U/L (p=0.07) in the Celsior and the Cold Blood group, respectively. Cold blood cardioplegia reduces perioperative myocardial damage compared to the Celsior solution in elective cardiac valve operations.

Clinical, angiographic, and intravascular ultrasound predictors of early stent thrombosis in patients with acute myocardial infarction

Risk factors reported for early stent thrombosis (EST) included acute coronary syndrome, suboptimal antiplatelet therapy, procedural factors such as residual dissection and underexpansion of stents, and smaller final lumen area and inflow/outflow disease (residual stenosis or dissection) by intravascular ultrasound (IVUS) [1–4]. However, the predictors of EST including all variables such as baseline characteristics, laboratory data, angiographic and IVUS findings in patients with acute myocardial infarction (AMI) are still not well known. From January 2007 to December 2009, we identified 418 consecutive patients with a first AMI who underwent pre-percutaneous coronary intervention (PCI) IVUS within 24 h from symptom onset, were stented successfully, and had post-PCI IVUS imaging. EST included acute (b24 h) and subacute ST (1 to 30 days) after stent implantation. Cardiac-specific troponin I (cTnI) levels were measured by a paramagnetic particle, chemiluminescent immunoenzymatic assay (Beckman, Coulter Inc., Fullerton, California). No-reflow was defined as postPCI TIMI grade 0, 1, or 2 flow. Tissue prolapse was defined as tissue extrusion through the stent strut at post-PCI. The baseline characteristics, angiographic and IVUS findings are summarized in Table 1. EST occurred in 16 patients (3.8%). Glycoprotein IIb/IIIa inhibitor was used more frequently in patients with EST compared with those without EST. Pre-PCI peak creatine kinase-MB and cTnI were significantly higher in patients with EST compared with those without EST. Pre-PCI TIMI flow grade was significantly lower in patients with EST compared with those without EST. More stents were deployed in patients with EST compared with those without EST. Noreflow during or after PCI was developed more frequently in EST group than in non-EST group (87.5% vs. 12.2%, p b 0.001). Plaque burden at the minimum lumen site was significantly greater in patients with EST compared with those without EST. Pre-PCI plaque rupture and IVUSdetected thrombuswere observedmore frequently in patients with EST compared with those without EST. Post-stenting tissue prolapse was observed more frequently in patients with EST compared with those without EST (68.8% vs. 32.6%, p= 0.003). Independent predictors of EST are summarized in Table 2. Multivariate analysis showed that noreflow, pre-PCI peak cTnI, and tissue prolapse were the independent predictors of EST. No-reflow can occur easily in lesions with various kinds of vulnerable plaque including plaque rupture and thrombus and this no-reflow is associated with microvascular damage which is likely to slow the epicardial coronary blood flow and to stagnate blood flow which may accelerate local thrombus formation [5]. The mechanism underlying the association between pre-PCI peak cTnI level and EST is not clear, although cTnI is associated with high thrombus grade with promoted thrombus formation in patients with AMI, who already have heightened systemic and intracoronary platelet reactivity, thrombin generation, and inflammation. Tissue prolapse may represent a source for thrombus accumulation in an environment that already has a high potential for thrombogenesis. Impaired arterial healing and ST have been associated with the prolapse of the necrotic core between stent struts. This is especially relevant in the setting of AMI, because such patients already have an increased risk for this devastating event [6]. In conclusion, the incidence of EST after stenting of infarct-related arteries was 3.8%. No-reflow, pre-PCI peak cTnI and tissue prolapse were associated with the development of EST after stent implantation in patients with AMI.

Impact of multivessel disease on myocardial perfusion and survival among patients undergoing primary percutaneous coronary intervention with glycoprotein IIb/IIIa inhibitors

Although primary angioplasty achieves thrombolysis in myocardial infarction (TIMI) 3 flow in most patients with ST-elevation myocardial infarction, epicardial recanalization does not guarantee optimal perfusion in a large proportion of patients. The influence of multivessel disease on myocardial reperfusion and survival after primary angioplasty has not been extensively investigated. To evaluate the impact of multivessel disease on myocardial perfusion and survival in a large cohort of patients with ST-elevation myocardial infarction treated with angioplasty and glycoprotein (GP) IIb/IIIa inhibitors. This analysis is based on 1494 patients undergoing primary angioplasty included in the EGYPT database. Myocardial perfusion was evaluated by angiography or ST-segment resolution, whereas infarct size was estimated by using peak creatine kinase-MB (CK-MB). Follow-up data were collected between 30 days and 1 year after primary angioplasty. Multivessel disease was observed in 870 patients (58.2%). The extent of coronary artery disease was associated with age, diabetes, hypertension, previous myocardial infarction, previous revascularization, abciximab treatment and longer ischaemic time, and was independently associated with impaired angiographic myocardial perfusion (adjusted odds ratio 1.18, 95% confidence interval [CI] 1.01-1.40, P=0.049). At 208±160 days, the extent of coronary artery disease was independently associated with higher mortality (adjusted hazard ratio 1.54, 95% CI 1.06-2.24, P=0.022). Among patients with ST-elevation myocardial infarction undergoing primary angioplasty with GP IIb/IIIa inhibitor treatment, the extent of coronary artery disease was independently associated with impaired myocardial perfusion and survival.

Analysis of factors related to short-term prognosis in patients undergoing percutaneous coronary intervention for acute myocardial infarction

The present study aimed to investigate the factors related to short-term prognosis in patients undergoing direct percutaneous coronary intervention (PCI) for acute ST-segment elevation myocardial infarction (STEMI). A total of 805 patients were included and divided into a control group and an adverse cardiovascular events group based on the prognosis, to compare risk factors and coronary angiographic characteristics in the two groups. In the adverse events group, the ages, admission blood glucose, uric acid (UA), homocysteine (HCY), creatine kinase (CK) and peak creatine kinase-MB (CKMB) isozyme levels were clearly higher compared with those in the control group, while the levels of total cholesterol (TC), triglycerides (TGs) and low-density lipoprotein (LDL) were lower compared with those in the control group. The incidence of hypertension in females in the adverse events group was markedly higher compared with that in the control group, while the diabetes rate was lower compared with that in the control group. Logistic regression analysis revealed that age, gender, hypertension, diabetes and admission blood glucose, HCY, TC and UA levels were independent risk factors of short-term prognosis in patients undergoing emergency PCI. The majority of the patients in the adverse events group were elderly females with hypertension, a large area of myocardial infarction and increased admission blood glucose, UA and HCY levels, as well as a low diabetes rate and decreased levels of acute-phase TC and LDL.

Ischemic Postconditioning may Increase Serum Fetuin-A Level in Patients with Acute ST-Segment Elevation Myocardial Infarction Undergoing Percutaneous Intervention

Fetuin-A inhibits inflammation and has a protective effect against myocardial ischemia. We investigated the influence of ischemic postconditioning on serum fetuin-A levels and high-sensitive C-reactive protein (hs-CRP) in patients with acute ST-segment elevation myocardial infarction undergoing percutaneous intervention. Forty-five patients undergoing percutaneous coronary intervention (PCI) were randomly assigned to a control (n = 21) or postconditioning (PC, n = 24) group within 90 minutes after admission. After predilatation, in the control group, no intervention was applied in the first 3 minutes of reperfusion, while in the postconditioning group, three cycles of 30-second angioplasty balloon deflation and 30-second inflation were repetitively applied. Blood samples were obtained and assayed for creatine kinase MB (CK-MB), fetuin-A and hs-CRP. The control group presented with higher peak CK-MB as compared with the PC group (123.67 +/- 44.19 vs. 93.08 +/- 35.29 U/L, p < 0.05). After PCI, PC was associated with a lower level of hs-CRP in comparison with the control group (6.07 +/- 1.35 vs. 7.03 +/- 1.27 mg/L, p < 0.05). Serum fetuin-A levels in the PC group was higher than in the control (161.06 +/- 23.98 mg/L vs. 144.59 +/- 22.76 mg/L, p < 0.05). Postconditioning may increase serum fetuin-A levels and decrease high-sensitive C-reactive protein in myocardial infarction patients.

Troponin T is a better predictor than creatine kinase-MB of long-term mortality after coronary artery bypass graft surgery

Elevations of creatine kinase-MB (CK-MB) and cardiac troponin T (cTnT) have an uncertain long-term prognostic value after coronary artery bypass graft (CABG) surgery. We aimed to test the hypothesis that CK-MB and cTnT are predictors of long-term survival after CABG and to assess which of these 2 biomarkers is the better predictor. A total of 1,350 consecutive patients undergoing isolated on-pump CABG had CK-MB and cTnT measured at 7, 20, and 44 hours, postoperatively. The end point was all-cause mortality, and during the median follow-up time of 6.1 years, 207 patients (15.3%) died. Both peak CK-MB and peak cTnT independently predicted long-term mortality (hazard ratio [HR] 1.003, 95% confidence interval [CI] 1.001-1.005, P = .007, and HR 1.31, 95% CI 1.17-1.46, P <.001, respectively) when analyzed in separate multivariate Cox models, adjusting for baseline demographic characteristics and perioperative risk factors. However, when analyzed simultaneously in the same Cox model, cTnT was a significant predictor (HR 1.31, 95% CI 1.13-1.51, P <.001), whereas CK-MB was not (P = .99). Similar results were found when the biomarkers were analyzed together in a Cox model adjusting for European System for Cardiac Operative Risk Evaluation. The differences in mortality between the biomarker groups were consistent also when analyzing strict quartiles of peak values of CK-MB and cTnT (P = .81 and P = .001, respectively). Both CK-MB and cTnT are predictors of mortality after CABG surgery; however, our data suggest that cTnT is a better predictor of long-term mortality after CABG surgery than CK-MB.

Prognostic Value of Total Bilirubin in Patients With ST-Segment Elevation Acute Myocardial Infarction Undergoing Primary Coronary Intervention

Previous studies have shown that the serum total bilirubin (TB) concentration was inversely related with stable coronary artery disease, diabetes mellitus, hypertension, and metabolic syndromes. The relation between TB levels and in-hospital and long-term outcomes in patients with ST-segment elevation myocardial infarction (STEMI) who undergo primary percutaneous coronary intervention (PCI) is not known. Data from 1,624 consecutive patients with STEMI who underwent primary PCI were evaluated. TB was measured after primary PCI, and the study population was divided into tertiles. The high TB group (n=450) was defined as a value in the upper third tertile (>0.9 mg/dl) and the low TB group (n= 1,174) as any value in the lower 2 tertiles (≤0.9 mg/dl). The in-hospital mortality rate was significantly greater in the high TB group than in the low TB group (4% vs 1.5%, p= 0.003). In the multivariate analyses, a significant association was noted between high TB levels and the adjusted risk of in-hospital cardiovascular mortality (odds ratio 3.24, 95% confidence interval 1.27 to 8.27, p= 0.014). In the receiver operating characteristic curve analysis, TB >0.90 mg/dl was identified as an effective cutpoint in patients with STEMI for in-hospital cardiovascular mortality (area under the curve 0.66, 95% confidence interval 0.55 to 0.76, p= 0.001). The mean follow-up period was 26.2 months. No differences wereseen in the long-term mortality rates between the 2 groups. In conclusion, high TBisindependently associated with in-hospital adverse outcomes in patients with STEMIwhoundergo primary PCI. However, no association was found with long-term mortality.

THE VALUE OF LEAD AVR IN IDENTIFYING THE INFARCTED-RELATED ARTERY AND PROGNOSIS IN PATIENTS WITH ACUTE ANTERIOR MYOCARDIAL INFARCTION

ObjectivesTO investigate the value of lead aVR in identifying the infarcted-related artery and prognosis in patients with acute anterior myocardial infarction.MethodsWe analysed electrocardiogram and coronary angiography in patients with acute...

Level and value of interleukin-18 in patients with acute myocardial infarction undergoing primary coronary angioplasty

The prognostic value of interleukin (IL)-18 in patients with ST-segment elevation acute myocardial infarction (STEMI) is currently unclear. Thus, the purpose of this study was to test whether the circulating IL-18 level can predict prognosis in patients with STEMI undergoing primary percutaneous coronary intervention (PCI). A prospective cohort study was conducted with 267 consecutive patients with STEMI of onset <12 h who were undergoing primary PCI. Blood samples for plasma IL-18 level were collected in the catheterization laboratory following vascular puncture. The plasma IL-18 level was also evaluated in 25 healthy and 30 at-risk control subjects. The plasma level of IL-18 was significantly higher in acute myocardial infarction (AMI) patients than in both groups of control subjects (all P < 0.0001). Patients with high plasma IL-18 level (⩾560 pg/ml) had significantly higher peak creatine kinase-MB levels, higher incidence of cardiogenic shock upon presentation, significantly lower left ventricular ejection fraction (LVEF), lower successful reperfusion and significantly higher incidence of 30-day composite major adverse clinical events (MACE) (advanced congestive heart failure ⩾class 3 or 30-day mortality) than those patients with low plasma IL-18 level (<560 pg/ml) (all P < 0.0001). Multiple stepwise logistic regression analysis demonstrated that high plasma IL-18 level (⩾560 pg/ml) along with low LVEF (<50%) and cardiogenic shock were the most independent predictors of 30- day MACE ( P < 0.0001). In patients with STEMI, plasma IL-18 level is a major independent inflammatory predictor of 30-day MACE. Evaluation of circulating IL-18 might improve the prediction of unfavorable clinical outcomes following AMI.

The “no-dissection” technique is safe for reoperative aortic valve replacement with a patent left internal thoracic artery graft

Management of a patent left internal thoracic artery graft during reoperation is controversial. The "no-dissection" technique avoids dissection and clamping of the left internal thoracic artery graft, and myocardial protection is achieved using adjunctive systemic hypothermia and hyperkalemia. We compared the postoperative outcomes after isolated reoperative aortic valve replacement in patients with previous coronary artery bypass grafting with a patent left internal thoracic artery graft using a no-dissection technique with the outcomes of patients with previous coronary artery bypass grafting without a left internal thoracic artery graft. The outcomes were analyzed for patients who underwent isolated reoperative aortic valve replacement with previous coronary artery bypass grafting from January 1, 2002, to June, 30, 2011. Patency of the left internal thoracic artery was confirmed using either coronary angiography or computed tomography angiography. The patent left internal thoracic artery group did not undergo dissection or clamping of the left internal thoracic artery graft, and myocardial protection was obtained using systemic hypothermia and hyperkalemia. The no left internal thoracic artery group underwent isolated aortic valve replacement with previous coronary artery bypass grafting but had no left internal thoracic artery graft. A total 174 patients were identified for the patent left internal thoracic artery group and 26 for the no left internal thoracic artery group. The perfusion and crossclamp times were similar. No differences were seen between the 2 groups in operative mortality (6.9% vs 7.7%, P = 1.00). The complication rates were similar, and the peak creatine kinase-MB values within 24 hours of surgery were not significantly different between the 2 groups (median, 27.4 vs 29 μ/mL; P = .72). Reoperative aortic valve replacement in patients with previous coronary artery bypass grafting and a patent left internal thoracic artery graft can be performed safely without dissection or clamping of the left internal thoracic artery using systemic hyperkalemia and hypothermia. We believe this method prevents unnecessary injury during dissection of the left internal thoracic artery graft.

Comparison of the Prognostic Value of Peak Creatine Kinase‐MB and Troponin Levels Among Patients With Acute Myocardial Infarction: A Report from the Acute Coronary Treatment and Intervention Outcomes Network Registry–Get With The Guidelines

Although peak creatine kinase-myocardial band (CK-MB) and troponin levels have been correlated with mortality among patients with acute myocardial infarction (AMI), the independent prognostic implications of these markers have not been compared. We hypothesized that in patients with AMI, peak troponin levels (as compared to peak CK-MB levels) would have greater prognostic value. We examined AMI patients in the National Cardiovascular Data Registry ACTION Registry-GWTG (Acute Coronary Treatment and Intervention Outcomes Network Registry-Get With The Guidelines) with CK-MB and troponin I levels recorded, excluding patients who were transferred in or out. Peak marker levels, standardized by the local laboratory upper limit of normal and assay standard deviation, were fitted into the previously validated ACTION Registry-GWTG mortality model to compare prognostic value. Between January 2007 and March 2009, 16 009 ST-segment elevation myocardial infarction (STEMI) and 26854 non-ST-segment elevation myocardial infarction (NSTEMI) patients were identified. Peak marker ratios were directly associated with in-hospital mortality in both STEMI and NSTEMI patients. Peak CK-MB had slightly greater discrimination compared with peak troponin I in predicting mortality in both STEMI (model C-statistic 0.881 vs 0.877, P = 0.011) and NSTEMI (C-statistic 0.831 vs 0.824, P = 0.001) patients. Both peak CK-MB and peak troponin I levels are independently associated with in-hospital mortality in this large contemporary database of AMI patients treated in routine practice. Peak marker values slightly improved model performance in prognosticating in-hospital mortality; the incremental value was higher with CK-MB than with troponin I. These findings may help to guide future risk stratification algorithms and contribute to more efficient use of serial cardiac marker measurements in clinical practice.

Interpretation of elevated plasma visfatin concentrations in patients with ST-elevation myocardial infarction

Visfatin is a cytokine that is expressed in many tissues, including the heart, and has been proposed to play a role in plaque destabilization leading to acute myocardial injury. The present study evaluates plasma levels of visfatin in acute ST-elevation myocardial infarction (STEMI) patients and examines the temporal changes in visfatin levels from the acute period to the subacute period to determine a correlation with the degree of myocardial ischemia. We evaluated 54 patients with STEMI. Circulating levels of visfatin and brain natriuretic peptide (BNP) were measured by ELISA. In addition, local expression of visfatin and BNP were detected by quantitative real-time polymerase chain reaction and immunohistochemical (IHC) analysis of left ventricular myocytes in a mouse model of myocardial infarction (MI). Plasma levels of visfatin were significantly increased in patients with STEMI on admission, relative to controls (effort angina patients and individuals without coronary artery disease). The visfatin levels reached a peak 24h after percutaneous coronary intervention (PCI) and then decreased toward the control range during the first week after PCI. The basal plasma visfatin levels were found to correlate with peak troponin-I, peak creatine kinase-MB, total white blood cell count, and BNP levels. Trend analyses confirmed that visfatin levels correlated with the number of diseased coronary arteries. Further, in MI mice, mRNA levels of visfatin and BNP were found to be higher than in sham-treated mice. IHC analysis showed that visfatin and BNP immunoreactivity was diffusely observable in left ventricular myocytes of the MI mice. This study indicates that plasma visfatin levels are significantly higher in STEMI patients and that these higher visfatin levels correlate with elevated levels of cardiac enzymes, suggesting that increased plasma visfatin may be closely related to the degree of myocardial damage.

Prognostic Implications of Creatine Kinase-MB Elevation After Percutaneous Coronary Intervention

Creatine kinase-MB (CK-MB) elevation after percutaneous coronary intervention (PCI) has been associated with increased risk for mortality. Although most studies have defined periprocedural myocardial infarction (pMI) as an elevation in CK-MB >3× upper limit of normal (ULN), use of different CK-MB assays and variation in site-specific definitions of the ULN may limit the value of such relative thresholds. We used data from the multicenter Evaluation of Drug-Eluting Stents and Ischemic Events (EVENT) registry to examine the impact of variations in site-specific thresholds for CK-MB elevation on the incidence of pMI as well as the relationship between absolute peak levels of CK-MB after PCI and 1-year mortality. The study cohort consisted of 6347 patients who underwent nonemergent PCI and had normal CK-MB at baseline. Across the 59 study centers, the ULN for CK-MB ranged from 2.6 to 10.4 ng/mL (median, 5.0 ng/mL), and there was an inverse relationship between the site-specific ULN and the incidence of pMI (defined as CK-MB elevation >3× ULN). Although any postprocedure elevation of CK-MB was associated with an adverse prognosis, in categorical analyses, only CK-MB ≥50 ng/mL was independently associated with increased 1-year mortality (hazard ratio, 4.71; 95% confidence interval, 2.42 to 9.13; P<0.001). Spline analysis using peak CK-MB as a continuous variable suggested a graded, nonlinear relationship with 1-year mortality, with an inflection point at ≈30 ng/mL. Among unselected patients undergoing PCI, there is a graded relationship between CK-MB elevation after PCI and 1-year mortality that is particularly strong for large CK-MB elevations (>30 to 50 ng/mL). Future studies that include pMI as a clinical end point should consider using a core laboratory to assess CK-MB (to ensure consistency) and raising the threshold for defining pMI above current levels (to enhance clinical relevance).

High admission levels of γ-glutamyltransferase predict poor myocardial perfusion after primary percutaneous intervention

OBJECTIVE:This retrospective study aimed to investigate the relationship between admission levels of serum γ-glutamyltransferase and poor myocardial perfusion after primary percutaneous coronary intervention in patients with acute myocardial infarction.INTRODUCTION:Reperfusion injury caused by free radical release and increased oxidative stress is responsible for the pathophysiology of the no-reflow phenomenon in patients with acute myocardial infarction undergoing primary percutaneous coronary intervention. Serum γ-glutamyltransferase is an established marker of increased oxidative stress.METHODS:The study population consisted of 80 patients (64 men and 16 women, mean age = 67.5±6.6 years) with thrombolysis in myocardial infarction 0/1 flow pre-procedurally. The patients were divided into two groups according to thrombolysis in myocardial perfusion grades that were assessed immediately following primary percutaneous coronary intervention. The two groups (group 1 and group 2) each consisted of 40 patients with thrombolysis in myocardial perfusion grades 0-1 and thrombolysis in myocardial perfusion grades 2-3, respectively.RESULTS:Admission pain to balloon time, γ-glutamyltransferase and creatine kinase-MB isoenzyme levels of group 1 patients were significantly higher than those of group 2 patients. Pain to balloon time, γ-glutamyltransferase, peak creatine kinase-MB isoenzyme, low left ventricular ejection fraction and poor pre-procedural thrombolysis in myocardial infarction grade were significantly associated with poor myocardial perfusion by univariate analysis. However, only pain to balloon time and γ-glutamyltransferase levels showed a significant independent association with poor myocardial perfusion by backward logistic regression analysis. Adjusted odds ratios were calculated as 4.92 for pain to balloon time and 1.13 for γ-glutamyltransferase.CONCLUSION:High admission γ-glutamyltransferase levels are associated with poor myocardial perfusion in patients with acute myocardial infarction undergoing primary percutaneous coronary intervention, particularly in patients with prolonged pain to balloon time.

Peripartal Myocardial Infarction Caused by Placenta Embolus

A-32-year old second gravid woman without known cardiovascular risk factors underwent an elective cesarean delivery during the 33rd week of gestation because of intrauterine growth retardation secondary to placenta insufficiency. The latter was most likely related to a previously diagnosed symptomatic antiphospholipid syndrome. Twenty hours after an uncomplicated delivery, the patient reported a sudden onset of typical chest pain after a severe cough attack. Pulmonary embolism was ruled out by computed tomography. Chest pain had subsided 1 hour after onset following the initiation of medical therapy. The ECG showed transient, nonsignificant ST-segment changes (Figure 1) in the inferior leads, and cardiac enzymes were slightly elevated, reaching peak values 12 hours later. The diagnosis of subacute non–ST-elevation myocardial infarction (peak troponin I 2.240 μg/L [<0.010 μg/L], peak creatine kinase 1316 U/L [<170 U/L], and peak creatine kinase MB 87.9 μg/L [<4.0 μg/L ]) was established, and the patient was transferred to the coronary care unit. Transthoracic echocardiography showed a modest inferolateral hypokinesia with preserved global systolic left ventricular function (Movie I in the online-only Data Supplement). The patient underwent coronary …

Relationship between TIMI frame count and admission glucose values in acute ST elevation myocardial infarction patients who underwent successful primary percutaneous intervention

Admission hyperglycemia is associated with poor prognosis in patients with acute myocardial infarction. Final Thrombolysis in Myocardial Infarction (TIMI) frame counts of culprit coronary arteries may show significant variability despite successful coronary reperfusion after primary percutaneous coronary intervention (PCI). In this prospective observational study, relationship between final TIMI frame counts of the culprit coronary artery and admission glucose values was investigated in patients who underwent successful primary PCI due to acute ST-elevation myocardial infarction (STEMI). During a 6- month period of time, 73 non-diabetic patients presented with acute STEMI who have undergone primary PCI with final TIMI 3 flow were consecutively included in the study. Patients were divided into two groups according to final TIMI frame counts. Group 1 (n=53) consisted of patients with final TIMI frame counts of the culprit coronary artery within the two standard deviation of predefined values and Group 2 (n=20) consisted of those with higher TIMI frame counts. Statistical analysis was performed using Chi-square, Mann-Whitney U tests and multiple linear regression analysis. Despite similar fasting glucose values, admission glucose levels were significantly higher in Group 2 as compared to Group 1 (138 [114-165] vs. 123 [97-143] mg/dl, p=0.03). In whole group, admission glucose values were significantly correlated with corrected TIMI frame counts of culprit coronary arteries (r=0.30, p=0.01). In addition, there were significant association between admission glucose values and peak creatine kinase-MB (r=0.36, p=0.007) values as well as left ventricular ejection fraction (r=-0.43, p=0.009). In multiple linear regression analysis, only admission glucose value was found to be significantly related to the final TIMI frame count of the culprit artery (β=0.04, 95%CI: 0.02-0.085, p=0.04). High admission glucose values were significantly associated with impaired coronary flow even after successful primary PCI in non-diabetic patients with STEMI.

The implications of serum enzymes and coagulation activities in postinfarction myocardial

Associations between cardiovascular diseases and serum enzymes or coagulation activities have been sufficiently documented in patients with myocardial infarction. However, the alterations of these biomarkers in patients with postinfarction myocardial rupture have rarely been reported. The aim of this study is to present the profiles of the markers in patients with postinfarction myocardial rupture. From 2004 to 2008, 19 consecutive patients were referred to this hospital for surgical repair of postinfarction myocardial rupture. Eight (42.1%) patients had free wall rupture, 5 (26.3%) had papillary muscle rupture, 5 (26.3%) had ventricular septal rupture, and 1 (5.3%) had double structure (ventricular septum + free wall) rupture. Thirteen patients survived the operation, and 6 died. Laboratory findings including serum enzymes and coagulation activities were collected and analyzed. The coagulation markers and serum enzymes except for fibrinogen increased significantly after the development of myocardial rupture. Statistical differences in D-dimer, partial thromboplastin time, peak lactate dehydrogenase, peak creatine kinase and creatine kinase fraction MB were found between non-survivors and survivors. Troponin I values were elevated significantly during the early days after the onset or surgical repair of myocardial rupture. Multivariant regression analysis did not show any significant relationship between creatine phosphokinase fraction MB (Y) and D-dimer (X1) or fibrinogen (X2). Myocardial rupture leads to extremely high serum enzyme and coagulation activities except for fibrinogen after the onset. The evaluation of these biomarkers may help in making diagnostic and treatment decisions and in judging the clinical prognosis of such patients.

Localization of culprit lesions in coronary arteries of patients with ST-segment elevation myocardial infarctions: Relation to bifurcations and curvatures

Although culprit lesions in ST-segment elevation myocardial infarction (STEMI) cluster in the proximal coronary arteries, their relationship to bifurcations and curvatures, where blood flow is disturbed, is unknown. We hypothesized that (a) culprit lesions localize to disturbed flow distal to bifurcations and curvatures and (b) the distribution of culprit lesions in the left (LCA) and right coronary arteries (RCA) and resulting infarct size are related to the location of bifurcations and curvatures. Emory University's contribution to the National Cardiovascular Data Registry was queried for STEMIs. Using quantitative coronary angiography, the distances from the vessel ostium, major bifurcations, and major curvatures to the culprit lesion were measured in 385 patients. Culprit lesions were located within 20 mm of a bifurcation in 79% of patients and closer to the bifurcation in the LCA compared with the RCA (7.4 ± 7.3 vs 17.7 ± 14.8 mm, P < .0001). Of RCA culprit lesions, 45% were located within 20 mm of a major curvature. Compared with those in the RCA, culprit lesions in the LCA were located more proximally (24.4 ± 16.5 vs 44.7 ± 28.8 mm, P = .0003) and were associated with larger myocardial infarctions as assessed by peak creatine kinase-MB (208 ± 222 vs 140 ± 153 ng/dL, P = .001) and troponin I (59 ± 62 vs 40 ± 35 ng/dL, P = .0006) and with higher in-hospital mortality (5.2% vs 1.1%, P = .04). In patients with STEMI, culprit lesions are frequently located immediately distal to bifurcations and in proximity to major curvatures where disturbed flow is known to occur. This supports the role of wall shear stress in the pathogenesis of STEMI.

Decreased Glomerular Filtration Rate is an Independent Predictor of In-Hospital Mortality in Patients With ST-Segment Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention

Background and ObjectivesPatients with renal dysfunction (RD) experience worse prognosis after myocardial infarction (MI). The aim of the present study was to investigate the impact of admission estimated glomerular filtration rate (eGFR) on clinical outcomes of patients undergoing primary percutaneous coronary intervention (PCI) for ST-segment elevation MI (STEMI).Subjects and MethodsWe retrospectively evaluated 4,542 eligible patients from the Korea Acute Myocardial Infarction Registry (KAMIR). Patients were divided into three groups according to eGFR (mL/min/1.73 m2): normal renal function (RF) group (eGFR ≥60, n=3,515), moderate RD group (eGFR between 30 to 59, n=894) and severe RD group (eGFR <30, n=133). Baseline characteristics, angiographic and procedural results, and in-hospital outcomes between the three groups were compared.ResultsAge, gender, Killip class ≥3, hypertension, diabetes, congestive heart failure, peak creatine kinase-MB, high sensitivity C-reactive protein, B-type natriuretic peptide, left ventricle ejection fraction, multivessel disease, infarct-related artery and rate of successful PCI were significantly different between the 3 groups (p<0.05). With decline in RF, in-hospital complications developed with an increasing frequency (14.1% vs. 31.8% vs. 45.5%, p<0.0001). In-hospital mortality rate was significantly higher in the moderate and severe RD groups as compared to the normal RF group (2.3% vs. 13.9% vs. 25.6%, p<0.0001). Using multivariate logistic regression analysis, adjusted odds ratio for in-hospital mortality was 2.67 {95% confidence interval (CI) 1.44-4.93, p=0.002} in the moderate RD group, and 4.09 (95% CI 1.48-11.28, p=0.006) in the severe RD group as compared to the normal RF group.ConclusionDecreased admission eGFR was associated with worse clinical courses and it was an independent predictor of in-hospital mortality in STEMI patients undergoing primary PCI.