Creatine kinase-MB Elevation Research Articles

Predictive Risk Factors for Upper Gastrointestinal Bleeding with Simultaneous Myocardial Injury

The aims of this study were to: (1) evaluate the epidemiology of simultaneous upper gastrointestinal bleeding (UGIB) and myocardial injury using parameters including troponin I (TnI); and (2) investigate the predictive risk factors of this syndrome. One hundred and fifty-five patients (101 men, 54 women; mean age, 64.7+/-10.4 years; range, 38-94 years) at the emergency department (ED) with the major diagnosis of UGIB were included. They underwent serial electrocardiography (ECG) and cardiac enzyme follow-up. Emergent gastroendoscopy was performed within 24 hours in most patients except for those who refused or were contraindicated. Mild myocardial injury was defined as the presence of any of the following: typical ST-T change on ECG, elevated creatine kinase-MB (CK-MB)>12 U/L, or TnI>0.2 ng/dL. Moderate myocardial injury was defined as the presence of any two of the previously mentioned conditions. In total, 51 (32.9%) and 12 (7.74%) patients developed mild and moderate myocardial injuries, respectively. Myocardial injury was more common among patients with variceal bleeding (20/25=80.0%) than those with ulcer bleeding (23/112=20.5%). It could partially be attributed to a higher baseline TnI level in cirrhotic patients. After adjusting for significant risk factors revealed by the univariate analysis, UGIB patients with a history of liver cirrhosis and more than three cardiac risk factors comprised a high-risk group for simultaneously developing myocardial injury. Other factors including age, gender, the color of nasogastric tube irrigation fluid, history of nonsteroidal anti-inflammatory drug use, vasopressin or terlipressin administration, vital signs, and creatinine recorded at the ED were not significant predictors. Those who developed myocardial injury had a longer hospital stay (mean duration, 8.73+/-6.94 vs. 6.34+/-2.66 days; p=0.03) and required transfusion of more units of packed erythrocytes.

Isolated cTnT Elevation After PCI

A large creatine kinase-MB (CK-MB) elevation after percutaneous coronary intervention (PCI) predicts a reduced chance of survival. Now, researchers

Frequency and Significance of Troponin T Elevation in Acute Ischemic Stroke

Elevated levels of troponin have been reported in patients with acute ischemic stroke. In this prospective study, the prevalence and characteristics of troponin elevation were examined in 244 patients with acute ischemic stroke but without overt ischemic heart disease. Troponin T (TnT) and creatine kinase-MB (CK-MB) concentrations were measured and 12-lead electrocardiograms obtained daily during the first 5 days of admission. Myocardial perfusion scintigraphy was performed in patients with TnT levels of 0.10 micro g/L and in comparable controls without elevation of TnT. Patients were followed for a mean of 19 +/- 7 months, with all-cause mortality as the clinical end point. Elevated levels of TnT (>0.03 micro g/L) and creatine kinase-MB (> or =10 micro g/L) were observed in 10% and 9% of patients, respectively. Patients with elevated TnT had higher frequencies of heart and/or renal failure. Perfusion abnormalities on myocardial perfusion scintigraphy at rest were not more frequent or pronounced in patients with TnT levels of > or =0.10 micro g/L than in the control group. Only 7 patients (3%) had elevations of TnT or creatine kinase-MB and electrocardiographic changes suggesting acute myocardial infarctions. According to univariate and multivariate analyses, elevation of TnT was significantly associated with mortality. In conclusion, elevated levels of TnT are rare in patients presenting with ischemic stroke but without overt ischemic heart disease. Heart and renal failure rather than myocardial infarction are the most likely causes. When present, elevation of TnT seems to be useful in identifying patients who are at increased risk of dying within the following 2 years.

Clinical importance of elevated CK-MB and troponin I levels in congestive heart failure

Myocyte necrosis has been considered to play a fundamental role in the pathophysiology of congestive heart failure (CHF), which has usually evolved as a consequence of depletion of compensatory mechanisms and contractile reserve of myocardium. Elevated levels of creatine kinase MB (CK-MB) and troponin I (Tn-I) have been regarded as biochemical markers of myocyte necrosis. This study was planned to investigate the specificity and sensitivity of Tn-I and CK-MB in CHF and to examine the correlation of these markers with disease severity. A total of 104 patients (38 female, 66 male; mean age, 66 y [range, 36-89]) with symptoms and signs of heart failure on admission and with a reduced left ventricular ejection fraction (EF; by transthoracic echocardiography) were labeled "the patient group," and 58 patients (40 female,18 male; mean age, 61 y [range, 34-77]) with no signs or symptoms of CHF and with a normal EF detected by transthoracic echocardiography were included in the study as "the control group." Left ventricular EFs, end-diastolic diameters, and end-systolic diameters of patients in both groups were measured. Blood samples were drawn from all patients in both groups on admission, so that levels of CK-MB and Tn-I could be measured. All patients in both groups also underwent coronary angiography. Conditions leading to elevation of CK-MB or Tn-I were considered exclusion criteria. The 2 groups failed to show any significant differences in terms of mean age and the presence of coronary artery disease, hypertension, or diabetes mellitus (P>.05). Mean EF in the patient group was lower than that in the control group (P<.05). Mean CK-MB and Tn-I in the patient group were significantly higher than in the control group (P<.05). In the patient group, hypertensive patients were found to have significantly higher mean values of CK-MB than were seen in normotensive patients in the same group (P<.05). In the patient group, 52 cases were considered to be class I-II (New York Heart Association [NYHA]) (group 1), and 52 were considered to be class III-IV (group 2). Group 1, group 2, and the control group did not differ significantly from one another with regard to the presence of coronary artery disease, hypertension, and diabetes mellitus (P>.05). The mean EF in group 2 was significantly lower than that in group 1 and in the control group (P<.05); the mean EF in group 1 was significantly lower than that in the control group (P<.05). Group 1 values did not differ significantly from those of group 2 or the control group in terms of enzymatic markers (P>.05), but group 2 had significantly higher mean values of CK-MB and Tn-I than were noted in the control group (P<.05). The uphill course of CK-MB and Tn-I values from the control group to group 2 (NYHA class III-IV) was statistically significant (P<.05). Serum concentrations of CK-MB and Tn-I may become elevated in severely symptomatic patients with CHF (particularly NYHA class III-IV), demonstrating a relationship between clinical severity of the disease and elevation of myocardial enzymes (CK-MB and Tn-I).

Below Radar

Below Radar

Protective role of chronic statin therapy in reducing myocardial damage during percutaneous coronary intervention

Percutaneous coronary intervention (PCI) is frequently associated with troponin I (TnI) elevation. Experimental studies suggest that statins may reduce ischaemia-reperfusion myocardial injury. The study objective was to verify whether chronic treatment with statins might reduce the occurrence and the extent of periprocedural myocardial damage in patients undergoing PCI. Five hundred and fifty-two consecutive patients undergoing PCI were included: 279 were not on statins before PCI, 273 were on statins. TnI levels >or= 0.3 ng/ml were considered indicative of myocardial injury. Statin-treated patients had a higher prevalence of hyperlipidaemia, previous myocardial infarction, and revascularization procedures. Coronary angiography also documented a higher prevalence of multivessel disease. No difference between the two groups was observed regarding the PCI-treated vessel, type of lesions, use of stents and of anti-IIb/IIIa inhibitors. Patients on statins showed the lowest incidence of TnI >or= 0.3 ng/ml (29 vs. 48%, P = 0.00001) and of creatine kinase-MB elevation (7 vs. 12%, P = 0.04). The mean peak TnI levels were significantly lower in patients on statins (1.07 +/- 3.8 vs. 2.73 +/- 12.3, P = 0.00006). Multivariate analysis identified preprocedural statin therapy as the only independent negative predictor of postprocedural abnormal TnI levels (odds ratio = 0.52; 95% confidence intervals 0.34-0.79; P = 0.003). This study shows that chronic therapy with statins reduces the incidence of periprocedural myocardial damage after PCI. The beneficial effect of statins was independent of either the most important clinical and angiographic characteristics or the use of other cardiovascular drugs including beta-blockers. These data support the specific cardioprotective role of statins.

Left Main Coronary Revascularization at the Crossroads

Percutaneous revascularization of left main coronary artery (LMCA) disease has remained controversial for more than 25 years, since LMCA balloon angioplasty was first performed by Andreas Gruentzig in 1978. Summarizing his experience, Gruentzig concluded, “We have not been too successful with dilating left main stems…although the procedure is relatively simple, the potential complications are both sudden and serious.”1 Following the evolution of percutaneous catheter-based therapies to include both bare metal stent and, more recently, drug-eluting stent (DES) platforms in conjunction with advances in periprocedural and postprocedural adjunctive pharmacotherapies, interest in percutaneous LMCA revascularization, particularly unprotected left main, has been renewed. Although studies performed with bare metal stents demonstrated a low rate of in-hospital mortality, the incidence of late coronary restenosis remained high.2–6 In the Unprotected Left Main Trunk Intervention Multi-Center Assessment (ULTIMA) registry, which enrolled 279 patients with unprotected LMCA disease who had percutaneous coronary revascularization (69% bare metal stent), mortality at a 1-year follow-up was proportional to clinical risk stratification (40% in high-risk versus 3.5% in low-risk patient cohorts), and repeated revascularization was required in 34% of cases.6 The experience gleaned from these studies continued to support the American College of Cardiology/American Heart Association (ACC/AHA) guideline recommendations that in reasonable surgical candidates with LMCA disease, coronary bypass surgery is the preferred therapeutic option.7 After the introduction of DES, several small clinical series demonstrated the feasibility and short-term safety of LMCA stenting, while late clinical/angiographic outcomes appeared favorable as compared with historical (nonrandomized) patient cohorts treated with bare metal stents.3,8–11 The cumulative experience with DES treatment for LMCA demonstrated an apparent marked reduction in major adverse cardiovascular events, including target vessel revascularization, during 6 to 12 months of follow-up as compared with the precedent experience after bare metal stent deployment. Article p 2542 The clinical …

Angiographic Adverse Events, Creatine Kinase-MB Elevation, and Ischemic End Points Complicating Percutaneous Coronary Intervention (a REPLACE-2 Substudy)

Several angiographic adverse events during coronary balloon angioplasty have been associated with increased creatine kinase-MB (CK-MB) enzymes and adverse clinical outcomes. The significance of angiographic adverse events in the stent era has not been widely studied. We analyzed 10 types of angiographic adverse events that were reported in the 6,010-patient Second Randomized Evaluation in PCI Linking Angiomax to Reduced Clinical Events (REPLACE-2) trial to determine their relation to CK-MB elevation and clinical ischemic end points after percutaneous coronary intervention (PCI). Angiographic adverse events occurred in 9.1% of REPLACE-2 patients. Most (8 of 10) types of angiographic adverse events were associated with an increased risk of increased CK-MB (p <0.001 for each), and 47% of all patients with an angiographic adverse event developed increased CK-MB. Logistic regression analysis showed that the strongest predictor of death, myocardial infarction, or revascularization at 6 months was the occurrence of an angiographic adverse event during PCI (odds ratio 1.9, 95% confidence interval 1.6 to 2.4, p <0.001). Side branch closure, abrupt closure, any decreased flow during the procedure, angiographic distal embolization, and perforation or tamponade were individual predictors of the occurrence of the combined clinical ischemic end point at 6-month follow-up (p <0.005 for each). In conclusion, most angiographic adverse events during PCI are associated with increased CK-MB and are powerful predictors of adverse clinical events within 6 months.

Diastolic dysfunction in stunned myocardium: a state of abnormal excitation–contraction coupling that is limited by Na+–H+ exchange inhibition

The systolic and diastolic effects of myocardial stunning were studied to evaluate the contributions of the endocardial and epicardial segments of the ventricular myocardial band, and determine if preconditioning by Na+-H+ exchange (NHE) inhibition effected post-stunning dysfunction. Thirteen Yorkshire-Duroc pigs (27.3-38.2 kg) underwent 15 min of mid-LAD clamping. Seven had no protective measures and six were pretreated with IV Cariporide 5 mg/kg 15 min before ischemia. Sonomicrometer crystals evaluated systolic dysfunction (impaired regional shortening) and diastolic dysfunction (contraction extending into early diastole). Before ischemia, contraction started first on the endocardial side followed 82+/-23 ms later by the subepicardium. Endocardial shortening stopped first, coinciding with negative dP/dt onset, while epicardial shortening phase persisted for 92+/-33 ms more during occurrence of rapid LVP descent and development of peak negative dP/dt. Ischemia produced paradoxical bulging of both segments. Sixty minutes after ischemia systolic segment shortening recovered 36+/-24% of baseline values without pretreatment, compared to 75.8+/-15% with Cariporide (p<0.05). Global ejection force (maximum dP/dt) fell 32+/-20% in the unprotected group, but was maintained by Cariporide pretreatment. Diastolic dysfunction always showed continued endocardial contraction into early diastole (occupying 38+/-16% of diastole in untreated hearts), whereas Cariporide treatment reduced this dysfunction to 5+/-10% (p<0.05). Persistent diastolic dysfunction raised left ventricle end diastolic pressure (LVEDP) 4 mmHg in untreated hearts, whereas Cariporide returned LVEDP to normal. Less elevation of creatine kinase MB (CK-MB) and conjugated dienes followed Cariporide pretreatment. Temporary LAD ischemia alters the normal sequential pattern of contraction responsible for ejection and suction by (a) reducing systolic contractile force, and (b) prolonging endocardial contraction into early diastole to disrupt the normal endocardial-epicardial sequence responsible for ventricular suction. NHE inhibition before ischemia limits postischemic systolic and diastolic dysfunction by re-establishing the expected shortening sequences within the ventricular myocardial band model.

Elevated creatine kinase-MB with normal creatine kinase predicts worse outcomes in patients with acute coronary syndromes: Results from 4 large clinical trials

The degree to which elevated creatine kinase (CK)-MB in the presence of normal CK is predictive of outcome is not well understood despite having been studied for decades. This analysis examined whether normal CK with elevated CK-MB in patients with non-ST-segment elevation acute coronary syndrome (NSTE ACS) is an independent predictor of worse outcomes. A concomitant goal was to contribute insight to the debate over how patients with NSTE ACS should be managed. Data for 25,960 patients from the GUSTO IIb, PARAGON A and B, and PURSUIT trials were analyzed. Of these patients, 6402 were excluded from primary analysis because of missing (unmeasured) biomarkers. Patients with complete laboratory data (n = 19,558) were grouped by CK and CK-MB results. To confirm the primary analysis results, data from patients with missing biomarkers were used in an imputation model. Patients were categorized in 1 of 4 groups: normal CK + normal CK-MB; normal CK + elevated CK-MB; elevated CK + normal CK-MB; or elevated CK + elevated CK-MB. For the primary outcome, 180-day death, or myocardial infarction, Kaplan-Meier estimates were 14.9%, 20.8%, 14.5%, and 18.2%, respectively. Regardless of total CK, elevated CK-MB was associated with a 25% to 49% increased relative risk of worse outcomes. Findings from the analyses were verified by the multivariable model. CK-MB remains a reliable marker for myocardial necrosis and a strong predictor of worse prognosis. All patients with ACS should have CK-MB measurement to search for cardiac ischemia. Patients with elevated CK-MB should receive aggressive management commensurate with their increased risks.

Aspirin and Clopidogrel Drug Response in Patients Undergoing Percutaneous Coronary Intervention: The Role of Dual Drug Resistance

Aspirin and Clopidogrel Drug Response in Patients Undergoing Percutaneous Coronary Intervention: The Role of Dual Drug Resistance Eli I. Lev, Rajnikant T. Patel, Kelly J. Maresh, Sasidhar Guthikonda, Juan Granada, Timothy DeLao, Paul F. Bray, Neal S. Kleiman We evaluated the response to clopidogrel among aspirin-resistant versus aspirin-sensitive patients undergoing elective coronary stenting. Patients (n = 150) treated with aspirin but not clopidogrel had blood samples drawn at baseline and 24 h after clopidogrel loading. Depending on the definition used, 9% to 15% were resistant to aspirin and 24% to clopidogrel. About half of the aspirin-resistant patients were also resistant to clopidogrel. As a group, aspirin-resistant patients had lower response to clopidogrel (assessed by platelet aggregation and activation markers) than aspirin-sensitive patients. Both aspirin- and clopidogrel-resistant patients had higher incidence of creatine kinase-MB elevation than the respective sensitive patients. We sought to evaluate the response to clopidogrel among aspirin-resistant versus aspirin-sensitive patients undergoing percutaneous coronary intervention (PCI). Wide variability has been reported in response to aspirin and clopidogrel. There are limited data on the simultaneous responses to both drugs. Elective PCI patients (n = 150) who received aspirin for ≥1 week but not clopidogrel were included. All patients received bivalirudin during PCI. Blood samples were drawn at baseline and 20 to 24 h after a 300-mg clopidogrel dose. Aspirin resistance was defined by ≥2 of 3 criteria: rapid platelet function analyzer-ASA score ≥550, 5 μmol/l adenosine diphosphate (ADP)-induced aggregation ≥70%, and 0.5 mg/ml arachidonic acid-induced aggregation ≥20%. Clopidogrel resistance was defined as baseline minus post-treatment aggregation ≤10% in response to 5 and 20 μmol/l ADP. Nineteen (12.7%) patients were resistant to aspirin and 36 (24%) to clopidogrel. Nine (47.4%) of the aspirin-resistant patients were also clopidogrel resistant. Aspirin-resistant patients were more likely to be women and have diabetes than were aspirin-sensitive patients. They also had lower response to clopidogrel, assessed by platelet aggregation and activation markers (flow cytometry-determined PAC-1 binding and P-selectin expression). Elevation of creatine kinase-myocardial band after stenting occurred more frequently in aspirin-resistant versus aspirin-sensitive patients (38.9% vs. 18.3%; p = 0.04) and in clopidogrel-resistant versus clopidogrel-sensitive patients (32.4% vs. 17.3%; p = 0.06). Aspirin-resistant patients as a group have reduced response to clopidogrel. Furthermore, we have identified a unique group of dual drug-resistant patients who may be at increased risk for thrombotic complications after PCI.

Plasma interleukin-18 concentration: a novel marker of myocardial ischemia rather than necrosis in humans

Myocardial ischemia contributes to cytokine expression in the myocardium in animals; therefore, plasma interleukin-18 concentration may be a good marker of myocardial ischemia/injury in patients with possible acute coronary syndrome. We sought to determine whether increases in plasma interleukin-18 concentrations might be indicative of myocardial ischemia in patients with acute coronary syndrome. Plasma interleukin-18 concentrations were assessed in 27 acute coronary syndrome patients in whom creatine kinase activity was within normal range on admission, in addition to 10 controls. Myocardial infarction was retrospectively evidenced in 15 of the 27 patients. All patients with acute coronary syndrome were treated by emergent coronary interventions just after admission. Blood sampling was done immediately after admission to determine plasma IL-18 concentration and biochemical markers of myocardial infarction. An increase in plasma interleukin-18 concentration was observed in acute coronary syndrome patients on admission, regardless of the retrospective evidence of myocardial necrosis. Plasma interleukin-18 elevation preceded creatine kinase-MB elevation in myocardial infarction patients. Plasma interleukin-18 concentrations on admission did not correlate with peak creatine kinase-MB (r=0.38, P=n.s.) or with left ventricular ejection fraction (r=-0.14, P=n.s.). Plasma interleukin-18 concentration elevates quickly after severe myocardial ischemic event regardless of evolving myocardial necrosis. Thus, plasma interleukin-18 concentration may be a good and early marker to identify whether the symptom is due to myocardial ischemia, and therefore, may be used in deciding the therapeutic strategy in individual patients with possible acute coronary syndrome.

Prediction of Complications Following Nonemergency Percutaneous Coronary Interventions

Previous models for prediction of complications after percutaneous coronary interventions (PCIs) have included in-hospital mortality and major in-hospital complications. In general, these models have excluded elevated cardiac biomarkers as a complication. We sought to determine whether a risk model could predict complications, including biomarker elevation, in patients undergoing nonemergency PCI. We examined the outcomes of nonemergency PCI performed on patients at Mayo Clinic from 2000 to 2003. The primary end point was in-hospital complications of death, myocardial infarction (MI) (Q-wave MI, or post-PCI creatine kinase-MB elevation >or=3 times the upper limit of normal), emergency coronary artery bypass grafting, or stroke. We used the Hosmer-Lemeshow test to demonstrate the adequacy of the model fit, and the c-index for discriminatory ability of the model. Of 2,894 nonemergency PCIs, the end point was noted in 232 (8%). The final prediction model included vein graft intervention (odds ratio [OR] 2.19), angiographic thrombus (OR 2.12), preprocedure stenosis of a minor (OR 1.98) or major (OR 1.62) side branch, and type C lesion (OR 1.48). The model had modest ability to discriminate between event and nonevent patients (c = 0.641). In the 500 bootstrap samples for internal validation, the c-index was 0.642 +/- 0.020, indicating only fair discriminatory ability. The average number of observed events was 232.0 +/- 14.7 compared with 232.1 +/- 2.5 expected events (average difference -0.06 +/- 14.5). In conclusion, the 5 risk variables associated with an increased risk of complications in patients undergoing elective PCI included vein graft intervention, presence of angiographic thrombus, stenosis of a major or minor side branch, and type C lesion; however, the discriminatory ability of the model derived from the variables was only modest.

Relation of Aspirin Resistance to Coronary Flow Reserve in Patients Undergoing Elective Percutaneous Coronary Intervention

Previous studies have shown that more complete platelet inhibition improves the coronary flow reserve (CFR), a measure of microvascular integrity, in patients undergoing percutaneous coronary intervention (PCI). We hypothesized that patients with aspirin resistance would have impaired CFR after elective PCI. We used VerifyNow Aspirin to determine the response to aspirin in 117 consecutive patients who underwent elective single-lesion PCI. The assay results are expressed quantitatively in Aspirin Reaction Units based on the degree of platelet aggregation. All patients received a 300-mg loading dose of clopidogrel >12 hours before and a 75-mg maintenance dose the morning of PCI. CFR was estimated using the Thrombolysis In Myocardial Infarction frame count method. Of the 117 patients, 22 (18.8%) were aspirin resistant. The clinical, angiographic, and procedural characteristics of the aspirin-sensitive and -resistant patients were balanced. All patients underwent successful PCI with <50% residual diameter stenosis and Thrombolysis In Myocardial Infarction grade 3 flow after PCI. Aspirin-resistant patients had a lower CFR than the aspirin-sensitive patients (1.42 +/- 0.35 vs 1.80 +/- 0.64, p = 0.018). Univariate correlates of CFR included the Aspirin Reaction Unit (r = -0.227, p = 0.014) and post-PCI creatine kinase-MB elevation (p = 0.048). Multivariate linear regression analysis revealed the Aspirin Reaction Unit to be the only independent determinant of CFR after PCI (r2 = 0.051, p = 0.014). Thus, aspirin resistance was associated with impaired CFR in patients who underwent elective PCI, implicating insufficient aspirin-induced platelet inhibition as a cause of microvascular dysfunction by distal atherothrombotic embolization and/or spasm.

Impact of the elevation of biochemical markers of myocardial damage on long-term mortality after percutaneous coronary intervention: results of the CK-MB and PCI study

Retrospective studies and post hoc analyses have suggested that mild elevations in the creatine kinase-MB (CK-MB) isoenzyme following percutaneous coronary intervention (PCI) may be associated with an increased risk of death in the long term. However, this finding is still controversial, and the prognostic significance of elevations of more sensitive markers of myocardial damage, such as the cardiac troponins, has not been established. In this multicentre prospective cohort study, we evaluated the influence of post-procedural elevations of CK-MB and troponin I (cTnI) on long-term mortality. The CK-MB and PCI study included 3494 consecutive patients undergoing PCI from February 2000 to October 2000 in 16 Italian tertiary centres. Blood samples were collected at baseline, and at 8-12 and 18-24 h after the procedure, and were analysed in a core biochemistry laboratory. CK-MB elevation was detected in 16% of the patients, and was associated with increased 2-year mortality [7.2 vs. 3.8%; odds ratio (OR): 1.9; 95% confidence interval (CI): 1.3-2.8; P<0.001). The degree of CK-MB elevation (peak CK-MB ratio) independently predicted the risk of death (adjusted OR per unit: 1.04; 95% CI: 1.01-1.07; P=0.009). A cTnI elevation was detected in 44.2% of the cases and was not associated with a significant increase in mortality (4.9 vs. 4.0%; OR: 1.2; 95% CI: 0.9-1.7; P=0.2). Post-procedural elevations of CK-MB, but not cTnI, influence 2-year mortality.

Creatine kinase-MB enzyme elevation and long-term clinical events after successful coronary stenting in lesions with ruptured plaque

Patients with acute coronary syndrome are at increased risk of acute and long-term events after stent implantation. We compared the impact of intravascular ultrasound detected plaque rupture on creatine kinase-MB (CK-MB) isoenzyme release and clinical outcomes by comparing 62 patients with ruptured plaques with 62 matched control patients who underwent stent implantation. Two thirds of the patients in each group presented with an acute coronary syndrome. There were no differences in procedural complications between groups, although patients with ruptured plaque had higher CK-MB elevation rates than those without ruptured plaque (1 to 3 times the upper limit of normal CK-MB, 35% vs 10%, p <0.001; >3 times the upper limit, 15% vs 2%, p = 0.02). Independent predictors of CK-MB elevation were presence of ruptured plaque (p = 0.03) and unstable angina (p = 0.04). Patients with ruptured plaque had higher composite rates of late events (target lesion revascularizations/myocardial infarctions/cardiac deaths) than controls (25% vs 9%, p = 0.03). These results were similar when only patients with acute coronary syndrome were studied. Plaque rupture morphology is associated with higher periprocedural CK-MB release and worse 1-year clinical outcome in patients treated with coronary stenting.

Differential mortality risk of postprocedural creatine kinase-MB elevation following successful versus unsuccessful stent procedures

Concrete structures are referred to as the basis of contemporary technical civilization. They support transportation, storage of goods, and shelter humans in large numbers. Despite their long endurance, they have ceased to be considered as maintenance-free. They are subject to long-term loading due to own weight, dynamic loading scenarios including earthquakes, as well as environmental degradation.

Are Patients With Unstable Angina Being Transformed in Acute Myocardial Infarction?

Background: Several patients with chest pain suspicious of acute myocardial ischemia and found to have elevated troponins but normal creatine kinase-MB (CKMB) are now being diagnosed as acute myocardial infarction (AMI). We undertook a prospective study to determine if these patients have the same clinical characteristics and prognosis of patients with CKMB (± troponin) elevation AMI. Methods: A total of 969 consecutive patients evaluated in our chest pain unit and presenting without ST-segment elevation on admission were submitted to serial measurements of CKMB (normal value <5 ng/mL, immunofluorescence assay, Dade-Behring) and troponin-I (normal value considered <1.0 ng/mL, immunofluorescence assay, Dade-Behring) followed by a stress test (for non-AMI and nonhigh-risk unstable angina patients) according to a probability stratification and diagnostic algorithm. Patients were then followed by 1 month for cardiac events: in-hospital death and urgent revascularization, and 30-day death, AMI, unstable angina, and urgent revascularization. Results: AMI was diagnosed in 114 patients: with CKMB elevation in 77 (classic-AMI) and with troponin-I elevation in 102. Seven of these patients did not measure all necessary CKMB and/or troponin I. Of the 107 AMI patients doing all measurements, 32 did not have CKMB elevation (troponin-AMI), whereas 9 did not have troponin-I elevation. Sensitivities of CKMB and troponin-I for AMI were 71% and 92%, respectively (P = 0.0000) and negative predictive values were 91% and 98%, respectively (P = 0.0000). As expected, specificities and positive predictive values were 100%. No significant differences in rates of clinical risk factors, admission indices of risk of events (as electrocardiogram changes, Killip class, blood pressure, heart rate, B-type natriuretic peptide level) and 30-day cardiac events (6.5% vs 9.2%, respectively) were seen between troponin-AMI and classic-AMI. Conclusions: 1) At the cutoff level of 1.0 ng/mL, troponin-I has significantly greater diagnostic sensitivity and negative predictive value for AMI than CKMB in patients with chest pain and no ST-segment elevation, identifying 28% more patients not recognized solely by CKMB. 2) Patients with troponin-AMI have similar clinical characteristics and 30-day event rate as classic-AMI, suggesting that they are true AMI.

Differential mortality risk of postprocedural creatine kinase-MB elevation following successful versus unsuccessful stent procedures

This study was designed to evaluate the effect of periprocedural myocardial infarction (MI) on mortality according to success of the stent procedure. The mortality effect of periprocedural MI relative to successful versus unsuccessful procedures has not been examined. All-cause mortality during the first year was evaluated prospectively among 5,850 patients from coronary stent clinical trials. Myocardial infarction was classified according to creatine kinase-MB level as type 1 (>1 but <3 times normal), type 2 (>or=3 but <or=8 times normal), or type 3 (>8 times normal or Q-wave MI). Procedures were classified as successful unless there was a final diameter stenosis >50%; final Thrombolysis In Myocardial Infarction flow grade <3; final National Heart, Lung, and Blood Institute dissection grade >or=D; repeat revascularization within 24 h; or stent thrombosis within 24 h. Myocardial infarction was more frequent after unsuccessful procedures (69.6% vs. 20.4%, p < 0.001). Mortality during the first year was higher in patients with MI (2.8% vs. 1.7%, p = 0.01), but the effect was significant only for type 3 MI (4.7% vs. 1.7%, p = 0.008). Moreover, the mortality difference for any MI was confined to patients with unsuccessful procedures (13.1% vs. 0%, p = 0.03), with no significant effect among patients with otherwise successful procedures (2.1% vs. 1.7%, p > 0.20). The independent predictors of mortality were unsuccessful procedure (p < 0.001), diabetes mellitus (p = 0.001), history of prior MI (p = 0.003), multivessel disease (p = 0.006), and advancing age (p < 0.001), but not periprocedural MI. The association of periprocedural MI with increased mortality during the first year following stent placement was confined to patients with unsuccessful procedures.

Protective effect of total flavones from Elsholtzia blanda (TFEB) on myocardial ischemia induced by coronary occlusion in canines

This study was undertaken to determine the effect of total flavones from Elsholtzia blanda (Benth.) Benth. (TFEB), a traditional Chinese medicine, on myocardial ischemia induced by coronary occlusion in Beagle dogs. Infarct size of left ventricle, serum activity of creatine kinase-MB (CK-MB) and malondialdehyde (MDA), hemorrheologic variables and homodynamic parameters including mean arterial pressure (MAP), coronary blood flow (CBF), coronary vascular resistance (CVR), end-diastolic pressure of left ventricle (LVEDP), rate of rise and decline of left ventricular pressure (±dp/dtmax) were measured in this study. Administration with TFEB produced a dose-dependent reduction in infarct size. TFEB 100 mg/kg exerted notable inhibition in the elevation of serum CK-MB and MDA activity. TFEB significantly reduced MAP and CVR. The decrease in CBF also tended to be smaller in treated dogs. TFEB improved the recovery of myocardial function by depressing the degree of reduction in ±dp/dtmax and LVEDP. TFEB also showed a capacity to resist ischemic damage through lowering blood viscosity. The results indicated that TFEB kept heart from ischemic damage due to coronary occlusion in Beagle dogs.