Creatine Kinase MB Mass Research Articles

Partial Inhibition of Platelet Thromboxane A 2 Synthesis by Aspirin Is Associated With Myonecrosis in Patients With ST-Segment Elevation Myocardial Infarction

Heterogeneity in response to aspirin (ASA) treatment, or "aspirin resistance," could be of importance in patients with ST-segment elevation myocardial infarction (STEMI). Decreased effects of ASA in platelets could be due to partial inhibition of cyclo-oxygenase-1 (COX-1) or to COX-1-independent mechanisms. We evaluated the effect of ASA treatment in patients with STEMI for (1) platelet thromboxane A(2) (TXA(2)) synthesis, (2) platelet recruitment elicited by TXA(2)-dependent and -independent mechanisms, and (3) a possible association of these aspects of platelet reactivity with serum markers of myonecrosis. We studied 62 ASA-treated patients within 48 hours of onset of the acute event and 69 ASA-free and 10 ASA-treated controls. TXA(2) synthesis and platelet recruitment (fluid-phase proaggregate activity of cell-free releasate) were assessed after collagen stimulation (1 micro g/ml) of whole blood. Partial inhibition of TXA(2) by ASA was found in 21 patients (34%). This was associated with significant increases in troponin T, creatine kinase-MB mass, creatine kinase, and recruiting activity versus 41 patients with blocked TXA(2) production. This was independent of fibrinolysis, and platelet COX-2 expression was not augmented. TXA(2) blockade was achieved after subsequent daily treatments or platelet incubation with ASA in vitro, suggesting lower sensitivity of COX-1 to ASA. In addition, 28 patients (45%) had an abnormally increased recruiting activity despite TXA(2) blockade, which was also associated with increased myonecrosis. In conclusion, ASA resistance, elicited by TXA(2)-dependent and TXA(2)-independent mechanisms, was prevalent in patients with STEMI. This study describes, for the first time, the association of partial platelet TXA(2) inhibition with myonecrosis.

Invited commentary

Isoenzyme cardiac troponin T (cTnT) is one component of a complex of three separate proteins that, together with tropomyosin, confers calcium sensitivity to the process of actin-myosin cross-bridge formation in the myocardial cell. Found exclusively in the myocardium, it is a potent inhibitor of these interactions and is a more sensitive and specific index of myocardial cell damage than creatine kinase-MB (CK-MB) fraction, CK-MB mass, and myoglobin level. Therefore, cTnT has emerged as a strong predictive variable of complications and clinical outcome after cardiac surgery.

Cardiac Troponin T Levels for Risk Stratification in Pediatric Open Heart Surgery

Cardiac troponin T has been found to be accurate predictor of complications and adverse clinical events after pediatric cardiac surgery. Contrary to adult cardiac surgery, the relationship of troponin T to patient survival after pediatric heart surgery has not been previously studied. The purpose of this study was to determine whether troponin T could predict death after pediatric open cardiac surgery. This was a retrospective cohort study in which data from 1001 consecutive children having cardiac surgery during a 5-year period were studied. Perioperative variables that could influence death at 30 postoperative days were evaluated. Multivariate analysis, using a forward stepwise logistic regression, showed that troponin T measured on the first postoperative day was a strong independent predictor of death at 30 days. Level of troponin T greater than 5.9 microg/L on the first postoperative day predicted death (odds ratio, 10.7; 95% confidence interval: 5.2 to 22.1) as did admission lactate level greater than 5.2 mmol/L (odds ratio, 22.2; 95% confidence interval: 9.7 to 50.8) No other variable, including postoperative creatine kinase-MB mass concentration, age, diagnosis, surgical procedure, presence of cyanosis, chromosomal anomaly or ventriculotomy, duration of cardiopulmonary bypass, or aortic cross-clamp, had any independent effect on 30-day survival. Cardiac troponin T level on the first postoperative day is a powerful independent risk marker of death in pediatric cardiac surgery.

Importância da proteína C-reativa no diagnóstico e no prognóstico intra-hospitalar em pacientes com dor torácica na sala de emergência

To test immediate diagnostic and prognostic values of C-reactive protein (CRP) in patients admitted to the emergency room (ER) with chest pain (CP) without ST-segment elevation on the electrocardiogram (ECG). From January 2002 to December 2003, 980 patients were consecutively seen in the ER with CP suggestive of acute coronary syndrome (ACS) (age = 64.9 +/- 14.3, men = 55%, diabetic = 18%, normal ECG = 84%). Serial CRP, creatine kinase MB mass (CKMB-mass) and troponin I determinations were performed on admission, in addition to serial ECG. CRP measurements were standardized (s-CRP) by the upper limit of normal (ULN) of the test used (3.0 mg/L for high-sensitivity C-reactive protein [hs-CRP] and 0.1 mg/dL for titrated CRP [t-CRP]). One hundred and twenty-five patients were diagnosed with acute myocardial infarction (AMI), and their s-CRP values were 1.31 +/- 2.90 (median = 0.47) compared to 0.79 +/- 1.39 (0.30) in no-AMI patients (p = 0.031). The s-CRP > 1.0 showed 30% sensitivity and 80% specificity, plus negative and positive predictive values of 6.1% and 96.7%, respectively, for AMI diagnosis. There were forty in-hospital cardiac events (16 deaths, 22 urgent revascularizations, and 2 acute myocardial infarction). In the first quartile of the s-CRP (< 0.10), three events were recorded, while in the fourth quartile (> 0.93) 15 events (p = 0.003) occurred. In the logistic regression model, masculine gender and s-CRP > 0.32 (odds ratio 7.6, 2.8 and 2.2, respectively) were independent predictors of cardiac events and left ventricular failure. In patients with chest pain presenting at the emergency room, s-CRP was not a good marker of AMI, although this diagnosis is virtually excluded by a normal value; in addition, values one-third above the upper limit of normal (>1 mg/L for hs-CRP or >0.33 mg/dL for t-CRP) were predictive of in-hospital adverse cardiac events.

Diagnostic Efficiency of Creatine Kinase (CK), CKMB, Troponin T and Troponin I in Patients with Suspected Acute Myocardial Infarction

The goal of this research was to assess the performance of serum creatine kinase (CK), creatine kinase MB (CKMB) [mass and activity], troponin I (TnI) and troponin T (TnT) in the diagnosis of acute myocardial infarction in patients admitted to the Coronary Care Unit at Queen Alia Heart Institute, Amman, Jordan, between March and July 2001. Blood samples collected for cardiac enzyme determination (CK, CKMB activity) were stored at -20°C for later determination of CKMB mass [Abbott Axsym, Ortho Clinical Diagnostics (OCD) ECi and Roche Elecsys], TnI (Abbott Axsym) and TnT (Roche Elecsys). The relative index (RI = CKMB mass/CK), for CKMB mass measurements, was calculated. Clinical notes and/or discharge diagnosis for each patient were reviewed to obtain the diagnosis of acute myocardial infarction. Fifty samples were from acute myocardial infarction (AMI) patients. Area under Receiver Operating Curve values were: CK 0.56, CKMB activity 0.72, percentage of CKMB activity 0.73, CKMB mass (Abbott) 0.76, CKMB mass (Roche) 0.77, CKMB mass (OCD) 0.78, RI (Roche) 0.83, RI (Abbott) 0.87, RI (OCD) 0.86, TnI 0.95, TnT 0.94. Sensitivity: TnI 88%, TnT 93%; specificity TnI 99%, TnT 99%. There was no significant difference in performance between TnI and TnT assays or between any of the CKMB mass measurements. Present results show that TnI and TnT are better cardiac markers than CK and CKMB, mass or activity.

The relationship between trace elements and cardiac markers in acute coronary syndromes

Previous studies have demonstrated increased serum copper and iron levels and decreased selenium and zinc levels in patients with myocardial infarction. Furthermore, the prognostic value of the levels of trace elements in myocardial infarction has been stressed. We examined serum levels of Cu, Fe, Zn and Se, as well as glutathione peroxidase (GPx), a selenoenzyme with antioxidant properties, and C-reactive protein (CRP), a marker of inflammation, in acute coronary syndromes (ACS) regarding their relationship to cardiac troponins and creatine kinase-MB mass (CK-MBm), important prognostic markers. Serum trace elements, GPx activity and CRP were determined in 70 patients with ACS who were admitted within 12 h after the onset. Differences in these parameters were evaluated in three groups of patients divided according to the levels of cardiac markers: group III consisted of patients with high increases in cTnT, cTnI and CK-MBm (⩾0.9 ng/mL, ⩾1.0 ng/mL, ⩾30 ng/mL, respectively), patients with milder increases in these markers were included in groups II and I consisted of patients with values just above the upper reference limits. Serum Fe levels increased significantly in group II and even more prominently in group III compared to group I ( p = 0.04 , 0.002 , respectively). There was no significant difference between groups II and III. The increase in serum Cu was significant in group III compared to both groups II and I ( p = 0.04 , 0.001 , respectively). There was no significant difference between groups I and II regarding Cu and Zn. The decrease in serum Se and GPx levels was significant only between groups III and I ( p = 0.004 for Se and p = 0.0001 for GPx). CRP levels showed a significant increase in group III compared to groups II and I ( p = 0.03 and 0.001). CRP showed a significant positive and GPx a significant negative correlation to the cardiac markers cTnT, cTnI and CK-MBm. Cu was positively correlated to all cardiac markers, while the positive correlation between Fe and cardiac markers was significant only for cTnI. Both Zn and Se were negatively correlated to cTnT, and Se was also to cTnI. In conclusion, the increase in serum levels of Cu and Fe and the decrease in serum levels of Zn and Se in patients with higher levels of troponins and CK-MBm imply that trace element levels are related to the degree of myocardial damage and thus may play a role in the pathogenesis of ischemic heart disease. The strong correlations between cardiac markers and both CRP and GPx suggest that these parameters are promising prognostic factors in acute coronary syndromes.

Cardiac Troponin and Creatine Kinase MB Monitoring during In-Hospital Myocardial Reinfarction

Cardiac troponin monitoring for detection of myocardial injury has been designated the new standard for differentiating the diagnosis of unstable angina and non-ST-elevation myocardial infarction (NSTEMI) in acute coronary syndrome patients (1)(2)(3)(4). Increased cardiac troponin I (cTnI) or T (cTnT) in the clinical setting of ischemia is defined as an acute MI and has been endorsed by the European Society of Cardiology, American College of Cardiology, the American Heart Association, the IFCC, and the Epidemiology World Council (1)(2)(3)(4)(5)(6). One of the challenges that confronts cardiac troponin monitoring encompasses the clinical setting of myocardial reinfarction within a short time period after an initial MI. Because cardiac troponins can remain increased in the circulation for up to 5 (cTnI) or 10 days (cTnT) after an acute MI, in theory, the role for monitoring cardiac troponins during reinfarction has been questioned. The European Society of Cardiology/American College of Cardiology consensus document notes that in the clinical setting of a reinfarction, creatine kinase MB (CKMB) may be more useful for monitoring for MI because CKMB remains increased for only 2–4 days after an acute MI (1)(2)(3)(4). There are only two case reports in the literature, both from a previous report from our laboratory, that readdressed the role of cardiac troponin monitoring in reinfarction (7). The purpose of this study was to compare the patterns of increases and decreases in cTnI and CKMB mass in a series of nine MI patients who experienced an in-hospital myocardial reinfarction (MI extension) within 4 days of the initial MI event. Over a period of 16 months (September 1999 through February 2001), nine MI patients were identified who experienced a myocardial …

Rates of positive cardiac troponin I and creatine kinase MB mass among patients hospitalized for suspected acute coronary syndromes.

Cardiac troponin I (cTnI) is a more specific and sensitive biomarker than creatine kinase MB (CKMB) for detection of myocardial damage. We report the prevalence of positive cTnI and CKMB mass among patients hospitalized with suspected acute coronary syndrome (ACS) and the potential impact of use of different reference cutoffs, particularly those proposed by European Society of Cardiology/American College of Cardiology (ESC/ACC) consensus guidelines, on rates of diagnosis of acute myocardial infarction (AMI). We analyzed 1719 consecutive patients with suspected ACS admitted to an urban acute care hospital over a 6-month period. Patients (> or = 18 years of age) had at least two separate sets of plasma biomarkers (cTnI and CKMB) measured more than 12-24 h after admission to determine the potential rates of AMI based on different biomarker cutoff concentrations. The prevalence of cTnI-positive cases ranged from 10.6%, based on a cutoff of twice the ROC curve (cTnI < or =1.2 microg/L), to 25.0%, using the ESC/ACC-recommended 99th percentile cutoff (cTnI <0.1 microg/L). The prevalence of CKMB-positive cases ranged from 10.4%, with the cutoff of twice the ROC curve (CKMB < or =10.0 microg/L) to 21.7%, with the 99th percentile cutoff (CKMB <3.9 microg/L). Use of the 10% CV cutoff (cTnI < or =0.3 microg/L and CKMB <3.9 microg/L) instead of the ROC cutoff produced a 26% increase in all cTnI-positive cases. Use of the 99th percentile reference cutoff instead of the ROC curve-derived cutoff produced an 85% increase in all cTnI-positive cases. A substantial proportion of the increase in total cTnI-positive cases was derived from cTnI-positive/CKMB-negative cases: 71 (4.1%), 73 (4.2%), 98 (5.7%), and 209 (12.2%) of cTnI-positive cases were CKMB-negative, as determined by the twice the ROC, ROC, 10% CV, and 99th percentile reference cutoffs, respectively. At the 99th percentile cutoffs, 8.8% of cases were CKMB-positive/cTnI-negative. Use of lower reference cutoffs for plasma biomarkers, as recommended by ESC/ACC guidelines, markedly increases the rates of cTnI-positive cases overall. A substantial proportion of the increase in total cTnI-positive cases was derived from the creation of additional cTnI-positive/CKMB-negative cases. CKMB-positive/cTnI-negative cases are likely false positive for myocardial injury.

Utility of biochemical markers in the follow-up of heart transplant recipients

Endomyocardial biopsy (EMB) is currently the standard method to diagnose acute graft rejection. However, considering the potential complications of this procedure, a noninvasive marker of rejection would be an ideal alternative or at least a helpful adjunct to posttransplant management. We measured myoglobin (Myo), creatine kinase MB mass (CK-MBm), troponin T (cTnT), serum amyloid A (SAA), and C-reactive protein (CRP) in 57 patients (mean age 37.5 years) who underwent orthotopic heart transplantation for end-stage cardiac failure between January and December 2001. Endomyocardial biopsies were performed routinely after surgery and histologically diagnosed rejection was graded according to the criteria of the International Society of Heart and Lung Transplantation. Concomittant with the biopsies, blood samples were drawn from the coronary sinus (central blood samples) and from a peripheral vein (peripheral blood samples) to assay biochemical markers. Among 149 EMB evaluated, 87 were negative (grade 0); 28 showed grade 1a rejection; 26 showed grade 1b; and 8 showed grade > 1b (2 were grade 2, 6 were grade 3a). Grades 0 and 1a were considered to be negative, while grades 1b and >1b were considered positive indicating potential acute graft rejection. cTnT, Myo, CK-MBm, SAA, and CRP levels were measured in 149 central blood samples and 149 peripheral blood samples. Myo and CK-MBm did not show significant changes. cTnT seems to be a potentially useful addition to the EMB results, while SAA and CRP showed variations with respect to EMB grade both in central and peripheral samples.

Interleukin-6 and tumor necrosis factor alpha in relation to myocardial infarct size and collagen formation

Background: Interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) levels increase after acute myocardial infarction (AMI) in humans. Experimental data suggest that these cytokines regulate the initiation of scar formation after AMI. We investigated the interrelationships of IL-6 and TNF-α, tissue injury, infarct size, cardiac function, and collagen formation in humans. Methods: Serum and plasma samples were taken on 93 patients receiving thrombolytic treatment for their first AMI. Collagen formation was evaluated by measuring concentrations of serum aminoterminal propeptide of type III procollagen (PIIINP). Results: IL-6 levels increased by 44% (P <.001) and peaked at 24 hours. Peak IL-6 levels correlated positively with area under the curve of creatine kinase MB mass (r =.31, P <.01), peak troponin T level (r =.34, P <.005), and PIIINP measured at discharge (r =.46, P <.001). There were no changes in TNF-α levels, and patients with left ventricular dysfunction (EF < 40 %) had similar TNF-α levels as those with preserved left ventricular function. Conclusions: IL-6 may regulate collagen formation and thus remodeling of the left ventricle after AMI. In addition, TNF-α measurement is useless in the assessment of infarct size or left ventricular function during the immediate post-infarction period.

Serum cardiac troponin and subclinical cardiac status in pediatric chronic renal failure.

Patients with uremia often have elevated serum cardiac troponin T (cTnT) even without clinical heart damage. Pediatric patients are ideal for studies of the relationship between uremia and heart disease because they are unlikely to have cardiac risk factors other than uremia. To determine the relationship between uremia and cTnT levels. Echocardiograms and blood chemistry results were obtained from 50 pediatric patients with chronic renal failure and without clinical heart disease. Levels of cTnT were tested for correlation with cardiac dysfunction. In multivariate analysis, biochemical aspects of renal disease and its treatment were tested for correlation with cardiac dysfunction. Forty-nine patients had cardiovascular abnormalities, including increased left ventricular function and mass, elevated heart rate and blood pressure, and reduced LV afterload. LV contractility was inversely correlated with cTnT level (r = -0.36). Higher cTnT also correlated with higher serum creatine kinase-MB mass, lower serum parathyroid hormone, higher blood urea nitrogen and bicarbonate levels, and the use of diuretics, but not with higher cardiac troponin I. Left ventricular contractility was inversely related to serum creatinine, phosphorus, and the use of beta-blockers. Elevated cTnT levels are not artifactual, but are genuine indicators of cardiomyocyte damage. Cardiac damage, indicated by either elevated cTnT or low LV contractility, is related to uremia, deranged calcium and phosphorus metabolism, and bicarbonate levels. Serum cTnT and LV contractility identify subclinical cardiac damage that could be treated to hopefully reduce cardiovascular morbidity and mortality in this high-risk population.

Ischemic preconditioning does not improve myocardial preservation during off-pump multivessel coronary operation

Background The value of ischemic preconditioning during coronary operations has remained controversial. The aim of this study was to evaluate the effects of ischemic preconditioning on myocardial energy metabolism and tissue injury during off-pump multivessel coronary surgery. Methods Eleven patients with preceding preconditioning were compared with 11 patients without it. The preconditioning group underwent a 5-minute period of ischemia followed by a 5-minute reperfusion period before coronary occlusion for each of the first two anastomoses. Results The transmyocardial differences (coronary sinus – arterial) in inosine and the sum of adenine degradation products increased in both groups, but the differences in xanthine and hypoxanthine increased only in the preconditioning group. Myocardial lactate production increased to a maximum of 0.09 mmol/L with preconditioning and to a maximum of 0.17 mmol/L without it. Transmyocardial pH differences increased to 0.03 U in both groups. The maximum postoperative concentration of creatine kinase-MB mass was 14.8 μg/L with preconditioning and 6.3 μg/L without preconditioning, and that of troponin I 7.4 μg/L and 5.2 μg/L, respectively. There were no statistically significant differences between the groups, however. Conclusions Ischemic preconditioning of 5 minutes followed by reperfusion of 5 minutes during off-pump multivessel coronary artery surgery did not prevent myocardial metabolic derangement and tissue injury and thus cannot be routinely recommended.

The relative utility of cardiac troponin i, creatine kinase‐mbmass, and myosin light chain‐1 in the long‐term risk stratification of patients with chest pain

Sensitive and specific cardiac markers convey important short-term prognostic information about patients with an acute coronary syndrome. There are, however, few data assessing their value as long-term predictors. The aim of the current study was to assess the relative value of three such markers and clinical characteristics in determining the long-term prognosis of patients with chest pain. Cardiac troponin I (cTnI), myosin light chain-(MLC-1), and creatine kinase-MBmass levels were obtained on admission (0 h) and at 4, 8, 16, and 24 h in 208 patients with chest pain. Eligible subjects were determined, at the time of hospital admission, to be at >7% risk of acute myocardial infarction (MI), but without new ST-segment elevation on their presenting electrocardiogram. Follow-up was performed a median of 28 (range 1-46) months later. The primary study endpoint was death or nonfatal MI, subsequent to the index admission. Cardiac TnI levels > or = 0.2 ng/ml (odds ratio [OR] 1.93, 95% confidence interval [CI] 1.09-3.40) and MLC-1 levels > or = 1 ng/ml (OR 3.24, 95% CI 1.83-5.73) were both significant predictors of death or MI during long-term follow-up; MLC-1 was, however, the only independent biochemical predictor (OR 2.11,95% CI 1.14-3.93). Both cTnl and MLC-1 predict the long-term outcome of patients with chest pain, but, in this cohort, MLC-1 proved to be a better predictor of mortality and nonfatal acute MI.

Aplicabilidad de la nueva definición de infarto de miocardio y opinión de los cardiólogos españoles

The Working Group on Ischemic Heart Disease and Coronary Care Units of the Spanish Society of Cardiology evaluated the applicability of a new definition of infarction in Spanish hospitals, its current use, and the opinion of Spanish cardiologists. A telephone survey was made (from late 2001 to early 2002) in Spanish hospitals to evaluate the availability of troponin or creatine kinase MB mass determinations. A questionnaire was sent to all members of the Spanish Society of Cardiology to query about the availability of determinations of cardiac necrosis markers at their respective hospitals, use of the new definition, and whether they agreed with the new definition. An important proportion of Spanish hospitals cannot determine myocardial necrosis markers (troponin or creatine kinase MB mass), mainly due to low-volume activity (fewer than 200 beds). The new definition of myocardial infarction was used by Spanish cardiologists always (24%), frequently (31%), sometimes (17%), seldom (14%), and never (11%). Agreement with the definition was complete in 21%, almost complete in 33%, half and half in 26%, rare in 10%, and absent in 7% of Spanish cardiologists. A large percentage of Spanish hospitals cannot use the new definition of myocardial infarction because they cannot determine specific cardiac necrosis markers. Spanish cardiologists are not generally using the new definition and many do not agree with it.

Biochemical and clinical predictors of long-term outcome in patients with nonspecific chest pain and nondiagnostic electrocardiograms

Background There are few data assessing the relative value of clinical factors and sensitive cardiac markers in determining the long-term prognosis of patients with chest pain. Likewise, little information exists about the long-term outcome of patients with chest pain who have negative markers of myocardial cell necrosis. This study addresses these issues in a cohort of patients with nonspecific chest pain and nondiagnostic electrocardiograms (ECGs). Methods Eligible subjects (n = 501) had experienced >15 minutes chest pain at rest during the previous 24 hours, but were found to be at low-risk for acute myocardial infarction (AMI) by means of a well-validated clinical algorithm. Cardiac troponin I, creatine kinase MB mass, myoglobin, and myosin light chain-1 were collected at presentation and 3, 6, and 12 hours later. Patients were observed for a median of 31 months. The composite end point was death or AMI subsequent to the index admission. Results Cardiac troponin I was the best single biochemical predictor of outcome (risk ratio 2.34, 95% CI 1.31-4.17, P = .004), but was of less independent prognostic value than age and an abnormal presenting ECG. It was also inferior to a combination strategy, using all 4 markers tested (risk ratio 2.37, 95% CI 1.44-3.91, P < .001). Fifty of 428 patients (12%) with a cardiac troponin I level ≤0.2 ng/mL and 25 of 287 patients (9%) without elevation of any marker tested sustained an adverse event during follow-up. Conclusions Cardiac troponin I is the most useful single biochemical predictor of long-term outcome, but the best determinants are age, an abnormal presenting ECG, and an “any marker positive” strategy. Patients without elevated cardiac markers have an adverse event rate of approximately 10% in the subsequent 31 months. (Am Heart J 2003;145:88-94.)

Elevated cardiac troponin T in peritoneal dialysis patients is associated with CRP and predicts all-cause mortality and cardiac death.

Cardiac troponin T (cTnT) is a highly sensitive and specific marker of myocardial damage. In sera from patients with end-stage renal disease, cTnT may be elevated without other signs of acute myocardial injury. It has been shown that elevated cTnT in haemodialysis patients is associated with poor prognostic outcome. The aim of the present study was to test the hypothesis that elevated cTnT in a single serum sample from peritoneal dialysis (PD) patients is of prognostic importance. Blood samples were taken from 26 randomly selected PD patients without signs of acute myocardial ischaemia. Sera were analysed for: cTnT with the second generation TnT ELISA on ES 300; cardiac troponin I (cTnI) with Opus Plus; and for creatine kinase-MB (CKMB) mass and C-reactive protein (CRP). After 4 years, clinical outcomes were evaluated by chart review. The influence on survival was tested with Kaplan-Meier analysis and Cox's proportional regression analysis. Concentrations of cTnT >/=0.04 micro g/l and CRP >/=10 mg/l were strong predictors of all-cause mortality in univariate analysis. Twelve out of 14 patients with cTnT >/=0.04 micro g/l died compared with three out of 12 with cTnT <0.04 micro g/l. Other factors that influenced survival were age and the presence of ischaemic heart disease (IHD). There was a significant positive correlation between cTnT and CRP, and between cTnT and age. Cardiac troponin T was an independent predictor compared with age but not compared with CRP and IHD. Neither cTnI nor CKMB mass concentrations were related to survival. Elevated serum concentrations of cTnT significantly predicted poor outcome and there was a correlation between cTnT and CRP concentrations in samples from PD patients. Cardiac troponin I and CKMB mass had no prognostic value.

Myoglobin, creatine kinase MB isoforms and creatine kinase MB mass in early diagnosis of myocardial infarction in patients with acute chest pain

Objectives Measurements of myoglobin and creatine kinase (CK)-MB isoforms have been suggested to be sensitive tests for the early diagnosis of myocardial infarction (MI). We have investigated the utility of myoglobin, creatine kinase (CK)-MB isoforms and creatine kinase MB mass (CK-MBm) in early diagnosis of MI using cardiac troponin T (cTnT) positivity as a reference. Design and methods The study population comprised 440 patients who had had chest pain for less than 12 h. Patients were divided into cTnT negative (cTnT-) or cTnT positive (cTnT+) patients (concentration of cTnT >0.1 μg/L at two different time points during 72 h). Results At the time of admission to the emergency department receiver operating characteristics (ROC) curves of CK-MB isoforms and CK-MBm were not better than that of myoglobin. Six hours after admission CK-MB isoforms and CK-MBm provided statistically significantly larger areas under the curve (AUC) than myoglobin ( p < 0.01). When ROC curves were related to the onset of chest pain (< 3 h, 3–6 h, and > 6 h) there were no significant differences between the cardiac markers studied. Conclusions According to the present findings, CK-MB isoforms or myoglobin offer no advantage over CK-MBm as early markers of myocardial infarction.

ACUTE EFFECT OF HAEMODIALYSIS ON SERUM MARKERS OF MYOCARDIAL DAMAGE

SUMMARYCardiac markers are more likely to be elevated in dialysis patients than in patients with renal failure not on dialysis. In this study, 31 patients (20 males, 11 females) undergoing chronic haemodialysis were enrolled. The effect of haemodialysis on cardiac troponin T (cTnT), I (cTnI), creatine kinase MB (CKMB) mass, CKMB activity and myoglobin assays was assessed by comparing pre‐ and post‐haemodialysis determinations. After correcting for haemoconcentration, significant differences were observed (mean ± SEM, pre‐ vs post‐dialysis) for myoglobin (178.9 ± 19.3 vs 225.0 ± 28.4 ng/ml; p=0.006) for cTnT (0.111 ± 0.028 vs 0.148 ± 0.037 ng/ml; p=0.004), for CKMB mass (2.75 ± 0.37 vs 2.59 ± 0.37 ng/ml; p=0.000) and CKMB activity (14.8 ± 0.9 vs 13.1 ± 0.9 U/l; p=0.000) assays. Our study questions the reliability of cardiac markers in dialysis patients and suggests that the clinical threshold value and diagnostic efficiency of each assay needs to be validated. Although these differences exceeded clinical threshold values in only a few patients, serum markers of myocardial damage in dialysis patients should be interpreted with caution.

Cardiovascular prevention before admission reduces mortality following acute myocardial infarction in patients with diabetes.

Previous studies have shown that patients with diabetes mellitus have an increased mortality after suffering from acute myocardial infarction (AMI). Patients with diabetes have several risk factors for cardiovascular disease. Our objective was to quantify the prevalence of pharmacological cardiovascular prevention at admission and relate such treatment to short and long-term mortality following AMI in patients with and without diabetes. All patients discharged from the Department of Internal Medicine at Helsingborg Hospital in 1996 and 1997 with a principal diagnosis of AMI were included in the study. Patients were divided into two groups according to the presence or absence of diabetes. Cardiovascular risk factors, on-going medication, type of ward following admission, peak creatine kinase MB mass (CKMB) and immediate treatment were registered. Information about death was obtained from the national register. Kaplan-Meier analysis was performed for life-expectancy. A total of 673 patients with AMI were registered, of which 117 (17.4%) had diabetes. No differences in 30 days (17.1% vs. 15.3%) or 1-year (24.8% vs. 27.4%) mortality were seen between the diabetes and control groups, whereas the 2-year mortality was significantly higher in the diabetes group (40.2% vs. 29.1%). Cardiovascular risk factors occurred more often in the diabetes group and the use of aspirin, ACE-inhibitors, statins and diuretics was significantly more frequent. In patients treated with aspirin, in combination with either statin or angiotensin converting enzyme (ACE)-inhibitor, or both, no differences were seen in 30 days, 1 or 2-year mortality between groups. In contrast to earlier studies we did not find an increased 30 days and 1-year mortality in patients with diabetes suffering from AMI. This discrepancy was linked to a higher frequency of pharmacological cardiovascular prevention, a finding supporting the hypothesis that survival of a diabetes patient after AMI could be affected by factors operating before the infarction.

Elevated soluble P-selectin levels are associated with an increased risk of early adverse events in patients with presumed myocardial ischemia

Background Cell adhesion molecules (CAMs) play a pivotal role in the interactions between leukocytes, platelets, and vascular endothelium. Soluble CAMs (sCAMs) are shed from cell surfaces and reflect cellular activation. Elevated levels of sCAMs have been reported in the acute coronary syndromes. We hypothesized, therefore, that sCAMs might prove of prognostic value in patients with acute chest pain presumed to be the result of myocardial ischemia. Methods One hundred twenty-six consecutive patients with chest pain, thought clinically to represent myocardial ischemia, were studied prospectively. Soluble intercellular adhesion molecule-1 (sICAM-1), vascular cell adhesion molecule-1 (sVCAM-1), E-selectin (sE-selectin) and P-selectin (sP-selectin) levels were assayed at presentation, as were cardiac troponin I (cTnI) and creatine kinase-MBmass (CK-MBmass). The primary study end point was the occurrence of a serious cardiac event (SCE) during the index admission or the subsequent 3 months. Results sP-selectin and cTnI levels were significantly higher among patients who had an early SCE (P =.006 and P <.001, respectively). Both remained independently predictive (P <.001) in a multivariate regression equation. The other independent predictor was a history of vascular disease (P <.05). No other markers were significant predictors of early outcome. Conclusion Elevated sP-selectin levels, but not those of other sCAMs, are predictors of early adverse events in patients with chest pain presumed caused by myocardial ischemia. Their utility in predicting the outcome of individual patients is, however, limited. (Am Heart J 2002;143:235-41.)