Clinical evaluation of the first medical whole blood, point-of-care testing device for detection of myocardial infarction. (1/344)

BACKGROUND: Validation of whole blood, point-of-care testing devices for monitoring cardiac markers to aid clinicians in ruling in and ruling out myocardial infarction (MI) is necessary for both laboratory and clinical acceptance. METHODS: This study evaluated the clinical diagnostic sensitivity and specificity of the First Medical Cardiac Test device operated by nursing and laboratory personnel that simultaneously measures cardiac troponin I (cTnI), creatine kinase (CK) MB, myoglobin, and total CK on the Alpha Dx analyzer in whole blood for detection of MI. Over a 6-month period, 369 patients initially presenting to the emergency department with chest pain were evaluated for MI using modified WHO criteria. Eighty-nine patients (24%) were diagnosed with MI. RESULTS: In whole blood samples collected at admission and at 3- to 6-h intervals over 24 h, ROC curve-determined MI decision limits were as follows: cTnI, 0.4 microgram/L; CKMB, 7.0 microgram/L; myoglobin, 180 microgram/L; total CK, 190 microgram/L. Based on peak concentrations within 24 h after presentation, the following sensitivities (+/- 95% confidence intervals) were found: cTnI, 93% +/- 5.5%; myoglobin, 81% +/- 9.7%; CKMB, 90% +/- 6.3%; total CK, 86% +/- 7.5%. Sensitivities were maximal at >90% for both cTnI and CKMB at >12 h in MI patients, without differences between ST-segment elevation and non-ST-segment elevation MI patients. CONCLUSIONS: The First Medical point-of-care device provides cardiac marker assays that can be used by laboratories and clinicians in a variety of hospital settings for ruling in and ruling out MI.  (+info)

Selective antioxidant enzymes during ischemia/reperfusion in myocardial infarction. (2/344)

The study of ischemia/reperfusion injury included 25 patients in the acute phase of myocardial infarction (19 perfused, 6 remained non-reperfused as evaluated according to the time course of creatine kinase and CK-MB isoenzyme activity) and a control group (21 blood donors). Plasma level of malondialdehyde was followed as a marker of oxidative stress. Shortly after reperfusion (within 90 min), a transient increase of malondialdehyde concentration was detected. The return to the baseline level was achieved 6 h after the onset of therapy. The activity of a free radical scavenger enzyme, plasma glutathione peroxidase (GPx), reached its maximum 90 min after the onset of treatment and returned to the initial value after 18 h. The specificity of the GPx response was confirmed by comparing with both non-reperfused patients and the control group, where no significant increase was detected. The erythrocyte Cu,Zn-superoxide dismutase (SOD) did not exhibit significant changes during the interval studied in perfused patients, probably due to the stability of erythrocyte metabolism. In non-reperfused patients, a decrease of SOD was found during prolonged hypoxia. These results help to elucidate the mechanisms of fast activation of plasma antioxidant system during the reperfusion after myocardial infarction.  (+info)

Safe discharge from the cardiac emergency room with a rapid rule-out myocardial infarction protocol using serial CK-MB(mass). (3/344)

OBJECTIVE: To determine whether a new protocol, using a rapid and sensitive CK-MB(mass) assay and serial sampling, can rule out myocardial infarction in patients with chest pain and decrease their length of stay in the cardiac emergency room without increasing risk. DESIGN: The combined incidence of cardiac death and acute myocardial infarction at 30 days, six months, and 24 months of follow up were compared between patients discharged home from the cardiac emergency room after ruling out myocardial infarction with a CK-MB(activity) assay in 1994 and those discharged home after a rapid CK-MB(mass) assay in 1996. SETTING: Cardiac emergency room of a large university hospital. PATIENTS: In 1994 and 1996, 230 and 423 chest pain patients, respectively, were discharged home from the cardiac emergency room with a normal CK-MB and an uneventful observation period. RESULTS: The median length of stay in the cardiac emergency room was significantly reduced, from 16.0 hours in 1994 to 9.0 hours in 1996 (p < 0.0001). Mean event rates in patients from the 1994 and 1996 cohorts, respectively, were 0.9% (95% confidence interval (CI) -0.3% to 2.1%) v 0.7% (95% CI -0.1% to 1. 5%) at 30 days, 3.0% (95% CI 0.8% to 5.2%) v 2.8% (95% CI 1.2% to 4. 4%) at six months, and 7.0% (95% CI 3.7% to 10.3%) v 5.7% (95% CI 3. 5% to 7.9%) at 24 months. Kaplan-Meier survival analysis showed no difference in mean event-free survival at 30 days, six months, and 24 months of follow up. CONCLUSIONS: Using a rule-out myocardial infarction protocol with a rapid and sensitive CK-MB(mass) assay and serial sampling, the length of stay of patients with chest pain in the cardiac emergency room can be reduced without compromising safety.  (+info)

Assessment of coronary reperfusion in patients with myocardial infarction using fatty acid binding protein concentrations in plasma. (4/344)

OBJECTIVE: To examine whether successful coronary reperfusion after thrombolytic treatment in patients with confirmed acute myocardial infarction can be diagnosed from the plasma marker fatty acid binding protein (FABP), for either acute clinical decision making or retrospective purposes. DESIGN: Retrospective substudy of the GUSTO trial. SETTING: 10 hospitals in four European countries. PATIENTS: 115 patients were treated with thrombolytic agents within six hours after the onset of acute myocardial infarction. Patency of the infarct related artery was determined by angiography within 120 minutes of the start of thrombolysis. MAIN OUTCOME MEASURES: First hour rate of increase in plasma FABP concentration after thrombolytic treatment, compared with increase in plasma myoglobin concentration and creatine kinase isoenzyme MB (CK-MB) activity. Infarct size was estimated from the cumulative release of the enzyme alpha hydroxybutyrate dehydrogenase in plasma during 72 hours, or from the sum of ST segment elevations on admission. Logistic regression analyses were performed to construct predictive models for patency. RESULTS: Complete reperfusion (TIMI 3) occurred in 50 patients, partial reperfusion (TIMI 2) in 36, and no reperfusion (TIMI 0+1) in 29. Receiver operating characteristic (ROC) curve analyses showed that the best performance of FABP was obtained when TIMI scores 2 and 3 were grouped and compared with TIMI score 0+1. The performance of FABP as a reperfusion marker was improved by combining it with alpha hydroxybutyrate dehydrogenase infarct size, but not with an early surrogate of infarct size (ST segment elevation on admission). In combination with infarct size FABP performed as well as myoglobin (areas under the ROC curve 0.868 and 0.857, respectively) and better than CK-MB (area = 0.796). At optimum cut off levels, positive predictive values were 97% for FABP, 95% for myoglobin, and 89% for CK-MB (without infarct size, 87%, 88%, and 87%, respectively), and negative predictive values were 55%, 52%, and 50%, respectively (without infarct size, 44%, 42%, and 34%). CONCLUSIONS: FABP and myoglobin perform equally well as reperfusion markers, and successful reperfusion can be assessed, with positive predictive values of 87% and 88%, or even 97% and 95% when infarct size is also taken into account. However, identification of non-reperfused patients remains a problem, as negative predictive values will generally remain below 70%.  (+info)

Detection of minor myocardial injury after successful percutaneous transluminal coronary angioplasty with or without stenting. (5/344)

Cardiac troponins are sensitive and specific markers for the detection of minor myocardial injury. However, they have been rarely used to monitor myocardial injury after coronary stenting. The purpose of the study was to measure cardiac troponin I (cTnI) and cardiac troponin T (cTnT) levels after apparently successful percutaneous transluminal coronary angioplasty (PTCA) with or without coronary stenting and to compare their results with serum creatine kinase (CK) and its isoform, creatine kinase-MB (CKMB). CTnI and cTnT levels were compared with those of CK or CKMB in 50 consecutive patients with stable angina undergoing visually successful PTCA with stenting (n = 35) or without stenting (n = 15). Cardiac TnI, cTnT, CK and CKMB levels were measured before and 6, 24, and 48 hours after the procedures was performed. None of the patients had abnormal cTnI or cTnT levels, CK activity, or CKMB levels before the procedures. Moreover, no patient showed electrocardiographic evidence of myocardial infarction. 13 patients (26%) had abnormal peak values of one or more markers at 24 hours after coronary intervention. Troponin I was elevated in 10/35 patients after coronary stenting (29%) and in 2/15 patients after PTCA (13%) (P = 0.327). Troponin T was elevated in 6 patients (17%) and CKMB activity was elevated in 3 patients (9%) of the coronary stenting group. CTnI was more significant than CKMB (P = 0.023) in detecting minor myocardial injury. When compared with cTnI and CKMB, cTnT did not reach significance (P = 0.129 and 0.489, respectively). 5 out of the 13 patients with abnormal markers (38%) developed side branch occlusion after stenting. In conclusion, cTnI was a very sensitive marker in detecting minor myocardial injury after coronary angioplasty with or without stenting. The frequency of increased serum levels of cardiac troponins was higher in patients undergoing stent implantation than in those treated with angioplasty alone but did not reach significance. Side branch occlusion may have accounted for some, but not all, periprocedural minor myocardial injury in the stent group.  (+info)

Effects of implantable cardioverter defibrillator implantation and shock application on biochemical markers of myocardial damage. (6/344)

BACKGROUND: Implantable cardioverter defibrillator (ICD) implantation is a common approach in patients at high risk of sudden cardiac death. To check for normal function, it is necessary to test the ICD. For this purpose, repetitive induction and termination of ventricular fibrillation by direct current shocks is required. This may lead to minor myocardial damage. Cardiac troponin T (cTnT) and I (cTnI) are specific markers for the detection of myocardial injury. Because these proteins usually are undetectable in healthy individuals, they are excellent markers for detecting minimal myocardial damage. The objective of this study was to evaluate the effect of defibrillation of induced ventricular fibrillation on markers of myocardial damage. METHODS: This study included 14 patients who underwent ICD implantation and intraoperative testing. We measured cTnT, cTnI, creatine kinase MB (CK-MB) mass, CK activity, and myoglobin before and at definite times after intraoperative shock application. RESULTS: Depending on the effectiveness of shocks and the energy applied, the cardiac-specific markers cTnT and cTnI, as well as CK-MB mass, showed a significant increase compared with the baseline value before testing and peaked for the most part 4 h after shock application. In contrast, the increases in CK activity and myoglobin were predominantly detectable in patients who received additional external shocks. CONCLUSIONS: ICD implantation and testing leads to a short release of cardiac markers into the circulation. This release seems to be of cytoplasmic origin and depends on the number and effectiveness of the shocks applied.  (+info)

Production of recombinant human creatine kinase (r-hCK) isozymes by tandem repeat expression of M and B genes and characterization of r-hCK-MB. (7/344)

BACKGROUND: Serum creatine kinase-MB isoenzyme (CK-MB) is widely used as a marker of myocardial injury. We prepared recombinant human CK (r-hCK) MB isoenzyme and examined its potential for use as a control material for assay of CK-MB in serum. METHODS: cDNAs encoding CK-M and CK-B subunits were inserted into the same plasmid vector, followed by transformation of Escherichia coli. The resulting three types of CK isoenzymes were purified by conventional chromatography. RESULTS: The ratio of MB to MM to BB was 50:40:10 on the basis of CK activity. Highly purified CK-MB with a specific activity of 533 U/mg was produced in a yield of 5.7 mg/g of packed cells. Purified r-hCK-MB had the isoelectric point (pI 5.3) and molecular size (46 kDa for the subunit) of native CK-MB. Its immunoreactivity in an ELISA using antibody against native heart enzyme was similar to that of cardiac CK-MB. The r-hCK-MB retained >90% activity for at least 4 months at 11 degrees C in a delipidated serum matrix in a liquid form at a concentration of 118 U/L. CONCLUSIONS: r-hCK-MB shows key properties of the native cardiac isoenzyme and may be useful as a control and calibrator for serum assays of CK-MB.  (+info)

Reactivation of ischemic events in acute coronary syndromes: results from GUSTO-IIb. Gobal Use of Strategies To Open occluded arteries in acute coronary syndromes. (8/344)

OBJECTIVES: We sought to determine the incidence of and risk factors for thrombotic events early after discontinuing antithrombin therapy in patients with acute coronary syndromes. BACKGROUND: Discontinuation of treatment with heparin and other thrombin inhibitors in patients with unstable coronary syndromes has related to clinical and biochemical evidence of early reactivation of thrombosis. METHODS: We studied 8,943 of the 12,142 patients with acute coronary syndromes enrolled in the Global Use of Strategies To Open occluded arteries in acute coronary syndromes trial of hirudin versus heparin. We excluded patients who received no study drug, lacked timing data, died or had myocardial (re)infarction [(re)MI] during study-drug infusion, or began heparin treatment within 2 h after treatment with the study drug was stopped. We assessed the incidence and timing of (re)MI by type and timing of antithrombin treatment. RESULTS: In all, 215 patients (2.4%) suffered (re)MI, 49 within 12 h of antithrombin therapy discontinuation and 166 between hour 12 and hospital discharge. The duration of infusion did not differ between the hirudin and heparin groups. The rate of early re(MI) after drug therapy discontinuation was significantly higher in patients given heparin versus hirudin (0.8% vs. 0.3%, p = 0.002). Patients with (re)MI had higher mortality at 30 days (23.6% vs. 2.4%, p = 0.001) and 1 year (35.2% vs. 6.7%, p = 0.001) compared with patients without (re)MI. CONCLUSIONS: The incidence of (re)MI was clustered within 12 h of heparin therapy discontinuation, with the greatest risk within 4 h. There was no evidence of early reactivation of thrombotic events after hirudin. Patients who had (re)infarction had worse outcomes. Better understanding of the mechanism and possible prevention of recurrent thrombosis is needed.  (+info)

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