Cardiac specific troponin-I release in canine experimental myocardial infarction: development of a sensitive enzyme-linked immunoassay

A canine model of experimental myocardial infarction has been used to investigate the release of troponin-I as a specific diagnostic indicator of cardiac necrosis. An enzyme-linked immunoassay was established to detect canine cardiac troponin-I in serum. Polyclonal antisera to cardiac troponin-I showed low cross-reactivity with skeletal muscle troponin-I which was completely removed by immunoadsorption. The cardiac specific ELISA time was 5 to 6 h. Assay sensitivity was 4 ng cardiac troponin-I/ml with an upper limit of 200 ng/ml in neat serum. Mean normal circulating levels of cardiac troponin-I were 15.6 ng/ml compared with an estimated 11 ng/ml in man [Cummins, B. et al. Am Heart J 113, 1333-1344 (1987)]. After experimental infarction, cardiac troponin-I was detectable within 4 to 6 h and peaked between 10 to 16 h post-ligation. Cardiac specific creatine kinase-MB isoenzyme was released with a similar initial time course. Mean peak cardiac troponin-I and CK-MB were elevated 6- and 10-fold respectively. Cardiac troponin-I levels were elevated for up to 200 h post-ligation compared to a maximum of 100 h for CK-MB. The prolonged time course of troponin-I release was comparable to that seen clinically [Cummins, B., et al. Am Heart J 113, 1333-1344 (1987)]. Histochemical infarct size correlated well with CK-MB but less so with troponin-I release. This may reflect the complex nature of intracellular troponin-I degradation and loss from necrotic cardiac tissue.     

Cardiac troponin I in patients with acute lower limb ischemia

The presence, cause, and clinical significance of elevated cardiac troponin I in patients with acute lower limb ischemia is yet unknown. Forty-six patients (20 men [43%]; mean age 72 +/- 10 years, range 42 to 92) with acute lower limb ischemia were enrolled in this study. Serial creatine kinase (CK), CK isoenzyme MB (CK-MB), and troponin I measurements were obtained in all consecutive patients. Peak levels were evaluated for each patient. Twenty-four patients (52%) had elevated peak troponin I levels (>0.2 ng/ml) during their hospitalization. Patients were divided into 3 groups according to their peak troponin I levels: 11 patients (24%) had peak troponin I levels >1 ng/ml (the high troponin I group), 13 (28%) had levels of 0.2 to 1 ng/ml (the intermediate troponin I group), and the remaining 22 (48%) had peak troponin I levels <0.2 ng/ml (the low troponin I group). The peak CK levels were 10,263 +/- 16,513, 1,294 +/- 1,512, and 934 +/- 1,045 IU/ml (p = 0.04) in the 3 different troponin I subgroups, respectively, and the peak CK-MB levels were 143 +/- 170, 38 +/- 31, and 38 +/- 43, respectively (p = 0.04). Troponin I was positively correlated with CK (R = 0.35, p = 0.017) and CK-MB (R = 0.38, p = 0.009). The mean length of hospitalization was 8.3 +/- 6.2 days for the whole study group and did not vary among the 3 troponin I groups (10.5 +/- 10.9 vs 8.6 +/- 4.9 vs 7.2 +/- 4.0 days, p = 0.762). There were no differences in mortality during hospitalization among the 3 groups (4 of 11 vs 1 of 13 vs 4 of 22 patients, p = 0.22). In conclusion, patients with acute lower limb ischemia often have elevated cardiac troponin I levels. Elevated troponin I levels were not associated with the duration of hospitalization or with in-hospital mortality in this group of patients.     

Cardiac troponin I elevation in paediatric cardiac catheterization.

OBJECTIVE: The aim of this study is to investigate prospectively whether intracardiac catheterization produces myocardial damage in paediatric heart. METHODS: The study was performed in all patients undergoing diagnostic cardiac catheterization at our institute. A baseline serum sample was drawn before the procedure. The second serum sample was obtained 4-6 hours after the procedure. Cardiac troponin-I and creatine kinase isoenzyme MB fraction levels were determined quantitatively. RESULTS: Diagnostic cardiac catheterization was performed in 30 patients. There were 17 males and 13 females in the study group. The median age was 12 months (range 1 to 204 months); the median body weight was 8 kilograms (range 2.1 to 45 kilograms). The increase in cardiac troponin I (0.21+/-0.04 ng/ml to 1.16+/-1.40 ng/ml, p<0.05) and creatine kinase isoenzyme MB (26.68+/-7.53 U/L to 41.65+/-22.12 U/L, p< 0.05) levels after the procedure was significant. CONCLUSION: This study shows that serum elevations of cardiac troponin I and creatine kinase isoenzyme MB occur after the most of paediatric diagnostic cardiac catheterization procedures.     

Immunological determination of serum m-AST activity in patients with acute myocardial infarction.

Serum m-AST (mitochondrial isoenzyme of AST) activity in patients with acute myocardial infarction was determined quantitatively by a new immunological technique which is sensitive and easily available. All 31 patients with acute myocardial infarction showed abnormally high levels of serum m-AST (more than 5 KU/ml); the mean serum m-AST activity attained its peak (42.0 +/- 4.9 KU/ml) on the first day after the onset of infarction 5 hours later than that of serum t-AST (total AST) activity in 15 patients whose peak m- and t-AST activities were identified clearly. The individual peak m-AST activity correlated with the total CK released (r = 0.83, n = 15), indicating that the release of m-AST also reflects the infarct size. The ratio of serum m-AST/t-AST increased following myocardial infarction and showed the maximal value (average 25.7%) on the third to seventh day after onset. This ratio in the patients with acute myocardial ifarction was also greater than that in patients with liver disease or with heart failure from causes other than acute myocardial infarction. In the patients who had the additional complication of heart failure and/or cardiogenic shock the ratio was also greater than that is the patients without these hazards. These results indicate that the ratio of serum m-AST/t-AST reflects the severity of the myocardial cellular damage in acute myocardial infarction.     

Myoglobin levels at 12 hours identify patients at low risk for 30-day mortality after thrombolysis in acute myocardial infarction: a Thrombolysis in Myocardial Infarction 10B substudy.

OBJECTIVE: We sought to identify, by use of serum cardiac markers, patients at low risk for 30-day mortality after ST-segment elevation myocardial infarction. BACKGROUND: Baseline cardiac markers are currently used to identify patients at increased risk for short-term events. We hypothesized that serum markers measured after treatment could identify patients at low risk for 30-day mortality. METHODS: A total of 839 patients from the Thrombolysis in Myocardial Infarction (TIMI) 10B study had myoglobin, cardiac-specific troponin-I, creatine kinase (CK)-MB measurements at the following time points; baseline, 90 minutes, and 3 and 12 hours after thrombolysis. By use of receiver operating characteristic analysis, thresholds were derived to predict 30-day mortality with at least 95% negative predictive value. RESULTS: Ninety minutes after thrombolysis myoglobin was superior to troponin-I or CK-MB in identifying patients at low risk for mortality. The 30-day mortality for 12-hour myoglobin < or = 239 ng/mL was 1.4% compared with 9.1% for levels > 239 ng/mL (P < .001). For 12-hour troponin-I (threshold 81.5 ng/mL), mortality was 1.9% versus 6.6% (P = .001) if above threshold; similarly for CK-MB at 12 hours (threshold 191 ng/mL) it was 3.3% versus 7.9% (P = .02). Multivariate analysis of baseline and posttreatment cardiac markers, age, sex, infarct artery location, and 90-minute TIMI flow grade identified only 12-hour myoglobin among the cardiac markers as independently predicting a low 30-day mortality (odds ratio 0.11, 95% confidence interval 0.02-0.50, P < .004). CONCLUSION: Serum cardiac markers can identify greater than two thirds of patients at low risk for 30-day mortality. A low 12-hour myoglobin level (< or = 239 ng/mL in this substudy) identifies such patients at low risk and could potentially assist in early risk stratification and triage after ST-segment elevation myocardial infarction.     

Plasma beta-thromboglobulin as a measure of platelet activity: Effect of risk factors and findings in ischemic heart disease and after acute myocardial infarction

The plasma concentration of beta-thromboglobulin (BTG), a platelet-specific protein released during platelet aggregation, is considered a sensitive marker of in vivo platelet activity. The mean plasma level in 133 asymptomatic individuals was 32.3 ± 1.1 ng/ml, and there was no difference between those with no risk factors (32.2 ± 1.2 ng/ml, n = 56), those who smoked (31.8 ± 1.8 ng/ml, n = 45), those with hyperlipidemia (32.8 ± 1.7 ng/ml, n = 15), and those exposed to both of these risk factors (34.1 ± 2.7 ng/ml, n = 17). The mean plasma BTG level in 104 patients with symptomatic ischemic heart disease was significantly elevated (40.9 ± 1.4 ng/ml, p < 0.01), but there was considerable overlap with normal levels. Although no difference was found between patients with no risk factors (38.1 ± 4.0 ng/ml, n = 13) and those with only 1 risk factor (37.0 ± 1.8 ng/ml, n = 44), patients with 2 or more risk factors had a significantly elevated plasma BTG level (45.2 ± 2.2 ng/ml, n = 47, p < 0.01). It is concluded that risk factors themselves do not increase platelet activity, but that patients with vascular disease have activated platelets that may contribute to the progression of the disease. Plasma BTG was also measured serially for 10 days in 29 patients after hospitalization with acute ischemic cardiac pain. Although the median plasma level was elevated above normal there were no acute changes in plasma BTG after either acute infarction (n = 22) or acute ischemia (n = 7), except in 2 patients in whom pericardial friction rubs developed. Thus, measurement of systemic plasma BTG did not detect platelet involvement in acute coronary occlusion or acute ischemia.     

Heart fatty acid binding protein in patients with ST-elevation acute coronary syndrome hospitalized within 6 hours after onset of pain

AIM: To compare diagnostic value of a novel marker of myocardial necrosis heart fatty acid binding protein (FABP) with that of troponin I (TnI) and total creatine kinase (CK) in patients admitted early after onset of ST-elevation acute coronary syndrome. MATERIAL: Fifty seven patients with ST-segment elevations justifying thrombolytic therapy admitted within 6 hours (29/57 within 3 and 12/57 - 2 hours) after onset of chest pain. In all patients myocardial infarction (MI) was eventually confirmed by development of Q waves and/or diagnostic increase of CK. METHODS: Samples of blood were taken at admission to coronary care unit. Cut-off values for an elevated level of FABP was 12 ng/ml, TnI - 1.2 and 0.4 ng/ml, CK - 400 IU/l. RESULTS: Overall FABP was elevated in 47 (83%), TnI - in 16 (28.1%), CK in 7 (12.3%) patients. Among patients admitted within first 3 and 2 hours FABP was elevated in 23/29 (79.3%) and 11/12 (91%), TnI - in 9/29 (31%) and 5/12 (41.7%), CK in 3/29 (10.3%) and 1/12 (8.3%) patients, respectively. The use of lower cut-off of abnormality (0.4 ng/ml) increased proportion of patients with elevated TnI up to 56.1% in the group as a whole, to 48.3% and 50% among patients admitted within first 3 and 2 hours, respectively. Nevertheless proportion of patients with elevated FABP remained higher with difference being significant for the whole group and patients admitted within first 3 hours (p=0.004 and 0.016, respectively). CONCLUSION: Most patients with ST-elevation acute coronary syndrome hospitalized within 2-6 hours after onset of pain had elevated levels of heart FABP.     

The incremental value of troponin-I testing in patients with intermediate risk unstable angina

BACKGROUND: Classification of patients with unstable angina (UA) by Agency for Health Care Policy and Research (AHCPR) guidelines in the emergency department reliably stratifies risk of death or myocardial infarction (MI) for triage to outpatient evaluation (low-risk), hospitalization (high-risk), or additional testing (intermediate-risk). Cardiac troponin-I elevation may identify patients at higher risk, but the incremental value may vary with AHCPR clinical risk. HYPOTHESIS: The objective of this study was to determine whether cardiac troponin-I had any additional value beyond triage based upon history, physical examination, and electrocardiogram, in the evaluation of patients with UA. METHODS: In all, 212 consecutive patients with UA and normal serum creatine kinase (CK)-MB levels and elevated troponin-I were risk stratified by AHCPR guidelines to evaluate the incremental value of adding routine troponin-I measurements to our current model for risk stratification. RESULTS: Primary events (death/nonfatal MI) occurred in 35% of high-risk, 15% of intermediate-risk, and 0% of low-risk patients (p < 0.001 by chi-square for trend). High troponin-I (> or =2.0 ng/dl) occurred in 48% of high-risk, 21% of intermediate-risk, and 19% of low-risk patients. The remaining patients in each risk group had indeterminate troponin-I levels (> or =0.4 < 2 ng/dl). Of those with high troponin-I, a primary event occurred in 36, 42, and 0% in the respective high-, intermediate-, and low-risk groups (p < 0.001). High troponin-I levels corresponded with a statistically significant increased rate of primary events only in patients at AHCPR intermediate risk: 42.4 vs. 7.3%, p < 0.001. CONCLUSION: The AHCPR guidelines risk stratify patients with UA. High troponin-I adds significant (p < 0.001) prognostic value in the patients at AHCPR intermediate risk and should be evaluated further in larger trials of such patients.     

Serum myoglobin level as diagnostic test in patients with acute myocardial infarction.

Serum myoglobin levels were measured in normal subjects and patients by means of a newly developed radioimmunoassay. Myoglobin was identified in all of 135 sera from normal adults and ranged between 6 and 85 ng/ml (mean +/- SE 31 +/- 1.3). Raised myoglobin levels were present in 62 of 64 patients with documented acute myocardial infarction, the mean serum concentration being 528 +/- 76 ng/ml. Serial determinations in 46 patients with acute infarct showed that maximum values usually occurred within 4 hours after admission. In 19 of 42 cases, raised myoglobin levels preceded the rise in creatine kinase (CK) values; in the remaining patients, both serum myoglobin and creatine kinase were increased on admission. Only 2 of an additional 44 patients admitted with chest pain but without subsequent electrocardiographic, enzyme, or technetium-99m stannous pyrophosphate myocardial scintigraphic evidence of acute myocardial infarction had raised myoglobin levels; the mean value for this group was within the normal range (44 +/- 6 ng/ml). Serum myoglobin values also were normal in patients with congestive heart failure without acute myocardial infarction, and in patients after moderate exercise and cardiac catheterisation. Trasient myoglobinaemia appears to be one of the earliest laboratory abnormalities occurring in acute myocardial infarction and, therefore, should prove useful as a diagnostic aid in patients.     

Changes of serum hepatocyte growth factor in coronary artery disease

Hepatocyte growth factor (HGF) is an endothelial cell specific growth factor involved in the repair of endothelial cells and collateral formation, however, the role for coronary artery disease is still unknown. We measured serum HGF level in various coronary artery diseases to examine the clinical significance. Serum HGF level was measured using the enzyme-linked immunosorbent assay method in patients with stable effort angina pectoris (n = 26), old myocardial infarction (n = 18), unstable angina pectoris (UAP; n = 10) and acute myocardial infarction (AMI; n = 21). As a control group, we selected 11 patients with neurocirculatory asthenia. Blood samples from peripheral veins were collected at cardiac catheterization before heparin administration. In the AMI group, blood samples were also collected at 48, 72 hr, 1, 2, 3 and 4 weeks from the peripheral veins and 48 and 72 hr after reperfusion from the coronary sinus. Serum HGF level was significantly higher in the UAP (0.41 +/- 0.12 ng/ml, p < 0.001) and AMI groups (0.38 +/- 0.26 ng/ml, p < 0.05) compared to the control group (0.19 +/- 0.09 ng/ml). Serum HGF level peaked 48 hr after reperfusion in both the peripheral veins (0.42 +/- 0.16 ng/ml) and coronary sinus (0.58 +/- 0.23 ng/ml) in the AMI group, with a significantly higher level in the coronary sinus than the peripheral veins (p < 0.05). No significant correlation between peak HGF level in the peripheral veins and peak creatine kinase (CK), CK-MB, ejection fraction and cardiac index was observed. Serum HGF was elevated in acute coronary syndrome, indicating advanced endothelial cell damage. HGF is produced, at least partially, in the heart in patients with AMI. Serum HGF level may be useful to detect endothelial cell damage rather than myocardial cell damage.     

Radioimmunoassay of creatine kinase-B isoenzyme in human sera: results in patients with acute myocardial infarction.

A radioimmunoassay was developed to measure serum levels of the B isoenzyme of creatine kinase(ATP: creatine N-phosphotransferase, EC 2.7.3.2) (CPK) in order to evaluate the time course and frequency of MB isoenzyme elevation in patients with acute myocardial infarction. The method can identify as little as 0.2 ng of the B portion of the CPK-MB isoenzyme, does not significantly crossreact with CPK-MM isoenzyme, and is not affected by storage of serum at --20 degrees CPK isoenzyme containing B subunits was detected in 48 out of 51 sera from normal adults; serum levels in these individuals ranged between 1.2 and 12.5 ng/ml [mean +/- SEM was 2.7 +/- 0.30 ng/ml]. The mean serum level of CPK-B isoenzyme in a pool of sera obtained from 100 normal subjects was 2.9 +/- 0.35 ng/ml; two patients with rhabdomyolysis that were studied had serum CPK-B isoenzyme levels of 2.5 and 3.5 ng/ml, respectively. In contrast, serum levels of the CPK-B isoenzyme were markedly elevated in sera from 18 patients with acute myocardial infarcts when obtained within 12 hr after hospital admission; the mean +/- SEM concentration was 56 +/- 7.8 ng/ml. We performed serial determinations on 14 patients with acute myocardial infarcts and demonstrated that maximal serum CPK-B levels occurred within the first 12 hr after admission and were lower thereafter. The serum concentration of B-containing CPK isoenzyme in 19 additional patients admitted with chest pain but without acute myocardial infarction was 3.4 +/- 0.50 ng/ml. Thus, radioimmunoassay measurement of CPK-B isoenzyme appears to be a useful and sensitive test for the detection of acute myocardial infarcts in patients.     

Prognostic value of cardiac troponin-I levels following catheter-based coronary interventions

This study has examined the prognostic significance of troponin-I (Tn-I) levels after catheter-based coronary interventions in coronary arteries and saphenous vein grafts lesions. Tn-I and creatine kinase-MB (CK-MB) fraction levels were measured at 6 and 18 to 24 hours after catheter-based coronary intervention in 1,129 consecutive patients with normal preintervention plasma levels of Tn-I, and CK-MB levels below the cutoff for myocardial infarction. Patients were stratified according to maximal postangioplasty Tn-I levels. Group I (n = 784) had no elevated Tn-I (<0.15 ng/ml), group II (n = 170) had Tn-I at 0.15 to 0.45 ng/ml, and group III (n = 175) had Tn-I elevation >0.45 ng/ml. Major in-hospital complications (death, 0-wave infarction, and emergent coronary bypass grafting) and out-of-hospital intermediate-term (8 months) outcomes were compared between the 3 groups. Tn-I elevation >0.45 ng/ml was associated with increased risk of mortality (group III, 1.6%; group II, 0.6%; and group I, 0.1%; p = 0.019) and major in-hospital complications (3.2%, 1.7%, and 0.5%; p = 0.004). There was no difference in death (1.8%, 3.2%, and 2.4%; p = 0.74), Q-wave infarction (0.6%, 0%, and 0.3%; p = 0.66), or target lesion revascularization (10.1%, 9.0%, and 9.3%; p = 0.86) between the 3 groups at follow-up. Cardiac event-free survival was similar between groups (p = 0.3). By multivariate analysis, Tn-I >0.45 ng/ml was an independent predictor for major in-hospital complications (odds ratio 2.1, 95% confidence interval 1.2 to 3.9, p = 0.01). The degree of risk was also associated with the conjoint elevation of Tn-I and CK-MB levels (odds ratio 1.1, 95% confidence interval 1.02 to 1.2, p = 0.01). We conclude that Tn-I levels >3 times the normal limit and conjoint elevation of Tn-I and CK-MB levels after coronary angioplasty are associated with increased risk of major in-hospital complications, but have no incremental risk of adverse intermediate-term (8 months) clinical outcomes.     

Usefulness of preoperative and postoperative Tc-99m (Sn)-pyrophosphate scans in patients with ischemic and valvular heart disease.

To assess the usefulness of myocardial imaging with technetium-99m-stannous pyrophosphate for detecting acute myocardial necrosis in patients undergoind cardiac surgery, 66 such patients were stldied. Tc-99m (Sn)-pyrophosphate scans were obtained in all patients 3 to 6 days postoperatively and in 45 preoperatively. Electrocardiograms and serum samples for measuring myocardial isoenzyme of creatine kinase (MB CK) levels were obtained before and serially after cardiac surgery. Seven of the 46 patients undergoing myocardial revascularization had a definite new myocardial infarction as indicated by electrocardiogram and MB CK isoenzyme concentrations, and postoperative pyrophosphate scans were abnormal in all but one. In addition, six of the eight patients with possible myocardial infarction (elevated MB CK levels and persistent ST-T wave depressions) had an abnormal scan postoperatively. Seven of the 20 patients undergoing aortic or mitral valve replacement, or both, had a possible postoperative myocardial infarction by electrocardiogram and MB CK criteria and the myocardial scan was positive in two. All the patients with a normal electrocardiogram and normal MB CK levels had a normal pyrophosphate scan. Preoperative scans were obtained in 22 patients wit; valvular heart disease and were positive in two with a heavy calcified mitral valve on fluoroscopy and in one with a calcified aortic valve. After valve replacement, the pyrophosphate scan became normal in two patients and remained abnormal in the third patient with electrocardiograms and MB CK levels suggesting acute myocardial infarction. We conclude that the Tc-99m (Sn)-pyrophosphate scan is useful for analyzing the occurrence of acute myocardial infarction in patients undergoing cardiac surgery and that, in conjunction with the electrocardiogram, it permits confirmation or exclusion of that diagnosis. Furthermore, false positive pyrophosphate scans may occur in patients with heavy valve calcifications.     

Prognostic significance of troponin T and MB creatine kinase elevations after percutaneous coronary interventions in patients with ischemic heart disease

AIM: To compare prognostic significance of troponin T (TnT) and MB creatine kinase (MB CK) elevations after percutaneous coronary interventions (PCI). MATERIAL AND METHODS: Patients with ischemic heart disease (n=122) were followed for 9+/-3 months after PCI. Coronary angiography was repeated in 79% of cases. Composite criterion of prognostic significance comprised coronary death or nonfatal myocardial infarction. RESULTS: Elevations of TnT , > or =0.03 ng/ml were noted in 55.5%, > or =0.1 ng/ml--in 21.9% of patients. Elevations of MB CK above upper limit of norm (ULN) were noted in 10.7% of patients. In 3 patients MB CK exceeded 3 ULN. Composite endpoint was registered in 53 patients (43.4%). There was no relation between any postprocedural elevation of MB CK and outcomes of follow-up. Levels of TnT between 0.03 and <0.1 hg/ml also were not related to prognosis. Post PCI TnT levels, > or =0.1 ng/ml were associated with significant worsening of prognosis during subsequent 6-12 months of follow-up.     

Specificity of cardiac troponin I and creatine kinase-MB isoenzyme in asymptomatic long-term hemodialysis patients and effect of hemodialysis on these cardiac markers

OBJECTIVES: The objectives of this study were: (1) to evaluate the specificity of cardiac troponin I and creatine kinase-MB isoenzyme in ambulatory asymptomatic chronic renal failure patients on long-term hemodialysis, and (2) to evaluate the effect of hemodialysis on the serum levels of cardiac troponin I and creatine kinase-MB isoenzyme. METHODS: One hundred and forty-four consecutive ambulatory asymptomatic chronic renal failure patients on hemodialysis for a minimum of 1 year were evaluated clinically. Serum cardiac troponin I and creatine kinase-MB isoenzyme levels were measured with specific monoclonal antibodies before and after dialysis using ACCESS Troponin I and ACCESS CK-MB assays. RESULTS: The specificity of serum cardiac troponin I was 83% with a cutoff level of 0.03 ng/ml, which is an expected level for healthy population, but it rose to 100% with a cutoff level of 0.15 ng/ml, which is a reference level for patients with acute myocardial infarction. Twenty-four (17%) patients had borderline elevation in cardiac troponin I (>0.03 to <0.15 ng/ml). A history of angina pectoris was more common in the borderline-elevated cardiac troponin I subgroup. In 28% of the patients, serum creatine kinase-MB isoenzyme levels were increased with a specificity of 72% at a cutoff level of 4 ng/ml, which is the upper limit of normal, but the specificity rose to 98% by increasing the cutoff level value to 10 ng/ml. There were no statistically significant differences in serum levels of cardiac troponin I and creatine kinase-MB isoenzyme before and after dialysis. CONCLUSIONS: Cardiac troponin I is highly specific in ambulatory asymptomatic chronic renal failure patients on long-term hemodialysis; borderline elevations in cardiac troponin I may represent microinjury to the myocardium. A serum level of creatine kinase-MB isoenzyme >2.5 times of the normal upper limit may be highly specific in this patient population. Hemodialysis per se does not significantly change the serum levels of cardiac troponin I and creatine kinase-MB isoenzyme.     

常温不停跳心内直视手术期间心肌损伤早期标志物的变化及其临床意义

目的探讨常温不停跳心内直视手术期间心肌损伤早期标志物的动态变化及其对预后的指导意义.方法选择48例择期二尖瓣置换术患者,分别于术前、术后即刻、术后12h、24h及48h等时点取静脉血检测C-反应蛋白(CRP)、肌酸激酶同工酶(CK-MB)、肌钙蛋白T(Tn-T)、肌钙蛋白I(Tn-I)浓度变化,同时记录心电图(ECG)、血流动力学指标及不良事件发生情况,并作相关分析.结果术前所有患者血浆CRP、CK-MB、Tn-T、Tn-I均在正常范围,术后即刻上述指标明显升高(P＜0.05 or 0.01),其中38例于术后12h达高峰,术后48h降至正常水平,9例患者CRP、CK-MB、Tn-T、Tn-I于术后即刻开始持续升高(P＜0.01),术后48h仍显著高于正常,其中2例死亡,7例发生术后低心排和/或严重心律失常;相关分析显示术后死亡及不良事件发生与血清Tn-T、Tn-I水平呈正相关(r分别为0,71和0.68,P＜0.001).结论常温不停跳心内直视手术后心肌损伤早期标志物明显升高,并于术后12h达峰值,其持续升高与术后不良事件的发生密切相关.     

血栓抽吸对急性ST段抬高心肌梗死患者的疗效

目的：探讨急性 ST 段抬高心肌梗死（STEMI）患者行急诊冠脉介入治疗（PCI）中使用血栓抽吸的临床疗效及对预后的影响。方法：STEMI 患者105例,其中应用血栓抽吸＋PCI 治疗34例（血栓抽吸＋PCI 组）,接受常规 PCI 治疗71例（常规 PCI 组）,比较两组患者术后血流恢复及心功能指标的变化以及术后1年内主要不良心血管事件（MACE）及再入院情况。结果：与常规 PCI 治疗组相比,血栓抽吸＋PCI 组血流恢复后的肌酸激酶同工酶[CK-MB,（236.62±133.00）ng/ml 比（186.47±69.20）ng/ml]、肌酸激酶（CK）[（2833.39±198.70）ng/ml 比（2129.59±199.40）ng/ml]峰值及 CK-MB [（12.38±6.70）h 比（9.65±3.90）h],CK [（12.80±8.10）h 比（9.68±3.50）h]峰值时间均显著降低（P 均＜0.05）;随访1年 MACE 事件发生率（19.7％比8.8％）及再入院率（66.2％比50.0％）有下降趋势,但无统计学意义（P ＞0.05）。两组血流恢复与心功能的差异无统计学意义（P ＞0.05）。结论：急诊 PCI 术中血栓抽吸有助于减轻病情,使酶学水平显著下降,可能还改善预后。     

Clinical outcomes after detection of elevated cardiac enzymes in patients undergoing percutaneous intervention

Objectives. We examined the relations of elevated creatine kinase (CK) and its myocardial band isoenzyme (CK-MB) to clinical outcomes after percutaneous coronary intervention (PCI) in patients enrolled in Integrilin (eptifibatide) to Minimize Platelet Aggregation and Coronary Thrombosis-II (trial) (IMPACT-II), a trial of the platelet glycoprotein IIb/IIIa inhibitor eptifibatide.Background. Elevation of cardiac enzymes often occurs after PCI, but its clinical implications are uncertain.Methods. Patients undergoing elective, scheduled PCI for any indication were analyzed. Parallel analyses investigated CK (n = 3,535) and CK-MB (n = 2,341) levels after PCI (within 4 to 20 h). Clinical outcomes at 30 days and 6 months were stratified by postprocedure CK and CK-MB (multiple of the site’s upper normal limit).Results. Overall, 1,779 patients (76%) had no CK-MB elevation; CK-MB levels were elevated to 1 to 3 times the upper normal limit in 323 patients (13.8%), to 3 to 5 times normal in 84 (3.6%), to 5 to 10 times normal in 86 (3.7%), and to >10 times normal in 69 patients (2.9%). Elevated CK-MB was associated with an increased risk of death, reinfarction, or emergency revascularization at 30 days, and of death, reinfarction, or surgical revascularization at 6 months. Elevated total CK to above three times normal was less frequent, but its prognostic significance paralleled that seen for CK-MB. The degree of risk correlated with the rise in CK or CK-MB, even for patients with successful procedures not complicated by abrupt closure.Conclusions. Elevations in cardiac enzymes, including small increases (between one and three times normal) often not considered an infarction, are associated with an increased risk for short-term adverse clinical outcomes after successful or unsuccessful PCI.     

Specificity of elevated serum MB creatine phosphokinase activity in the diagnosis of acute myocardial infarction.

Creatine phosphokinase (CPK) isoenzyme determinations are useful in the diagnosis of myocardial infarction. However, until suitably sensitive and precise quantitative procedures became available, the diagnostic specificity of serum CPK isoenzyme elevations could not be thoroughly examined. In this study an assay procedure capable of accurately determining activity of individual CPK isoenzymes even in serum samples with normal total CPK activity was employed to obtain two types of information. First, CPK isoenzyme profiles were examined in extracts of a spectrum of human tissues obtained at operation to determine whether the isoenzyme associated with myocardium is presented in other human tissues in quantities sufficient to produce increased activity in serum. In addition, CPK isoenzymes were analyzed quantitatively in serial serum samples from 50 hospitalized control subjects, 100 patients with acute myocardial infarction, 100 patients undergoing non-cardiac surgery and 50 patients undergoing cardiac catheterization to determine whether insult to tissues other than the heart is associated with increased "myocardial" CPK isoenzyme activity in serum. Results from analyses of tissue extracts indicated that myocardium is the only tissue surveyed containing sufficient MB CPK to account for substantial increases in serum MB activity. Results from analyses of serial serum samples indicated that MB CPK activity levels are consistently elevated after myocardial infarction, averaging 0.089 IU/ml. However, after cardiac cathetrization or noncardiac surgery peak serum MB activity remains low, averaging only 0.004 IU/ml despite marked elevations in total serum CPK activity. Thus, elevated serum MB CPK activity is a highly specific as well as sensitive criterion of myocardial injury.     

Effect on outcome of an increase of serum cardiac troponin T in patients with healing or healed ST-elevation myocardial infarction

Recently, an association between minimally elevated cardiac troponin levels and cardiovascular risk in the general population has been reported. However, the prevalence and clinical importance of elevated cardiac troponin T (cTnT) levels remain unclear in patients with histories of myocardial infarction (MI). In this study, 1,807 consecutive patients with ST-segment elevation MIs were prospectively studied (77.1% men; mean age 64.4 years). Venous blood samples were obtained in the chronic stage of MI (28 +/- 7 days after onset), and serum cTnT levels were determined. During the average follow-up of 1,042 days, 84 patients died and 83 had nonfatal reinfarctions. Patients with cTnT levels in the highest quartile (> or = 0.040 ng/ml [n = 353]) had a higher incidence of all-cause death (8.2% vs 5.2%, p = 0.049) and nonfatal reinfarction (8.3% vs 5.1%, p = 0.048) than patients with cTnT levels from the lower 3 quartiles (<0.040 ng/ml [n = 1,064]). Multivariate Cox regression analysis revealed that a minimally elevated cTnT level (> or =0.040 ng/ml) was a significant predictor of all-cause mortality (hazard ratio 1.79, 95% confidence interval 1.10 to 2.90, p <0.02) and nonfatal reinfarction (hazard ratio 1.50, 95% confidence interval 1.13 to 2.20, p <0.03). Subgroup analysis showed that an elevated cTnT level was also a predictor of all-cause mortality and nonfatal reinfarction in patients without heart failure. In conclusion, minimally elevated cTnT levels in the chronic stage of MI predicted long-term adverse clinical outcomes.