危重病患者心肌肌钙蛋白I测定的临床意义

目的 探讨危重病患者隐匿性心肌损伤的发生率以及心肌肌钙蛋白I(cTnI)在评价危重病患者预后中的作用。方法 通过检测159例危重病患者血清cTnI的水平,利用回顾性双盲的单中心研究方法,分析危重病(呼吸衰竭、脑血管意外、心力衰竭等)患者cTnI与心肌损伤、机械通气时间、ICU住院时间和死亡率的关系。结果 在159例危重病患者中有34例(21.4％)患者存在cTnI的升高,但34例患者中只有9例(26.5％)被诊断存在心肌梗死,有25例患者并未发现有明显的心肌损伤。cTnI升高患者的死亡率远远高于cTnI未升高的患者(41.2％vs 16.0％),机械通气的发生率(58.8％vs 23.2％)和持续时间(7.9 vs 3.1 d)也大大增加,ICU住院时间也明显延长(10.8 vs 4.3 d)。结论cTnI水平的升高表明危重病患者中并发心肌损伤和功能失调的发生率很高,特别是许多心电图正常的隐匿性心肌损伤。cTnI作为心肌损伤的特异性标志物,在评价危重病患者的预后中也发挥重要作用。特别cTnI水平升高患者的死亡率、心肌损伤、机械通气的发生率、ICU住院时间等方面都明显增加。     

Elevation of serum cardiac troponin I in noncardiac and cardiac diseases other than acute coronary syndromes.

This study evaluated the role of serum cardiac troponin I as a biochemical marker for the diagnosis of acute coronary syndromes in the presence of noncardiac diseases. Diagnostic characteristics were examined in 102 consecutive patients who were found to have serum cardiac troponin I levels higher than the upper reference limit of 0.6 ng/mL. Of 102 patients with cardiac troponin I levels of >0.6 ng/mL, 35 did not have the final diagnoses of acute coronary syndromes (myocardial infarction or unstable angina) but had various other final diagnoses, including nonischemic dilated cardiomyopathy, muscular disorders, central nervous system disorders, HIV disease, chronic renal failure, sepsis, lung diseases, and endocrine disorders. The mean value of serum cardiac troponin I in the patients with diseases other than acute coronary syndromes was significantly lesser than in those with acute coronary syndromes (2.0+/-1.9 [SD] v. 24.7+/-28.2 ng/mL; P<.0001). There were significantly fewer histories of chest pain and prior myocardial infarction in patients with diseases other than acute coronary syndromes than in those with acute coronary syndromes (history of chest pain, 3 v. 48 patients [P<.001]; history of prior myocardial infarction, 0 v. 30 patients [P<.001]). In conclusion, elevated serum levels of cardiac troponin I, especially in the lower ranges, should be interpreted with caution, particularly in patients suffering from acute illnesses who lack other diagnostic features suggestive of acute coronary ischemic events.     

The Etiology and Prognostic Significance of Cardiac Troponin I Elevation in Unselected Emergency Department Patients

Background: Cardiac troponin elevations are associated not only with acute coronary syndromes (ACS) but also with multiple other cardiac and non-cardiac conditions. Study Objectives: To investigate the etiology and clinical significance of cardiac troponin I elevations in an unselected Emergency Department (ED) patient cohort. Methods: The study population consisted of 991 consecutive troponin-positive patients admitted to the ED of a university hospital with ACS as the presumptive diagnosis. Cardiac troponin I was measured on admission and a follow-up sample was obtained at 6–12 h. Clinical diagnosis was ascertained retrospectively using all the available information including electrocardiogram, clinical data, laboratory tests, and available coronary angiograms. Results: At admission, 805 (81.2%) patients were already troponin positive; of these, the troponin elevation was related to myocardial infarction (MI) in 654 (81.2%) patients. Finally, 83.0% of the troponin elevations were due to MI, 7.9% were related to other cardiac causes, and 9.1% to non-cardiac diseases. The leading non-cardiac causes were pulmonary embolism, renal failure, pneumonia, and sepsis. Non-cardiac patients with elevated troponin I at admission showed significantly higher in-hospital mortality (26.7% vs. 13.4%, p = 0.002) compared to cardiac patients. Conclusion: Elevated troponin levels for reasons other than MI are common in the ED and are a marker of poor in-hospital prognosis.     

Elevated cardiac troponin levels in critically ill patients: prevalence, incidence, and outcomes.

BACKGROUND: Levels of cardiac troponin, a sensitive and specific marker of myocardial injury, are often elevated in critically ill patients. OBJECTIVES: To document elevated levels of cardiac troponin I in patients in a medical-surgical intensive care unit and the relationship between elevated levels and electrocardiographic findings and mortality. METHODS: A total of 198 patients expected to remain in the intensive care unit for at least 72 hours were classified as having myocardial infarction (cardiac troponin I level >or=1.2 microg/L and ischemic electrocardiographic changes), elevated troponin level only (>or=1.2 microg/L and no ischemic electrocardiographic changes), or normal troponin levels. Events were classified as prevalent if they occurred within 48 hours after admission and as incident if they occurred 48 hours or later after admission. Factors associated with mortality were examined by using regression analysis. RESULTS: A total of 171 patients had at least one troponin level measured in the first 48 hours. The prevalence of elevated troponin level was 42.1% (72 patients); 38 patients (22.2%) had myocardial infarction, and 34 (19.9%) had elevated troponin level only. After the first 48 hours, 136 patients had at least 1 troponin measurement. The incidence of elevated troponin level was 11.8% (16 patients); 7 patients (5.1%) met criteria for myocardial infarction, and 2 (1.5%) had elevated troponin level only. Elevated levels of troponin I at any time during admission were associated with mortality in the univariate but not the multivariate analysis. CONCLUSIONS: Elevated levels of cardiac troponin I in critically ill patients do not always indicate myocardial infarction or an adverse prognosis.     

Clinical predictors of 30-day cardiac events in patients with acute coronary syndrome at a community hospital

OBJECTIVE: We sought to determine predictors of coronary events (cardiac death, acute myocardial infarction, and urgent revascularization) within 30 days after admission. METHODS: We prospectively collected data on 400 patients admitted through our emergency room for unstable angina and acute coronary syndromes. Patients with ST-segment elevation myocardial infarction and those who required thrombolysis were excluded. RESULTS: Of 383 patients who were eligible, 120 patients had coronary events within 30 days. Statistically significant variables associated with coronary events were advanced age, male sex, family history of premature coronary artery disease (CAD), diabetes mellitus, tobacco abuse, prior congestive heart failure, prior myocardial infarction, and history of CAD. Symptoms at presentation associated with cardiac events were typical angina and shortness of breath. Objective measures of ischemia associated with cardiac events were elevated troponin T, elevated creatine kinase MB, and ischemic electrocardiographic changes. Using forward stepwise regression analysis, we generated a model to predict 30-day major adverse cardiac events. The strongest predicting variable was serum troponin T (accounting for 33% of predicting r2, P < 0.001) followed by typical angina (r2 increasing to 37%), ischemic electrocardiographic changes (40%), prior CAD (42%), family history of premature CAD (44%), shortness of breath (46%), and positive creatine kinase MB (48%). The positive predictive power of the complete model was r2 = 48%, P < 0.001. CONCLUSION: Our model incorporating elements from the patient's demographic, medical history, presentation, and ischemic assessment identified 48% of patients presenting with unstable angina and acute coronary syndromes who will suffer a major adverse cardiac event within 30 days of admission. Although the strongest predictor was identified as serum troponin T, other clinical criteria offered improvement in our predictive abilities. Therefore, good initial clinical evaluation in addition to simple tests such as serum cardiac markers and electrocardiography are valuable in risk stratification of patients presenting with acute coronary syndromes and cardiac chest pain. Additional testing may be necessary to improve the positive predictive value of the model. Cardiac enzymes and electrocardiographic changes have the highest negative predictive value for occurrence of major adverse cardiac events. Identification of high-risk patients is essential to direct resources toward these patients and to avoid unnecessary costs and risk to the low-risk population.     

Cardiac troponin elevations among critically ill patients

PURPOSE OF THE REVIEW: Elevated levels of cardiac troponins, indicative of the presence of cardiac injury, have been reported in critically ill patients. In this review, the incidence, significance, and clinical relevance of elevated troponin levels among this group of patients will be discussed. RECENT FINDINGS: It has been shown that elevated cardiac troponin levels can be present among critically ill septic patients without evidence of myocardial ischemia. Recent studies show that elevated troponin levels are also present in a diverse group of critically ill patients without sepsis or septic shock. In addition, several but not all studies show that the mortality rate of troponin-positive patients is significantly higher compared with troponin-negative patients. SUMMARY: Elevated troponin levels are not only present in patients suffering from acute coronary syndromes but can also be present in critically ill patients. Even minor elevations are specific for myocardial injury. However, every elevated troponin level in the critically ill patient should not be rigorously diagnosed or treated as a myocardial infarction.     

Moderately elevated serum troponin concentrations are associated with increased morbidity and mortality rates in surgical intensive care unit patients

OBJECTIVE: To determine the significance of moderate elevations of serum troponin I in a surgical intensive care unit patient population in terms of its impact on indexes of outcome including mortality, morbidity, and hospital and intensive care unit length of stay. DESIGN: Retrospective chart review and analysis of clinical data. SETTING: A surgical intensive care unit at a tertiary care hospital. PATIENTS: From the 27-month surgical intensive care unit database of admissions, 869 patients with serum troponin I determinations during their admission were identified. Patients who had cardiac surgery were excluded. INTERVENTIONS: None. MEASUREMENTS AND RESULTS: Patients were divided into four groups based on their maximum serum troponin I concentrations. Hospital mortality, incidence of myocardial infarction, and hospital and intensive care unit length of stays were compared. Patients with moderate elevations of serum troponin I (0.4-2.0 microg/L) had a significantly higher mortality rate (chi-square = 32.57, p <.0001) and longer length of intensive care unit and hospital stays (p <.0005) when compared with patients without similar elevations. Within the range of moderately elevated troponin concentrations, higher titers were associated with increasing mortality risk, longer hospital and intensive care unit stays, and a higher incidence of myocardial infarction. The use of a beta-blocker and aspirin was associated with better survival for patients with maximum serum troponin concentrations > or =2 microg/L. CONCLUSION: Moderate elevations of serum troponin I, which are below the threshold required to diagnose overt myocardial infarction, may reflect ongoing myocardial injury in the critically ill and are associated with a higher mortality rate and longer hospital and intensive care unit length of stays. The use of beta-blockers and aspirin is associated with better outcomes for this subset of patients.     

Myocardial ischemia, cardiac troponin, and long-term survival of high-cardiac risk critically ill intensive care unit patients

OBJECTIVES: To determine the incidence and association of myocardial ischemia with troponin elevation and survival in high-cardiac-risk intensive care patients. DESIGN: Prospective observational study. SETTING: Intensive care unit of a tertiary hospital. SUBJECTS: One-hundred one general intensive care unit patients having a history of coronary artery disease or at least two risk factors for coronary artery disease. INTERVENTIONS: Continuous 12-lead electrocardiographic monitoring with on-line ST-trend analysis, daily cardiac troponin measurements, clinical and physiologic assessment, and up to 2-yr follow-up for survival. MEASUREMENTS AND MAIN RESULTS: During 8,988 hrs or a mean +/- sd of 95 +/- 85 hrs/patient of continuous 12-lead electrocardiographic monitoring, 21 patients (21%) had ischemic ST-segment changes, characterized in most (19) by ST depression and lasting >60 mins in 15 (71.4%). Of the 38 patients (38%) with troponin elevation, myocardial infarction was clinically suspected in four and myocardial ischemia on continuous 12-lead electrocardiographic monitoring was observed in 14 (36.8%). Fourteen (66.7%) of the patients with ischemic ST changes and 12 (75%) of those with prolonged (>60 mins) ischemia had troponin elevation. The sensitivity, specificity, and positive and negative predictive values of prolonged (>60 mins) ischemia predicting troponin elevation were 31.6%, 95.2%, 80.0%, and 69.8%, respectively. Prolonged (>60 mins) ischemia was significantly associated with troponin elevation by both univariate and multivariate analyses (odds ratio = 9.0; p = .008). Acute Physiology and Chronic Health Evaluation II score, renal failure, and the use of norepinephrine also independently predicted troponin elevation. Troponin but not ischemia predicted increased 1-month, 6-month, and 2-yr mortality (odds ratio = 6.0, 3.2, and 2.99, respectively; p < .001). CONCLUSIONS: Silent ischemia is strongly associated with troponin elevation in high-cardiac-risk intensive care unit patients, and troponin elevation predicts both early and late mortality.     

Cardiac troponin I does not independently predict mortality in critically ill patients with severe sepsis

Objective: Patients with sepsis often have elevated cardiac troponin I even in the absence of coronary artery disease. The prognostic value of cardiac troponins in critically ill patients with sepsis remains debatable. Our objective was to evaluate the prognostic value of cardiac troponin I in critically ill patients with severe sepsis. Methods: In this retrospective study, we included patients with severe sepsis who had troponin assayed within 12 h of admission to intensive care over a 6 year period. Patients who had myocardial infarction at intensive care admission in the setting of sepsis were excluded. Included patients were classified into two groups based on their serum troponin I levels: low troponin group (troponin ≤ 0.1 µg/L) and elevated troponin group (troponin > 0.1 µg/L). The primary outcome of interest was hospital mortality. The secondary outcome measures included intensive care mortality, intensive care and hospital length of stay. Results: A total of 382 patients were admitted to intensive care with sepsis. Of these, 293 patients were included in analyses. There was a statistically significant difference in hospital (15% vs 36.1%; P < 0.01) and intensive care (11% vs 25%; P < 0.01) mortality, but not in intensive care and hospital duration of stay. Logistic regression analysis revealed temperature, simplified acute physiology score II and serum lactate to be independent predictors of hospital mortality. Cardiac troponin I was not an independent predictor of hospital mortality. Conclusion: Critically ill patients with severe sepsis who had elevated troponin had increased hospital and intensive care mortality. However, cardiac troponin I did not independently predict hospital mortality.     

Coronary angiographic findings in patients with cocaine-associated chest pain

Patients who present to the Emergency Department (ED) with chest pain associated with cocaine use are a common problem. The incidence and predictors of underlying significant coronary disease in patients with and without myocardial infarction (MI) has not been well described. Patients who underwent coronary angiography within 5 weeks of an ED evaluation for cocaine-associated chest pain were studied. Significant disease was defined as > or = 50% stenosis of a coronary artery or major branches or bypass graft. A total of 90 patients underwent coronary angiography. Significant disease was present in 45 (50%), with 1-vessel disease in 32%, 2-vessel disease in 10%, 3-vessel disease in 6%, with significant graft stenosis in 3%. Significant disease was present in 77% of patients with MI or troponin I elevations, compared to only 35% of patients without myonecrosis. Predictors of significant coronary disease included MI or troponin I elevations, prior MI, known coronary disease (prior MI or revascularization), and elevated cholesterol. Only 7 of the 39 patients (18%) without myonecrosis or a history of coronary disease had significant disease on angiography. In conclusion, significant disease is found in the majority of patients with cocaine-associated MI or troponin elevations. In contrast, only a minority of those without myonecrosis have significant coronary disease.     

Diagnosis and risk stratification of patients with anginal pain and non-diagnostic electrocardiograms

Patients with acute chest pain suggestive of myocardial ischaemia, and normal or non-diagnostic electrocardiograms, form a difficult subgroup for diagnosis and early risk stratification. We prospectively evaluated the role of troponin T (cTnT), troponin I (cTnI), CKMB mass and myoglobin, in the diagnosis and risk stratification of 214 patients with acute chest pain of < or = 24 h and non-diagnostic or normal ECGs admitted directly to the Cardiac Unit of the Royal Victoria Hospital Belfast from the Mobile Coronary Care Unit or the Accident/Emergency Department. This was a single-centre prospective study, and follow-up (3 months) was complete for all patients. Blood was assessed for quantitative cTnT, cTnI, CKMB mass and myoglobin, and qualitative cTnT on admission and at 12 h. Diagnosis of index event and incidence of new cardiac events (death, non-fatal myocardial infarction, revascularization, or readmission for unstable angina) over 3 months were assessed. Based on standard criteria, myocardial infarction occurred in 37/214 (17%), and unstable angina in 72/214 (34%). At 12 h from admission, cardiac troponins had higher sensitivity for the diagnosis of acute coronary syndromes (myocardial infarction and unstable angina) than conventional markers (cTnI 48%, cTnT 38%, CKMB mass 30% or myoglobin 27%). At 3 months, a new cardiac event had occurred in 42/214 (20%). Significantly higher event rates occurred when any of the biochemical markers was elevated, but the statistical significance was highest for patients with elevated cTnI (p < 0.0001). Whilst gender, history of ischaemic heart disease (IHD), stress test response, cTnT, cTnI, CKMB mass and myoglobin were univariate predictors, cTnI at 12 h and stress test response were the only two independent significant predictors for a subsequent cardiac event at 3 months. Raised cTnI at 12 h after admission had the highest sensitivity for the diagnosis of acute coronary syndromes, and was independently associated with a 2-3 times increased risk of future cardiac events within 3 months among patients with acute chest pain suggestive of myocardial ischaemia but with normal or non-diagnostic ECGs.     

Cardiac troponin elevations in chronic renal failure: prevalence and clinical significance

OBJECTIVES: The aim of the study was investigate the prevalence of abnormal values of cardiac troponin T (cTnT) and cardiac troponin I (cTnI) in patients with chronic renal failure (CRF) and their clinical significance. DESIGN AND METHODS: We investigated the concentrations of cTnT and cTnI in 49 CRF patients without heart disease or diabetes. Cardiac TnT values were measured with a second generation immunoassay and cTnI with two immunoassays with different analytical sensitivity. All CRF patients underwent regular clinical follow-up over a 18-month period. RESULTS: No patients with CRF had elevated values of cTnI when measured with one assay and only 2 patients displayed minimally elevated values with the second assay. In contrast, 23 CRF patients (47%) displayed cTnT concentrations elevated above the upper reference limit. The elevated cTnT values observed were below the values detected in acute myocardial infarction and were not associated with adverse cardiac events during follow-up. CONCLUSIONS: Mildly elevated cTnT concentrations are common in patients with CRF and do not appear to be associated with adverse coronary events.     

Utility of Troponin I in Patients with Cocaine-associated Chest Pain

Baseline electrocardiogram abnormalities and market elevations not associated with myocardial necrosis make accurate diagnosis of myocardial infarction (MI) difficult in patients with cocaine-associated chest pain. Troponin sampling may offer greater diagnostic utility in these patients. OBJECTIVE: To assess outcomes based on troponin positivity in patients with cocaine chest pain admitted for exclusion of MI. METHODS: Outcomes were examined in patients admitted for possible MI after cocaine use. All patients underwent a rapid rule-in protocol that included serial sampling of creatine kinase (CK), CK-MB, and cardiac troponin I (cTnI) over eight hours. Outcomes included CK-MB MI (CK-MB >or= 8 ng/mL with a relative index [(CK-MB x 100)/total CK] >or= 4, cardiac death, and significant coronary disease (>or=50%). RESULTS: Of the 246 admitted patients, 34 (14%) met CK-MB criteria for MI and 38 (16%) had cTnI elevations. Angiography was performed in 29 of 38 patients who were cTnI-positive, with significant disease present in 25 (86%). Three of the four patients without significant disease who had cTnI elevations met CK-MB criteria for MI, and the other had a peak CK-MB level of 13 ng/mL. Sensitivities, specificities, and positive and negative likelihood ratios for predicting cardiac death or significant disease were high for both CK-MB MI and cTnI and were not significantly different. CONCLUSIONS: Most patients with cTnI elevations meet CK-MB criteria for MI, as well as have a high incidence of underlying significant disease. Troponin appears to have an equivalent diagnostic accuracy compared with CK-MB for diagnosing necrosis in patients with cocaine-associated chest pain and suspected MI.     

Prognostic significance of admission cardiac troponin T in patients treated successfully with direct percutaneous interventions for acute ST-segment elevation myocardial infarction

BACKGROUND: Cardiac troponin T (cTnT) elevations at admission indicate a high-risk subgroup of patients with acute ST-segment elevation myocardial infarction, possibly due to a higher failure rate of reperfusion therapies. OBJECTIVE: We sought to determine the predictive role of admission cTnT in patients with ST-segment elevation myocardial infarction undergoing successful direct percutaneous coronary intervention. METHODS: A total of 218 consecutive patients with ST-segment elevation myocardial infarction were enrolled. Patients were stratified according to admission cTnT and infarct location. They were followed prospectively for short-term and long-term outcomes.RESULTS A positive cTnT (47.7%) was associated with higher mortality rates at 30 days (14.4% vs. 3.5%, p = .003) and 12 months (17.3% vs. 4.4%, p =.007). cTnT allowed discrimination of patients at high and low risk for cardiac death at 30 days and 12 months among anterior (19.2% vs. 7.9%, p = .19, and 25% vs. 13.2%, p = .22, respectively) and, more impressively, among nonanterior acute myocardial infarction (9.6% vs. 1.3%, p = .04, and 11.5% vs. 1.3%, p = .017, respectively). In multivariate analysis, older age, anterior infarct location, and depressed left ventricular function were the most potent independent predictors of future risk. Among clinical variables available at admission, cTnT indicated independently a higher risk of cardiac death (odds ratio, 3.1 [1.07-9.01], p =.038). This increased risk associated with a positive cTnT was almost independent of time delays from onset of symptoms to admission (3.8 vs. 2.3 hrs in cTnT-positive vs. cTnT-negative patients, p <.001). CONCLUSIONS: Admission cTnT is a strong predictor of future cardiac risk in patients with ST-segment elevation myocardial infarction, despite successful restoration of Thrombolysis in Myocardial Infarction grade 3 coronary flow by direct percutaneous coronary intervention.     

Early CK-MB Elevations Predict Ischemic Events in Stable Chest Pain Patients

ABSTRACT Objective : To demonstrate that creatine kinase-MB fraction (CK-MB) elevations within three hours of presentation in the emergency department (ED) are associated with subsequent ischemic events in clinically stable chest pain patients. Methods : Prospective cohort study at two university-affiliated teaching hospitals. Participants were consenting ED chest pain patients 25 years old or older without evidence of rhythm or hemodynamic instability (n = 449). Exclusions included ST-segment elevation ≥0.1 mV in ≥2 electrocardiogram leads, chest wall trauma, abnormal x-ray studies, and incomplete data collection. Measurements included presenting and three-hour CK-MB levels, presenting ECG, initial clinical impression of coronary care unit need, and clinical follow up. Monitored adverse events included myocardial ischemia necessitating coronary angioplasty or cardiac bypass surgery, recurrent in-hospital myocardial infarction, bradycardia requiring pacing, emergent cardioversion, cardiogenic shock, ventricular fibrillation, and death. Results : Overall, nine (2%) of 449 patients experienced an ischemic event within the first 48 hours. All nine patients required either coronary angioplasty or bypass surgery. Four (44%) of the nine patients with 48-hour ischemic events had elevated CK-MB levels. Of 23 patients who had complications within one week of ED presentation, seven (30%) had elevated ED CK-MB levels. An elevated CK-MB level was associated with an ischemic event both within 48 hours (risk ratio 9.5; 95% CI 2.7–33.7) and within one week (risk ratio 5.2; 95% CI 2.3–11.7). Conclusions : An elevated CK-MB level within three hours of ED presentation is associated with a subsequent ischemic event in the clinically stable chest pain patient without ST-segment elevation. However, the ED CK-MB identifies only a minority of otherwise low-risk patients who develop ischemic events; other markers for diagnosing myocardial ischemia in the ED are needed.     

Myocardial injury in children following resuscitation after cardiac arrest

BACKGROUND: Myocardial dysfunction occurs immediately after successful cardiac resuscitation. Our purpose was to determine whether measurement of cardiac troponin I in children with acute out-of-hospital cardiac arrest predicts the severity of myocardial injury. METHODS AND RESULTS: This prospective, observational study was performed in the Pediatric Intensive Care Unit (PICU) on 24 patients following arrest, ranging in age from 8 months to 17 years. Troponin measurements were obtained on admission, and at 12, 24, and 48 h. Transthoracic echocardiograms were performed within 24 h after admission. Survival to hospital discharge was 29% (7/24). The mean age was 5.9+/-4.6 years for survivors and 4.2+/-5.3 years for non-survivors. The median (range) duration of cardiac arrest times for survivors was 6 min (3 to 63 min) versus 34 min (4 to 70 min) for nonsurvivors (P=0.02). Survivors received 1.3+/-2.2 doses of epinephrine (adrenaline) compared with 2.9+/-1.6 doses for non-survivors (P=0.02). Only one patient had ventricular fibrillation and defibrillation was unsuccessful. The ejection fraction for survivors averaged 73.2+/-11.2%, but for nonsurvivors only 55.4+/-19.8% (P=0.04). Ejection fraction correlated inversely with troponin at 12 h (r=-0.54, P=0.01) and at 24 h (r=-0.59, P=0.02). Circumferential fiber shortening for survivors was 37.5+/-7.8 and 25.5+/-10.7% for nonsurvivors (P=0.02). It also correlated inversely with troponin (r=-0.46, P=0.03 for survivors and r=-0.65, P=0.01, for nonsurvivors). CONCLUSION: After cardiac arrest and resuscitation in pediatric patients, the severity of myocardial dysfunction was reflected in troponin I levels.     

The Prognostic Significance of Troponin I and Troponin T

Abstract. Objectives : To determine and compare the prognostic abilities of early, single-sample measurements of cardiac troponin I (cTn-I), cardiac troponin T (cTn-T), creatine kinase-MB (CK-MB) among ED patients with possible myocardial ischemia. Methods : Prospective collection of clinical and serologic data using an identity-unlinked technique from patients with possible myocardial ischemia at 2 urban EDs. Outcome data concerning the occurrence of adverse events (AEs) during the 14 days after enrollment were used to calculate and compare the relative risks (RRs) and predictive values (with 95% confidence intervals) of the 3 markers for predicting AEs. Results : Among the 401 study patients, 105 AEs occurred in 67 patients. cTn-I, cTn-T, and CK-MB were all significantly predictive of AEs, with RRs of 3.87 (2.39, 6.26), 3.03 (1.92, 4.79), and 6.45 (4.74, 8.77), respectively. For prediction of AEs, sensitivity for each of the 3 markers was low (cTn-I = 15.38, cTn-T = 24.62, CK-MB = 15.38), while specificity was high (cTn-I = 97.62, cTn-T = 93.15, CK-MB = 99.70). No significant difference in predictive ability was found between cTn-I and cTn-T. However, a positive CK-MB result was a stronger predictor of AEs than either cTn-I (p = 0.01) or cTn-T (p = 0.001). Conclusions : No significant difference in predictive abilities was found between cTn-I and cTn-T. However, routine testing for both CK-MB and either of the troponins may optimize early identification of high-risk patients so they may be targeted for a higher level of care and consideration of more aggressive therapies.     

Elevated plasma concentrations of the endogenous nitric oxide synthase inhibitor asymmetric dimethylarginine predict adverse events in patients undergoing noncardiac surgery

OBJECTIVE: In patients with cardiovascular disease or organ failure, elevated plasma concentrations of the endogenous nitric oxide synthase inhibitor asymmetric dimethylarginine (ADMA) are associated with an increased risk of future cardiovascular events. We aimed to investigate elevated plasma ADMA concentrations as a prospective risk marker for adverse events in patients undergoing noncardiac surgery. DESIGN: Prospective observational study. SETTING: Two tertiary care centers. PATIENTS: Four hundred and two patients scheduled for elective noncardiac surgery. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Patients were followed for 30 days after surgery for a predefined composite end point (death, myocardial infarction/acute coronary syndrome, acute heart failure, severe arrhythmia, embolism, or thrombosis). Plasma ADMA concentrations at baseline were determined by high-performance liquid chromatography. ADMA was only weakly (-0.2 < tau < 0.2) correlated with other risk markers and risk scores. In univariate logistic regression, per 0.1-micromol/L increment in plasma ADMA concentration, the odds ratio to experience the primary end point increased by 1.26 (95% confidence interval 1.10-1.45, p = .001). In a multivariate logistic regression model adjusting for age, gender, current smoking, plasma creatinine, hypertension, diabetes, ischemic heart disease, highly sensitive C-reactive protein, revised cardiac risk index, type of surgery, high-risk surgery, ASA class, and study center, ADMA was found to be an independent risk marker. The odds ratio to experience the primary end point was 1.33 (95% confidence interval 1.12-1.59, p = .001) per 0.1-micromol/L increase in the plasma ADMA concentration. CONCLUSIONS: Elevated plasma ADMA concentrations are independently associated with a higher risk for adverse events in the peri- and postoperative periods.     

Prognostic implications of myocardial necrosis triad markers' concentration measured at admission in patients with suspected acute coronary syndrome

The aim of the study was to analyze the prognostic implications of 3 myocardial necrosis markers measured at admission in short-term observation of patients with suspected acute coronary syndrome. The study group consisted of 336 consecutive patients whose concentration of cardiac troponin I, creatine kinase-MB fraction, and myoglobin were measured at admission. All patients referred due to chest pain and suspected acute coronary syndrome and were followed up for 30 days. The patients who died had statistically higher concentration of cardiac troponin I (8.7 +/- 17.2 vs 0.9 +/- 3.2 ng/mL; P = .0006), myoglobin (215.2 +/- 181.5 vs 109.7 +/- 151.5 ng/mL; P = .003), and creatine kinase-MB (21.9 +/- 30.7 vs 8.8 +/- 25.9 ng/mL; P = .005), compared to patients who stayed alive. There was statistically significant increase in 30-day all-cause mortality with increasing numbers of positive markers-0.6% for patients with nonpositive marker, 3.4% for patients with 1 positive marker, and 11.5% for patients with at least 2 positive markers (P = .001 for trend).     

Whole blood choline and plasma choline in acute coronary syndromes: prognostic and pathophysiological implications

BACKGROUND: Whole blood choline (WBCHO) and plasma choline (PLCHO) concentrations increase rapidly after stimulation of phospholipase D in acute coronary syndromes (ACS). Early risk-stratification was analyzed in 217 patients with suspected ACS and a negative admission troponin T (<0.03 microg/L). METHODS: WBCHO and PLCHO were measured using high-performance-liquid-chromatography mass spectrometry. Major cardiac events (MACE) were defined as cardiac death/arrest, coronary intervention or myocardial infarction (MI). RESULTS: WBCHO (> or = 28.2 micromol/L) was predictive for MACE (hazard ratio [HR] 2.7; p<0.001), cardiac death/arrest (HR 4.2; p=0.015), heart failure (HR 2.8; p=0.003), coronary intervention (HR 2.1; p=0.01) and MI (HR 8.4; p=0.002) after 30 days. PLCHO (> or = 25.0 micromol/L) was predictive for MACE (HR 2.6; p=0.005), cardiac death/arrest (HR 15.7; p<0.001), heart failure (HR 6.0; p<0.001) but not for coronary intervention and MI. WBCHO and PLCHO were predictive for MACE in multivariate analysis (Odds ratio [OR] 2.7, p=0.009 and OR 3.3, p=0.03) independently of age, gender, prior MI, coronary risk factors and ECG. CONCLUSIONS: WBCHO and PLCHO are significant and independent predictors of major cardiac events in admission troponin T negative acute coronary syndromes. Both are predictive for events related to tissue ischemia and WBCHO is capable of detecting risks associated with coronary plaque instability.