Cardiac involvement in patients with acute neurologic disease: confirmation with cardiac troponin I

BACKGROUND: Patients with acute neurologic illness often manifest findings suggestive of cardiac injury. Their proper interpretation is unclear. Accordingly, we conducted a blinded evaluation to assess the incidence of cardiac injury determined by elevations of cardiac troponin I (cTnI) in patients presenting within 24 hours of a neurologic event and to determine their short- and long-term prognostic effect. METHODS: Blood samples for measurement of cTnI levels were obtained on hospital admission and daily for 3 days and were run by immunoassay. Extensive clinical evaluations including electrocardiograms and echocardiograms were obtained from all patients; daily follow-up evaluations were performed. The clinical electrocardiographic, echocardiographic, and biochemical data were analyzed independently by blinded observers. RESULTS: Peak levels of cTnI were elevated (> or =0.4 microg/L) in 17 patients (19%) (mean + SD, 2.5 + 2.7 microg/L). All patients with elevated cTnI levels had clinical, electrocardiographic, or echocardiographic evidence of cardiac injury except those (n = 5) with minor elevations. One-year mortality was 29% (23/80). Early death (< or =30 days) accounted for 44% of total mortality (n = 10) and was significantly higher in patients with elevated cTnI levels (Wilcoxon P =.01; odds ratio, 6. 4). This difference was less marked by 1 year (Wilcoxon P =.07). CONCLUSIONS: There is a substantial prevalence of myocardial injury in patients with acute neurologic illness. Cardiac injury in this population, as in others, seems to adversely affect prognosis.     

Prevalence and clinical significance of an elevated cardiac troponin I in patients presenting to the Emergency Department without chest pain

BACKGROUND: Cardiac troponins are currently measured in patients presenting with chest pain. Little is known about routinely measured cardiac troponins in patients presenting without chest pain. The aim of this study was to determine the prevalence and clinical significance of an elevated cardiac troponin I (cTnI) in patients presenting to the Emergency Department without chest pain. METHODS: During a 6-month period, we routinely measured cTnI in all patients presenting to the internist, neurologist, or lung specialist for reasons other than chest pain. We followed patients with an elevated cTnI for 1 year and determined mortality and incidence of non-fatal myocardial infarction, percutaneous coronary intervention (PCI), and coronary artery bypass grafting (CABG). RESULTS: cTnI was elevated in 41 out of 1130 patients (3.6%). Patients with an elevated cTnI were older (78 vs. 62 years) and more often admitted to the hospital (95% vs. 78%) than those with a normal cTnI. Twenty-six patients (63%) with an elevated cTnI died within 1 year. Approximately 50% of these deaths were cardiac-related. Two patients (4.9%) suffered a non-fatal myocardial infarction, while no patient underwent PCI or CABG during follow-up. CONCLUSION: Routinely measured cTnI is seldom elevated in a general population of patients presenting to the Emergency Department without chest pain. Patients with an elevated cTnI are, on the average, 16 years older than those with a normal level. An elevated cTnI is clearly associated with an unfavorable outcome.     

Prognostic usefulness of marginal troponin T elevation

Marginal elevations of troponin T among patients with chest pain are often considered to be insignificant. We sought to define the prognostic value of marginal troponin T elevations in patients presenting to the emergency department with suspected myocardial ischemia. Four hundred twenty-eight consecutive patients presenting to the emergency department with ongoing chest pain were evaluated, followed through their hospital course, and contacted for follow-up 4 months after discharge. Two hundred ninety-nine patients had undetectable troponin T levels (<0.01 microg/L), 76 had marginal troponin T elevations (0.01 to 0.09 microg/L), and 53 had frank troponin T elevations (> or =0.1 microg/L). Patients with either marginally or frank elevated troponin levels were older and more likely to be men, but did not differ from patients with undetectable troponin levels with regard to the prevalence of coronary artery disease risk factors, history of coronary disease, or race. While in the hospital, the undetectable and marginal troponin groups were referred for cardiac testing in equal proportions (58% and 59%, respectively), whereas 87% of the elevated group underwent further testing. After adjustment for possible confounders, a significantly increased rate of death/myocardial infarction/revascularization was observed in the marginal troponin group compared with the undetectable troponin group (p = 0.004). Marginal elevations of troponin T identified a currently underevaluated high-risk subgroup of patients with suspected myocardial ischemia who are more likely to have adverse clinical outcomes than those with undetectable troponin levels.     

血肌钙蛋白Ⅰ、C-反应蛋白和D-二聚体水平与急性胸痛患者预后关系的评价

目的：前瞻性研究血清肌钙蛋白Ｉ（ｃＴｎＩ）、Ｃ－反应蛋白（ＣＲＰ）和血浆Ｄ－二聚体水平对急性胸痛患预后的评估作用。方法：９０例急性胸痛患，分别测定ｃＴｎＩ、ＣＲＰ和Ｄ－二聚体水平后，随诊３个月。随诊终点为心脏事件。结果：随诊期间１４例患发生心脏事件，其中８６％患ｃＴｎＩ水平升高，５０％ＣＲＰ升高，７９％Ｄ－二聚体升高，５０％患３项均升高。９０例患中，ｃＴｎＩ升高和正常组心脏事件发生率分别为２５％和５％（Ｐ〈０．０１），ＣＲＰ升高和正常组为３２％和１０％（Ｐ〈０．０１），Ｄ－二聚体升高和正常组为３３％和５％（Ｐ〈０．００１）。结论：急性胸痛患就诊时的ｃＴｎＩ、ＣＲＰ和Ｄ－二聚体水平分别与预后相关。     

Troponin I as a marker of right ventricular dysfunction and severity of pulmonary embolism.

BACKGROUND: Cardiac troponin I (cTnI) is a specific marker which allows detection of minor myocardial cell damage. In patients with severe pulmonary embolism (PE), the rise in pulmonary artery pressure can lead to progressive right ventricular dysfunction (RVD), and clinical studies have demonstrated the presence of ischemia and even right ventricular infarction. Our aims were to determine the prevalence and diagnostic utility of cTnI in identifying patients with RVD and to ascertain whether it correlates with severity of PE. METHODS: We studied 77 patients with PE diagnosed by pulmonary angiography, ventilation-perfusion lung scan, spiral computed tomography scan or a combination of abnormal echocardiogram with clinical presentation suggestive of PE or with positive subsidiary exams (d-dimers, venous Doppler of the lower limbs, ECG, blood gas analysis). We further classified the PE according to the European Society of Cardiology severity levels, the PE being: 1) massive, if there was shock and/or hypotension; 2) submassive, if we found right ventricular hypokinesis on the echocardiogram; and 3) non-massive, in the remaining cases. We considered the highest cTnI serum value from the admission to 24 hours and a normal value of < 0.10 ng/ml. RESULTS: Among the 60 patients with cTnI measurements, 42 had elevated values. Among those with RVD, 26 (81.3%) had increased cTnI levels and only 14 (35%) with elevated cTnI values did not have RVD, indicating that positive cTnI tests were significantly associated with RVD (p = 0.038). Patients with positive cTnI tests had earlier onset of symptoms (24.0 vs. 144.0 hours, p=0.02), higher prevalence of emboli in proximal vessels (pulmonary trunk and right or left main pulmonary arteries) (OR = 12, CI= 1.6-88.7), and received more thrombolytic therapy (OR = 5.4, CI = 1.1-26.8) than those with normal cTnI tests. cTnI levels were higher among patients with submassive PE (median: 0.77 ng/ml) and lower in those with non-massive PE (0.08 mg/ml, p < 0.05). CONCLUSIONS: Around 70% of patients with PE have elevated cTnI values and this test is significantly associated with RVD. cTnI measurements provide additional information in the evaluation of patients with PE by identifying more severe cases and those at increased risk of hemodynamic deterioration, who can benefit from more aggressive therapeutic strategies.     

Cardiac troponins in the elderly: interpretation of elevated levels

Elderly patients with myocardial infarction commonly present with symptoms other than chest pain. The clinician evaluation of the elderly may rely on laboratory methods more so than in younger patients. Fortunately,advances in laboratory science have brought newer biomarkers of cardiac injury to the clinical arena including cardiac troponins I and T(cTnI,cTnT) . These regulatory components of the contractile apparatus are sensitive indicators of myocardial injury. Their central role in the current definition of acute myocardial infarction highlights their utility in the diagnosis of acute myocardial ischemic syndromes. The troponins are also released in some clinical situations where thrombotic complications of coronary artery disease and resultant acute myocardial infarction have not occurred. Examples of these conditions include conditions like myocarditis,pulmonary embolism,sepsis,and acute stroke. Elevated troponins in these conditions are thought to emanate from injured myocardial cells and in most circumstances have been associated with adverse outcomes. Interpretation of elevated troponin in the elderly requires consideration of other possible conditions.     

A comparison of troponin T and troponin I as predictors of cardiac events in patients undergoing chronic dialysis at a Veteran's Hospital: a pilot study.

OBJECTIVE: The purpose of this study was to prospectively evaluate the usefulness of the cardiac troponins as predictors of subsequent cardiac events in patients with chronic renal failure undergoing dialysis. BACKGROUND: Cardiac troponin T (cTnT) and I (cTnI) are cardiac markers that are specific for cardiac muscle. They are also excellent prognostic indicators for patients presenting with chest pain. Although cardiac disease is the leading cause of death in dialysis patients, standard methods to diagnose acute coronary syndromes in patients with renal failure are often misleading. METHODS: A six-month prospective study was done in a university-affiliated Veterans Hospital's dialysis clinic. Forty-nine patients undergoing chronic dialysis with no complaints of chest pain were followed for cardiac events occurring in the six months after cardiac troponin measurements. These included unstable angina, acute myocardial infarction and cardiac death. An additional 83 patients with renal failure but who were not undergoing dialysis were also examined. RESULTS: Within six months all three dialysis patients with elevated cTnI at entry into the study suffered an adverse complication (specificity and positive predictive value = 100%). Twenty-five patients had cTnT elevated at >0.10 ng/ml (53%). Patients with diabetes were more likely to have elevated troponin T levels (64% vs. 25%, p = 0.01). All six patients developing cardiac events within three months had elevations of cTnT >0.1 ng/ml (sensitivity = 100%). Whereas the specificity of cTnT was only 56% for a near-term cardiac event, the negative predictive value of cTnT using a cutoff of < or = 0.1 ng/ml was 100%. On restratifying patients using a cutoff value of cTnT of >0.2 ng/ml, only nine of 49 dialysis patients (18%) had elevated levels. In patients with renal failure not undergoing dialysis, only three of 83 (4%) had elevated troponin I or T. None of these patients suffered a cardiac event in the next six months. CONCLUSIONS: This prospective pilot study clearly delineates the troponins as important prognosticators in asymptomatic otherwise "stable" patients on chronic dialysis, especially those with concomitant diabetes mellitus. It also appears that troponins are more likely to be elevated in dialysis patients than other patients with renal failure not on dialysis. The above suggests that the combination of cTnI and cTnT might be very effective in elucidating cardiac risks of patients with renal failure undergoing chronic dialysis.     

Elevated troponin level is not synonymous with myocardial infarction

BACKGROUND: Elevated troponin I in the absence of angiographically visible coronary lesions is seen in up to 10-15% of those undergoing angiography for suspected coronary artery disease. This study aims to elucidate the etiology of elevated cardiac troponin I in patients with normal coronary arteries on angiography. METHODS: We identified 1551 (8.6%) patients with normal coronary arteries from our catheterization database of 17,950 patients from Jan 2000 to Jun 2004. Elevated troponin I levels were found in 217 (14%) of 1551 patients with normal coronary arteries. Of these 217 patients, 73 surgical patients were excluded, and the remaining 144 patients formed the study population. The study population was compared with age and gender matched patients with myocardial infarction and coronary artery disease (Group II). RESULTS: The patients with elevated cardiac troponin I (cTnI) with normal coronary arteries had significantly lower prevalence of atherosclerotic risk factors and significantly higher left ventricular ejection fractions. The cTnI in patients with normal coronary arteries was elevated due to a number of causes including tachycardia, myocarditis, pericarditis, severe aortic stenosis, gastrointestinal bleeding, sepsis, left ventricular hypertrophy, severe congestive heart failure, cerebrovascular accident, electrical trauma, myocardial contusion, hypertensive emergency, myocardial bridging, pulmonary embolism, diabetic ketoacidosis, chronic obstructive pulmonary disease exacerbation and coronary spasm. CONCLUSIONS: Cardiac troponin I could be elevated in a number of conditions, apart from acute myocardial infarction, and could reflect myonecrosis. Acute myocardial infarction is a clinical diagnosis as the laboratory is an aide to, not a replacement for, informed decision making.     

Abnormal troponin I levels in acute pulmonary embolism without abnormal concentrations of D-dimer at admission

Serum troponin I is a sensitive indicator of myocardial damage but abnormal troponin I levels have been reported without acute coronary syndrome and without cardiac damage. It has been reported that right ventricular overload and hypoxia in acute pulmonary embolism may lead to right ventricular myocardium injury reflected by elevated cardiac troponin levels and that in patients with acute central sub-massive or non-massive pulmonary embolism, even mild increase in troponin I >0.03 mug/L may provide relevant short-term prognostic information independent to clinical, laboratory and echocardiographic data. It has also been reported that patients with acute small pulmonary embolism might present with relatively low concentrations of D-dimer and it might have implications regarding the diagnostic yield of D-dimer in patients who are suspected of having an acute pulmonary embolism. We present a case of abnormal troponin I levels without abnormal concentrations of D-dimer at admission in a 26-year-old Italian man with acute pulmonary embolism. Also this case focuses attention on the importance of a correct evaluation of abnormal troponin I levels and not elevated D-dimer levels in acute pulmonary embolism.     

A superior early myocardial infarction marker. Human heart-type fatty acid-binding protein

Human heart-type fatty acid-binding protein (FABP) has a high potential as an early marker for myocardial infarction (MI) being more specific than myoglobin. FABP is a low molecular mass cytoplasmic protein (15 kDa) that is released early after the onset of ischemia and it may be useful for rapid confirmation or exclusion of acute myocardial infarction (AMI). Immunochemically assayed FABP, cardiac troponin I (cTnI) and enzymatically assayed creatine phosphokinase (CPK) were determined serially in plasma and serum samples from 218 patients presenting with chest pain and suspected MI. In the 94 patients with confirmed MI, FABP rose to a maximum level (577.6 +/- 43.8 microg/L) 3 hours after the onset of symptoms and returned to normal within 30 hours. The FABP level peaked 7-9 hours earlier than CPK (2288 +/- 131 U/L) and cTnI (357.1 +/- 23.9 microg/L). CPK took 50-70 hours to return to normal level and cTnI returned to normal level over 70 hours. The areas under the receiver operating characteristic (ROC) curves for FABP were calculated as 0.871 at admission and 0.995 one hour after admission, whereas for CPK the areas were 0.711 and 0.856 and for cTnI the areas were 0.677 and 0.845, indicating that the FABP test gave a better diagnostic classification at the early stage being reached by cTnI (0.995) only 8 hours after admission. For FABP, both sensitivity and negative predictive value (NPV) increased quickly to 100% for samples monitored just one hour after admission. By using only two samples, one at admission and one 1 hour post admission, sequential FABP monitoring can reliably diagnose AMI patients 1 hour after admission and 100% of non-AMI patients can be excluded with no false negative results. The late markers cTnI and CPK have the similar diagnostic performance only 7 hours later. Thus measurement of FABP in plasma or serum allows the earliest immunochemical confirmation or exclusion of AMI.     

Superiority of combined CK-MB and troponin I measurements for the early risk stratification of unselected patients presenting with acute chest pain

BACKGROUND: Recent studies have suggested that positive troponin I tests are associated with an increased risk of cardiac death during short-term follow-up. However, it is unknown if troponin I tests alone or in addition to CK-MB measurements are superior to predict unfavorable outcome during long-term follow-up. PATIENTS AND METHODS: In a prospective, double-blind study we assessed the prevalence and prognostic value of combined troponin I and CK-MB tests in an unselected cohort of patients (n = 292) admitted to the emergency department for acute chest discomfort. Patients were grouped according to the diagnosis on discharge in those with acute myocardial infarction (1), unstable angina (2), and noncardiac chest pain (3). Six months after enrollment, death rates were obtained and follow-up interviews were performed with respect to survival, recurrence of chest pain, and myocardial infarction. RESULTS: In patients with evidence of coronary heart disease, the mortality rate for abnormal troponin I and normal CK-MB levels was 5.0%. Baseline troponin I and elevated CK-MB levels were associated with a mortality rate of 4.0%. However, the mortality rate was significantly higher (11.1%) in patients presenting with elevated troponin I and CK-MB values. In patients without myocardial infarction on admission, 10.5% with positive troponin I tests died compared to 1.6% with negative tests. The mortality rate in patients without myocardial infarction was 2.7% for patients with elevated CK-MB but normal troponin I values. In patients with both markers elevated a significantly higher mortality rate (16.7%) was found, representing a 6-fold increase in the death event rate. With the additional knowledge of troponin I values, it could be demonstrated that certain cases were misclassified as having noncardiac chest pain. At least some of the latter patients with above-normal values of troponin I were retrospectively to be reclassified as unstable angina. Acute non-Q-wave myocardial infarctions were occasionally misdiagnosed as either angina pectoris or nonischemic chest pain. CONCLUSIONS: Our data suggest the superiority of combined CK-MB and troponin I measurements in clinical practice for the early risk stratification of patients presenting with acute chest pain. In nonmyocardial infarctions, both CK-MB and troponin I convey independent prognostic information with regard to fatal outcome. Troponin I tests in addition to CK-MB measurements contribute to a lower rate of misdiagnoses.     

Diversity of the elevation of serum cardiac troponin I levels in patients during their first visit to the emergency room.

BACKGROUND: Although measurement of serum creatine kinase levels, as well as myoglobin levels, has been used for screening patients with acute coronary syndrome (ACS), the specificity of both is low. Measurement of cardiac troponin levels is now extensively used for the diagnosis of ACS because of their superior cardiac specificity. However, troponin levels are reportedly elevated not only in patients with ACS but also in those with other diseases. METHODS AND RESULTS: The clinical characteristics of 1,023 patients (mean age: 63.5+/-16.3 years; males: 665, females: 358) whose serum cardiac troponin I (cTnI) levels had been measured at the initial visit to the emergency room of Toyota Memorial Hospital between April 2004 and March 2005 were retrospectively analyzed. A positive elevation of cTnI was defined as cTnI > or =0.03 ng/ml. There were 432 patients (42.2%) with positive cTnI levels. The cTnI levels (8.48+/-2.64 ng/ml) in patients with acute myocardial infarction (AMI) were greater than those (0.25+/-0.07 ng/ml) in patients with unstable angina pectoris (AP), as well as those (0.04+/-0.01 ng/ml) in patients with stable AP. In terms of the diagnosis of AMI, the sensitivity was high enough (94.6%), but its specificity was relatively low (61.9%). Furthermore, the differentiation between AMI and unstable AP by the cTnI value alone was impossible. The cTnI levels were elevated in patients with a variety of diseases other than ACS, including heart failure, cardiomyopathies, myocarditis, renal failure, tachyarrhythmias, and pulmonary embolism. CONCLUSIONS: Elevation of the cTnI level is frequently observed in patients in the emergency room with common diseases other than ACS.     

A proposed strategy for utilization of creatine kinase-MB and troponin I in the evaluation of acute chest pain

In recent years, cardiac troponins have attracted great interest as a marker for myocardial injury. However, there are limited data on strategies for use of creatine kinase (CK)-MB and troponin I (cTnI) in clinical practice. We sought to develop a testing strategy using prospectively collected clinical data including serial CK-MB and cTnI levels from 1,051 patients aged > or = 30 years admitted to a teaching hospital for acute chest pain. Diagnostic performance was evaluated for peak values of CK-MB and cTnI obtained during the first 24 hours for the combined end point of acute myocardial infarction and/or major cardiac events within 72 hours. The overall diagnostic accuracy was similar for both cardiac markers alone, and for the combination of cTnI and CK-MB (receiver-operating characteristic curve 0.84, 0.86, and 0.87, respectively). In the multivariate analysis, models including cardiac markers showed that both CK-MB and cTnI added information to clinical data to predict the combined end point, but cTnI added significantly less. Using recursive partitioning analysis, we developed a strategy that would restrict routine cTnI use to patients with normal CK-MB results and findings on the electrocardiogram consistent with ischemia. This strategy would divide patients with suspected myocardial ischemia into 4 groups with risks for the combined end point of 4%, 13%, 26%, and 85%. Thus, cTnI adds information to CK-MB mass and clinical data for predicting major cardiac events, but this contribution is mainly in patients with evidence of myocardial ischemia on their electrocardiograms.     

Electrocardiography and prediction of myocardial damage in patients with acute pulmonary embolism

Acute pulmonary embolism (APE) may lead to myocardial necrosis detected by elevation of cardiac troponin levels. We tried to assess, if electrocardiographic abnormalities may help to define APE patients with myocardial damage and at high risk of complicated clinical course. Therefore we analyzed 50 patients (34F) aged 64.6 +/- 16.9 with confirmed APE. On admission 12-lead standard ECG was recorded and cardiac troponin T (cTnT) was determined quantitatively (Roche). Serum cTnT levels > 0.01 ng/ml, regarded to indicate myocardial injury, were detected in 29 (58%) patients. ST segment depression in ECG was found in 24% of all patients and was more frequent in cTnT + then in group without myocardial injury (41.4% vs 0%, p=0.004). Complicated clinical course and death in acute pulmonary embolism were also more frequently observed in group with ST segment depression (47.1% vs 12.1%, p = 0.03 and 75.0% vs 14.3%, p = 0.02 respectively). Although negative T waves were slightly more frequent in patients with elevated serum troponin T level (65.5% vs 42.9%) and in patients, who died of pulmonary embolism (62.5% vs 54.8%), the difference did not reach statistical significance. Conclusion: ST segment depression detected in standard ECG in patients with APE suggests myocardial injury and may indicate unfavourable clinical course.     

Chronic Myocardial Injury and Risk for Stroke

BACKGROUNDChronic myocardial injury, defined as persistent troponin levels >99th percentile values when measured with high-sensitivity assays (hs-cTn), is common. The association between chronic myocardial injury and stroke is unknown. This study aimed to investigate the association between chronic myocardial injury and stroke.METHODSFrom 2011 to 2014, we included patients with chest pain and high-sensitivity cardiac troponin T levels measured concurrently but without acute conditions associated with elevated high-sensitivity cardiac troponin T levels. Cox regression was used to calculate hazard ratios (HRs) with 95% confidence intervals (CIs) for stroke in patients with stable high-sensitivity cardiac troponin T levels of 5-9, 10-14, 15-29, 30-49, and ≥50 ng/L, using <5 ng/L as reference group. Categories >14 ng/L were defined as chronic myocardial injury.RESULTSA total of 19,460 patients were included, among whom 1528 (7.9%) had chronic myocardial injury. During a mean follow-up of 2.1 years, there were 244 (1.2%) strokes. With increasing high-sensitivity cardiac troponin T levels yearly stroke rates increased from 0.24% to 4.0%. Adjusted hazard ratios with 95% confidence intervals for stroke were 1.83 (1.27-2.64) in patients with high-sensitivity cardiac troponin T levels of 5-9 ng/L, increasing to 1.95 (1.21-3.14), 3.38 (1.80-6.35), and 4.32 (1.89-9.91) in patients with high-sensitivity cardiac troponin T levels of 15-29, 30-49, and ≥50 ng/L, respectively.CONCLUSIONSPatients with chronic myocardial injury have up to a 4-fold increased risk of stroke compared with patients with high-sensitivity cardiac troponin T levels <5 ng/L. Our findings indicate that patients with any detectable high-sensitivity cardiac troponin T level, in particular those with chronic myocardial injury, have an increased risk of stroke and require further attention.     

Cardiac troponin I predicts myocardial dysfunction in aneurysmal subarachnoid hemorrhage

OBJECTIVES: We studied the incidence of myocardial injury in aneurysmal subarachnoid hemorrhage (SAH) using the more sensitive cardiac troponin I (cTnI) assay, correlated changes in cTnI with creatine kinase, MB fraction (CK-MB), myoglobin, and catecholamine metabolite assays, and examined the predictive value of changes in cTnI for myocardial dysfunction. BACKGROUND: Myocardial injury in aneurysmal SAH as evidenced by elevated CK-MB fraction has been reported. Little published data exist on the value of cTnI measurements in aneurysmal SAH. METHODS: Thirty-nine patients were studied for seven days. Clinical cardiovascular assessment, electrocardiographic (ECG), echocardiography, cTnI, CK, CK-MB and CK-MB index, myoglobin and 24-h urinary catecholamine assays were performed in all patients. The ECG abnormalities were defined by the presence of ST-T changes, prolonged QT intervals, and arrhythmias. An abnormal echocardiogram was defined by the presence of wall-motion abnormalities and a reduced ejection fraction. The severity of SAH was graded clinically and radiologically. RESULTS: Eight patients demonstrated elevations in cTnI (upper limit of normal is 0.1 microg/liter with the immunoenzymatic assay and 0.4 microg/liter with the sandwich immunoassay), while five had abnormal CK-MB levels (upper limit of normal is 8 microg/liter). Patients with more severe grades of SAH were more likely to develop a cTnI leak (p < 0.05). Patients with cTnI elevations were more likely to demonstrate ECG abnormalities (p < 0.01) and manifest clinical myocardial dysfunction (p < 0.01) as evidenced by the presence of a gallop rhythm on auscultation and clinical or radiological evidence of pulmonary edema as compared to those with CK-MB elevations. The sensitivity and specificity of cTnI to predict myocardial dysfunction were 100% and 91%, respectively, whereas the corresponding figures for CK-MB were 60% and 94%, respectively. Elevations in myoglobin levels (upper limit of normal <70 microg/liter) and urinary catecholamine metabolites (urinary vanilmandelate/creatinine ratio upper limit of normal, 2.6) are a nonspecific finding. CONCLUSIONS: Measurements of cTnI reveal a higher incidence of myocardial injury than predicted by CK-MB in aneurysmal SAH, and elevations of cTnI are associated with a higher incidence of myocardial dysfunction. Thus, cTnI is a highly sensitive and specific indicator of myocardial dysfunction in aneurysmal SAH.     

经皮冠状动脉腔内成形术前后血清肌钙蛋白I的变化

目的：通过动态观察血清心肌肌钙蛋白Ｉ（ｃＴｎＩ）及肌酸激酶ＭＢ同工酶（ＣＫ－ＭＢ）的变化,以评价经皮冠状动脉腔内成形术对心肌的可能影响。方法：对５９例行经皮冠状动脉腔内成形术的冠心病患者,分别测定其术前,术后６、１２、２４、４８和７２小时的血清ｃＴｎＩ及ＣＫ－ＭＢ水平,并进行分组比较。结果：１８例患者术前血清ｃＴｎＩ正常,术后６小时升高,１２～２４小时达峰值,４８～７２小时渐降至正常;３１例患者术前、术后血清ｃＴｎＩ均正常;１０例患者术前、术后血清ｃＴｎＩ均高于正常值。全部病例中仅３例患者ＣＫ－ＭＢ增高。血清ｃＴｎＩ升高与球囊扩张总时间及扩张次数有关。结论：经皮冠状动脉腔内成形术可能会造成心肌微小损伤,ｃＴｎＩ为监测心肌损伤的可靠而灵敏指标。     

老年肺动脉血栓栓塞误诊70例临床分析

目的分析老年肺动脉血栓栓塞(肺栓塞)的特点及误诊原因,以提高对老年肺栓塞的早期识别和处理。方法回顾性分析70例老年肺栓塞误诊患者的临床表现、超声心动图、心肌酶、肌钙蛋白Ⅰ、血气分析、D-二聚体、胸部X线及其他影像等临床资料,总结分析误诊的原因。结果 70例老年肺栓塞患者中,临床表现胸闷、呼吸困难57例(81.4%),胸痛27例(38.6%),咳嗽15例(21.4%),晕厥13例(18.6%),误诊疾病主要为冠心病46例(65.7%),心功能不全7例(10.0%),肺部感染5例(7.1%),慢性阻塞性肺病3例(4.3%),脑梗死3例(4.3%)。肺栓塞临床分类大面积1 9例,次大面积37例,小面积14例。结论老年肺栓塞多合并基础疾病,患者非特异性的临床症状、心电图的改变、肌钙蛋白I及心肌酶的升高、胸部X线浸润阴影为误诊主要原因。     

Prediction of short-term outcome in patients with suspected myocardial infarction

STUDY OBJECTIVE: Although specific cardiac injury markers have enhanced early patient classification, the ECG remains a necessary investigation in the acute phase of chest pain. Combined use of both tests could further improve the diagnostic and prognostic accuracy. METHODS: We studied 311 consecutive patients who came to the emergency department of a regional referral hospital for the differential diagnosis of acute chest discomfort. The admission ECG was classified using an automated interpretation program and tested together with elevated admission creatine kinase isoform MB (CK-MB) and cardiac troponin I (TnI) concentration for prediction of final myocardial injury (44%) and in-hospital mortality (14%). RESULTS: Combining the information from the admission ECG and cardiac markers, the sensitivity for becoming final myocardial injury (maximal CK-MB >/=11 microg/L) was 90% and specificity 61%. The proportion of false-negative results (10%) was independent of symptom duration. Age, positive ECG findings, and increased admission TnI levels were predictive for in-hospital mortality. CONCLUSION: The commonly available biochemical and ECG criteria allow risk stratification of patients with a suspected acute ischemic event. The data analysis can easily be automated and is independent of patient delay.