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.     

A comparison of cardiac troponin T and cardiac troponin I in patients with acute coronary syndromes

The majority of studies have shown that the performance of assays for cTnT and cTnI is almost identical in detecting AMI in patients with coronary artery disease. Currently cTnT may have an advantage over cTnI because available laboratory and POC platforms are standardized to a single reference material. Nevertheless, the decision to use cTnT or cTnI a given laboratory will probably be made on the basis of cost and the availability of automated instrumentation within that institution, and not necessarily on assay performance. A laboratory is unlikely to purchase an instrument to perform a single test. Because cTnI will soon be available on all commercial immunoassay analyzers, it seems likely that cTnI will become the analyte of choice.     

Cardiac troponin I in acute pericarditis

OBJECTIVES: This study was designed to investigate the prognostic value of cardiac troponin I (cTnI) in viral or idiopathic pericarditis. BACKGROUND: Idiopathic acute pericarditis has been recently reported as a possible cause of nonischemic release of cTnI. The prognostic value of this observation remains unknown. METHODS: We enrolled 118 consecutive cases (age 49.2 +/- 18.4 years; 61 men) within 24 h of symptoms onset. A highly sensitive enzymoimmunofluorometric method was used to measure cTnI (acute myocardial infarction [AMI] threshold was 1.5 ng/ml). RESULTS: A cTnI rise was detectable in 38 patients (32.2%). The following characteristics were more frequently associated with a positive cTnI test: younger age (p < 0.001), male gender (p = 0.007), ST-segment elevation (p < 0.001), and pericardial effusion (p = 0.007) at presentation. An increase beyond AMI threshold was present in nine cases (7.6%), with an associated creatine kinase-MB elevation, a release pattern similar to AMI, and echocardiographic diffuse or localized abnormal left ventricular wall motion without detectable coronary artery disease. After a mean follow-up of 24 months a similar rate of complications was found in patients with a positive or a negative cTnI test (recurrent pericarditis: 18.4 vs. 18.8%; constrictive pericarditis: 0 vs. 1.3%, for all p = NS; no cases of cardiac tamponade or residual left ventricular dysfunction were detected). CONCLUSIONS: In viral or idiopathic acute pericarditis cTnI elevation is frequently observed and commonly associated with young age, male gender, ST-segment elevation, and pericardial effusion at presentation. cTnI increase is roughly related to the extent of myocardial inflammatory involvement and, unlike acute coronary syndromes, is not a negative prognostic marker.     

血清肌钙蛋白与结缔组织疾病损伤心脏的相关研究

目的 探讨血清肌钙蛋白Ｉ（ｔｒｏｐｏｎｉｎ,Ｉ,Ｔｎ－Ｉ）、肌钙蛋白Ｔ（ｔｒｏｐｏｎｉｎＴ,Ｔｎ－Ｔ）与结缔组织疾病ｃｏｎｎｅｃｔｉｖｅ ｔｉｓｓｕｅ ｄｉｓｅａｓｅｓ,ＣＴＤ）损伤心脏的关系。方法 本实验以酶联免疫吸附法（ＥＬＩＳＡ）检测了９９例ＣＴＤ患者的血清Ｔｎ－Ｉ、Ｔｎ－Ｔ浓度,与正常对照组进行了比较,其阳性率与ＣＫ－ＭＢ、ＵＣＧ、ＥＣＧ阳性率进行了比较。结果 ９９例ＣＴＤ患者,其中系统性     

Characteristics of elevated cardiac troponin I in patients with acute ischemic stroke

Objective To study prognostic characteristics of cardiac troponin I (cTnI) elevation in acute ischemic stroke. Methods We retrospectively studied patients (n = 248) with acute ischemic stroke, acute ST-segment elevation myocardial infarction, and acute non-ST-elevation myocardial infarction who were treated between January 2013 and October 2015. Baseline demographic data and changes in cTnI levels among these three groups were compared. Patients with acute ischemic stroke were assigned to either the cTnI elevation group (cTnI > 0.034 ng/mL) or the no cTnI elevation group (cTnI ≤ 0.034 ng/mL). Logistic regression analysis was used to identify risk factors associated with elevated serum cTnI in patients with acute ischemic stroke. Moreover, the duration of hospital stay and incidence of major cardiovascular outcomes were compared in patients with acute ischemic stroke, with or without elevated cTnI. Results In this study population of patients with acute ischemic stroke (n = 178), acute ST-segment elevation myocardial infarction (n = 35), and acute non-ST-elevation myocardial infarction (n = 35), patients with acute ischemic stroke with elevated cTnI comprised 18.54% of subjects. Patients with elevated cTnI were older and more likely to have a history of hypertension. In addition, these patients had higher levels of inflammatory markers, reduced renal functions, increased D-dimer levels, higher NIH stroke scores, and lower left ventricular ejection fractions. Logistic regression analysis showed that both percentage of neutrophil and NIH stroke scores were elevated; estimated glomerular filtration rate and left ventricular ejection fraction were decreased in patients with acute ischemic stroke who had elevated cTnI, and they had more frequent major cardiovascular events during hospital stay. Conclusion Elevated cTnI detected in patients with acute ischemic stroke, indicated a greater likelihood of poor short-term prognosis during hospital stay.     

Cardiac troponin I in aortic valve disease

BACKGROUND: Plasma cardiac troponin I levels may be higher than normal in conditions other than ischemic heart disease. We aimed at measuring troponin I levels in aortic valve patients, in which increased values for left ventricular dimensions and pressure are frequently found. METHODS: Plasma levels of troponin I, creatine kinase (CK) and the MB fraction of the same enzyme were measured in a group of 25 clinically stable aortic valve patients. Echocardiographic study was performed in all patients; hemodynamic and coronary angiographic study was performed in 19 patients. Troponin I was also measured in a control population (n=305). RESULTS: The mean value for troponin I was found to be higher in aortic valve patients (0.07+/-0.02 ng/ml), when compared to controls (0.01+/-0.02 ng/ml; P<0.05). Significant correlations were found between troponin I and both creatine kinase and its MB fraction. When the 25 patients were divided into two groups, with lower (up to 0.04 ng/ml; 12 patients) and higher (0.05 ng/ml or greater; 13 patients) values for troponin I, patients with higher values were found to have greater mean left ventricular wall thickness (9.9+/-0.3 mm, n=11, vs. 12.1+/-0.3 mm, n=13) and pulmonary artery systolic pressures (36.6+/-2.5 mmHg, n=7, vs. 53.7+/-3.4 mmHg, n=9). CONCLUSIONS: We conclude that slightly raised plasma levels of cardiac troponin I are relatively common in aortic valve patients with no evidence of ischemia. Higher left ventricular wall thickness and pulmonary artery systolic pressure may be related to slightly raised troponin I plasma levels.     

Cardiac troponin I elevation in hospitalized patients without acute coronary syndromes

Increase of cardiac troponins occurs in a variety of clinical situations in the absence of an acute coronary syndrome (ACS). Few data exist regarding the incidence, clinical characteristics, and predictive value of various cardiac diagnostic tests and outcome of patients with a non-ACS-related troponin increase. We studied 883 consecutive hospitalized patients with increased cardiac troponin I levels. The discharge diagnosis was reclassified and troponin increase attributed to ACS or another process. Clinical data and results of cardiac diagnostic tests were collected. Patients were followed for a median of 30 months. Three hundred eleven patients were classified as having a non-ACS-related troponin increase (35.2%). An alternative explanation for troponin increase was found in 99% of these patients. Troponin level had poor accuracy in discriminating patients with and without ACS (area under the receiver operating characteristics curve 0.63). Coronary angiography was frequently unhelpful in excluding a non-ACS-related troponin increase because 77% of patients in the non-ACS group had significant flow-limiting coronary artery disease. Patients with non-ACS-related troponin increase had significantly higher in-hospital (hazard ratio 2.8, 95% confidence interval 2.0 to 3.8) and long-term (hazard ratio 2.0, 95% confidence interval 1.6 to 2.5) mortalities compared with patients with ACS. In conclusion, cardiac troponin level is frequently increased in hospitalized patients in the absence of an ACS and portends poor short- and long-term outcomes. Most of these patients have an alternative explanation for cardiac troponin increase. Cardiac diagnostic procedures are frequently unhelpful in excluding a non-ACS-related troponin increase.     

Cardiac troponin T in patients with kidney disease

Atherosclerosis is accelerated in dialysis patients and cardiovascular mortality is up to 20 times higher than in the general population. Cardiac troponin T (cTnT) is a sensitive marker of myocardial necrosis and studies have confirmed the superiority of this marker over traditional cardiac enzymes. Elevated cTnT has been observed in patients with various degrees of renal failure and treatment modalities in the absence of an acute coronary event. The possibility that increased troponins reflect decreased clearance or analytical interference from uremic serum is unlikely. It is accepted that cTnT detected in serum from patients with end-stage renal failure is derived from myocytes and this effect could be caused by subclinical myocardial ischemic release of troponin, myocardial remodeling, or from uremic pericarditis or myocarditis. The significance of cTnT in patients with different degrees of renal failure and different treatment modalities is presented in this review.     

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.     

心肌肌钙蛋白I在急性冠状动脉综合征中的应用

急性冠状动脉综合征(ACS)是指不稳定型心绞痛(UA)、Q波型心肌梗死(QMI)、非Q波型心肌梗死(NQMI)和心源性猝死这样一组临床病征。心肌肌钙蛋白I(cTnI)是新近发展的心肌组织所特有的心肌酶学标志物。本文对cTnI的生物化学特点、检测方法、cTnI与ACS的联系进行评价。cTnI在诊断心肌损害方面敏感性高,特异性强,诊断时间窗口宽,明显优于传统心肌酶,对ACS可进行危险度分层及预后评价,并可预测UA患者复杂冠状动脉形态,值得推广使用。     

Serum cardiac troponin I and ST-segment elevation in patients with acute pericarditis.

OBJECTIVE: ST-segment elevation in acute pericarditis is believed to be caused by superficial myocardial inflammation or epicardial injury. We used cardiac troponin I, a sensitive and specific marker of myocardial injury, to assess myocardial lesions in idiopathic acute pericarditis and its relationship to ST-segment elevation. PATIENTS AND METHODS: Sixty-nine consecutive patients (53 men, 48+/-17 years) with idiopathic acute pericarditis were included. We used an enzymoimmunoflurometric method to measure serum cardiac troponin I on admission (myocardial infarction threshold was 1.5 ng. ml(-1)). RESULTS: Cardiac troponin I was detectable in 34 patients (49%) and was beyond the 1.5 ng. ml(-1)threshold in 15 (22%). Coronary angiography performed in seven of these 15 patients was normal in all of them. ST-segment elevation was observed in 93% of the patients with cardiac troponin I >1.5 ng. ml(-1)vs 57% of those without (P<0.01). Sensitivity of ST-segment elevation to detect myocardial injury was 93% and specificity 43%. Patients with a cardiac troponin I increase higher than 1.5 ng. ml(-1)were more likely to have had a recent infection (66% vs 31%;P=0.01) and were younger (37+/-14 vs 52+/-16 years;P=0.002). There was no significant relationship with other parameters such as pericardial friction rub, fever, PR segment abnormalities, echocardiographic findings or C-reactive protein. CONCLUSION: In patients with idiopathic acute pericarditis, an increase in cardiac troponin I is frequently observed, especially in younger patients and those with a recent infection. Although ST-segment elevation does not reliably indicate myocardial injury, a significant cardiac troponin I increase is only seen in these patients.     

Prevalence of increased cardiac troponin I levels in patients with and without acute pulmonary embolism and relation of increased cardiac troponin I levels with in-hospital mortality in patients with acute pulmonary embolism

Cardiac troponin I levels were increased in 24 of 147 patients (16%) with documented acute pulmonary embolism and in 20 of 594 patients (3%) without pulmonary embolism (p <0.001). In patients with acute pulmonary embolisms, 8 of 24 (33%) with increased cardiac troponin I levels and 9 of 123 (7%) with normal cardiac troponin I levels died during hospitalization (p <0.001).     

Prognostic value of cardiac troponin I in patients with non-ST elevation acute coronary syndrome

AIM: To elucidate relationship between initial blood levels of troponin I and occurrence of such events as death, myocardial infarction, coronary artery bypass surgery, and angioplasty in patients with non-ST elevation acute coronary syndrome. MATERIAL: One hundred one patients aged 32-78 years admitted to coronary care unit within 24 hours after onset of pain including 69 (68.3%) with unstable angina and 32 (31.7%) with non-ST elevation myocardial infarction. METHOD: Troponin I was determined by immunoassay, values below 0.4 ng/ml were considered normal. RESULTS. During 30 days of hospitalization there were 16 (35.5%) and 5 events (8.9%) events (p=0.001) among 45 patients who had elevated level of troponin I (group 1) and 56 patients with normal troponin I (group 2), respectively. By 6 months events occurred in 19 (42.2%) and 6 (10.7%) patients in groups 1 and 2, respectively (p=0.0004). CONCLUSION: Thus elevated blood level of troponin I in patients with non-ST elevation acute coronary syndrome has important value for prognosis.     

Elevated circulating cardiac troponin I in patients with cirrhosis

It has been shown that certain patients with cirrhosis have asymptomatic cardiac abnormalities that have not yet been explained. Thus, cardiac troponin I, a specific marker of myocardial injury, has been measured in patients with cirrhosis without previous cardiac disease. Thirty-two consecutive patients (age 49 +/- 11) with cirrhosis and normal ECG were selected, 22 of which were alcoholic. Hemodynamic investigations were performed. Left ventricular function and mass were evaluated by echocardiography. Serum creatine kinase MB mass, myoglobin, and cardiac troponin I concentrations were measured. Cardiac troponin I concentrations were elevated in 10 patients (32%) (range 0.06-0.25 microg/L) whereas creatine kinase MB mass and myoglobin were normal in all patients. Abnormal troponin I values were not related to the severity of cirrhosis, to the degree of portal hypertension, or to other hemodynamic values. In contrast, elevated serum cardiac troponin I concentrations were related to a decreased stroke-volume index (P <. 05) and a decreased left ventricular mass (P <.05). These results show a high prevalence of slightly elevated serum cardiac troponin I in patients with cirrhosis, especially in those with alcoholic cirrhosis. Elevated troponin I is associated with subclinical left ventricular myocardial damage. These findings may be linked to a lack of left ventricular adaptation in certain patients with cirrhosis and alcoholic cardiomyopathy.