Cardiac troponin I elevation in acute pulmonary embolism is associated with right ventricular dysfunction

OBJECTIVES: The purpose of this study was to evaluate the prevalence and diagnostic utility of cardiac troponin I to identify patients with right ventricular (RV) dysfunction in pulmonary embolism. BACKGROUND: Right ventricular overload resulting from elevated pulmonary resistance is a common finding in major pulmonary embolism. However, biochemical markers to assess the degree of RV dysfunction have not been evaluated so far. METHODS: In this prospective, double-blind study we included 36 study patients diagnosed as having acute pulmonary embolism. RESULTS: Among the whole study population, 14 patients (39%) had positive troponin I tests. Ten of 16 patients (62.5%) with RV dilatation had increased serum troponin I levels, while only 4 of 14 patients (28.6%) with elevated troponin I values had a normal RV diameter as assessed by echocardiography, indicating that positive troponin I tests were significantly associated with RV dilatation (p = 0.009). Patients with positive troponin I tests had significantly more segmental defects in ventilation/perfusion lung scans than patients with normal serum troponin I (p = 0.0002). CONCLUSIONS: Our data demonstrate that more than one-third of patients clinically diagnosed as having pulmonary embolism presented with elevated serum troponin I concentrations. Troponin I tests helped to identify patients with RV dilatation who had significantly more segmental defects in lung scans. Thus, troponin I assays are useful to detect minor myocardial damage in pulmonary embolism.     

Clinical usefulness and prognostic value of elevated cardiac troponin I levels in acute pulmonary embolism

Background

Right ventricular myocardial ischemia and injury contribute to right ventricular dysfunction and failure during acute pulmonary embolism. The objective of this study was to evaluate the clinical usefulness of cardiac troponin I (cTnI) in the assessment of right ventricular involvement and short-term prognosis in acute pulmonary embolism

Methods

Thirty-eight patients with acute pulmonary embolism were included in the study. Clinical characteristics, right ventricular involvement, and clinical outcome were compared in patients with elevated levels of serum cTnI versus patients with normal levels of serum cTnI.

Results

Among the study population (n = 38 patients), 18 patients (47%) had elevated cTnI levels (mean ± SD 1.6 ± 0.7 ng/mL, range 0.7-3.7 ng/mL, median, 1.4 ng/mL), and comprised the cTnI-positive group. In the other 20 patients, the serum cTnI levels were normal (≤0.4 ng/mL), and they comprised the cTnI-negative group. In the cTnI-positive group (n = 18 patients), 12 patients (67%) had right ventricular dilatation/hypokinesia, compared with 3 patients (15%) in the cTnI-negative group (n = 20 patients, P = .004). Right ventricular systolic pressure was significantly higher in the cTnI-positive group (51 ± 8 mm Hg vs 40 ± 9 mm Hg, P = .002). Cardiogenic shock developed in a significantly higher number of patients with elevated serum cTnI levels (33% vs 5%, P = .01). In patients with elevated cTnI levels, the odds ratio for development of cardiogenic shock was 8.8 (95% CI 2.5-21).

Conclusions

Patients with acute pulmonary embolism with elevated serum cTnI levels are at a higher risk for the development of right ventricular dysfunction and cardiogenic shock. Serum cTnI has a role in risk stratification and short-term prognostication in patients with acute pulmonary embolism.     

Elevated cardiac troponin levels in patients with submassive pulmonary embolism.

BACKGROUND: Cardiac troponins are reliable markers of myocardial injury that are being used increasingly in patients presenting with undifferentiated chest pain or dyspnea to diagnose an acute coronary syndrome. If elevated cardiac troponin levels also occur in patients with pulmonary embolism because of right ventricular dilation and myocardial injury, such patients could be misdiagnosed. We performed a prospective cohort study to determine the prevalence of elevated cardiac troponin I (cTnI) levels in patients with submassive pulmonary embolism. METHODS: Consecutive patients with objectively confirmed submassive pulmonary embolism and no previous history of ischemic heart disease, other cardiac disease, or renal insufficiency were included. Creatine kinase and cTnI levels were measured within 24 hours of clinical presentation on 2 occasions 8 to 12 hours apart. RESULTS: Of 24 patients with submassive pulmonary embolism, 5 (20.8%) had elevated cTnI levels of 0.4 microg/L or higher (95% confidence interval, 7.1-42.2%). One of these patients had a cTnI level higher than 2.3 microg/L that was suggestive of myocardial infarction. CONCLUSION: Pulmonary embolism should be considered in the differential diagnosis of patients presenting with undifferentiated chest pain or dyspnea and an elevated cardiac troponin level.     

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.     

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.     

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).     

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.     

Troponin levels as a guide to treatment of pulmonary embolism

Right ventricular dysfunction in hemodynamically stable patients with acute pulmonary embolism may be a harbinger of adverse outcomes and may potentially result in the early use of thrombolytic therapy. Risk stratification of these patients is an area of recent and intense investigation with a focus on the assessment of right ventricular function after the embolic event. Echocardiography has been used to identify right ventricular dysfunction but is potentially hampered by a number of limitations. With the onset of right ventricular dilation and possible ischemia in acute pulmonary embolism, elevated serum troponins may be an early and reliable marker of right ventricular dysfunction. In acute pulmonary embolism, both right ventricular dysfunction by echocardiogram and elevated troponin levels have been shown to predict an adverse outcome. Therefore, serum troponin levels should help stratify patients with submassive acute pulmonary embolism into a group in which aggressive medical or surgical intervention would be considered.     

Evidence for lack of myocardial injury in children with acute rheumatic carditis

Despite pathologic evidence of myocardial inflammation, the significance of myocarditis in children with acute rheumatic carditis remains controversial. Elevations in cardiac troponin I have been demonstrated in other forms of myocarditis. The purpose of our study was to determine if levels of cardiac troponin I are elevated, suggesting myocardial injury, in patients with acute rheumatic carditis. We identified all those patients with acute rheumatic fever, presenting between July 1998 and December 2000, who had clinical evidence of carditis, such as a new murmur of mitral or aortic regurgitation, and who had an echocardiogram, measurements of levels of cardiac troponin I, erythrocyte sedimentation rate, and/or C-reactive protein performed at the time of presentation. Their charts were reviewed for demographic and clinical data. Echocardiograms were reviewed for severity of aortic and mitral regurgitation, and measurements made of left ventricular ejection fraction, fractional shortening, and end-diastolic dimension. We found 16 patients with acute rheumatic carditis, ranging in age from 2.0 to 16.1 years, with just over one-third having symptoms of congestive heart failure. All patients had evidence of acute inflammation. There was a significant relationship between symptoms and severity of mitral regurgitation. No patient had elevated levels of cardiac troponin I level. The fact that levels of cardiac troponin I are not elevated in the serum of children with acute rheumatic carditis suggests that there is minimal myocytic necrosis in this setting. This supports the concept that acute valvar regurgitation is the major hemodynamic abnormality in these patients.     

QR in V1--an ECG sign associated with right ventricular strain and adverse clinical outcome in pulmonary embolism.

AIMS: To test the hypothesis that Qr in V(1)is a predictor of pulmonary embolism, right ventricular strain, and adverse clinical outcome. METHODS AND RESULTS: ECG's from 151 patients with suspected pulmonary embolism were blindly interpreted by two observers. Echocardiography, troponin I, and pro-brain natriuretic peptide levels were obtained in 75 patients with pulmonary embolism. Qr in V(1)(14 vs 0 in controls; p<0.0001) and ST elevation in V(1)> or =1 mV (15 vs 1 in controls; p=0.0002) were more frequently present in patients with pulmonary embolism. Sensitivity and specificity of Qr in V(1)and T wave inversion in V(2)for predicting right ventricular dysfunction were 31/97% and 45/94%, respectively. Three of five patients who died in-hospital and 11 of 20 patients with a complicated course, presented with Qr in V(1). After adjustment for right ventricular strain including ECG, echocardiography, pro-brain natriuretic peptide and troponin I levels, Qr in V(1)(OR 8.7, 95%CI 1.4-56.7; p=0.02) remained an independent predictor of adverse outcome. CONCLUSIONS: Among the ECG signs seen in patients with acute pulmonary embolism, Qr in V(1)is closely related to the presence of right ventricular dysfunction, and is an independent predictor of adverse clinical outcome.     

Pulmonary embolism: CT signs and cardiac biomarkers for predicting right ventricular dysfunction

The aim of this study was to prospectively evaluate the accuracy of quantitative cardiac computed tomography (CT) parameters and two cardiac biomarkers (N-terminal-pro-brain natriuretic peptide (NT-pro-BNP) and troponin I), alone and in combination, for predicting right ventricular dysfunction (RVD) in patients with acute pulmonary embolism. 557 consecutive patients with suspected pulmonary embolism underwent pulmonary CT angiography. Patients with pulmonary embolism also underwent echocardiography and NT-pro-BNP/troponin I serum level measurements. Three different CT measurements were obtained (right ventricular (RV)/left ventricular (LV)(axial), RV/LV(4-CH) and RV/LV(volume)). CT measurements and NT-pro-BNP/troponin I serum levels were correlated with RVD at echocardiography. 77 patients with RVD showed significantly higher RV/LV ratios and NT-pro-BNP/troponin I levels compared to those without RVD (RV/LV(axial) 1.68 ± 0.84 versus 1.00 ± 0.21; RV/LV(4-CH) 1.52 ± 0.45 versus 1.01 ± 0.21; RV/LV(volume) 1.97 ± 0.53 versus 1.07 ± 0.52; serum NT-pro-BNP 6,372 ± 2,319 versus 1,032 ± 1,559 ng · L(-1); troponin I 0.18 ± 0.41 versus 0.06 ± 0.18 g · L(-1)). The area under the curve for the detection of RVD of RV/LV(axial), RV/LV(4-CH), RV/LV(volume), NT-pro-BNP and troponin I were 0.84, 0.87, 0.93, 0.83 and 0.70 respectively. The combination of biomarkers and RV/LV(volume) increased the AUC to 0.95 (RV/LV(volume) with NT-pro-BNP) and 0.93 (RV/LV(volume) with troponin I). RV/LV(volume) is the most accurate CT parameter for identifying patients with RVD. A combination of RV/LV(volume) with NT-pro-BNP or troponin I measurements improves the diagnostic accuracy of either test alone.     

Usefulness of combined assessment with computed tomographic signs of right ventricular dysfunction and cardiac troponin T for risk stratification of acute pulmonary embolism

The aim of this study was to evaluate the incremental value of combined assessment with computed tomographic (CT) signs of right ventricular (RV) dysfunction and cardiac troponin T level for predicting early death or adverse outcomes due to acute pulmonary embolism (PE). One hundred seventy-three non-high-risk patients with acute PE, confirmed by CT pulmonary angiography, were retrospectively evaluated. The area under the curve and hazard ratio of CT signs and troponin T levels were compared for predicting early death or adverse outcomes. Patients were classified into intermediate- and low-risk groups on the basis of CT signs and troponin T levels, and mortality was compared. Seventeen patients (9.8%) died within 3 months. Early mortality of intermediate-risk patients (14% to 19%) was higher than that of low-risk patents (2% to 6%). A ratio of RV volume to left ventricular volume > 1.5 had the highest area under the curve (0.709) and hazard ratio (5.402) for predicting early death. The combination of CT signs and elevated troponin T level had an increased area under the curve and hazard ratio for predicting early death and adverse outcomes compared to those of CT signs or elevated troponin T level alone. In conclusion, the combined assessment of the ratio of RV volume to left ventricular volume and an elevated troponin T level provided incrementally more prognostic information in non-high-risk patients with acute PE compared to the single predictor of CT signs or troponin T level.     

Right ventricle injury during acute pulmonary embolism leads to its remodeling

Right ventricular (RV) overload and hypoxia in acute pulmonary embolism (APE) may lead to RV myocardium injury reflected by elevated cardiac troponin levels. We studied 26 patients aged 57.2+/-17.8 years with first episode of APE. On admission troponin T (TnT) was measured. Transthoracic echocardiography was performed after 6 months of anticoagulation. Myocardial injury (TnT > or =0.03 ng/ml) was observed in 8 (30.8%) patients at the diagnosis. At follow up RV diastolic area tended to be larger in group with myocardial injury (25.0 (20.8-38.6) vs 18.4 (17.7-23.3) cm(2), p=0.06). Tricuspid annulus systolic velocity at tissue Doppler was lower in group with myocardial injury (0.12 (0.11-0.13) vs 0.15 (0.13-0.21) m/s, p=0.04), while no such a relationship was found for mitral annulus systolic velocity. TnT concentration correlated with RV diastolic area (r=0.61) and tricuspid annulus systolic velocity (r=-0.58) although not significantly (p=0.08 and p=0.09. respectively). Our data suggest that RV injury in acute phase of PE may lead to its remodeling.     

Characteristics of a subset of patients with reversible systolic dysfunction in chronic kidney disease

There exists a subgroup of uremic cardiomyopathy patients who experience resolution of heart failure symptoms with recovery of normal cardiac geometry following hemodialysis. The authors studied 52 patients with chronic kidney disease on hemodialysis over a period of 190 days. There were 29 patients with systolic dysfunction (left ventricular ejection fraction <40%). Twenty-three patients with preserved systolic function had diastolic dysfunction. Of the 29 patients with systolic dysfunction, 10 patients had significant improvement in New York Heart Association functional class and left ventricular internal diameter in diastole (LVIDd: 59.8 ± 2.6-55.92 mm and left ventricular internal diameter in systole [LVIDs]: 51.8 ± 1.8-34 ± 1.2 mm; P < .001) with significant increases in left ventricular ejection fraction (30.55%-50.14%; P < .001). These patients had the highest baseline serum levels of troponin I (P = .024), which decreased significantly with recovery of cardiac function. When the entire study group was regrouped as those below and those above the median change of C-reactive protein (CRP), patients with CRP greater than the median change had significant improvements in LVIDs and ejection fraction. A subgroup of patients with uremic cardiomyopathy who demonstrated reversible left ventricular systolic dysfunction had high levels of serum troponin I levels at presentation, which regressed with recovery of ventricular function in parallel with CRP levels.     

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.     

Cardiac troponins T and I in patients with end-stage renal disease: the relation with left ventricular mass and their prognostic value

BACKGROUND: Cardiac troponins are frequently elevated in patients with end-stage renal disease (ESRD) in the absence of acute myocardial ischemia. The cause and prognostic value of cardiac troponin elevations in such patients are controversial. HYPOTHESIS: The aims of this study were (1) to define the incidence of cTnT and cTnI elevations in patients with ESRD, (2) to evaluate the relationship between troponin elevations and left ventricular mass index (LVMI), and (3) to evaluate the prognostic value of elevations in cTnT and cTnI prospectively. METHODS: We included 129 patients with ESRD (71 men, age 44 +/- 16 years) with no clinical evidence of coronary artery disease. All patients underwent cardiac examinations, including medical history, physical examination, electrocardiogram, and transthoracic echocardiography. Left ventricular mass index was calculated and all patients were followed for 2 years. RESULTS: The cTnT concentration was > 0.03-0.1 ng/ml in 27 (20.9%) and > 0.1 ng/ml in 27 (20.9%) of the 129 patients. The cTnI concentration was > 0.5 ng/ml in 31 (24%) of 129 patients. Multiple logistic regression analysis identified LVMI (p < 0.001), diabetes (p = 0.001), and serum albumin level (p = 0.009) as a significant independent predictor for elevated cTnT. Left ventricular mass index was the only significant independent predictor for elevated cTnI (p = 0.002). There were 25 (19.4%) deaths during follow-up. Multivariable analysis showed that elevation of cTnT and cTnI did not emerge as an independent predictor for death. Serum albumin level (p < 0.001) was the strongest predictor of mortality, followed by age (p = 0.002) and LVMI (p = 0.005). CONCLUSIONS: Cardiac troponin T and I related significantly to the LVMI. The increased serum concentration of cardiac troponins probably originates from the heart; however, they are not independent predictors for prognosis.     

Prognostic significance of troponin elevation and right ventricular enlargement in acute pulmonary embolism

The troponin I values and echocardiographic data of 141 patients with acute pulmonary embolism (PE) were correlated with 30-day mortality. Patients with elevated troponin and right ventricular enlargement are at significantly greater risk for death after PE than patients with only 1 or with neither adverse prognostic marker.     

Is acute pulmonary embolism more severe in the presence of obstructive sleep apnea? Results from an observational cohort study

Obstructive sleep apnea (OSA) might influence disease severity in acute pulmonary embolism (PE). 253 survivors of acute PE were evaluated for sleep-disordered breathing by portable monitoring and nocturnal polysomnography. PE patients with an apnea-hypopnoea index (AHI)?≥?15/h were significantly older (p?<?0.001), had significantly impaired renal (p?<?0.001) and left ventricular functions (p?=?0.003), showed significantly elevated troponin I (p?=?0.005) and D-dimer levels (p?=?0.024), were hospitalised significantly longer (p?<?0.001), and had significantly elevated PE severity scores (p?=?0.015). Moderate or severe OSA was significantly (p?=?0.006) more frequent among intermediate- and high-risk PE patients (81.0%) compared to the low-risk PE cohort (16.3%). Multiple logistic regression analysis revealed that PE patients in the AHI?≥?15/h cohort were at significant risk for myocardial injury (p?=?0.015). Based on clinical risk stratification models, patients with no relevant OSA syndrome tended to be at a lower risk for short-term mortality (p?=?0.068). Acute PE might present more severely in OSA patients, possibly due to nocturnal hypoxemia or OSA-related hypercoagulability.     

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.     

心脏型脂肪酸结合蛋白对急性肺栓塞早期危险分层和预后预测的价值

目的:探讨急性肺栓塞(APE)患者起病24 h内,心脏型脂肪酸结合蛋白(H-FABP)对危险分层和预后预测的价值。方法:选择2009年6月至2010年10月至急诊就诊的发病24 h内的APE患者,按危险分层分为高危组、中危组和低危组,记录各组基线资料,以及超声心动图右心室腔径、估测肺动脉收缩压、心率、动脉血氧分压等结果,对各组H-FABP和肌钙蛋白I(cTNI)阳性率进行统计分析,并分析各因素与住院期间不良事件(死亡、气管插管和心肺复苏)发生率之间的相关性。结果:共有55例符合条件的APE患者入选,女性患者共30例;高危组12例,中危组25例,低危组18例;3组入院时心率、动脉血氧分压、肺动脉收缩压、溶栓二聚体(D-Dimer)在各组间差异有显著统计学意义。高危组患者入院时间显著早于中危组和低危组(中位数分别为4 h vs.8 h vs.14 h,P=0.001),右心室腔径更大[(32.3±9.1)mm vs.(29.1±7.8)mm vs.(22.6±8.4)mm,P=0.017),肺动脉收缩压更高(中位数分别为40 mmHg vs.20 mmHg vs.15 mmHg,P=0.033,1 mmHg=0.133 kPa),住院期间不良事件发生率也显著高于中低危组。H-FABP阳性率显著高于cTNI阳性率(78.2%vs.43.6%,P=0.017)。相关性分析显示,H-FABP阳性率与不良事件发生率显著相关(r=0.875,P=0.037),而cTNI与不良事件发生率的相关性未达统计学意义(r=0.115,P=0.059)。结论:APE发病后早期H-FABP敏感性显著高于cTNI,且与住院期间不良事件发生率显著相关。