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.     

Incremental prognostic value of troponin I and echocardiography in patients with acute pulmonary embolism.

BACKGROUND: To test the hypothesis that troponin I and echocardiography have an incremental prognostic value in patients with pulmonary embolism (PE). METHODS AND RESULTS: In 91 patients with acute PE, echocardiography was performed within 4h of admission. Troponin I levels were obtained on admission and 12h thereafter. The 0.06 microg/l troponin I cut-off level was identified as the most useful, high-sensitivity cut-off level for the prediction of adverse outcome by receiver operating characteristic analysis with a sensitivity and specificity of 86%, respectively. Twenty-eight (31%) patients had elevated troponin I levels (4.9+/-3.8 microg/l). Twenty-one (23%) patients had adverse clinical outcomes including in-hospital death in five, cardiopulmonary resuscitation in four, mechanical ventilation in six, pressors in 14, thrombolysis in 14, catheter fragmentation in three, and surgical embolectomy in three. The area under the receiver operating characteristic curve from multivariate regression models for predicting adverse outcome without troponin I and echocardiography (0.765), with troponin I (0.890) or echocardiography alone (0.858), and the combination of both tests (0.900) was incremental. Three-month survival rate was highest in patients with both a normal troponin I level and a normal echocardiogram (98%). Positive predictive value for adverse clinical outcomes of the combination of echocardiography and troponin I was higher (75% (95%CI 55-88%)) compared with each test alone (echocardiography: 41%, 95% CI 28-56%; troponin I: 64%, 95% CI 46-79%). CONCLUSIONS: While troponin I measurements added most of the prognostic information for identifying high-risk patients, a normal echocardiogram combined with a negative troponin I level was most useful to identify patients at lowest risk for early death.     

预测肺栓塞患者临床结果的因素

肺栓塞是病死率较高的疾病之一,病死率因病情严重程度而异。影响肺栓塞患者预后的因素众多,研究预测肺栓塞患者临床结果的因素有助于优化肺栓塞的治疗。血流动力学不稳定（动脉收缩压低于90mmHg或休克）（1mmHg：0．133kPa）、右心功能不全（右心室扩大、收缩期室间隔反向运动）、心电图异常、血浆心肌肌钙蛋白水平升高和血浆脑利钠肽水平升高是肺栓塞患者预后不良的预测因素。除了血流动力学不稳定采用的收缩压判断值（低于90mmHg）之外,其他预测因素的判断标准各研究均不一致,使其临床应用受到限制。     

Risk stratification of acute pulmonary embolism

Acute pulmonary embolism (PE) is a potentially life-threatening condition, with an overall 3-month mortality rate of 15% and with right ventricular failure as the most common cause of early death. Risk stratification facilitates identification of high-risk patients and may be helpful in guiding the initial and long-term management. In patients with massive PE and hemodynamic instability, rapid risk assessment is paramount and bedside echocardiography and multislice chest computed tomography (CT) are useful for identifying patients who may benefit from thrombolysis or embolectomy. Cardiac biomarkers, including troponin and the natriuretic peptides, are sensitive markers of right ventricular function. Low levels of troponin, B-type natriuretic peptide (BNP), and NT-terminal proBNP are all highly sensitive assays for identifying patients with an uneventful clinical course. Multislice chest CT is not only useful to diagnose or exclude PE; it also is useful for risk assessment. A right-to-left ventricular dimension ratio > 0.9 on the reconstructed CT four-chamber view identifies patients at increased risk of early death. This article focuses on risk stratification tools, including the clinical examination, electrocardiography, echocardiography, cardiac biomarkers, and chest CT.     

Risk factors for pulmonary embolism in patients preliminarily diagnosed with community-acquired pneumonia: a prospective cohort study

D-dimer levels are increased in patients with acute pulmonary embolism (PE). However, D-dimer levels are also increased in patients with community-acquired pneumonia (CAP). The aim of this prospective cohort study was to examine the incidence and clinical features of patients preliminarily diagnosed with CAP and with increased D-dimer levels, and who finally were diagnosed with PE. Patients diagnosed with CAP and hospitalized in the Respiratory Department of the Tenth People’s Hospital Affiliated to Tongji University between May 2011 and May 2013 were enrolled. D-dimer levels were measured routinely after admission. For patients with increased D-dimer levels, those suspected with PE underwent computed tomography pulmonary angiography (CTPA). A total of 2387 patients with CAP was included: 724 (30.3 %) had increased D-dimer levels (median of 0.91 mg/L). CTPA was performed for 139 of the 724 patients (median D-dimer levels of 1.99 mg/L). Among the 139 patients, 80 were diagnosed with PE, and 59 without PE; D-dimer levels were 2.83 and 1.41 mg/L, respectively (p < 0.05). Multivariate analysis showed that age, coronary heart disease, chronic obstructive pulmonary disease (COPD), lower limb varicosity, chest pain, shortness of breath, hemoptysis, fever, and increased levels of troponin I were independent risk factors for PE. Presentation of PE and CAP are similar. Nevertheless, these results indicated that for hospitalized patients with CAP and elevated D-dimer levels, PE should be considered for those >60 years; with CHD, COPD, or lower limb varicosity; with chest pain, shortness of breath, hemoptysis, increased troponin I, or low fever.     

Pulmonary embolism and cardiac enzymes

BACKGROUND: Pulmonary embolism (PE) is often associated with chest pain, electrocardiographic changes, and right ventricular (RV) dysfunction on echocardiogram. There have been reports of elevated troponin levels with PE. RV dysfunction and elevated troponin levels have prognostic implications in acute PE. The purpose of this retrospective analysis was to determine whether PE was associated with elevated cardiac enzymes and whether there was any difference among patients who presented with or without chest pain. METHODS: Records of 93 consecutive patients with high-probability ventilation/perfusion lung scan results for PE were analyzed for the presence or absence of chest pain on presentation, abnormalities in cardiac enzymes, and evidence of RV dysfunction on echocardiogram. RESULTS: A total of 56 of 93 patients had cardiac enzymes evaluated; 24 of these 56 patients had chest pains, and 32 did not. Only 1 patient of the 56 had abnormal cardiac enzymes. This patient had a known history of coronary artery disease (CAD) and had experienced an acute anterior myocardial infarction. Echocardiograms were performed in 36 of 93 patients. Evidence of RV dysfunction on echocardiograms was found in 22 of these patients. No significant relationship was found between RV dysfunction and chest pains (P > .10). CONCLUSION: We found no significant relationship between high-probability ventilation/perfusion scan results and abnormalities in cardiac enzymes irrespective of the presence or absence of chest pain. Patients with a history of CAD or RV dysfunction did not have a higher incidence of chest pain when compared with those with no known history of CAD or RV dysfunction.     

Risk stratification of normotensive patients with acute symptomatic pulmonary embolism

Treatment guidelines recommend strong consideration of thrombolysis in patients with acute symptomatic pulmonary embolism (PE) that present with arterial hypotension or shock because of the high risk of death in this setting. For haemodynamically stable patients with PE, the categorization of risk for subgroups may assist with decision-making regarding PE therapy. Clinical models [e.g. Pulmonary Embolism Severity Index (PESI)] may accurately identify those at low risk of overall death in the first 3 months after the diagnosis of PE, and such patients might benefit from an abbreviated hospital stay or outpatient therapy. Though some evidence suggests that a subset of high-risk normotensive patients with PE may have a reasonable risk to benefit ratio for thrombolytic therapy, single markers of right ventricular dysfunction (e.g. echocardiography, spiral computed tomography, or brain natriuretic peptide testing) and myocardial injury (e.g. cardiac troponin T or I testing) have an insufficient positive predictive value for PE-specific mortality to drive decision-making toward such therapy. Recommendations for outpatient treatment or thrombolytic therapy for patients with PE necessitate further development of prognostic models and conduct of clinical trials that assess various treatment strategies.     

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.     

Laboratory tests in the diagnosis of pulmonary embolism

The diagnosis of pulmonary embolism (PE) requires objective testing. However, all imaging techniques have their own limitations and costs and cannot be performed in every patient with suspected PE. After decades of unfruitful research, several laboratory tests have been evaluated for suspected PE, the most promising being the D-dimer test. As a general rule, the specificity of D-dimers is too low to confirm PE. Conversely, several (but not all) D-dimer assays have a high sensitivity for diagnosing PE. Outcome studies indicate that the Vidas D-dimer and SimpliRED D-dimer can be used safely to withdraw anticoagulation when the pretest probability of PE is low (SimpliRED) or when it is low or moderate (Vidas). These results may however not apply to other D-dimer assays and clinicians should know the characteristics of the test used in their hospital. Blood gas analysis does not have sufficient sensitivity and specificity to confirm or exclude PE, but it may be used to evaluate the clinical probability of PE before other testing is done. The diagnostic value of the alveolar dead space fraction in patients with suspected PE is currently investigated. Initial data suggest that it needs to be combined with a D-dimer test to safely exclude PE. Brain natriuretic peptide and cardiac troponin have limited usefulness for diagnosing PE, but both tests may identify patients with a poor prognosis, in whom more aggressive treatment may be warranted.     

Outpatient treatment of patients with pulmonary embolism

Very few treatment studies have included patients with pulmonary embolism (PE) but there have been many enrolling patients with deep vein thrombosis (DVT). Should treatment for PE be different from treatment for DVT? Post-mortem and clinical studies have shown a strong association between PE and the presence of venous thrombosis in the lower limbs but some recent data suggest that certain clinical factors will predict patients at higher risk of death from PE. Unfortunately, it is not clear that identifying patients as high risk will affect outcome. Two large studies recently compared treatment with unfractionated heparin to treatment with low-molecular-weight heparin in patients with PE. Combining the two studies, the rates of recurrent DVT or PE were 2.9% (13/442) in the low-molecular-weight heparin group and 3.2% (14/441) in the unfractionated heparin group, and major hemorrhage occurred in fewer than 3% of patients. The feasibility of providing outpatient care to many patients presenting to tertiary care hospitals with acute PE has become evident. In our institutions, the data suggest about 50% of patients with PE could be treated as outpatients. Until further knowledge is available, it is not unreasonable to perform echocardiography and cardiac troponin T on patients with PE if they are not completely stable or if concern over concomitant cardiopulmonary disease exists. If they meet criteria demonstrated to result in early death, it is of course reasonable not to treat such patients on a solely outpatient basis. Evidence is accumulating that patients with PE as their initial symptom complex of their venous thromboembolic disease have a worse prognosis, specifically, higher risk of recurrence and higher risk of death, but there are no data to suggest outpatient therapy will affect their prognosis. Low-molecular-weight heparin or intravenous unfractionated heparin, followed by oral anticoagulant therapy, provide adequate therapy in most patients with PE, and many can be treated as outpatients.     

Pulmonary embolism

Pulmonary embolism (PE) is a common illness that can cause death and disability. It is difficult to detect because patients present with a wide array of symptoms and signs. The clinical setting can raise suspicion, and certain inherited and acquired risk factors predispose susceptible individuals. D-dimer concentration in blood is the best laboratory screening test, and chest CT has become the most widespread imaging test. Treatment requires rapid and accurate risk stratification before haemodynamic decompensation and the development of cardiogenic shock. Anticoagulation is the foundation of therapy. Right-ventricular dysfunction on echocardiography and higher than normal concentrations of troponin identify high-risk patients who might need escalation of therapy with thrombolysis or embolectomy even if the blood pressure is normal on presentation. When patients are admitted to medical wards or when patients undergo surgery, their physicians should prescribe prophylactic measures to prevent PE. After hospital discharge, prophylaxis should continue for about a month for patients at high risk of thromboembolism.     

某三甲医院近10年肺栓塞诊治现况及科室间诊治差异调查

目的分析我院近10年肺栓塞(PE)诊治现况,探讨科室间对PE的诊治差异。方法分析2006年01月至2015年10月出院诊断为PE的患者资料,调查PE病例数、首诊科室、诊断方法;分析确诊PE患者的高危因素、临床表现、辅助检查(心电图、心脏彩超、心肌酶谱、肌钙蛋白、脑钠肽、下肢血管彩超、D-二聚体、动脉血气)、抗凝药物、抗凝开始时间、误诊以及转归等。结果 (1)共375例患者诊断为PE(确诊231例、临床诊断144例),CT肺动脉造影为确诊PE的主要方法[诊断221例(95.67%)];随年限增加,PE病例数逐年增加,其中呼吸内科、心血管内科、普外科和急诊科为诊断较多的前四位科室(分别为36.80%、23.81%、17.75%和8.23%);确诊PE患者死亡8例(3.46%),24例(10.39%)自动出院/转院;确诊PE首诊时误诊率为10.39%(24例);(2)确诊PE患者前三位临床表现是呼吸困难(77.49%)、咳嗽(35.93%)和下肢肿胀(35.93%);(3)确诊PE前四位危险因素是卧床(20.35%)、癌症(16.02%)、深静脉血栓形成史(9.96%)和骨科术后(9.52%);(4)确诊PE患者中186例(80.52%)给予低分子肝素治疗,32.03%患者确诊后第1天开始LMWH治疗;163例(70.56%)予华法林治疗;24例(10.39%)仅给予对症处理;出院时77例(33.33%)国际标准化比值达2~3;(5)呼吸科与其他科室比较:D-二聚体(χ2=4.025,P=0.045)、动脉血气(χ2=5.953,P=0.015)、心电图(χ2=5.682,P=0.017)和出院时患者INR达2~3执行情况(χ2=26.143,P0.001)优于其他科室,但心脏超声(χ2=2.153,P=0.142)、脑钠肽(χ2=0.019,P=0.891)、心肌酶谱(χ2=1.357,P=0.244)、肌钙蛋白(χ2=1.772,P=0.183)、下肢血管彩超检查(χ2=0.722,P=0.395)、对症处理(χ2=0.670,P=0.413)、确诊后第一天华法林抗凝(χ2=1.417,P=0.234)、确诊后第一天LMWH抗凝(χ2=3.362,P=0.067)、确诊后肝素与华法林同日重叠抗凝(χ2=3.482,P=0.062)并不优于其他科室。结论 PE患者高危因素多、临床表现不典型;我院临床医师对PE的诊断意识有增加,但辅助检查和危险分层意识尚较差,治疗水平尚有待提高。     

Venous thromboembolism: past, present and future

Over the last four decades there have been remarkable advances in the diagnosis and treatment of venous thromboembolism (VTE)-pulmonary embolism (PE) and deep venous thrombosis (DVT). We have moved from no objective documentation to a plethora of ever improving imaging studies. Evolving treatment modalities have reduced the mortality due to PE to approximately 2%. Shorter hospitalizations followed by outpatient therapy are a growing reality. The use of primary prophylaxis is increasing, but more widespread use must be encouraged. Despite the many accomplishments, too many patients with VTE with its high mortality without treatment remain undiagnosed. There is a critical need to improve the role of the patient's history in identifying patients who warrant objective testing. The ideal would be the development of a biological marker of VTE, similar to the creatinine kinase-MB, creatinine kinase-MM, or troponin I in acute myocardial infarction.     

The Incidence of Acute Pulmonary Embolism with COVID-19 Pneumonia in Saudi Arabia: A Retrospective Single-Center Study

Acute pulmonary embolism (APE) is a common and prognostically significant complication of COVID-19 infection. We investigated the clinical characteristics and chest CT findings of COVID-19 positive patients complicated with APE. A retrospective, record-based, case-series study was performed examining 483 patients admitted to King Saud Medical City during the pandemic, from April 2020 to June 2020. Of these, 92 patients who underwent chest CT scans were included in the final analysis. The incidence of APE, clinical presentations, radiological patterns, and patient outcomes were assessed and compared against those for patients without PE. The incidence of APE was 22% [95% confidence interval (95% CI): 19%–39%], detected by chest CT. Men constituted 85.0% of patients, with a mean age of 48.9 ± 16.7 years. For most patients with APE, risk factors for thromboembolism were established but did not differ significantly from those without PE. The mean D-dimer level of 9.1 (range 7.0–10.2) was significantly higher among patients diagnosed with APE (OR: 1.021; 95% CI: 1.012–1.028; P = 0.001) compared with that in patients without PE. Moreover, the mean levels of lactate dehydrogenase (LDH, 628.5; range: 494.0–928.3; OR: 1.002; 95% CI: 1.000–1.003; P = 0.02), C-reactive protein (CRP; 158.5; range: 105.3–204.5; OR: 1.025; 95% CI: 1.015–1.035; P = 0.001), and cardiac troponin (3.5; range; 2.6–3.8; OR: 1.016; 95% CI: 0.971–1.067; P = 0.01) were also significantly higher in patients with APE than those in patients with PE. The chest CT presentations of APE included massive, segmental, and sub-segmental APE. The need for Intensive Care Unit admission was higher among patients diagnosed with APE, who presented a fatality rate of 10%.. Our study pointed to the incidence and predictors of APE in COVID-19 patients. High levels of D-dimer, CRP, cardiac troponin, and LDH should alert the clinician to the possibility of APE in COVID-19 patients..     

Normal D-dimer levels in emergency department patients suspected of acute pulmonary embolism

OBJECTIVES: We sought to determine:1) whether normal D-dimer enzyme-linked immunosorbent assay (ELISA) assays predicted the absence of pulmonary embolism (PE) in the high-volume emergency department (ED) of the Brigham and Women's Hospital, and 2) whether ED physicians accepted normal D-dimer levels as confirmation of no PE without further diagnostic testing such as lung scanning, chest computed tomography (CT) scanning, or pulmonary angiography. BACKGROUND: Although the plasma D-dimer ELISA is a sensitive screening test for excluding acute PE, this laboratory marker has not been widely integrated into clinical algorithms such as creatine kinase-MB fraction or troponin testing for acute myocardial infarction. METHODS: We mandated that ED physicians order D-dimer ELISA tests on all patients suspected of acute PE. We reviewed the clinical record of each ED patient initially evaluated for suspected PE during the year 2000. We determined whether additional imaging tests for PE were obtained and whether the final diagnosis was PE. RESULTS: Of 1,106 D-dimer assays, 559 were elevated and 547 were normal. Only 2 of 547 had PE despite a normal D-dimer. The sensitivity of the D-dimer ELISA for acute PE was 96.4% (95% confidence interval [CI]: 87.5% to 99.6%), and the negative predictive value was 99.6% (95% CI: 98.7% to >99.9%). Nevertheless, 24% of patients with normal D-dimers had additional imaging tests for PE. CONCLUSIONS: The D-dimer ELISA has a high negative predictive value for excluding PE. By paying more attention to normal D-dimer results, fewer chest CT scans and lung scans will be required, and improvements may be realized in diagnostic efficiency and cost reduction.     

Prognosis based on creatine kinase isoenzyme MB, cardiac troponin I, and right ventricular size in stable patients with acute pulmonary embolism

Prognosis of stable patients with acute pulmonary embolism (PE) has been assessed with cardiac troponin I (cTnI) and right ventricular (RV) function or size. Whether creatine kinase-MB isoenzyme (CK-MB) would add to the prognostic assessment is uncertain. We retrospectively assessed in-hospital mortality from PE in 392 stable patients to test the hypothesis that CK-MB would be of greater prognostic value than cTnI or RV size and we assessed whether combinations would increase prognostic value. CK-MB was high in 29 patients (7.4%); cTnI was high in 76 patients (19%) and intermediate in 78 patients (20%). The right ventricle was dilated in 128 patients (33%). Trends showed highest in-hospital mortality from PE in 4 of 29 (14%) with high CK-MB compared to 6 of 76 (7.9%) with high cTnI and 8 of 128 (6.3%) with RV dilatation (differences NS). High CK-MB and high cTnI provided added prognostic information only in patients with RV dilatation. Mortality with high CK-MB plus RV dilatation (4 of 19, 21%) tended to exceed mortality with high cTnI plus RV dilatation (5 of 39, 13%, NS). When CK-MB and cTnI were high and the right ventricle was dilated, PE mortality tended to be highest (4 of 14, 29%, NS). In conclusion, cardiac biomarkers contributed to prognosis only in patients with RV dilatation. CK-MB was the strongest predictor of death from PE but its prevalence was low, thus limiting its value as a single prognostic indicator. The combination of high CK-MB, high cTnI, and RV dilatation tended to indicate the highest mortality.     

Troponin I and right ventricular dysfunction for risk assessment in patients with nonmassive pulmonary embolism in the Emergency Department in combination with clinically based risk score

To determine whether troponin I (cTnI) and right ventricular (RV) dysfunction predict adverse in-hospital outcomes in patients admitted to the Emergency Department (ED) with definite nonmassive pulmonary embolism (PE) independent of and in addition to a recently validated clinical prognostic risk score. From a pool of 168 patients with suspected PE, 89 had nonmassive PE confirmed by spiral lung angio-computed tomography. By the clinical prognostic score, in our study sample, 14% had very low risk; 17% had low risk, 20% had intermediate risk, whereas high risk and very high risk were identified in 29 and 20%, respectively. Prevalence of elevated cTnI (>0.1 microg/L, 57%) at admission was comparable among patients grouped by clinical prognostic score (P = NS); echocardiographic RV dysfunction (54%) was more prevalent with intermediate or high clinical risk score (P < 0.02). Increased cTnI predicted primary end-point (development of hemodynamic instability, overall 33 cases, 37%) independent of and in addition to the clinical risk class and RV dysfunction (P < 0.01 for interaction). Fatal events (12 cases, 14%, 5 definite, 7 possible PE-related) were predicted by higher clinical risk score (P < 0.05). In patients with nonmassive central PE admitted to the ED, increased cTnI contributed to identifying those with increased risk of development of hemodynamic instability independent of and in addition to a validated clinically based risk score.     

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.     

Safety and efficacy of fondaparinux as an adjunctive treatment to thrombolysis in patients with high and intermediate risk pulmonary embolism

No data are available on the efficacy and safety of a combination of fondaparinux and thrombolysis in the setting of high to intermediate risk pulmonary embolism (PE). Patients submitted to thrombolysis and fondaparinux, presenting with ≥1 of the following criteria were included: (1) cardiogenic shock, (2) syncope, (3) ≥1 proximal thrombo-embolus at CT scan, (4) positive troponin test, (5) echocardiographic findings indicating right ventricular (RV) dysfunction. In-hospital results included death, recurrent PE, persistent RV dysfunction at 48 h echocardiography, bleeding complications. Twenty seven patients were included; 22 received a 2 h infusion of rt-PA and 5 received a 2 h infusion of streptokinase. Ten patients presented with cardiogenic shock (37%), 8 with syncope (30%), all had RV dysfunction. 82% of patients had an uneventful in-hospital course. One patient died during hospital stay from refractory shock. Thrombolysis failed in 2 patients (7%), requiring successful rescue surgical embolectomy. Bleeding events occurred in 2 patients (7%), of whom 1 required blood transfusion. Despite the small sample size, our data suggest that fondaparinux procures adequate tolerability compared to standard current therapy in combination with thrombolysis in high to intermediate risk PE.