Episode Of Acute Pulmonary Embolism Research Articles

Right Ventricular Thrombus and Pulmonary Thromboembolism/Thrombosis in Behçet's Disease: A Case Report

Behçet's disease (BD) is a multisystemic, chronic, inflammatory disease of unknown origin characterized by alternation of exacerbation and quiescence phases. Cardiac involvement in BD is infrequent. We report a case of a young man with BD with right ventricular thrombus and pulmonary thromboembolism. A 20-year-old man was admitted to our hospital with a 6-month history of dyspnea at rest, asthenia, and fever. Transthoracic echocardiography showed right wall thickened and presence of floating masses in the right outflow tract. Transesophageal echocardiography confirmed the presence of diffuse thrombosis in the right ventricle, with mobile ramifications in its outflow tract. Cardiovascular magnetic resonance and computed tomography of heart confirmed the presence of thrombi, the increased thickness of endocardiac tissue, and altered cardiac wall signal transmission. Computed tomography scan showed multiple pulmonary thrombi. Myocardial biopsy specimen showed diffused subendocardial thrombosis with damage of cardiac myocytes and presence of granulocytes. Six months after discharge, no cardiac masses were detected by transthoracic echocardiography. However, a few weeks after this last echocardiogram, the patient was again hospitalized for a new episode of acute pulmonary embolism. The patient was discharged with increasing dose of oral anticoagulant, with no evidence of cardiac masses at transthoracic echocardiography and thrombosis at computed tomography. The patient is still healthy on anticoagulant, immunosuppressive, and steroid therapy. This case provides a rare example of BD, in which we found-at the same time-heart and pulmonary manifestations, with the presence of right ventricular thrombus and pulmonary thrombi in situ.

Elevated D-dimer concentration identifies patients with incomplete recanalization of pulmonary artery thromboemboli despite 6 months anticoagulation after the first episode of acute pulmonary embolism

Background Despite long-term anticoagulation in some patients after acute pulmonary embolism (APE) pulmonary thrombi are not completely resolved. We hypothesized that elevated D-dimer concentration reflecting increased endogenous fibrinolysis may indicate incomplete pulmonary thrombi resolution after the first episode of PE. Methods 55 patients aged 54.7 ± 18.6 years were anticoagulated for 6 months with acenocumarol (74.5% patients) or low molecular weight heparin (25.5% patients) when control spiral computed tomography (sCT), lung perfusion scintigraphy and D-dimer assessment were performed. Results Incomplete recanalization of pulmonary circulation was found in 39 (70.9%) patients — thrombi at sCT and/or ≥ 1 wedge-shaped perfusion defect at scintigraphy. Age, sex, rate of unprovoked APE, malignancies, thrombolysis in the acute phase and type of long-term anticoagulation were similar in patients without and with complete recanalization. D-dimer at follow-up but not on admission was higher in patients with then without incomplete recanalization (median 340 (80–2280) vs 160 (60–390) ng/mL, p = 0.02). All 11 (20%) patients with D-dimer level > 500 ng/mL at follow-up did not resolve thromboemboli completely. ROC analysis showed that D-dimer at follow-up identified patients with incomplete recanalization (AUC 0.709, 95% CI (0.560–0.831), p = 0.007). Multivariable analysis confirmed that D-dimer > 350 ng/mL at follow-up and right ventricle dysfunction at the diagnosis were independent predictors of incomplete recanalization (OR 18.58 (95% CI 1.97–175.19) and 7.03 (95% CI 1.43–34.6), respectively, p = 0.0006). Conclusion Elevated D-dimer after 6 months anticoagulation and right ventricular dysfunction at the diagnosis predict incomplete recanalization of pulmonary circulation after first episode of APE.

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 ≥ 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.

The association between the proximal extension of the clot and the severity of pulmonary embolism (PE): a proposal for a new radiological score for PE

The aim of the study was to investigate the association between the proximal level of the clot and the severity of pulmonary embolism (PE). The cohort consisted of 99 consecutive patients with PE diagnosed by multi-detector computed tomography. A new score was constructed by calculating the mean value of the largest affected vessel [sub-segmental = 1, segmental = 2, lobar = 3, main pulmonary artery (MPA) = 4] in each lung. A significant association was found between the most proximal level of PE and pulmonary artery obstruction index (PAOI) (P < 0.0001), right ventricular (RV)/left ventricular (LV) ratio (P < 0.0001), and PaO(2) (P = 0.004). No significant association was found between systolic blood pressure and the level of PE. Troponin-T was elevated in none of the sub-segmental, 5% of segmental, 20% of lobar, and in 56% of PEs in the MPA (P = 0.001). Significant association was found between the proposed score and PAOI (P < 0.0001), RV/LV ratio (P < 0.0001), PaO(2) (P < 0.008). Troponin-T was elevated in 10% of level 1, 0% of level 2, 43% level of 3, 66% of level 4 PE (P < 0.0001). Cut-off level score 4 yielded a sensitivity of 84% and a specificity of 74% for the detection of elevated troponin-T. In conclusion, the study indicates that both the most proximal level of PE and the proposed score are related to the severity of PE as determined by blood oxygenation, biochemical and radiological parameters and could therefore be of value for rapid risk stratification of PE. However, the prognostic value of these classifications and their clinical significance needs to be evaluated in properly designed studies.

Association of Persistent Right Ventricular Dysfunction at Hospital Discharge After Acute Pulmonary Embolism With Recurrent Thromboembolic Events

In patients with acute pulmonary embolism, right ventricular dysfunction (RVD) on hospital admission is a predictor of adverse short-term clinical outcome. The aim of this study was to evaluate the prognostic value of RVD persistence at hospital discharge with regard to the likelihood of recurrent venous thromboembolism (VTE). Echocardiography was used to assess RVD on admission and before hospital discharge in 301 consecutive patients with the first episode of acute pulmonary embolism occurring from January 1998 through July 2004. Right ventricular dysfunction was diagnosed in the presence of 1 or more of the following: right ventricular dilation (without hypertrophy), paradoxical septal systolic motion, and Doppler evidence of pulmonary hypertension. Patients were followed up at 2, 6, and 12 months and yearly thereafter. The primary end point was symptomatic, recurrent fatal or nonfatal VTE. Patients were categorized as those (1) without RVD (155 patients [51.5%]), (2) with RVD regression (RVD on admission but not at discharge; 87 patients [28.9%]), and (3) with persistent RVD (RVD on admission and at discharge; 59 patients [19.6%]). After a mean +/- SD of 3.1 +/- 2.7 years, patients with RVD persistence showed an increased risk of recurrent VTE (14 patients, 9.2% patient-years) compared with those without RVD (15 patients, 3.1% patient-years) or RVD regression (3 patients, 1.1% patient-years) (P = .001). Six of 8 deaths related to pulmonary embolism occurred in patients with RVD persistence. At multivariate analysis, adjusted by anticoagulant treatment duration, RVD persistence was an independent predictor of recurrent VTE (hazard ratio, 3.79; P<.001). Persistent RVD at hospital discharge after an acute pulmonary embolism is associated with recurrent VTE.

Usefulness of bedside testing for brain natriuretic peptide to identify right ventricular dysfunction and outcome in normotensive patients with acute pulmonary embolism: Pieralli P, Olivotto I, Vanni S, et al. Am J Cardiol 2006;97:1386–90

This study from Florence, Italy demonstrated the usefulness of brain natriuretic peptide (BNP) in identifying right ventricular dysfunction in normotensive patients with acute pulmonary embolism (PE) and without evidence of left ventricular dysfunction as a cause. It also used elevated BNP levels to predict outcome and mortality in the inpatient setting. Sixty-one patients with a first documented episode of acute PE by spiral computed tomography of the chest without evidence of shock or left ventricular dysfunction were studied. All patients underwent BNP testing upon diagnosis and echocardiography within 1 h of admission. Patients were divided into three equal groups (tertiles) based on increasing BNP levels. Thereafter, the relationship of BNP was related to the presence of right ventricular dysfunction as measured by echocardiography. The lowest BNP tertile values ranged from 1.1 to 85 pg/mL (20 patients); the middle BNP tertile ranged from 88.7 to 487 pg/mL (21 patients); and the highest BNP tertile ranged from 527 to 1300 pg/mL (20 patients). Overall, 35 patients out of 61 had evidence of right ventricular dysfunction. No patients in the lower tertile had right ventricular dysfunction compared with 75% in the middle tertile and 100% in the upper tertile. Eleven patients had PE-related clinical deterioration and developed cardiogenic shock. All these patients belonged to the upper tertile. This study suggests that a BNP value less than 85 pg/mL adequately excludes the presence of right ventricular dysfunction with 100% negative predictive value. A BNP level greater than 487 was identified as the optimal cutoff to predict right ventricular dysfunction and PE-related clinical deterioration or death.

Chronic Thromboembolic Pulmonary Hypertension

Since the last World Symposium on Pulmonary Hypertension in 2008, we have witnessed numerous and exciting developments in chronic thromboembolic pulmonary hypertension (CTEPH). Emerging clinical data and advances in technology have led to reinforcing and updated guidance on diagnostic approaches to pulmonary hypertension, guidelines that we hope will lead to better recognition and more timely diagnosis of CTEPH. We have new data on treatment practices across international boundaries as well as long-term outcomes for CTEPH patients treated with or without pulmonary endarterectomy. Furthermore, we have expanded data on alternative treatment options for select CTEPH patients, including data from multiple clinical trials of medical therapy, including 1 recent pivotal trial, and compelling case series of percutaneous pulmonary angioplasty. Lastly, we have garnered more experience, and on a larger international scale, with pulmonary endarterectomy, which is the treatment of choice for operable CTEPH. This report overviews and highlights these important interval developments as deliberated among our task force of CTEPH experts and presented at the 2013 World Symposium on Pulmonary Hypertension in Nice, France.

Usefulness of Bedside Testing for Brain Natriuretic Peptide to Identify Right Ventricular Dysfunction and Outcome in Normotensive Patients With Acute Pulmonary Embolism

Echocardiographic right ventricular (RV) dysfunction is a well-established prognostic indicator in patients with acute pulmonary embolism. However, the possibility of implementing a rapid and effective triage with biohumoral markers such as brain natriuretic peptide (BNP) may be of value. Sixty-one patients with a first documented episode of acute pulmonary embolism without shock and previous left ventricular dysfunction were prospectively studied. All patients underwent echocardiography and rapid BNP testing on admission. Patients were followed up for in-hospital death, progression to shock, and nonfatal pulmonary embolism recurrence. Overall, 35 patients (57%) had echocardiographic evidence of RV dysfunction on admission, and its prevalence increased progressively with increasing levels of BNP. A BNP level <85 pg/ml was highly accurate in excluding RV dysfunction. No patient in the lower tertile of BNP values (1.1 to 85.0 pg/ml) had RV dysfunction, compared with 75% in the middle tertile (88.7 to 487.0 pg/ml) and 100% in the upper tertile (527 to 1,300 pg/ml). Overall, 11 patients (18%), belonging to the upper tertile, progressed to shock during admission, 4 of whom died. The association of RV dysfunction with a BNP level in the upper tertile (>or=527 pg/ml) showed incremental prognostic value over RV dysfunction alone (in-hospital death and progression to shock were 55% and 31%, respectively). In the present study, BNP represented a powerful predictor of in-hospital clinical deterioration, with substantial incremental prognostic value over echocardiography alone.

Incidence of chronic thromboembolic pulmonary hypertension after pulmonary embolism.

Chronic thromboembolic pulmonary hypertension (CTPH) is associated with considerable morbidity and mortality. Its incidence after pulmonary embolism and associated risk factors are not well documented. We conducted a prospective, long-term, follow-up study to assess the incidence of symptomatic CTPH in consecutive patients with an acute episode of pulmonary embolism but without prior venous thromboembolism. Patients with unexplained persistent dyspnea during follow-up underwent transthoracic echocardiography and, if supportive findings were present, ventilation-perfusion lung scanning and pulmonary angiography. CTPH was considered to be present if systolic and mean pulmonary-artery pressures exceeded 40 mm Hg and 25 mm Hg, respectively; pulmonary-capillary wedge pressure was normal; and there was angiographic evidence of disease. The cumulative incidence of symptomatic CTPH was 1.0 percent (95 percent confidence interval, 0.0 to 2.4) at six months, 3.1 percent (95 percent confidence interval, 0.7 to 5.5) at one year, and 3.8 percent (95 percent confidence interval, 1.1 to 6.5) at two years. No cases occurred after two years among the patients with more than two years of follow-up data. The following increased the risk of CTPH: a previous pulmonary embolism (odds ratio, 19.0), younger age (odds ratio, 1.79 per decade), a larger perfusion defect (odds ratio, 2.22 per decile decrement in perfusion), and idiopathic pulmonary embolism at presentation (odds ratio, 5.70). CTPH is a relatively common, serious complication of pulmonary embolism. Diagnostic and therapeutic strategies for the early identification and prevention of CTPH are needed.

Duration of anticoagulation treatment after an acute episode of pulmonary embolism

Duration of anticoagulation treatment after an acute episode of pulmonary embolism

Late prognosis of acute pulmonary embolism.

Sixty consecutive patients who survived an episode of acute pulmonary embolism documented by pulmonary angiography were assessed one to seven years later (average follow-up period, 29 months) to determine long-term prognosis. Thirty-nine were alive, 19 (32 per cent) had died, and two were lost to follow-up study. Survival largely depended on cardiac status before embolism. Of 42 patients without left ventricular failure, 36 survived. However, of 16 with failure before embolism, only three survived. Follow-up lung scans and arterial-blood gases in the survivors and autopsy in those who died demonstrated resolution of embolism in most patients. Of 43 with adequate follow-up data, resolution was complete in 28 (65 per cent) and partial in 10 (23 per cent); unresolved embolism persisted in only five patients (12 per cent), with resultant chronic cor pulmonale in only one. Recurrent embolism was documented in only one. The long-term prognosis of patients who survive acute embolism thus appears to be dependent on the presence or absence of prior heart disease. (N Engl J Med 289:55–58, 1973)

Normalization of Prolonged IV Conduction Time in a Patient with Acute Pulmonary Embolism

A patient is presented in whom an ECG pattern of left bundle branch block temporarily disappeared following an episode of acute pulmonary embolism. Clinical improvement was associated with a return of the ECG pattern to the pre-embolization configuration. It is postulated that the original left bundle branch block pattern was due to delayed conduction along the left bundle branch, which was “normalized” by the occurrence of delay in conduction along the right bundle secondary to pulmonary embolism. Recovery from pulmonary embolism resulted in reappearance of the left bundle branch block pattern.

Hypoxemia in pulmonary embolism, a clinical study.

The cause of hypoxemia was studied in 21 patients with no previous heart or lung disease shortly after an episode of acute pulmonary embolism. The diagnosis was based on pulmonary angiography demonstrating distinct vascular filling defects or "cutoffs." It was found that virtually all of the hypoxemia in patients with previously normal heart and lungs could be accounted for on the basis of shunt-like effect. The magnitude of the shunting did not correlate with the percent of the pulmonary vascular bed occluded nor with the mean pulmonary artery pressure. The shunts tended to gradually recede over about a month after embolism. Patients without pulmonary infarction were able to inspire 80-111% of their predicted inspiratory capacities, and this maneuver temporarily diminished the observed shunt. Patients with pulmonary infarcts were able to inhale only to 60-69% of predicted inspiratory capacity, and this did not reverse shunting. These data suggest that the cause of right-to-left shunting in patients with pulmonary emboli is predominantly atelectasis. When the elevation of mean pulmonary artery pressure was compared to cardiac index per unit of unoccluded lung, it fell within the range of pulmonary hypertension predicted from published data obtained in patients with exercise in all except one case. This observation suggests that pulmonary vasoconstriction following embolism is not important in humans, although these data are applicable only during the time interval in which our patients were studied and in patients receiving heparin.