Pulmonale Thromboembolie hemoptysis

Pulmonale Thromboembolie hemoptysis



Incidence of Chronic Thromboembolic Pulmonary Hypertension after Pulmonary Embolism — NEJM Pulmonale Thromboembolie hemoptysis

N Engl J Med ; Chronic thromboembolic pulmonary hypertension CTPH is associated with considerable morbidity and mortality, pulmonale Thromboembolie hemoptysis.

Its incidence after pulmonary embolism and associated risk factors are not well documented. Full Text of Background We conducted a prospective, pulmonale Thromboembolie hemoptysis, 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, pulmonale Thromboembolie hemoptysis. Full Text of Methods The cumulative incidence of symptomatic CTPH was 1.

No cases occurred after two years among the patients with more than two years of follow-up data. The following increased the pulmonale Thromboembolie hemoptysis of CTPH: Full Text of Results CTPH is a relatively common, serious complication of Warum erhalte ich Krampfadern embolism.

Diagnostic and therapeutic strategies for the early identification and prevention of CTPH are needed. Full Text of Discussion Chronic pulmonary hypertension pulmonale Thromboembolie hemoptysis considered a relatively rare complication of pulmonary embolism but is associated with considerable morbidity and mortality.

However, the true frequency estimated at 0. It has been hypothesized that in situ thrombosis and pulmonary arteriopathy are common causes of vascular occlusion leading to chronic thromboembolic pulmonary hypertension CTPH and that pulmonary embolism is unlikely to be a common cause of Oberhausen kaufen Varison disease.

The purpose of this prospective, long-term follow-up study was to assess the incidence of symptomatic CTPH in a large series of consecutive patients with an adequately treated episode of acute symptomatic pulmonary embolism without prior pulmonary embolism or venous thrombosis. We also evaluated potential risk factors for CTPH. The University Hospital in Padua, Italy, serves as a primary referral center for patients with suspected pulmonary embolism.

Patients undergo a standardized diagnostic workup. Patients with an episode of acute symptomatic pulmonary embolism without prior pulmonary embolism or venous thrombosis were included in the cohort study, whereas patients with acute pulmonary embolism who had had a pulmonary embolism or venous thrombosis were also included in the assessment of risk factors.

The institutional review board approved the study protocol, and each patient provided written informed consent. Patients were treated with adjusted-dose unfractionated heparin, preceded in those with severe pulmonary embolism by thrombolytic drugs or, rarely, pulmonale Thromboembolie hemoptysis, thromboembolectomy. The dose was adjusted to maintain an activated partial-thromboplastin time that was 1.

The activated partial-thromboplastin time was measured approximately six hours after the start of heparin treatment, about six hours after each measurement of the activated partial-thromboplastin time that was subtherapeutic or supratherapeutic, and otherwise daily. Oral anticoagulants were started during the first week and continued for at least six months; the target international normalized ratio INR was 2, pulmonale Thromboembolie hemoptysis. The INR was usually monitored daily until the therapeutic range had been achieved, then twice or three times weekly during the first two weeks, pulmonale Thromboembolie hemoptysis then once a week or less often, depending on the stability of the results.

Prolongation of anticoagulant treatment beyond six months was individualized, depending on the presence of a perceived risk of recurrent venous thromboembolism. Follow-up was performed prospectively at least every 6 months during the first 2 years and then yearly for up to 10 years. The minimal period of follow-up was one year. For patients who died during follow-up, the date and cause of death were documented.

An autopsy was to be requested for any patient in whom pulmonary embolism pulmonale Thromboembolie hemoptysis not be excluded as a cause of death. An independent, expert committee assessed all study outcomes. Patients who had otherwise unexplained persistent dyspnea on exertion or at rest during follow-up were considered to have thromboembolic pulmonary hypertension.

These patients underwent transthoracic echocardiography. CTPH was considered to be present if the systolic and mean pulmonary-artery pressures exceeded 40 mm Hg and 25 mm Hg, respectively; the pulmonary-capillary wedge pressure was normal; and there was angiographic evidence of pouching, webs, pulmonale Thromboembolie hemoptysis, or bands with or without poststenotic dilatation, intimal irregularities, abrupt narrowing, or total occlusion, pulmonale Thromboembolie hemoptysis.

Each of these findings is consistent with the presence of CTPH. Patients were classified as having pulmonary embolism related to transient risk factors recent trauma, fracture, surgical intervention, hospitalization, pregnancy, and the use of oral contraceptives or hormone-replacement therapy or permanent risk factors deficiency of antithrombin, protein C, or protein S; mutation in the factor V Leiden or prothrombin gene; and the presence of lupus Varizen und Kinder, active cancer, immobilization from chronic medical illness, or two or more first-degree relatives with venous thromboembolism.

The following potential risk factors for CTPH were considered: All previous episodes of pulmonary embolism and venous thrombosis were pulmonale Thromboembolie hemoptysis and accepted if confirmed by objective diagnostic testing 6 or if anticoagulant treatment had been administered for at least three months. Patients with suspected recurrent pulmonary embolism during the study underwent objective testing. In the cohort study, Kaplan—Meier survival estimates and their 95 percent confidence intervals were calculated to estimate the cumulative incidence of CTPH, recurrent venous thromboembolism, and mortality among patients who entered the study with a first episode of pulmonary embolism without prior venous thromboembolism.

In addition, potential risk factors for CTPH were evaluated in the entire cohort with the use of univariate logistic-regression analysis. Then, all variables with a univariate level of significance of less than 0. All calculations were performed with the pulmonale Thromboembolie hemoptysis of SAS software, version 6. Pengo, Lensing, and Prandoni conceived the study design, oversaw its conduct, and wrote the initial protocol and first draft of the article. Prins and Marchiori contributed elements of the study design, did the statistical pulmonale Thromboembolie hemoptysis, and helped write and revise the article.

Davidson, Tiozzo, Albanese, Biasiolo, Pegoraro, and Iliceto helped design and conduct the study, interpret the data, and write or revise the article. We identified consecutive patients with acute pulmonary embolism.

Of these, 81 were excluded because they had conditions potentially responsible for nonthromboembolic pulmonary hypertension, preexisting exertional dyspnea, or both 38 had chronic obstructive pulmonary disease, 13 had valvular heart diseases, 5 had dilated cardiomyopathy, and 1 patient each had rheumatoid lung, left atrial myxoma, and patent ostium secundum or because they lived too far from the study center to be followed prospectively 22 patients.

Ten additional patients declined to participate in the study. The median follow-up was No patient was lost to follow-up. Of the patients, 32 During the initial recurrence, 16 patients presented with pulmonary embolism pulmonale Thromboembolie hemoptysis of whom died and pulmonale Thromboembolie hemoptysis with deep-vein thrombosis only.

Twenty of the 32 initial recurrences of thromboembolism Kaplan—Meier analysis showed that the cumulative incidence of recurrent venous thromboembolism was 4. Of the patients, 18 died as a direct consequence pulmonale Thromboembolie hemoptysis the acute episode, 17 on the first day and 1 on the second day after admission case-fatality rate, 8, pulmonale Thromboembolie hemoptysis.

During follow-up, 23 additional patients died: In 5 of the 12 patients who died of cancer, the cancer became clinically evident after the diagnosis of pulmonary embolism. The cumulative mortality rate was 9. The cumulative incidence of CTPH was 0. Of the patients with an acute episode of pulmonary embolism who were included in the analysis of risk factors, had a first pulmonary embolism, 58 had had a previous deep-vein thrombosis, and 24 had already had a pulmonary embolism Table 1.

Symptomatic CTPH developed in 3 of the 58 patients with previous deep-vein thrombosis 5. The INR was subtherapeutic i. In the multivariate model, pulmonale Thromboembolie hemoptysis, younger age per decadea previous pulmonary embolism, and a larger perfusion defect per decile decrement in perfusion remained significantly associated with an increased risk of CTPH, and idiopathic presentation became significantly associated with an increased risk.

Of the 18 patients with a diagnosis of CTPH, pulmonale Thromboembolie hemoptysis underwent bilateral pulmonary thromboendarterectomy.

The pulmonale Thromboembolie hemoptysis patients who were in NYHA class II pulmonale Thromboembolie hemoptysis surgery, one because of life-threatening hemoptysis, pulmonale Thromboembolie hemoptysis, and the other because of rapidly increasing pulmonary-artery pressure. All patients had clinically significant hemodynamic improvement, and all but one were in NYHA class I after discharge. The condition of these eight patients remained stable after a median follow-up of 22 months range, 7 to In one patient, surgery was considered unsuitable owing to extensive distal obstructions.

Two other patients died, pulmonale Thromboembolie hemoptysis, and autopsy revealed extensive unresolved chronic emboli, pulmonale Thromboembolie hemoptysis. The condition of the other seven patients remained stable all were in NYHA class II after a median follow-up of 38 months range, 17 to We found that symptomatic CTPH affects approximately 4 Varizen Wette Topf of patients within two years after a first episode of symptomatic pulmonary embolism, with no subsequent increase in incidence.

These results challenge the current belief that CTPH pulmonale Thromboembolie hemoptysis rare after an episode of pulmonary embolism and occurs long after the acute episode. We attempted to minimize bias by adhering to rigorous methodologic and clinical standards. A substantial number of consecutive patients with a first episode of confirmed pulmonary embolism and without a previous deep-vein thrombosis were included in the cohort, pulmonale Thromboembolie hemoptysis, and the median follow-up was almost eight years.

Patients received state-of-the-art treatment for pulmonary embolism, and the average length of anticoagulation was more than one year. All patients with dyspnea underwent a diagnostic workup in which both recurrent pulmonary embolism and CTPH were considered.

Moreover, independent experts used prespecified criteria to diagnose both recurrent pulmonary embolism and CTPH. Since symptoms of dyspnea were elicited during the routine follow-up visits, it is likely that we identified all patients with symptomatic CTPH. However, we may have missed patients with fewer symptoms and those who were asymptomatic. Hence, our estimate of the incidence of CTPH should be viewed as the lower limit. For our incidence estimates, we excluded patients who presented with recurrent pulmonary embolism or previous venous thrombosis to avoid spurious inflation of complication rates based on case finding and referral bias.

We also excluded patients who had a history of other diseases that are known to be associated with pulmonary hypertension and those who had preexisting exertional dyspnea. However, we cannot exclude the possibility that the patients in whom symptomatic CTPH developed had a compromised pulmonary circulation before pulmonale Thromboembolie hemoptysis first episode of pulmonary embolism, pulmonale Thromboembolie hemoptysis.

Taking into account these considerations, we believe that our results represent a reasonably precise estimate of the incidence of symptomatic CTPH. The clinical course of pulmonary embolism has been described in two previous studies that followed patients for one year and six months, respectively. Our estimates of the incidence of recurrent venous thromboembolism 8. However, the mortality rate in our pulmonale Thromboembolie hemoptysis appears lower Since CTPH occurred in only a limited number of patients with acute pulmonary embolism without prior thrombotic episodes, we also included patients with acute pulmonary embolism who had had prior thrombotic episodes in the analysis of risk factors for CTPH.

Among potential risk factors evaluated, pulmonale Thromboembolie hemoptysis, multiple episodes of pulmonary embolism, a larger perfusion defect, a younger age, and idiopathic presentation of pulmonary embolism were associated with an increased risk of CTPH in the final multivariate regression model.

Use of thrombolytic treatment was related in the univariate model to an increased risk of CTPH but not after adjustment for other risk factors. This is likely due to the blau Jod Thrombophlebitis of patients with extensive pulmonary embolism for this treatment.

Recurrent pulmonary embolism was clearly associated with an increased risk of CTPH. However, it should be noted that some of the patients with previous episodes of pulmonary embolism had had multiple episodes that had sometimes been inadequately treated, contributing to the size of this increase in risk.

However, even without the recurrence of pulmonary embolism, the risk of CTPH is not negligible but amounts to 3 to 4 percent after proper diagnosis and treatment.


Pulmonale Thromboembolie hemoptysis

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