My New Year Resolution. Read only if critical thinking is employed!
So very little is known about the long term prognoses of PEs that I've decided to start a collection of articles that touch on that. Rose-tinted glasses were not used during this quest. I also recognize that for every 'bad' prognosis there's a 'good' prognosis; those are easily found and not the thrust of this effort.
This collection might contain studies/articles that are lacking in good science/study design. This is a 'collection' only. If anyone can point to the scientific/statistical faults in any article, please do so. Testimonials not accepted. (grin)
Patient Outcomes after Acute Pulmonary Embolism
A Pooled Survival Analysis of Different Adverse Events
Frederikus A. Klok1,
Wendy Zondag1,
Klaas W. van Kralingen2,
Arie P. J. van Dijk3,
Jouke T. Tamsma1,
Fenna H. Heyning4,
Hubert W. Vliegen5and
Menno V. Huisman1
+Author Affiliations
1Section of Vascular Medicine, Department of General Internal Medicine-Endocrinology, 2Department of Pulmonary Medicine, and 5Department of Cardiology, LUMC, Leiden; 3Department of Cardiology, Radboud University Nijmegen Medical Centre, Nijmegen; 4Department of Hematology, Medical Center Haaglanden, The Hague, The Netherlands
Correspondence and requests for reprints should be addressed to Frederikus A. Klok, M.D., LUMC (C4-70) Albinusdreef 2, Postbus 9600 2300 RC Leiden, The Netherlands. E-mail:F.A.Klok@LUMC.nl
Next Section
Abstract
Rationale: There is a lack of information on the long-term prognosis of patients with acute pulmonary embolism (PE).
Objectives: To assess the long-term risk for adverse events after PE.
Methods: Consecutive patients diagnosed with PE between January 2001 and July 2007, and patients in whom PE was ruled out from a previous study were followed until July 2008 for the occurrence of adverse clinical events: mortality, symptomatic recurrent venous thromboembolism, cancer, arterial cardiovascular events and chronic thromboembolic pulmonary hypertension. Hazard ratios (HR) for all endpoints and a combined endpoint were calculated and adjusted for potential confounders.
Measurements and Main Results: Three hundred eight patients with unprovoked, 558 with provoked, and 334 without PE were studied with a median follow-up period of 3.3 years. Patients with unprovoked PE had a lower overall risk for mortality than patients with provoked PE (HR, 0.59; 95% confidence interval [CI], 0.43–0.82), but a higher risk for nonmalignancy-related mortality (HR, 1.8; 95% CI, 1.3–2.5), recurrent venous thromboembolism (HR, 2.1; 95% CI, 1.3–3.1), cancer (HR, 4.4; 95% CI, 2.0–10), cardiovascular events (HR, 2.6; 95% CI, 1.5–3.8) and chronic thromboembolic pulmonary hypertension (1.5 vs. 0%). The risk for the combined endpoint did not differ between both groups (HR, 0.98; 95% CI, 0.82–1.1). Patients without PE had similar risks for malignancy and cardiovascular events than patients with provoked PE, but lower risks for the remaining outcomes. The fraction of both patients with provoked and unprovoked PE without events after 1 year was only 70% and decreased to fewer than 60% after 2 years and fewer than 50% after 4 years, whereas this latter was 84% for the control patients.
Conclusions: The clinical course of acute PE is complicated by high rates of serious adverse events, which occur in half of the patients within 4 years.
http://ajrccm.atsjournals.org/content/181/5/501.full
This collection might contain studies/articles that are lacking in good science/study design. This is a 'collection' only. If anyone can point to the scientific/statistical faults in any article, please do so. Testimonials not accepted. (grin)
Patient Outcomes after Acute Pulmonary Embolism
A Pooled Survival Analysis of Different Adverse Events
Frederikus A. Klok1,
Wendy Zondag1,
Klaas W. van Kralingen2,
Arie P. J. van Dijk3,
Jouke T. Tamsma1,
Fenna H. Heyning4,
Hubert W. Vliegen5and
Menno V. Huisman1
+Author Affiliations
1Section of Vascular Medicine, Department of General Internal Medicine-Endocrinology, 2Department of Pulmonary Medicine, and 5Department of Cardiology, LUMC, Leiden; 3Department of Cardiology, Radboud University Nijmegen Medical Centre, Nijmegen; 4Department of Hematology, Medical Center Haaglanden, The Hague, The Netherlands
Correspondence and requests for reprints should be addressed to Frederikus A. Klok, M.D., LUMC (C4-70) Albinusdreef 2, Postbus 9600 2300 RC Leiden, The Netherlands. E-mail:F.A.Klok@LUMC.nl
Next Section
Abstract
Rationale: There is a lack of information on the long-term prognosis of patients with acute pulmonary embolism (PE).
Objectives: To assess the long-term risk for adverse events after PE.
Methods: Consecutive patients diagnosed with PE between January 2001 and July 2007, and patients in whom PE was ruled out from a previous study were followed until July 2008 for the occurrence of adverse clinical events: mortality, symptomatic recurrent venous thromboembolism, cancer, arterial cardiovascular events and chronic thromboembolic pulmonary hypertension. Hazard ratios (HR) for all endpoints and a combined endpoint were calculated and adjusted for potential confounders.
Measurements and Main Results: Three hundred eight patients with unprovoked, 558 with provoked, and 334 without PE were studied with a median follow-up period of 3.3 years. Patients with unprovoked PE had a lower overall risk for mortality than patients with provoked PE (HR, 0.59; 95% confidence interval [CI], 0.43–0.82), but a higher risk for nonmalignancy-related mortality (HR, 1.8; 95% CI, 1.3–2.5), recurrent venous thromboembolism (HR, 2.1; 95% CI, 1.3–3.1), cancer (HR, 4.4; 95% CI, 2.0–10), cardiovascular events (HR, 2.6; 95% CI, 1.5–3.8) and chronic thromboembolic pulmonary hypertension (1.5 vs. 0%). The risk for the combined endpoint did not differ between both groups (HR, 0.98; 95% CI, 0.82–1.1). Patients without PE had similar risks for malignancy and cardiovascular events than patients with provoked PE, but lower risks for the remaining outcomes. The fraction of both patients with provoked and unprovoked PE without events after 1 year was only 70% and decreased to fewer than 60% after 2 years and fewer than 50% after 4 years, whereas this latter was 84% for the control patients.
Conclusions: The clinical course of acute PE is complicated by high rates of serious adverse events, which occur in half of the patients within 4 years.
http://ajrccm.atsjournals.org/content/181/5/501.full
Replies
Curr Opin Hematol. 2008 Sep;15(5):499-503. doi: 10.1097/MOH.0b013e3283063a51.
Long-term outcome of pulmonary embolism.
Meyer G, Planquette B, Sanchez O.
Source
Division of Respiratory and Intensive Care, Hopital Europeen Georges Pompidou, Assistance Publique Hopitaux de Paris and Universit Paris Descartes, Facult de Medecine, Paris, France. guy.meyer@egp.aphp.fr
Abstract
PURPOSE OF REVIEW:
Until recently, little was known about the long-term outcome of pulmonary embolism. Long-term mortality and recurrence rates, the case fatality rate of recurrent events, and the frequency of persistent vascular defects remained largely unknown. Improvements in our knowledge of these aspects may help to define the optimal long-term treatment of pulmonary embolism. This review will address these issues.
RECENT FINDINGS:
The death rate after pulmonary embolism is less than 5% during 3-6 months of anticoagulant treatment, provided that the patient is hemodynamically stable and free of major underlying disease. The rate of recurrent thromboembolism is less than 5% on anticoagulant therapy, reaching 30% after 10 years. Recurrences are more likely to take the form of a new pulmonary embolism than deep venous thrombosis. Chronic thromboembolic pulmonary hypertension occurs in less than 5% of the patients.
Most patients have persistent perfusion defects after the initial episode and further studies are required to determine the long-term significance of this finding.
SUMMARY:
Pulmonary embolism has a higher mortality rate than deep venous thrombosis. Patients with pulmonary embolism have no higher risk of recurrence, but any recurrence is more likely to be a new pulmonary embolism than a deep venous thrombosis. A significant number of patients develop persistent perfusion defects after pulmonary embolism.
PMID: 18695374 [PubMed - indexed for MEDLINE]
http://radiology.rsna.org/content/242/3/889.full
Technical article (radiology) with \'embolic burden\' and where it was located. I confess that I\'m not familiar with this but will certainly look into it.
Another abstract found while trying to find out what embolic burden meant.
http://journal.publications.chestnet.org/article.aspx?articleid=1216035
Abstract
Background: In patients with acute pulmonary embolism (PE), the correlation between the embolic burden assessed by multidetector CT (MDCT) scan and clinical outcomes remains unclear. Patients with symptomatic acute PE diagnosed based on MDCT angiography were included in a multicenter study aimed at assessing the prognostic role of the embolic burden evaluated with MDCT scan.
Methods: Embolic burden was assessed as (1) localization of the emboli as central (saddle or at least one main pulmonary artery), lobar, or distal (segmental or subsegmental arteries) and (2) the obstruction index by the scoring system of Qanadli. The primary outcome was 30-day all-cause death or clinical deterioration. Predictors of all-cause death or clinical deterioration were identified by Cox regression statistics.
Results: Overall, 579 patients were included in the study; 60 (10.4%) died or had clinical deterioration at 30 days. Central localization of emboli was not associated with all-cause death or clinical deterioration (hazard ratio [HR], 2.42; 95% CI, 0.77-7.59; P = .13). However, in 516 hemodynamically stable patients, central localization of emboli (HR, 8.3; 95% CI, 1.0-67; P = .047) was an independent predictor of all-cause death or clinical deterioration, whereas distal emboli were inversely associated with these outcome events (HR, 0.12; 95% CI, 0.015-0.97; P = .047). No correlation was found between obstruction index (evaluated in 448 patients) and all-cause death or clinical deterioration in the overall study population and in the hemodynamically stable patients.
Conclusions: In hemodynamically stable patients with acute PE, central emboli are associated with an increased risk for all-cause death or clinical deterioration. This risk is low in patients with segmental or subsegmental PE.
[Note: \'remains unclear\'.]
AND NOW---- for a completely different opinion. (Gotta love these studies!)
\"Conclusion
These results suggest that CT pulmonary embolic burden are not associated with risk of death due to APE. Serum level of D-dimer may
represent amount of pulmonary clot burden.\"
http://ajrccm.atsjournals.org/cgi/reprint/181/1_MeetingAbstracts/A1929
[Curious! \"This abstract is funded by: None\". Huh?]
http://qjmed.oxfordjournals.org/content/103/2/91.full
\"There are several limitations to our study\"
\"Further prospective studies combining clinical, radiological and biological data, perhaps with the use of scoring systems that incorporate haemodynamic parameters, D-dimers and troponin as well radiological parameters of severity, may allow for the development and validation of a measure of risk stratification for patients with acute PE. This will aid the physician in accurately assessing prognosis and help guide optimal management.\"
Low or high leptin and PE outcomes
Int J Obes (Lond). 2012 Mar 20. doi: 10.1038/ijo.2012.36. [Epub ahead of print]
BMI-independent inverse relationship of plasma leptin levels with outcome in patients with acute pulmonary embolism.
Dellas C, Lankeit M, Reiner C, Schfer K, Hasenfu G, Konstantinides S.
Source
Department of Cardiology and Pulmonology, Heart Center, University of Gttingen, Gttingen, Germany.
Abstract
Objective:The adipocytokine leptin is an independent cardiovascular risk factor and exerts prothrombotic effects, both in arterial and venous thrombosis. We therefore investigated the relationship between leptin levels and clinical outcome in patients with acute pulmonary embolism (PE).
Design:We prospectively studied consecutive patients with confirmed acute PE admitted at the University Hospital of Goettingen (Germany) between 2003 and 2009.Subjects:The study subjects were a total of 264 patients with PE (median age, 68 years; interquartile range, 53-75; 60% women; body mass index (BMI) 27kgm(-2) (24.1-31.2)). Leptin levels were determined by a commercially available enzyme-linked immunosorbent assay. Patients were followed for an adverse 30-day outcome, that is, death, circulatory collapse with need for catecholamines, intubation or resuscitation, and for long-term survival.Results:The median leptin level was 10.1ngml(-1) (3.7-25.2). Patients (n=49; 18.6%) with a complicated 30-day course had significantly lower leptin levels (5.3ngml(-1) (1.8-19.7) compared with patients without complications (10.4ngml(-1) (4.7-25.5), P=0.02). When leptin was analyzed as a continuous variable, there was a significant 36% increase in the relative risk for early complications for every decrease in the natural logarithm of leptin by one s.d. (odds ratio (OR) 1.36 (1.06-1.76), P=0.017), independently of BMI (BMI-adjusted OR, 1.52 (1.13-2.05), P=0.006). In addition, patients within the lowest leptin tertile had a 2.8- and 2.3-fold increased risk for 30-day-complications, compared with those in the middle (P=0.011) and high tertile (P=0.030), and a worse probability of long-term survival (log-rank; P=0.018).
Conclusion:
Low plasma leptin concentration is a predictor for a complicated course and high mortality in patients with acute PE. This association is independent of known factors affecting leptin levels, including gender and obesity.International Journal of Obesity advance online publication, 20 March 2012; doi:10.1038/ijo.2012.36.
PMID: 22430305
http://emedicine.medscape.com/article/300901-overview
I\'m including these links even though I haven\'t dug deeply into the sources.
The link to Hemex Lab especially needs investigating since they\'re selling their services.
Dr Crist\'s article may be more reliable but he doesn\'t dig very deep into hypercoagulation--- e.g. DVTs and PEs but that\'s not his specialty. Treatment for Borreliosis MAY prevent hypercoagulation. As a \'study of one\' I\'d never had any problems with coag. until I had to go off antibiotics due to moving to a state where the doctors won\'t treat Lyme properly. Less than a year of off abx I got my first PE. Cause? I can\'t say but it is suspicious.
http://drcharlescrist.net/Borreliosis/Hypercoagulation/
http://www.diagnose-me.com/symptoms-of/hypercoagulation-thickened-blood.html