Patient Outcomes after Acute Pulmonary Embolism: A Pooled Survival Analysis of Different Adverse Events

Abstract

A number of studies have linked chronic exposure to infectious agents such as Helicobacter pylori, Chlamydia pneumoniae, and herpes viruses to coronary artery disease and stroke (Wimmer MLJ, et al [Stroke 1996;27:2207-10] and Ridker PM et al [Circulation 1998;98: 2796-2799) with atherosclerosis. It has been thought that chronic infections may lead to an inflammatory process through remote signaling of inflammatory mediators that ultimately begin the process of atherosclerosis. The authors postulate that it is more likely that an aggregate of infectious burden, rather than a single infection, would lead to such a proinflammatory state.This study measured antibody titers to common infectious microorganisms (Chlamydia pneumoniae, Helicobacter pylori, cytomegalovirus, and herpes viruses 1 and 2) in community participants who were stroke free. A weighted index of infectious burden was then calculated based on Cox models derived from the association of each infection with stroke risk. Maximum carotid plaque thickness was then determined with highresolution carotid artery duplex scanning. The association between infectious burden and maximum carotid plaque thickening after adjustment for other risk factors was determined using weighted least squares regression.Serologic results for all five infectious organisms were available for 861 participants (mean age, 67.2 Ϯ 9.6 years) in whom maximum carotid plaque thickness measurements were also available. The infectious burden index was a mean of 1.0 Ϯ 0.35 (median, 1.08), and 52% of the participants had detectible plaque (mean, 0.90 Ϯ 1.04 mm). Infectious burden was associated with maximum carotid plaque thickness (adjusted increase in maximum carotid plaque thickness 0.09 mm; 95% confidence interval, 0.03-0.15 mm per standard deviation increase of infectious burden).Comment: An implication of the study is that infectious burden may be a modifiable risk of atherosclerosis and that measurement of carotid plaque thickness may provide a way to assess the effects of an anti-infective strategy. A weakness of the study is that serologic measurements of infection and carotid plaque thickness were determined at only a single time. Temporal relationships between carotid plaque thickness and infectious burden cannot be determined from these data. Another problem with the infectious etiology of atherosclerosis theory is that clinical trials of antibiotic therapy for infectious agents thought to be associated with atherosclerosis have not been shown to reduce vascular risk (O'Connor CM, et al [JAMA 2003;2901: 1459 and Cameron CP, et al [N Engl J Med 2005;352:1646-54]). Limb-Shaking Transient Ischaemic Attacks in Patients WithInternal Carotid Artery Occlusion: A Case-Control Study Persoon S, Kappelle LJ, Klijn CJM. Brain 2010;133:915-22.

30-Year Mortality After Venous Thromboembolism

“…[1][2][3][4][5][6][7][8][9] A recent study reported an 8-year mortality risk of 12%, 1 whereas in an earlier study, mortality risk reached 50% after 8 years of follow-up. 5 Previous studies were limited by short follow-up time (maximum, 10 years), [1][2][3][4][6][7][8][9][10][11] age restrictions (<70 years of age 1 or between 65 and 89 years of age 7 ), lack of adjustment for comorbidity 3,12 or calendar period, 3,5 and failure to examine mortality for DVT and PE separately. 1,8,12 Only a few studies have compared long-term mortality between VTE patients and a comparison cohort from the general population, with inconsistent results.…”

The optimal duration of anticoagulant therapy after unprovoked venous thromboembolism – still a challenging issue

“…Platelets and markers of platelet [62,63]. The combined results of two randomized, double-blind trials, WARFA-SA and ASPIRE, showed that aspirin, compared with placebo, reduced the rate of recurrence to 32 % (P = 0.007) in patients with a fi rst unprovoked VTE who had completed at least six months of standard therapy, without increased risk of major bleeding [64,65].…”

“…VTE is characterised by a persistent higher mortality, leading to 6-12 % of deaths within one month from the diagnosis and a yearly rate of mortality up to 8.5 % in patients aff ected by PE [2].…”

The connection between pulmonary embolism and chronic thromboembolic pulmonary hypertension: research session at the American Thoracic Society 2016 Meeting

“…While many patients recover completely after acute pulmonary embolism (PE), some go on to develop serious cardiopulmonary disabilities (1). PE that fails to resolve can be remodeled into progressive intravascular scars that cause persistent lung perfusion defects, which some have called chronic thromboembolic disease.…”