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Master Class & workshop
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Chronic Venous Disease
August 14 -15, 2009
Manipal Hospital Bangalore, India
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| Weekly Venous News |
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ACS, Deep-Vein Thrombosis Linked to Idiopathic Pulmonary Fibrosis
Patients with idiopathic pulmonary fibrosis (IPF) are two to three times as likely as the general population to experience acute coronary syndromes (ACS) and are at a similarly increased risk of developing deep-vein thrombosis (DVT), report investigators who saw the relationships in both a case-control analysis and a longitudinal follow-up of IPF cases [1]. Both increased incidences of vascular disease were more pronounced after the IPF diagnosis was made than before.
Their data don't show that the lung disorder causes vascular disease or the reverse, nor do they say much about the etiology of IPF, according to Dr Richard B Hubbard (University of Nottingham, UK), who led the study. But he suspects that IPF may somehow be associated with a propensity for thrombosis that may increase the risk of ACS and DVT.
What they do suggest, he said, is that the possibility of cardiovascular disease should be routinely explored in patients diagnosed with IPF.
"The interesting parallel is perhaps diabetes, where, even if you allow for other risk factors, people with diabetes have a marked increase in risk of vascular disease. Once they've got the diagnosis, then maybe you should consider primary-prevention strategies. And I think the same is probably true for people with IPF."
Hubbard et al also write that the findings "provide further support for a possible trial of anticoagulation in people with IPF to determine whether this has a beneficial effect on the outcome of this devastating disease."
As reported in the December 15, 2008, issue of the American Journal of Respiratory and Critical Care Medicine, 920 patients with newly diagnosed IPF were identified in the Health Improvement Network, a longitudinal primary-care database in the UK.
In one analysis, the patients and 3593 control subjects matched for age, sex, and the community in which they lived were compared for clinical events, smoking status, and exposure to cardiovascular drugs during the average of eight years prior to IPF diagnosis.
The cases were about 1.5 to two times as likely, compared with controls, to have had a diagnosis of ACS, DVT, or angina; there was no significant difference in risk of either atrial fibrillation or stroke.
Odds ratio (95% CI) for cardiovascular diagnoses in patients vs matched controls prior to IPF diagnosis
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End point |
OR (95% CI) |
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ACS |
1.53 (1.15 - 2.03) |
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Deep-vein thrombosis |
1.98 (1.13 - 3.48) |
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Angina |
1.84 (1.48 - 2.29) |
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Use of warfarin, aspirin, and angiotensin-converting enzyme (ACE) inhibitors were each significantly increased among the patients compared with controls, but use of beta blockers and statins was comparable.
In a second analysis, the patients and controls were prospectively followed for averages of 2.7 years and 3.9 years, respectively, after the index diagnosis.
The increased incidences of ACS and DVT were more pronounced after the diagnosis than before, although it was no longer present for angina, nor, once again, were there significant increases for atrial fibrillation or stroke.
The results were about the same, according to the authors, after adjustment for smoking and use of statins, aspirin, amiodarone, beta blockers, warfarin, or ACE inhibitors.
Relative risk (95% CI) of cardiovascular diagnoses in patients vs matched controls after diagnosis of IPF |
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End point |
RR (95% CI) |
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ACS |
3.14 (2.02 - 4.87) |
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Deep-vein thrombosis |
3.39 (1.57 - 7.28) |
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Special attention was paid to use of amiodarone, for which pulmonary fibrosis is just one possible side effect. Among the patients there were 34 who had been exposed to the drug, for a rate of 4%, vs 2% among controls. The group concedes that some cases of IPF might actually have been caused by the drug.
In a post hoc analysis that followed patients and controls that excluded all who had been exposed to amiodarone, the relative risk of ACS among patients was still 3.29 (95% CI 2.11 - 5.13).
"My hope is that physicians will look more widely in people with IPF, to try to treat other aspects of them as well, and not just focus on their lungs," Heffner commented.
In an accompanying editorial [2], Dr David A Zisman (University of California, Los Angeles) and Dr Steven M Kawut (Columbia University, New York, NY) note that the analyses from Hubbard et al do "imply" a causal relationship between IPF and vascular disease. If such a relationship is confirmed in other studies, they write, "the presence of IPF itself could constitute a sufficiently potent risk factor for CAD [coronary artery disease] such that more aggressive goals in risk-factor modification would be warranted."
A press release from the American Thoracic Society, which sponsors the journal in which the study appears, provided a statement from a past president, Dr John E Heffner (Oregon Health and Science University, Portland), regarding the study's implications for the treatment of IPF patients.
"As with other chronic, progressive respiratory disorders, the lungs in IPF may be the bellwether of other more systemic pathogenic events," Heffner says. "What is first expressed in the lung becomes manifest later in other organ systems. This perspective will both realign research efforts and also direct more comprehensive healthcare to patients diagnosed with early IPF."
The study authors have disclosed no relevant financial relationships.
Dr. Zisman has received income from serving on the advisory board of Gilead Sciences and research grants from Intermune and Actelion Pharmaceuticals. Dr. Kawut has received lecture and consulting fees and course funding from Actelion Pharmaceuticals and Gilead Sciences and participating in research sponsored by Actelion Pharmaceuticals, Gilead Sciences, and Intermune. |
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Sources
• Hubbard RB, Smith C, Le Jeune I, et al. The association between idiopathic pulmonary fibrosis and vascular disease: a population-based study. Am J Respir Crit Care Med. 2008;178:1257-1261.
• Zisman DA, Kawut SM. Idiopathic pulmonary fibrosis. A shot through the heart? Am J Respir Crit Care Med. 2008;178:1192-1193.
American Journal of Respiratory and Critical Care Medicine, December 15, 2008.
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