A new study from UCLA and the University of Pennsylvania shows that patients with pulmonary fibrosis, a progressive lung disease, are more likely also to develop heart disease. The study may lead to a greater understanding of both diseases and the role of inflammation, as well as help develop new treatments.
Published in the March 8 issue of the Archives of Internal Medicine, the study showed that patients with pulmonary fibrosis were four times more likely to have extensive coronary artery disease compared with patients without this type of lung condition.
“We were very surprised by the large number of pulmonary fibrosis patients who had also developed advanced coronary artery disease,” said Dr. David A. Zisman, senior author and director of the Interstitial Lung Disease Program and assistant professor of the Division of Pulmonary and Critical Care Medicine at the David Geffen School of Medicine at UCLA.
This is the first study of its kind, and researchers note that pulmonary fibrosis and coronary artery disease may prove very similar — both cause inflammation that leads to scarring and/or plaque development. “Visually the disease processes look very much the same,” Zisman said.
According to Zisman, this study adds to the growing body of research taking a closer look at the impact of the inflammation process throughout the body. “Inflammation plays a key role in so many diseases, from Alzheimer’s disease and heart disease to cancers as well as pulmonary fibrosis,” Zisman said. “The more we learn about the interaction of such diseases, the better we will be able to direct treatments.”
“In the next step of research, we will look more closely at the processes that underlie development of these two diseases,” said Dr. Robert M. Strieter, a study author, chief of the Division of Pulmonary and Critical Care Medicine, and vice chair of medicine at the David Geffen School of Medicine at UCLA. He adds that the disease process generating pulmonary fibrosis in the lungs may have more systemic effects — causing similar inflammation processes in other areas of the body, such as development of coronary artery disease.
According to Strieter, researchers will next try to identify which substances a pulmonary fibrosis lung makes that may reach the heart to produce or exacerbate heart disease.
Study investigators reviewed coronary angiograms of 630 patients at the University of Pennsylvania, who were being evaluated for lung transplant. Although patients had a wide range of lung disorders, those with pulmonary fibrosis had twice the risk of having coronary artery disease and four times the risk of having more extensive coronary artery disease than patients without this condition.
The most common form of pulmonary fibrosis is idiopathic pulmonary fibrosis that affects 5 million worldwide and 100,000 in the United States. The progressive disease causes inflammation and scarring of the lungs and most patients are eventually referred for lung transplant.
Heart disease or coronary artery disease — the No. 1 killer in the United States — causes blockages of the arteries that feed the heart muscle, which could lead to a heart attack.
The study was funded by the National Institutes of Health and a private donation.
Additional study authors include Dr. Jorge R. Kizer, Division of Cardiology, Departments of Medicine and Public Health, Weill Medical College of Cornell University, New York City; Nancy P. Blumenthal, Dr. Robert M. Kotloff and Dr. John Hansen-Flaschen, Pulmonary, Allergy and Critical Care Division, University of Pennsylvania School of Medicine, Philadelphia; Dr. Stephen E. Kimmel; Dr. Victor A. Ferrari, Cardiovascular Division of the Department of Medicine and the Department of Epidemiology and Biostatistics, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania School of Medicine, Philadelphia; and Dr. Selim M. Arcasoy, Division of Pulmonary, Allergy and Critical Care, Department of Medicine, Columbia University College of Physicians and Surgeons, New York City.
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