Pulmonary effects leave cardiac red herring in COPD, emphysema
medwireNews: US researchers have found evidence that impaired left ventricular (LV) filling in patients with chronic obstructive pulmonary disease (COPD) and emphysema is caused by reduced LV preload due to upstream pulmonary causes, as opposed to intrinsic diastolic dysfunction.
Using magnetic resonance imaging, R Graham Barr (University of Columbia, New York) and colleagues show that patients with COPD have a significantly reduced pulmonary vein cross-sectional area, indicating reduced LV filling pressure. Conversely, increased pulmonary vein area would have pointed to intrinsic LV dysfunction, explain the authors.
They say that patients with the respiratory conditions, who are commonly identified as having LV dysfunction by echocardiography, may in fact be misdiagnosed.
The findings were based on data from 165 people with a history of smoking, recruited primarily from the Multi-Ethnic Study of Atherosclerosis, of whom 53% had COPD.
The authors found that the mean total cross-sectional pulmonary vein area was around 10.4% smaller in patients with COPD, at 562 mm2 compared with 618 mm2 in controls, after adjusting for confounders.
Additionally, percent emphysema, as measured on computed tomography scan, was significantly inversely related to pulmonary vein area, such that those in the highest quartile (mean 40% voxels below -910 Hounsfield Units [HU]) had a predicted total area of 526 mm2 compared with 652 mm2 in the lowest quartile (mean 4.6% voxels below -910 HU).
The authors found that the association between emphysema and pulmonary vein area was true even in patients without COPD.
"These findings suggest that impaired LV filling in COPD, and also in emphysema in the absence of clinical COPD, may be predominantly due to reduced LV preload from upstream pulmonary causes rather than intrinsic diastolic dysfunction," they write in Chest.
They say that signs on echocardiography, such as reversed E/A ratio, may be misinterpreted as LV dysfunction in patients with COPD, when they in fact represent increased stiffness of the left ventricle or states of low LV filling pressure. Indeed, in their study, patients with COPD were 2.6-fold more likely to have an abnormal E/A ratio than controls.
Additionally, the researchers estimate that around 13% of the controls in their study appeared to have diastolic dysfunction on echocardiography, which was actually emphysema-related low LV preload.
Nevertheless, they acknowledge that cardiopulmonary interactions in COPD and emphysema are likely, and that the rate of intrinsic LV dysfunction in COPD patients is probably greater in real-world populations due to the exclusion of cardiac patients from their study.
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By Kirsty Oswald, medwireNews Reporter