Pulmonary vascular volume, impaired left ventricular filling and dyspnea: The MESA Lung Study

Carrie P. Aaron, Eric A. Hoffman, Joao A.C. Lima, Steven M. Kawut, Alain G. Bertoni, Jens Vogel-Claussen, Mohammadali Habibi, Katja Hueper, David R. Jacobs, Ravi Kalhan, Erin D. Michos, Wendy S. Post, Martin R. Prince, Benjamin M. Smith, Bharath Ambale-Venkatesh, Chia Ying Liu, Filip Zemrak, Karol E. Watson, Matthew Budoff, David A. BluemkeR. Graham Barr

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34 Scopus citations

Abstract

Background Evaluation of impaired left ventricular (LV) filling has focused on intrinsic causes of LV dysfunction; however, pulmonary vascular changes may contribute to reduced LV filling and dyspnea. We hypothesized that lower total pulmonary vascular volume (TPVV) on computed tomography (CT) would be associated with dyspnea and decrements in LV end-diastolic volume, particularly among ever-smokers. Methods The Multi-Ethnic Study of Atherosclerosis recruited adults without clinical cardiovascular disease in 2000±02. In 2010±12, TPVV was ascertained as the volume of arteries and veins in the lungs detectable on non-contrast chest CT (vessels -1 mm diameter). Cardiac measures were assessed by magnetic resonance imaging (MRI). Dyspnea was selfreported. Results Of 2303 participants, 53% had ever smoked cigarettes. Among ever-smokers, a lower TPVV was associated with a lower LV end-diastolic volume (6.9 mL per SD TPVV), stroke volume, and cardiac output and with dyspnea (all P-values <0.001). Findings were similar among those without lung disease and those with 0-10 pack-years but were mostly non-significant among never-smokers. TPVV was associated smaller left atrial volume but not with LV ejection fraction or MRI measures of impaired LV relaxation. In a second sample of eversmokers, a lower pulmonary microvascular blood volume on contrast-enhanced MRI was also associated with a lower LV end-diastolic volume (P-value = 0.008). Conclusion Reductions in pulmonary vascular volume were associated with lower LV filling and dyspnea among ever-smokers, including those without lung disease, suggesting that smokingrelated pulmonary vascular changes may contribute to symptoms and impair cardiac filling and function without evidence of impaired LV relaxation.

Original languageEnglish (US)
Article numbere0176180
JournalPloS one
Volume12
Issue number4
DOIs
StatePublished - Apr 2017

Bibliographical note

Funding Information:
Dr. Aaron reports research grants from the Alpha-1 Foundation and Stony Wold-Herbert Fund. Dr. Hoffman is a founder and shareholder of VIDA Diagnostics, a company commercializing lung image analysis software developed in part at the University of Iowa. Dr. Kawut reports unrestricted educational grants to his institution from Actelion, United Therapeutic, Gilead, Lung Biotech, Pfizer, Ikaria, Merck, Bayer and the Pulmonary Hypertension Association, grant support from Actelion, Gilead and GeNO, travel reimbursement from the American College of Chest Physicians and the American Thoracic Society, and personal fees from the European Respiratory Journal. Dr. Vogel-Claussen has received personal fees from Novartis and Boehringer Ingelheim. Dr. Hueper has participated in research with Seimens Healthcare and received grant support from Deutsche Forschungsgemeinschaft. Dr. Kalhan has received grant support from Boehringer Ingelheim, GlaxoSmithKline, PneumRx/BTG and Spiration and personal fees from Forest Laboratories, Boehringer Ingelheim and Merck. Dr. Prince has patent agreements with GE Healthcare, Siemens, and Bayer. Dr. Ambale-Venkatesh has received personal fees from Biomet. Dr. Budoff reports grant support from GE. Dr. Barr reports research grants from the Alpha-1 Foundation and personal fees from UpToDate. The other authors report no conflicts. This does not alter our adherence to PLOS ONE policies on sharing data and materials.

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