Poster Presentations: Wednesday, October 26, 2011 |

Is Pericardial Fat a Regional Risk Factor for Pulmonary Vascular Health? The Association Between Pericardial Fat and Pulmonary Artery Systolic Pressure (The Jackson Heart Study) FREE TO VIEW

DeMarc Hickson, PhD; Heba Abed, MPH; Ravi Gawalapu, PhD; Marcy Petrini, PhD; Demondes Haynes, PhD; Jiankang Liu, MD; J. Jeff Carr, MD; Herman Taylor, MD
Chest. 2011;140(4_MeetingAbstracts):731A. doi:10.1378/chest.1120174
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PURPOSE: Pericardial fat has been shown to have local effects on neighboring anatomic structures. We recently demonstrated that pericardial fat was associated with a restrictive lung pattern, independent of C reactive protein (CRP) and abdominal visceral fat (VAT) (Hickson, 2011). Given the close proximity to the pulmonary vasculature, pericardial fat may have mechanical or paracrine effects on the pulmonary circulation; however, the nature of this relationship is unknown.

METHODS: In a cross-sectional analysis of data from 839 Jackson Heart Study participants (mean age: 55.4±11.0 years; 69.4% female), we examined the association between pericardial fat and pulmonary artery systolic pressure (PASP) estimated from Doppler echocardiography. We hypothesized that higher pericardial fat volumes would be associated with higher PASP, independent of systemic blood pressure, CRP and VAT.

RESULTS: Women had lower pericardial fat volumes (64.5±25.5 versus 76.8±30.9 cm3) but higher PASP (27.7±6.9 versus 25.8±6.7 mmHg) than men. In mutivariable adjusted models, pericardial fat was positively associated with PASP, but this association did not persist after individual adjustments for CRP and VAT. Participants in the highest quartile of pericardial fat volume had the highest odds of pulmonary hypertension (PASP ≥30 mmHg), but this association was attenuated after adjustment for CRP and VAT.

CONCLUSIONS: Pericardial fat is correlated with PASP in women and men, but the association was mediated after controls for CRP and VAT. The attenuation of this relationship by CRP is consistent with a potential inflammatory contribution to pulmonary hypertension, which may be influenced by adiposity both locally and remotely from the pulmonary vasculature.

CLINICAL IMPLICATIONS: Obesity has been linked to respiratory health. The findings reported in this study suggest a pathway through which cardiac adiposity may alter pulmonary circulation, although not independent of visceral abdominal fat.

DISCLOSURE: The following authors have nothing to disclose: DeMarc Hickson, Heba Abed, Ravi Gawalapu, Marcy Petrini, Demondes Haynes, Jiankang Liu, J Jeff Carr, Herman Taylor

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