Abstract: Poster Presentations |

Pericardial Morphology in Vibroacoustic Disease FREE TO VIEW

Nuno Castelo Branco, MD; José I. Fragata, MD, PhD; Ana P. Martins, MD; Emanuel Monteiro, BSc; Mariana Alves-Pereira, PhD Candidate
Author and Funding Information

Research, Center for Human Performance, Alverca, Portugal


Chest. 2003;124(4_MeetingAbstracts):213S-b-214S. doi:10.1378/chest.124.4_MeetingAbstracts.213S-b
Text Size: A A A
Published online


PURPOSE:  Pericardial thickening in the absence of an inflammatory process and with no diastolic dysfunction is the hallmark of vibroacoustic disease (VAD): a whole-body pathology caused by long-term (years) exposure to low frequency noise (LFN) (≤500 Hz, including infrasound). This study explores the morphological features of the human pericardial response to LFN exposure.

METHODS:  Pericardial fragments were removed from 11 VAD patients with their informed consent, at the beginning of cardiac surgery (for other reasons), and always from the same location: anterior, ventral portion of the parietal leaflet. Specimens were prepared for light and electron microscopy

RESULTS:  All fragments were over 2mm thick (normal: less than 0.5 mm thick). A newly formed loose tissue layer, sandwiched between both thickened layers of fibrosa, was quite evident. No cilia were identified in the mesothelial layer. Both fibrosa layers, on either side of the loose tissue layer, were distinctly composed of wavy collagen bundles, with numerous elastic fibers. The loose tissue layer contained adipose tissue cells, neural and blood vessels, and collagen and elastic fibers. None of the layers had the typical cellularity of an inflammatory process. However, a large amount of burst cells and cellular debris is scattered throughout both fibrosa layers and the new loose tissue layer.CONCLUSIONS: Although the response of the pericardium to LFN seems to be an adaptation response, this does not exclude the loss of functional capabilities, i.e., not a single cilium was identified. Possibly, this newly formed loose tissue layer, with numerous elastic components, plays an important pneumatic role, to maintain normal function heart in these patients. The observed cellular death was not necrotic, and apoptotic processes were not evident except for the phagocytosis. This may be an explanation for the frequent auto-immune disorders seen in LFN-exposed individuals. Immunohistochemical studies are underway to study cell proliferation, cell death, and auto-immune processes.

CLINICAL IMPLICATIONS:  Cardiovascular problems, namely thickening of cardiac structures, and collagenous diseases can be related to LFN exposure.

DISCLOSURE:  N. Castelo Branco, None.

Wednesday, October 29, 2003

12:30 PM - 2:00 PM




Citing articles are presented as examples only. In non-demo SCM6 implementation, integration with CrossRef’s "Cited By" API will populate this tab (http://www.crossref.org/citedby.html).

Some tools below are only available to our subscribers or users with an online account.

Related Content

Customize your page view by dragging & repositioning the boxes below.

CHEST Journal Articles
PubMed Articles
  • CHEST Journal
    Print ISSN: 0012-3692
    Online ISSN: 1931-3543