Introduction: Vibroacoustic disease (VAD) is a heterogeneous and systemic entity, caused by long term (> or =10 yr) exposure to noise environments characterized by large pressure amplitude and low frequency (LPALF) (> or =90 dB SPL, < or = 500 Hz), and not explained by other possible etiologic agents. The goal of this study was to identify possible structural changes in hearts of men with suspected VAD.

Methods: A total of 485 men were divided into 3 noise groups: no noise exposure (< or =70 dB), n = 48 (Group I); moderate noise exposure, (>70dB and < 90 dB), n = 113 (Group II); and intense noise exposure (> or =90 dB), n = 324 (Group III). Echo-Doppler studies were performed (HP SONOS 1500) and recorded on coded videotapes. Three observers performed blinded evaluations of 26 echo-Doppler parameters. For the purpose of the present study only 12 morphological parameters were compared among the groups: thickening of the mitral, aortic, tricuspid, and pulmonary valves, pericardium and endocardium; mitral valve regurgitation, prolapse and ruptured chordae tendinae; and inflow velocities. Thickness and severity of the applicable parameters were scored in seven-grade scale (0,0.5,1, ...,3).

Results: All evaluated parameters were statistically significantly different in Group I vs. Group III, except flow velocity E. Comparison of Group I vs. Group II revealed statistically significant differences in mitral, aortic, tricuspid and pericardial thickening, with the strongest evidence for mitral and pericardial structures.

Conclusions: This confirms the results of previous studies. Occupational exposure to noise environments characterized by LPALF noise causes structural changes in the heart. Mitral valve and pericardial thickening constitute the first signs of VAD.

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