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Introduction: Constrictive pericarditis is a rare complication of asbestos exposure and few cases have been reported in the literature., Case Report: We report two cases of constrictive pericarditis in subjects previously exposed to asbestos. The first case, a 62 years old man, had occupational asbestos exposure whilst working for seven years in an electric plant 23 years before the diagnosis. The second case, a 76 years old man, had worked 21 years as a lagger up until 20 years before. The initial presentation in both cases was of sub-acute right heart failure. Both underwent pericardectomy which revealed pericardial thickening due to collagen fibrosis. Both patients died, one and five years respectively after surgery. Eight other cases of pericardial effusion and/or thickening, some with calcification, have been reported in association with previous asbestos exposure. Most of these cases had coexisting pleural lesions., Conclusions: As the prognosis is guarded (three of the eight reported cases died), making an early diagnosis is desirable.

Asbestos-related benign pleural lesions can involve the parietal pleura (pleural plaques), and/or visceral pleura as focal or diffuse (diffuse pleural thickening) fibrosis. Benign asbestos pleurisy and rounded atelectasis are linked with visceral pachypleuritis, the former as a cause, the latter as a consequence. The prevalence of these lesions, particularly pleural plaques, is very high, reaching 25% in populations of workers exposed intermittently to asbestos. Conventional radiology has a sensitivity less than 50% for detection of plaques, and a specificity less than 85%. Tomodensitometry is today the reference diagnostic tool: availability, cost and irradiation have to be considered before its use in mass screening. Pleural plaques are most often asymptomatic and a functional impairment cannot be proven usually on an individual basis. Visceral pleural thickening is more often accompanied by symptoms (dyspnea, pain) and functional impairment. There is no treatment susceptible to produce a regression of pleural lesions. Asbestos exposure increases the risk of pulmonary and pleural cancers. However there is no evidence of an increased risk in subjects with plaques compared with subjects without plaques but an equivalent asbestos exposure. The cost and the risk of diagnostic procedures induced by the screening, as well as the anxiety provoked by the detection of radiologic abnormalities are to be considered. Finally it is difficult today to justify the screening of benign pleural lesions by arguing an improvement of the life expectancy or of the quality of life of former asbestos exposed workers. It is probable that benefit of a screening will be of a social type, at an individual or a collective level.

The involvement of the apical pleura is infrequent in diffuse pleural thickening secondary to asbestos exposure. Most often diffuse pleural thickening is accompanied by an obliteration of the costophrenic angle and the posterior and paraspinous pleural surfaces of the pleura are involved to the greatest extent. Unlike this typical form, we observed in five patients exposed to asbestos an apical pleural fibrosis, uni or bilateral, accompanied with lung retraction, hilar ascension and tracheal attraction. Apical pleural thickening with upper lobe changes in asbestos-exposed persons should be regarded as due to the asbestos exposure, after exclusion of other causes like tuberculosis and the apex tumors. Usually the evolution of the lesions is slowly progressive over several years or even decade, and results in mild restrictive defect.

The aim of this study was to estimate the evolution of the incidence of mesothelioma in the Loire-Atlantique department since 1956 and to register all the cases diagnosed between 1985 and 1992 and to complete the data of earlier studies carried out between 1956 and 1984. The cases were indexed from the files of the pathology department and also from demographic and occupational data concerning the patients which had been gathered retrospectively from an inquiry of patients attached either to private physicians or to a hospital service. From 1956 to 1984 there were 125 cases (119 men, 6 women) who had been diagnosed; 92 cases were registered between 1985 and 1992 (79 men and 13 women). An increase in the annual number of cases was significant. The incidence during the period 1985-1992 was 10.9 per million inhabitants (men 19.4, women 3) against 8.7 (men 17.2, women 0.8) for the period 1975 to 1984 and 2.6 (men 5.2, women 0.2) for the period 1956-1974. The mean age of the subjects at the time of diagnosis rose during the period studied (59.2 +/- 9.4 between 1956-1974 to 63.1 +/- 11.9 between 1975-1984 and 67.0 +/- 9.7 between 1985-1992). Occupational exposure to asbestos was certain or probable in 85 per cent of cases with a median duration of exposure of 25 years (range 2 months to 48 years) with a median interval between the first exposure to diagnosis of 44 years (range 10-70 years). The industrial sector most often implicated was naval construction (127 cases).(ABSTRACT TRUNCATED AT 250 WORDS)