Non-ischemic myocardial fibrosis after long-term asbestos exposure

Our plain-English summary of Non-ischemic myocardial fibrosis after long-term asbestos exposure, by A. Kohama, T. Masuyama, M. Hori, et al (Internal Medicine, 1996).

The study

• Authors: A. Kohama, T. Masuyama, M. Hori, J. Tanouchi
• Journal: Internal Medicine
• Published: 1996;35(8):605-10
• Cited by: 1 article, as counted by NIH iCite
• Read it: PubMed · Publisher

Abstract

To determine whether or not myocardial fibrosis in the left ventricle increases after exposure to asbestos fiber, we studied myocardial fibrosis in 42 autopsied hearts; 17 of asbestosis (AS) and 18 of chronic pulmonary disease (CP) without pneumoconiosis. Seven patients with extracardiopulmonary disease were used as a control group (CONT). The extent of myocardial fibrosis in the left ventricle was significantly greater in the AS group compared to the other groups (AS 3.6 +/- 1.3% vs. CP 2.4 +/- 1.0% vs. CONT 1.6 +/- 0.8%). There was a significant difference in the appearance ratio of focal fibrosis between the asbestosis group and the other groups. Focal fibrosis was observed in none of 7 control patients, in 3 of 18 patients with chronic pulmonary disease and in 9 of 17 patients with asbestosis. We concluded that characteristic myocardial fibrosis was observed in humans after long-term asbestos exposure.

In plain English

This Japanese autopsy study compared heart muscle scarring (fibrosis) in 42 hearts: 17 from people with asbestosis, 18 with other chronic lung diseases but no pneumoconiosis, and 7 controls who died of diseases outside the heart and lungs. Most asbestosis patients had worked in asbestos spinning, for 10 to 34 years. Average left-ventricle fibrosis was 3.6% of tissue area in the asbestosis group, 2.4% in the lung disease group and 1.6% in controls. The asbestosis figure was significantly higher than both others. Scattered (focal) fibrosis appeared in 10 of 17 asbestosis patients, 3 of 18 lung disease patients and 0 of 7 controls. No asbestos bodies were found in the asbestosis group's hearts, which the authors said does not rule out asbestos fibers. The authors concluded that left-ventricle fibrosis changes in pattern and amount after long-term asbestos exposure and accompanying respiratory failure, without coronary sclerosis. They suggested asbestos fiber may be one cause. Their stated limitations included no established way to measure percent fibrosis in autopsied hearts, cancer-related wasting in most controls, and studying only asbestosis patients who died of respiratory failure or chronic cor pulmonale.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Autopsy (pathology) comparison of hearts from three patient groups
• Who was studied: 42 autopsied hearts from three groups. 17 were from asbestosis patients (13 males, 4 females, ages 34 to 78, mean 60) who died of respiratory failure and/or chronic cor pulmonale. 18 were from patients with chronic pulmonary disease without pneumoconiosis (16 males, 2 females, mean age 63). 7 were from controls with extra-cardiopulmonary disease (5 males, 2 females, mean age 58). The authors were based in Osaka, Japan. The article does not state the dates of the autopsies.
• Exposure: Occupational asbestos exposure in the asbestosis group. Jobs were spinning (14 patients), asbestos cement (1), electric welding (1), and casting, mining and grinding (1). Exposure lasted 10 to 34 years according to Table 1. Fiber types were not specified.
• Main results:
  • Percent fibrosis in the left ventricle (mean, with standard deviation) was 3.6 (1.3)% in the asbestosis group, 2.4 (1.0)% in the chronic pulmonary disease group and 1.6 (0.8)% in the control group.
  • Left-ventricle percent fibrosis was significantly greater in the asbestosis group than in the chronic pulmonary disease group (p less than 0.01).
  • In the right ventricle and the ventricular septum, percent fibrosis was significantly greater in the asbestosis group than in the control group. It was only slightly greater than in the chronic pulmonary disease group, and that difference was not statistically significant.
  • Focal fibrosis was found in none of 7 control patients, 3 of 18 chronic pulmonary disease patients and 10 of 17 asbestosis patients. The difference between the asbestosis group and the control group was reported as significant.
  • Heart muscle fiber diameter was larger in both the asbestosis and chronic pulmonary disease groups than in controls. It did not differ between the asbestosis and chronic pulmonary disease groups.
  • No asbestos bodies were found in any heart specimen from the asbestosis group. The authors said this does not necessarily mean asbestos fibers were completely absent.
• The authors' conclusion: The authors concluded that the pattern of distribution and the amount of collagen fiber in the left ventricle change after long-term exposure to asbestos fiber and also after concomitant respiratory failure, without coronary sclerosis. They supposed asbestos fiber may be one of the causes of the myocardial fibrosis.
• Limitations the authors state:
  • There is no established method for measuring percent fibrosis in autopsied hearts.
  • Most control subjects were cachectic (wasted) because of cancer, and it is unknown whether cachexia causes less myocardial fibrosis.
  • Only hearts of asbestosis patients who died of respiratory failure and/or chronic cor pulmonale were examined.
  • Lung fibrosis was not measured quantitatively, so it could not be correlated with myocardial fibrosis.
  • The presence of asbestos fibers in the heart specimens was not confirmed. The authors said electron microscopy studies are needed.

Topics

The National Library of Medicine indexes this study under subjects our site covers: Asbestosis.

Medical terms in this study, explained in our Lexicon: Fibrosis, Asbestos Exposure, Pneumoconiosis.

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