The Pathology of Cor Pulmonale

Our plain-English summary of The Pathology of Cor Pulmonale, by G.W.H. Schepers (1957).

The study

• Author: G.W.H. Schepers
• Published: Transactions of the American College of Cardiology, Volume 7. (1957)
• Type of article: Journal article
• Our copy: from Johns-Manville's own medical library. The article is still under copyright, so we describe it here rather than post it.

In plain English

This 1957 article reviewed the pathology of cor pulmonale, a strain on the right side of the heart linked to impaired lung circulation. It reported no new patient study, drawing instead on published autopsy, clinical and experimental work. The author argued the apparent rise in cor pulmonale might partly reflect better diagnosis but was probably also real. The author proposed classifying it by onset, by cause (in the lung itself, in heart valve or muscle disease, or elsewhere in the body), and by three anatomical stages. Emphysema and bronchitis were described as the dominant causes, with dust diseases (pneumoconioses) more important in industrial communities. For asbestosis, the author described diffuse scarring engulfing lung blood vessels; growth of vein-wall outer layers and elastic fibers, often with asbestos bodies nearby; capillary overgrowth; and, in advanced cases, pleural thickening and mediastinal adhesions limiting backup circulation. The author noted that pathologists' criteria were subjective and based on end-stage cases. The author concluded that much remained unknown. The author also expected earlier diagnosis and treatment of chronic bronchitis, emphysema and the pneumoconioses to reduce 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: Narrative review of the pathology of cor pulmonale (no new patient data)
• Who was studied: No study population of its own; the article reviewed published autopsy, clinical and experimental (animal) literature on cor pulmonale
• Exposure: Causes of cor pulmonale in general, including emphysema, bronchitis, tuberculosis and pneumoconioses (silicosis, anthracosilicosis, berylliosis, asbestosis). For asbestosis, the article said extensive parts of the lung may be diffusely fibrosed, with blood vessels incorporated in scar tissue.
• Main results:
  • The author stated that the apparently increasing prevalence of cor pulmonale may be partly illusory because of better diagnosis, but is probably real to a material degree
  • The author described emphysema (with bronchitis) as a dominant cause, and said cor pulmonale is more likely in industrial communities where pneumoconioses are more prevalent
  • The author proposed classifying chronic cor pulmonale by type (primary, secondary, tertiary) and into at least three anatomical stages
  • The author described secondary cor pulmonale as arising from many kinds of heart disease (right-sided heart disease mediated via the lung through valvular or myocardial disease)
  • The author described a tertiary (miscellaneous) group of cor pulmonale that originates in structures outside the lungs, such as pulmonary embolism from thrombosed veins elsewhere in the body
  • The author wrote that inhaled dusts with a high percentage of free silica provoke inflammation and fibrosis around lung arteries, making cor pulmonale a logical sequel to prolonged inhalation
  • The author stated that pneumoconiosis alone appears to be the less important factor, with complicating emphysema or concomitant lung infection playing a major role
  • In asbestosis, the author described growth of the outer layer (adventitia) and elastic fibers of lung veins, with asbestos bodies often demonstrable in these zones
  • The author listed asbestosis among pneumoconioses showing hyperplasia of the capillaries in the alveolar walls, which the author said reduces effective oxygenation
  • The author stated that in advanced asbestosis, marked pleural thickening and mediastinal adhesions reduce the opportunity for collateral circulation, further burdening the lung circulation
• The authors' conclusion: The author concluded that much more needs to be discovered about the pathology of cor pulmonale. The author stated that earlier diagnosis and treatment of chronic bronchitis, emphysema and the pneumoconioses, which the author called probably preventable or capable of amelioration, would prove effective in reducing its prevalence or effects. The author also said research should be concentrated on emphysema.
• Limitations the authors state:
  • The author noted that pathologists' anatomical criteria are based mostly on end-stage disease
  • The author noted that subjective factors largely determine what pathologists report, contributing to disagreement between institutions
  • The author noted that most experimental information comes from cats and dogs, whose cardiopulmonary circulation may not be fully comparable to humans'

Topics

Medical terms in this study, explained in our Lexicon: Pathology, Cor Pulmonale, Autopsy, Emphysema, Asbestos Bodies, Pleural Thickening.

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