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Published on: June 14, 2016
Myocardial hypertrophy induces carotid body hyperplasia
Efthimios Sivridis1, Pavlos Pavlidis, Aliki Fiska
1Department of Pathology, Democritus University of Thrace, University General Hospital of Alexandroupolis, Greece.
Insights
Cardiac hypertrophy is linked to enlarged carotid bodies, primarily due to an increase in sustentacular cells. This suggests long-standing hypoxia from cardiopulmonary disease drives carotid body hyperplasia.
Area of Science:
- Cardiovascular Pathology
- Respiratory Physiology
- Cell Biology
Background:
- Carotid bodies (CBs) are known to enlarge in response to chronic cardiopulmonary disease.
- The relationship between cardiac hypertrophy and CB hyperplasia requires further investigation.
Purpose of the Study:
- To determine if cardiac hypertrophy is associated with carotid body (CB) hyperplasia.
- To analyze the cellular changes within CBs in cases of cardiac hypertrophy.
Main Methods:
- Autopsy examination of 15 cases with cardiac hypertrophy and 2 control groups (16 cases).
- Morphometric analysis of CB volume and cellular composition (progenitor, dark, light, sustentacular cells) via serial sections.
- Dissection of carotid bifurcations.
Main Results:
- Significant increase in CB volume and sustentacular cells in individuals with cardiac hypertrophy.
- Sustentacular cell hyperplasia was observed irrespective of drug induction.
- Focal accumulation of dark or light cells was infrequent (3 cases).
Conclusions:
- Generalized sustentacular cell hyperplasia in CBs is likely a response to long-standing hypoxia associated with cardiac hypertrophy.
- Focal increases in dark or light cells may indicate proliferative or metaplastic changes due to short-term hypoxia.
Abstract:
The carotid bodies tend to enlarge after long-standing cardiopulmonary disease. Our objective was to investigate whether cardiac hypertrophy is associated with carotid body hyperplasia. Fifteen autopsy cases with combined left and right ventricular hypertrophy were examined and compared with two control groups (16 cases). The study involved a meticulous dissection of carotid bifurcations, thin serial sections, and morphometric analysis of carotid body volume and cell types (progenitor, dark, light, and sustentacular). There was a significant increase in sustentacular cells in all individuals with cardiac hypertrophy, which was not drug-induced, and accompanied by a similar increase in carotid body volume. Dark or light cell accumulation was detected focally and only in three instances. It appears that the generalized sustentacular cell hyperplasia is the result of long-standing hypoxia, while a superimposed focal prominence of dark or light cells may be proliferative or metaplastic in nature and attributed to short-term hypoxia.
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