Heart disease is common in humans and chimpanzees, but is caused by different pathological processes

Heart disease is common in both humans and chimpanzees, manifesting typically as sudden cardiac arrest or progressive heart failure. Surprisingly, although chimpanzees are our closest evolutionary relatives, the major cause of heart disease is different in the two species. Histopathology data of aff...

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Veröffentlicht in:Evolutionary applications 2009-02, Vol.2 (1), p.101-112
Hauptverfasser: Varki, Nissi, Anderson, Dan, Herndon, James G, Pham, Tho, Gregg, Christopher J, Cheriyan, Monica, Murphy, James, Strobert, Elizabeth, Fritz, Jo, Else, James G, Varki, Ajit
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Sprache:eng
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Zusammenfassung:Heart disease is common in both humans and chimpanzees, manifesting typically as sudden cardiac arrest or progressive heart failure. Surprisingly, although chimpanzees are our closest evolutionary relatives, the major cause of heart disease is different in the two species. Histopathology data of affected chimpanzee hearts from two primate centers, and analysis of literature indicate that sudden death in chimpanzees (and in gorillas and orangutans) is commonly associated with diffuse interstitial myocardial fibrosis of unknown cause. In contrast, most human heart disease results from coronary artery atherosclerosis, which occludes myocardial blood supply, causing ischemic damage. The typical myocardial infarction of humans due to coronary artery thrombosis is rare in these apes, despite their human-like coronary-risk-prone blood lipid profiles. Instead, chimpanzee 'heart attacks' are likely due to arrythmias triggered by myocardial fibrosis. Why do humans not often suffer from the fibrotic heart disease so common in our closest evolutionary cousins? Conversely, why do chimpanzees not have the kind of heart disease so common in humans? The answers could be of value to medical care, as well as to understanding human evolution. A preliminary attempt is made to explore possibilities at the histological level, with a focus on glycosylation changes.
ISSN:1752-4571
1752-4571
DOI:10.1111/j.1752-4571.2008.00064.x