心肌梗塞
心脏病学
内科学
医学
心力衰竭
炎症
骨折
骨质疏松症
放射科
作者
Priscilla M. Tjandra,Crystal M. Ripplinger,Blaine A. Christiansen
出处
期刊:American Journal of Physiology-heart and Circulatory Physiology
[American Physiological Society]
日期:2024-02-02
卷期号:326 (3): H845-H856
被引量:2
标识
DOI:10.1152/ajpheart.00576.2023
摘要
Myocardial infarction (MI) and osteoporotic fracture (Fx) are two of the leading causes of mortality and morbidity worldwide. Although these traumatic injuries are treated as if they are independent, there is epidemiological evidence linking the incidence of Fx and MI, thus raising the question of whether each of these events can actively influence the risk of the other. Atherosclerotic cardiovascular disease and osteoporosis, the chronic conditions leading to MI and Fx, are known to have shared pathoetiology. Furthermore, sustained systemic inflammation after traumas such as MI and Fx has been shown to exacerbate both underlying chronic conditions. However, the effects of MI and Fx outside their own system have not been well studied. The sympathetic nervous system (SNS) and the complement system initiate a systemic response after MI that could lead to subsequent changes in bone remodeling through osteoclasts. Similarly, SNS and complement system activation following fracture could lead to heart tissue damage and exacerbate atherosclerosis. To determine whether damaging bone-heart cross talk may be important comorbidity following Fx or MI, this review details the current understanding of bone loss after MI, cardiovascular damage after Fx, and possible shared underlying mechanisms of these processes.
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