The heart-bone connection: relationships between myocardial infarction and osteoporotic fracture
Priscilla M Tjandra1,2, Crystal M Ripplinger2,3, Blaine A Christiansen2,4
1Department of Orthopaedic Surgery, University of California San Francisco, San Francisco, California, United States.
Insights
Myocardial infarction (MI) and osteoporotic fractures (Fx) are linked. This review explores how MI impacts bone health and how Fx affects the heart, suggesting shared mechanisms influence both conditions.
Area of Science:
- Cardiovascular Medicine
- Orthopedics
- Immunology
Background:
- Myocardial infarction (MI) and osteoporotic fractures (Fx) are leading causes of mortality and morbidity.
- Epidemiological data suggest a link between MI and Fx incidence, challenging their independent treatment.
- Shared pathoetiology exists between atherosclerotic cardiovascular disease and osteoporosis.
Purpose of the Study:
- To investigate the potential influence of MI on bone health and Fx on cardiovascular health.
- To explore shared underlying mechanisms, including systemic inflammation, sympathetic nervous system (SNS), and complement system activation.
- To determine the significance of bone-heart cross-talk in comorbidities following MI or Fx.
Main Methods:
- Review of current literature on bone loss post-MI.
- Review of current literature on cardiovascular damage post-Fx.
- Analysis of shared pathoetiological mechanisms and systemic responses.
Main Results:
- MI can trigger systemic responses (SNS, complement) affecting bone remodeling via osteoclasts.
- Fx can induce systemic responses (SNS, complement) leading to cardiac damage and atherosclerosis.
- Sustained systemic inflammation post-trauma exacerbates underlying chronic conditions.
Conclusions:
- MI and Fx may actively influence each other's risk through systemic effects.
- Bone-heart cross-talk represents a significant factor in the comorbidity of MI and Fx.
- Understanding shared mechanisms is crucial for managing these prevalent conditions.
Abstract:
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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