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Updated: Aug 28, 2025

Imaging of the Microstructural Failure Mechanism in the Human Hip
Published on: September 29, 2023
Cardiac alterations following experimental hip fracture - inflammaging as independent risk factor
Ina Lackner1,2, Birte Weber2,3,4, Jochen Pressmar1,2
1Department of Trauma and Orthopedic Surgery, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nuremberg, Erlangen, Germany.
Insights
Hip fractures cause secondary cardiac injury, especially in older mice. Age-related inflammation exacerbates these cardiac changes, highlighting a critical risk factor in trauma patients.
Area of Science:
- Cardiovascular Research
- Trauma Medicine
- Gerontology
Background:
- Trauma can cause secondary cardiac injuries without direct heart damage.
- Hip fractures are increasing in the elderly, often linked to cardiac events.
- This study investigates hip fracture effects on the heart in young and middle-aged mice.
Purpose of the Study:
- To determine the impact of hip fractures on cardiac function in healthy young and middle-aged mice.
- To investigate age-related differences in cardiac response to hip fracture.
- To explore the role of inflammation and molecular changes in secondary cardiac injury post-hip fracture.
Main Methods:
- Hip fracture or sham surgery in young (12-week) and middle-aged (52-week) female mice.
- Analysis of systemic inflammation and myocardial tissue at 6 and 24 hours post-fracture.
- Utilized multiplex analysis, RT-qPCR, and immunohistochemistry for molecular and structural assessments.
Main Results:
- Hip fracture increased systemic IL-6 and KC levels, more pronounced in middle-aged mice.
- Middle-aged mice exhibited heightened myocardial expression of inflammatory markers (HMGB1, TLR2/4, TNF, IL1β, NLRP3).
- Significant alterations in myocardial metabolism (glucose/fatty acid transporters), calcium handling (SERCA), and structure (desmin, troponin I) were observed in middle-aged mice.
Conclusions:
- Hip fractures induce myocardial alterations in both young and middle-aged mice, potentially leading to secondary cardiac injury.
- Aging and 'inflammaging' act as independent risk factors, worsening cardiac alterations after hip fracture.
- These findings underscore the vulnerability of the aging heart to trauma-induced cardiac complications.
Background:
Cardiac injuries following trauma are associated with a worse clinical outcome. So-called trauma-induced secondary cardiac injuries have been recently described after experimental long bone fracture even in absence of direct heart damage. With the progressive aging of our society, the number of elderly trauma victims rises and therefore the incidence of hip fractures increases. Hip fractures were previously shown to be associated with adverse cardiac events in elderly individuals, which have mainly been attributed to pre-conditioned cardiac diseases. The aim of the present study was to investigate the effect of hip fractures on the heart in healthy young and middle-aged mice.
Materials And Methods:
Young (12-week-old) and middle-aged (52-week-old) female C57BL/6 mice either received an intramedullary stabilized proximal femur fracture or sham treatment. The observation time points included 6 and 24 h. Systemic levels of pro-inflammatory mediators as well as local inflammation and alterations in myocardial structure, metabolism and calcium homeostasis in left ventricular tissue was analyzed following hip fracture by multiplex analysis, RT-qPCR and immunohistochemistry.
Results:
After hip fracture young and middle-aged mice showed increased systemic IL-6 and KC levels, which were significantly elevated in the middle-aged animals. Furthermore, the middle-aged mice showed enhanced myocardial expression of HMGB1, TLR2/4, TNF, IL1β and NLRP3 as well as considerable alterations in the myocardial expression of glucose- and fatty acid transporters (HFABP, GLUT4), calcium homeostasis proteins (SERCA) and cardiac structure proteins (desmin, troponin I) compared to the young animals following hip fracture.
Conclusion:
Young and middle-aged mice showed local myocardial alterations, which might predispose for the development of secondary cardiac injury following hip fracture. Age and the age-associated phenomenon of 'inflammaging' seemed to be an independent risk factor aggravating and accelerating cardiac alterations following hip fracture.
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