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Spinal cord injury-induced cardiomyocyte atrophy and impaired cardiac function are severity dependent
Jordan W Squair1,2, Jie Liu1, Wolfram Tetzlaff1,3,4
1International Collaboration of Repair Discoveries (ICORD), University of British Columbia, Vancouver, BC, Canada.
Insights
Severe spinal cord injury (SCI) causes cardiomyocyte atrophy and impaired cardiac function, unlike moderate SCI. This study reveals how SCI severity impacts heart mechanics and cardiomyocyte structure.
Area of Science:
- Cardiovascular Physiology
- Neuroscience
- Regenerative Medicine
Background:
- Spinal cord injury (SCI) can impact cardiovascular health, but the relationship between injury severity and cardiac function is not fully understood.
- Left ventricular (LV) mechanics and cardiomyocyte structure are crucial for maintaining cardiac output.
- Previous research has not clearly delineated how varying degrees of SCI affect cardiac parameters.
Purpose of the Study:
- To investigate the effect of SCI severity on left ventricular (LV) mechanics, cardiac function, and cardiomyocyte morphology.
- To determine if moderate versus severe spinal cord contusions elicit different cardiac responses.
- To establish the correlation between structural cardiomyocyte changes and LV function post-SCI.
Main Methods:
- Experimental SCI was induced in Wistar rats using T3 spinal cord contusions of moderate (200 kdyn) and severe (400 kdyn) intensity, alongside a SHAM group.
- In vivo cardiac function and deformation (radial strain) were assessed using standard echocardiography and speckle tracking analyses.
- Ex vivo analysis examined structural changes in cardiomyocytes, including length, width, and length/width ratio.
Main Results:
- Severe SCI led to a significant reduction in LV chamber size and systolic radial strain compared to pre-injury levels.
- Cardiomyocytes in severe SCI rats exhibited atrophy, characterized by decreased length and width, and an increased length/width ratio.
- Moderate SCI did not result in any significant changes in LV mechanics, cardiac function, or cardiomyocyte structure compared to the SHAM group.
Conclusions:
- The severity of spinal cord injury is a critical determinant of cardiac remodeling and functional impairment.
- Severe SCI induces cardiomyocyte atrophy and alters LV mechanics, directly correlating with reduced cardiac function.
- These findings highlight a direct link between SCI severity, cardiomyocyte structural integrity, and impaired left ventricular performance.
New Findings:
What is the central question of this study? How does the severity of spinal cord injury affect left ventricular mechanics, function and the underlying cardiomyocyte morphology? What is the main finding and its importance? Here, we show that severe, but not moderate, spinal cord injury causes cardiomyocyte atrophy, altered left ventricular mechanics and impaired cardiac function. The principal aim of the present study was to assess how the severity of spinal cord injury (SCI) affects left ventricular (LV) mechanics, function and underlying cardiomyocyte morphology. Here, we used different severities of T3 spinal cord contusions (MODERATE, 200 kdyn contusion; SEVERE, 400 kdyn contusion; SHAM) and combined standard echocardiography with speckle tracking analyses to investigate in vivo cardiac function and deformation (contractility) after experimental SCI in the Wistar rat. In addition, we investigated changes in the intrinsic structure of cardiac myocytes ex vivo. We demonstrate that SEVERE SCI induces a characteristic decline in LV chamber size and a reduction in in vivo LV deformation (i.e. radial strain) throughout the entire systolic portion of the cardiac cycle [25.6 ± 3.0 versus 44.5 ± 8.1% (Pre-injury); P = 0.0029]. SEVERE SCI also caused structural changes in cardiomyocytes, including decreased length [115.6 ± 7.63 versus 125.8 ± 6.75 μm (SHAM); P = 0.0458], decreased width [7.78 ± 0.71 versus 10.78 ± 1.08 μm (SHAM); P = 0.0015] and an increase in the length/width ratio [14.88 ± 0.66 versus 11.74 ± 0.89 (SHAM); P = 0.0018], which was significantly correlated with LV flow-generating capacity after SCI (i.e. stroke volume, R2 = 0.659; P = 0.0013). Rats with MODERATE SCI exhibited no changes in any metric versus SHAM. This is the first study to demonstrate that the severity of SCI determines the course of changes in the intrinsic structure of cardiomyocytes, which are directly related to contractile function of the LV.
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