Spinal Cord Injury Causes Systolic Dysfunction and Cardiomyocyte Atrophy

JOURNAL OF NEUROTRAUMA, 2018 · DOI: 10.1089/neu.2017.4984 · Published: February 1, 2018

Simple Explanation

Spinal cord injury (SCI) can lead to heart problems, specifically affecting the heart's ability to pump blood effectively (systolic dysfunction). This study aimed to determine if this dysfunction is directly caused by SCI, independent of other factors. The researchers used a rat model of SCI and found that SCI does indeed impair the heart's systolic function, regardless of loading conditions. This means the heart's pumping ability is weakened even when accounting for changes in blood volume and pressure. The study also found that the heart muscle cells (cardiomyocytes) in SCI rats were smaller, and there were changes in the heart's extracellular matrix, suggesting structural changes contribute to the dysfunction. The loss of sympathetic control of the heart due to SCI appears to be a key factor.

Study Duration

5 weeks

Participants

24 male Wistar rats

Evidence Level

Not specified

Key Findings

1
SCI impairs systolic function independent of loading conditions, as evidenced by a significant reduction in end-systolic elastance.
2
SCI leads to cardiomyocyte atrophy, with reductions in both the width and length of the cells, and alterations in the left ventricular extracellular matrix.
3
The reduction in the rate of LV pressure rise (dP/dtmax) can be offset by beta-adrenergic stimulation, implicating the loss of descending sympatho-excitatory control as a cause of LV dysfunction.

Research Summary

This study investigates the impact of spinal cord injury (SCI) on cardiac function in a rat model, focusing on load-independent systolic dysfunction and changes in cardiomyocytes. The key findings reveal that SCI impairs systolic function regardless of loading conditions, induces cardiomyocyte atrophy, and affects the left ventricular extracellular matrix. The study highlights the role of sympathetic control in maintaining cardiac inotropy and suggests that therapies targeting the preservation of descending sympathetic pathways are needed to prevent cardiac dysfunction after SCI.

Practical Implications

Therapeutic Targets

Future therapies should focus on preserving descending sympathetic pathways to prevent cardiac contractile dysfunction post-SCI.

Rehabilitation Strategies

Rehabilitation strategies need to normalize ventricular filling and address other aspects of cardiac dysfunction after SCI to prevent early heart disease.

Clinical Practice

PV relationships can aid diagnosis and provide novel mechanistic understanding in the setting of heart failure with preserved ejection has shown that PV relationships can aid diagnosis and provide novel mechanistic understanding.

Study Limitations

1
The exact mechanism causing impaired contractile function remains to be elucidated.
2
The causal relationship with respect to the relative temporal changes in LV contractility and myocyte/matrix remodeling is not conclusively demonstrated.
3
The study did not seek to investigate the temporal response of contractile indices.

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