SCI impairs heart function due to impaired sympathetic control


Lay summary by Noah Kaiser, Malachy Frey, Chris West

Edited by Jocelyn Chan

This is a lay summary of the original Nature Communications research article by Mary Fossey, Shane Balthazaar, Jordan Squair, Alexandra Williams, Malihe-Sadat Poormasjedi-Meibod, Tom Nightingale, Erin Erskine, Brian Hayes, Mehdi Ahmadian, Garett Jackson, Diana Hunter, Katharine Currie, Teresa Tsang, Matthias Walter, Jonathan Little, Matt Ramer, Andrei Krassiokov, Chris West.

The goal of this study was to describe the upper-body movement patterns during seated boxing and battling rope exercises in individuals with motor-complete spinal cord injury (SCI). Specifically, the researchers looked at trunk muscle activation patterns and upper-body kinematics (motion analysis without considering force). Trunk muscles can generally be thought of as upper-body muscles since the trunk refers to the torso, which contains the chest, abdomen, pelvis and back. Therefore, trunk muscles are very important for both breathing and movement.

Why is this study important?

This study is significant because it demonstrates how and why the heart changes after spinal cord injury (SCI). The findings from this work could help us to design therapies to reduce the risk of cardiovascular disease and improve heart function in individuals with a SCI.

How was the study done and what were the results? 

This paper was split into two separate parts:

Part 1

The research in part one was performed via clinical trials on individuals with SCI and other experimental models. The clinical trials were performed on individuals with a high-level spinal cord injury (SCI). Non-invasive methods were used to image the heart, and the outcome was that there is a gradual drop in left ventricle (LV) structure. The left ventricle is one of the four large chambers of the heart. Specifically, there was no change in the heart structure at 6 months post-SCI but structure was reduced by 2 years post-injury. This highlights a plausible window for intervention within the first 6 months before heart structure starts to change.

In the experimental laboratory studies, invasive as well as non-invasive strategies were used to determine the effects of SCI on the heart. The non-invasive tests produced results similar to the clinical trial, with a gradual reduction of LV structure. The invasive tests showed an immediate reduction of LV function. It was also discovered that there is an immediate reduction in sympathetic neural control. Sympathetic neural control refers to the control of our sympathetic system, which is also known as our fight and flight system.

Part 2

Multiple experiments were devised in part 2 to understand the role that the reduction in sympathetic (SP) neural control has on the decreased cardiac function post-SCI seen in Part 1. To test the role of the SP system in LV function, the rodent models were put under anesthesia while data was assessed at three points, pre-intervention (control), post-SCI, and post-SCI after a receptor-blocking drug was administered. SCI caused a drastic decrease in LV pressure generating capacity (PGC; I.e., heart function) that was not further reduced with the drug. This study provided initial proof that damage to SP nerves is a direct cause of decreased cardiac function after SCI.

To further demonstrate the role of the SP nervous system, the next experiment explored whether a SCI at varying locations could cause a different level of LV impairment. The rodent model cohort was randomized into 3 groups and received one of three procedures: a high-SCI (near complete loss of SP control), a low-SCI (preserves SP control), or no procedure (i.e. control group). They were then monitored for 12 weeks afterwards to collect data using invasive methods. LV PGC, contractility (heartbeat strength), and heart efficiency were lower in the high-SCI group relative to both the low-SCI and control. There was also no notable difference in LV function between the control group and the low-SCI group, where the SP pathways were intact. This further demonstrates that a SCI can impair LV function based on location, which dictates how severely it affects the SP system.

This final experiment was to verify the previous one, as it could be argued that other factors, such as in cage activity, may have differed between rodent models with different levels of injuries. To isolate the SP variable, the high-SCI group was further divided into 2 groups. One group received a drug that preserves descending SP pathways, while the other group did not receive any drugs (i.e. the control group). After 8 weeks their LV function was assessed using invasive methods. LV contractility and PGC were all higher in the group that received the drug. However, there was no difference in the average arterial pressure. This proved once more that a loss in LV function seen in after SCI was caused by damage to the SP system.


This study demonstrated that there is an immediate decrease in cardiac function after a SCI, and a gradual decrease in cardiac structure, which is caused by damage to SP nervous system that controls the LV. This opens the door for future studies to investigate how strategies that target the SP pathways impact heart function following SCI.

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