Lightning Presentation Sydney Spinal Symposium 2026

Cardiovascular Imbalances and Risk Characterisation Using Integrated Technologies following Spinal Cord Injury (CIRCUIT Study) (#138)

Ryan M Dorrian 1 , Nashwa Najib 1 , Ryan O'Hare Doig 1 , Ryan Quarrington 2 , Annabel Sorby-Adams 3 , Hugh McCloskey 1 , Lyndsey Collins-Praino 4 , Anna V Leonard 1 , Jillian Clark 5 , Taha Ali 5 , Marie-claire Seeley 6 , Peter Psaltis 7 , Ashish Diwan 1
  1. SpineLabs, Adelaide University, Adelaide, South Australia, Australia
  2. SpineLabs, Adelaide University, Adelaide, South Australia, Australia
  3. Massachusetts General Hospital, Harvard Medical School, Bostom, MA, USA
  4. Cognitive Ageing and Neurodegenerative Disease Laboratory, Adelaide University, Adelaide, South Australia, Australia
  5. South Australian Spinal Cord Injury Service, Central Adelaide Local Health Network, Adelaide, South Australia, Australia
  6. Rosemary Bryant AO Research Centre, Adelaide University, Adelaide, South Australia, Australia
  7. Cardiology, Royal Adelaide Hospital, Adelaide, South Australia, Australia

Introduction

Individuals with traumatic spinal cord injury (SCI) may experience daily cardiovascular imbalances (CI) that are potentially life-threatening. While long-term consequences are poorly characterised, they may include cognitive decline and increased cardiovascular disease (CVD) risk – a leading cause of death after SCI. As CI typically emerge between 3-6 months post-SCI, early intervention may prevent poor long-term outcomes.

Aim

To identify biological signatures in subacute biospecimens associated with frequent and severe CI, long-term CVD risk, and cognitive decline following SCI.

Method

Adults (18+) with subacute SCI (1-3 months) will be recruited from the Royal Adelaide Hospital. Participants will undergo subacute and yearly biospecimen collection (blood, urine, stool, saliva), autonomic and cognitive assessments, and annual CVD screening over a 5-year follow-up. Cardiovascular autonomic testing will involve 24-hour ambulatory ECG and blood pressure monitoring, and continuous ECG and blood pressure monitoring during deep breathing, Valsalva, and head-up tilt table tests. Cognitive assessment will use the CANTAB battery paired with transcranial Doppler to examine cerebral perfusion. CVD screening will include QRISK3 lifetime risk estimation and blood biochemistry. Echocardiography, carotid-femoral pulse wave velocity, and flow-mediated dilation will examine cardiac function, arterial stiffness, and endothelial function as mechanisms. Subacute biospecimens collected pre-CI development will be examined via multi-omics approach, integrating proteomics, metabolomics, and transcriptomics to extract biological signatures unique to individuals who develop CI, cognitive decline, and high CVD risk.

Hypothesised Results

Individuals with frequent and severe CI will demonstrate greater lifetime CVD risk and cognitive decline due to impaired left ventricle mechanisms, maladaptive vascular remodelling, and impaired cerebral perfusion. Biospecimen analysis will identify biological signatures that distinguish individuals who develop CI and poor long-term outcomes.

Conclusion

By characterising biological signatures of at-risk individuals, this study may facilitate early intervention to alter long-term trajectories of CI, extending lifespan and restoring quality of life following SCI.