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Author Spotlight: Evaluating Traditional Chinese Therapy for Ankylosing Spondylitis in Mice
Published on: October 27, 2023
Left Ventricular Systolic Myocardial Function in Ankylosing Spondylitis
Helga Midtbø1, Anne G Semb2, Knut Matre3
1Haukeland University Hospital, Bergen, Norway.
Patients with ankylosing spondylitis (AS) show subclinical myocardial dysfunction, indicated by lower global longitudinal strain (GLS), independent of cardiovascular disease risk factors. This dysfunction is linked to aortic root diameter in AS patients.
Area of Science:
- Cardiology
- Rheumatology
- Medical Imaging
Background:
- Subclinical left ventricular (LV) myocardial dysfunction is a known cardiovascular disease (CVD) risk factor.
- The presence of subclinical LV dysfunction in ankylosing spondylitis (AS) patients, independent of traditional CVD risk factors, remains unclear.
Purpose of the Study:
- To investigate whether patients with ankylosing spondylitis (AS) exhibit subclinical left ventricular (LV) myocardial dysfunction.
- To determine if this dysfunction is independent of common cardiovascular disease (CVD) risk factors.
Main Methods:
- 106 patients with AS and 106 matched controls underwent conventional and speckle tracking echocardiography.
- Left ventricular (LV) systolic myocardial function was evaluated using peak systolic global longitudinal strain (GLS).
Main Results:
- Global longitudinal strain (GLS) was significantly lower in patients with AS compared to controls (-17.7 ± 2.5% vs. -18.4 ± 2.3%, P = 0.03).
- Ankylosing spondylitis (AS) was independently associated with lower GLS, even after adjusting for cardiovascular disease (CVD) risk factors.
- In AS patients, lower GLS correlated with a larger aortic root diameter (β = 0.24, P = 0.02).
Conclusions:
- Patients with ankylosing spondylitis (AS) demonstrate impaired left ventricular (LV) systolic function (lower GLS) compared to controls, independent of confounders.
- Lower GLS in AS patients is associated with aortic root dilation.
- Further research is needed to confirm if this subclinical dysfunction contributes to the elevated CVD risk observed in AS.
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