Key result
Cardiac MRI-derived global longitudinal strain was reduced in patients with aortic stenosis but did not independently predict all-cause mortality.
Why the study?
The study investigated global longitudinal strain measured by cardiac MRI as a marker of left ventricular decompensation in aortic stenosis and its relationship with myocardial fibrosis, symptoms, remodeling, and clinical outcomes.
Does global longitudinal strain measured by cardiac MRI predict clinical outcomes and correlate with myocardial fibrosis in patients with aortic stenosis?
Cohort (n=200)
No
Does global longitudinal strain measured by cardiac MRI predict clinical outcomes and correlate with myocardial fibrosis in patients with aortic stenosis?
While cardiac MRI-derived GLS correlates with myocardial fibrosis in aortic stenosis, it does not independently predict clinical outcomes beyond established markers.
Answers are grounded in this paper and cite their sources.
CMR GLS correlates with fibrosis in aortic stenosis but lacks specificity and independent prognostic value; leaves open its utility for decompensation assessment.
Purpose To use global longitudinal strain (GLS) as a marker of left ventricular decompensation in aortic stenosis and to investigate the relationship of GLS measured with cardiac MRI with markers of myocardial fibrosis, symptom development, remodeling, and clinical outcomes. Materials and Methods Patients with aortic stenosis and healthy control subjects were assessed. GLS was assessed by using cardiac MRI feature tracking, diffuse fibrosis by T1 mapping, and replacement fibrosis using late gadolinium enhancement. Follow-up was prospective for the primary endpoint of all-cause mortality. Results GLS was reduced in aortic stenosis (n = 159) compared with control subjects (n = 41) (−17.6% ± 3.1 [standard deviation] vs −18.9% ± 2.6, P = .02). GLS demonstrated weak associations with aortic stenosis severity (Vmax; r = 0.24, P = .0005) but showed moderate correlation with T1 mapping measures of myocardial fibrosis (eg, indexed extracellular volume [iECV]; r = 0.43, P < .0001). Moreover, GLS was reduced in patients with midwall fibrosis compared with control subjects (P < .001), although values were similar to those of patients with myocardial infarction (P = .25). In adjusted analyses, GLS was associated with total myocardial fibrosis burden (iECV) and ejection fraction (both P < .001). GLS offered poor discrimination between disease states, inability to distinguish between control subjects and patients (area under the curve [AUC], 0.60), presence or absence of fibrosis (AUC, 0.63), or symptomatic severity (left ventricular decompensation AUC, 0.64). At follow-up (median, 1466 days), 21 patients died. GLS did not independently predict clinical outcomes. Conclusion GLS correlates with established markers of myocardial fibrosis. However, widespread utility of single GLS measurements may be limited by overlap between disease states and its inability to predict clinical outcomes beyond current established markers.
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Spath et al. (2019) conducted a cohort in Aortic stenosis (n=200). Global longitudinal strain (GLS) measured by cardiac MRI vs. Healthy controls / baseline variables was evaluated on All-cause mortality (HR 1.03, 95% CI 0.86-1.22, p=0.8). Cardiac MRI-derived global longitudinal strain was reduced in patients with aortic stenosis but did not independently predict all-cause mortality.
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