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Magnetic Resonance Derived Myocardial Strain Assessment Using Feature Tracking
Published on: February 12, 2011
Layer-Specific Strain Analysis in Patients with Dilated Cardiomyopathy
Despina-Manuela Toader1, Alina Paraschiv2, Georgică Târtea3,4
1EuroEchoLab, Craiova Cardiology Center, Emergency Hospital Craiova, 200642 Craiova, Romania.
Insights
Layer-specific strain analysis in dilated cardiomyopathy can predict cardiac mortality. Circumferential strain at the endocardium (CSPMend) is a key indicator for identifying patients at higher risk of death within two years.
Area of Science:
- Cardiology
- Echocardiography
- Cardiac Imaging
Background:
- Dilated cardiomyopathy (DCM) is a significant cause of heart failure.
- Etiology of DCM (ischemic vs. non-ischemic) influences disease presentation.
- Predicting cardiac mortality in DCM patients with heart failure decompensation is crucial.
Purpose of the Study:
- To evaluate layer-specific strain in DCM based on etiology.
- To determine if longitudinal and circumferential layer strain predict cardiac mortality in DCM patients.
- To assess the prognostic value of strain parameters in a two-year follow-up.
Main Methods:
- Recruited 97 DCM patients (LVEF ≤ 40%), divided by ischemic (n=51) and non-ischemic (n=46) etiologies.
- Performed conventional and 2D speckle-tracking echocardiography (2D-STE) during compensated heart failure.
- Assessed layer-specific longitudinal and circumferential strain (endocardium, mid-myocardium, epicardium) and calculated gradients.
Main Results:
- Non-ischemic DCM patients showed lower global and layer strain than ischemic patients.
- Decreased GLS, GLSend, GLSend-GLSepi, CSPMend, CSPMend-CSPMepi, CSAP, CSAPend, and CSAPend-CSAPepi were observed in non-survivors.
- Multivariate analysis identified CSPMend as an independent predictor of two-year mortality; a cut-off of -10.8% showed 80% sensitivity and 61.05% specificity.
Conclusions:
- Layer-specific strain analysis revealed reduced values in non-ischemic DCM and in non-survivors.
- Circumferential strain at the endocardium (CSPMend) emerged as the most sensitive parameter for predicting mortality risk in DCM patients.
Background/Objectives:
This study aimed to evaluate layer-specific strain according to etiology and assess whether subtle changes in longitudinal and circumferential layer strain are involved in predicting cardiac mortality during a two-year follow-up in patients with dilated cardiomyopathy admitted with heart failure decompensation.
Methods:
97 patients with dilated cardiomyopathy and a left ventricle ejection fraction ≤ 40% were recruited, 51 with ischemic and 46 with nonischemic etiologies. Conventional and two-dimensional speckle-tracking echocardiography (2D-STE) were conducted in dilated cardiomyopathy patients with a compensated phase of heart failure before discharge. Layer-specific longitudinal and circumferential strain was assessed from the endocardium, mid-myocardium, and epicardium by two-dimensional (2D) speckle-tracking echocardiography. The gradient between the endocardium and epicardium was calculated.
Results:
Patients with nonischemic etiology of dilated cardiomyopathy presented smaller values of global and layer strain than patients in the ischemic group. GLS, GLSend, GLSend-GLSepi, CSPMend, CSPMend-CSPMepi, CSAP, CSAPend, and CSAPend-CSAPepi were the parameters with statistically significant decreased values in non-survivors compared with survivors. In multivariate analysis, only CSPMend showed an independent value in predicting mortality at two-year follow-up. Receiver operator curve analysis provided CSPMend of -10.8% as a cut-off value with a sensitivity of 80% and specificity of 61.05% in identifying the dilated cardiomyopathy and heart failure patients with a risk of death at two-year follow-up.
Conclusions:
GLS, GCS, and layer-specific strain analysis showed decreased values in nonischemic compared with ischemic dilated cardiomyopathy and also in non-survivors compared with survivors. CSPMend was the most sensitive strain parameter to identify patients with increased mortality risk at two-year follow-up.
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