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Early Assessment of Left Ventricular Function by Layer-Specific Strain and Its Relationship to Pulsatile Arterial
Jing Shi1, Yumeng Xing1, Juying Qian2
1Department of Echocardiography, Zhongshan Hospital of Fudan University, Shanghai Institute of Medical Imaging, Shanghai Institute of Cardiovascular Diseases.
Insights
Patients with coronary slow flow (CSF) exhibit impaired left ventricular (LV) systolic function, particularly in the endocardium and mid-myocardium layers. Increased arterial load, indicated by lower arterial compliance, is linked to this reduced LV contractility in CSF patients.
Area of Science:
- Cardiology
- Cardiovascular Physiology
- Medical Imaging
Background:
- Controversy exists regarding left ventricular (LV) function impairment in patients with coronary slow flow (CSF).
- Increased arterial load may negatively impact coronary anatomy and LV function.
- Layer-specific strain analysis offers a novel approach to assess LV contractility.
Purpose of the Study:
- To investigate LV systolic function using layer-specific strain technology in patients with CSF.
- To assess the association between pulsatile arterial load and LV contractility in CSF.
- To explore the relationship between layer-specific strain and coronary microvascular function markers.
Main Methods:
- Utilized two-dimensional speckle tracking imaging (2D-STI) to assess layer-specific global longitudinal strain (GLS) (endocardium, mid-myocardium, epicardium).
- Measured indexed arterial compliance (ACI) to estimate pulsatile arterial load.
- Included 70 patients with CSF and 50 controls; correlated strain parameters with coronary artery disease severity (number of affected arteries, thrombolysis in myocardial infarction frame count).
Main Results:
- Layer-specific GLS was significantly reduced in the endocardium and mid-myocardium of CSF patients compared to controls.
- Layer-specific longitudinal strain correlated with the number of affected coronary arteries and thrombolysis in myocardial infarction frame count.
- Patients with CSF had lower indexed arterial compliance (ACI), which negatively correlated with layer-specific GLS.
Conclusions:
- Layer-specific LV evaluation reveals impaired longitudinal function in CSF patients, particularly in inner myocardial layers.
- Increased pulsatile arterial load, indicated by lower ACI, is associated with worse LV longitudinal function in CSF.
- This study highlights the utility of layer-specific strain analysis in understanding LV pathophysiology in coronary slow flow.
Abstract:
Previous studies reported a controversial left ventricular (LV) function impairment and pathophysiology in patients with coronary slow flow (CSF). Greater arterial load has been shown to increase aortic impedance and endothelial shear stress, potentially affecting coronary anatomy and function. We investigated LV systolic function by a new layer-specific strain technology and assessed the association between pulsatile arterial load and contractility.A total of 70 patients with CSF and 50 controls with normal coronary angiography were included in the study. Layer-specific longitudinal and circumferential strains were assessed from endocardium, mid-myocardium, and epicardium (global longitudinal strain (GLS)-endo, GLS-mid, GLS-epi and GCS-endo, GCS-mid, GCS-epi) by two-dimensional speckle tracking imaging (2D-STI). Pulsatile arterial load was estimated by indexed arterial compliance (ACI). Layer-specific GLS showed a decreasing gradient from the endocardium to the epicardium in both the controls and CSF group. GLS-endo and GLS-mid in the CSF group were significantly lower than the control group (all P < 0.05). Layer-specific longitudinal strain showed a good correlation with the number of affected coronary arteries (all P < 0.05) and the mean thrombolysis in the myocardial infarction frame count (TFC) (all P < 0.05). ACI was lower in patients with CSF (P = 0.005), and ACI was correlated negatively with layer-specific GLS (all P < 0.05).Layer-specific evaluation of the LV provides an understanding of the layer-specific properties of the LV wall and the possible process of the LV impairment in patients with CSF. Greater pulsatile arterial load, as manifested by a lower ACI, is coupled with worse LV longitudinal function in patients with CSF.
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