Factors influencing the end-diastolic vortex assessed by using vector flow mapping
Xiaoxia Zhang1, Jun Niu2, Ling Wu1
1Postgraduate Training Base of Jinzhou Medical University, PLA 967th Hospital, Dalian, China.
Insights
Late diastolic vortex formation in the left ventricle (LV) is influenced by filling patterns and heart rate. Atrial contraction may enhance this vortex, improving diastolic-systolic coupling, especially in enlarged ventricles.
Area of Science:
- Cardiovascular Physiology
- Cardiac Imaging
- Hemodynamics
Background:
- The end-diastolic vortex plays a crucial role in left ventricular (LV) diastolic function.
- Understanding factors influencing vortex dynamics is key to assessing cardiac health.
Purpose of the Study:
- To investigate the determinants of the late diastolic vortex in normal and abnormal ventricles.
- To analyze the relationship between vortex characteristics and hemodynamic parameters.
Main Methods:
- Vector flow mapping analysis of Color Doppler data from the LV apical long-axis view.
- Study included 57 patients with coronary artery disease, 57 with dilated cardiomyopathy, and 53 healthy volunteers.
Main Results:
- In healthy individuals, vortex area and flux correlated with transmitral A velocity and heart rate.
- Transmitral A velocity and heart rate were independent predictors of vortex flux.
- LV size influenced vortex dynamics in patients with LV dysfunction and enlargement.
Conclusions:
- Late LV filling significantly impacts end-diastolic vortex formation.
- Compensatory atrial contraction can enhance the end-diastolic vortex, aiding diastolic-systolic coupling.
- LV size is a critical factor affecting the end-diastolic vortex in pathological conditions.
Objectives:
The purpose of this study was to assess the factors influencing the late diastolic vortex in normal and abnormal ventricles.
Methods:
Color Doppler data in left ventricle (LV) were acquired from apical long-axis view and analyzed using vector flow mapping in 57 patients with coronary artery disease, 57 patients with dilated cardiomyopathy, and 53 healthy volunteers.
Results:
In normals, corrected area and flux of the end-diastolic vortex were positively correlated with transmitral A velocity and heart rate. Subjects with E/A <1 had higher vortex flux than those with E/A >1. Heart rate was the only independent predictor of corrected vortex area (R2 = .170, P = .004), and transmitral A velocity and heart rate were the independent predictors of corrected vortex flux (R2 = .490, P < .001). Patients with various mitral filling patterns showed significant differences in vortex area and flux. The vortex area and flux were positively correlated with transmitral i velocity and a'. Transmitral A velocity was the only independent predictor of corrected vortex area (R2 = .180, P < .001), while transmitral A velocity, heart rate, LV end-systolic short diameter, and end-diastolic long diameter were the independent determinants of corrected vortex flux (R2 = .593, P < .001).
Conclusions:
The end-diastolic vortex is formed and mainly affected by the late LV filling. The compensatory atrial contraction may enhance the end-diastolic vortex that facilitates coupling between diastole and systole. LV size can influence the end-diastolic vortex in patients with LV dysfunction and enlargement.
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