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J Am Coll Cardiol, 2005; 46:2223-2228, doi:10.1016/j.jacc.2005.09.015
© 2005 by the American College of Cardiology Foundation
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Magnetic Resonance Imaging Assessment of Ventricular Dyssynchrony

Current and Emerging Concepts

Albert C. Lardo, PhD, FAHA*, Theodore P. Abraham, MD, FACC and David A. Kass, MD

Division of Cardiology, Johns Hopkins University, Baltimore, Maryland



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Figure 1 (A) Temporal series of images demonstrating magnetic resonance imaging myocardial tagging during systole (upper panels) and diastole (lower panels) and (B) an illustration showing the direction of myocardial strains. (C) Individual phases from the cardiac cycle showing the spatial and temporal evolution of three-dimensional circumferential strain for a normal healthy human heart (upper panels) and a patient with severe cardiomyopathy and left bundle branch-type conduction delay (lower panels). Time moves from left (end-diastole) to right (end-systole). During systolic contraction, the spatial and temporal distribution of circumferential strain are visualized by the color changes, where red corresponds to the neutral (end-diastolic) strain, blue is shortening, and yellow is lengthening or stretch. ECC = circumferential strain; ELL = longitudinal strain; ERR = radial strain; LV = left ventricle; RV = right ventricle.

 


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Figure 2 (A) Illustration showing the relationship between local strain and tag frequency for harmonic phase-based strain measurements. The contraction of a tagged fiber in the middle would increase the tagging frequency (density of tag lines) as shown in the top fiber. Stretching causes a reduction in local frequency. (B) Two-dimensional segmentation of the heart and mesh generation (top panel) and regional strain versus time plots over the cardiac cycle; (C) complete regional strain versus time plots over the cardiac cycle for all segments. ECC = circumferential strain.

 


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Figure 3 Comparison of a strain-encoded circumferential strain image (A) and the corresponding phase matched steady-state free precession sequence in a normal healthy volunteer (B). Note the uniform transmural strain gradient at the septum and left ventricular lateral wall.

 


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Figure 4 (A) Schematic model of hearts with delayed segments clustered in one region versus spaced about the myocardium. Depending on how one indexes dyssynchrony, the result could be the same for both situations, despite markedly different impacts on dyssynchrony. (B) Calculation of a vector-dyssynchrony index. Values of regional shortening (strain) or time of peak shortening are determined at various positions in the cross section. These are then multiplied by a unit vector pointing in that direction, and the vectors are summed to generate the net (gray) vector magnitude. Greater net vector magnitude reflects dyssynchrony. (C) Determination of the temporal uniformity of strain or circumferential uniformity ratio estimate index. A measure of wall motion or timing value is plotted versus location. Overall dyssynchrony appears as a sine-wave (analogous to the situation shown at top panel of A). If delays are dispersed through the wall (lower panel of A), the plot appears as the dotted line. By determining the low-frequency content of these plots, one derives the dyssynchrony index.

 


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Figure 5 Representative images illustrating lead artifacts seen in magnetic resonance images.

 




 
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