Myocardial tissue tagging with cardiovascular magnetic resonance

Abstract

Cardiovascular magnetic resonance (CMR) is currently the gold standard for assessing both global and regional myocardial function. New tools for quantifying regional function have been recently developed to characterize early myocardial dysfunction in order to improve the identification and management of individuals at risk for heart failure. Of particular interest is CMR myocardial tagging, a non-invasive technique for assessing regional function that provides a detailed and comprehensive examination of intra-myocardial motion and deformation. Given the current advances in gradient technology, image reconstruction techniques, and data analysis algorithms, CMR myocardial tagging has become the reference modality for evaluating multidimensional strain evolution in the human heart. This review presents an in depth discussion on the current clinical applications of CMR myocardial tagging and the increasingly important role of this technique for assessing subclinical myocardial dysfunction in the setting of a wide variety of myocardial disease processes.

Figure 1

Short axis tagging at the mid ventricular level covering the cardiac cycle (A-F). Tagging is applied upon detection of QRS complex at end diastole (A). Tag lines follow the myocardial deformation during systole (B, C, and D) and relax in diastole (E, F). Fading of tag lines occurs near end diastole (F) due to T1 tissue relaxation.

Figure 2

1.5 and 3T mid ventricular short axis tagging covering the cardiac cycle (F1-F4). Note better tag-tissue contrast and longer tag persistence (F4) on 3T MRI system.

Figure 3

Schematic diagram demonstrating the three dimensional circumferential - radial - longitudinal (RCL) coordinate system used for strain calculation. Normal strains (dark solid arrows) are described with respect to the short axis plane: E_CC represents circumferential shortening tangential to epicardial surface, E_RR represents myocardial thickening radially towards the center of the ventricle and E_LL represents basal to apical shortening along the ventricular long axis.E_RC, E_RL and E_CL (dotted and curved arrows) represent change in angle caused by shear. Torsion represents the wringing motion caused by an apical counterclockwise rotation (curved arrow A) and a basal clockwise rotation (curved arrow B) around the ventricular long axis at end systole. Torsional deformation compensates for the opposing vectors in the subepicardium and subendocardium created by opposing myofiber arrangement in both layers.

Figure 4

Myocardial infarction at the infero-septal region of left ventricle (A-D). Inversion recovery mid ventricular short axis image (A) demonstrates subendocardial delayed enhancement at the infero-septal region of the left ventricle (white arrow) in the distribution of right coronary artery. Corresponding tagged image and strain analysis curves (B & D) demonstrate reduced E_CC at the infarct region (blue curve 1) compared to lateral wall (red curve 2) and adjacent non enhanced myocardium (green curve 3). Color coding (C) of tagged image aids visual assessment of regional dysfunction (dysfunctional infarcted myocardium in green). See additional file 3: Movie 3 for the original data used.

Figure 5

Pulmonary Arterial Hypertension (A-C). Cine gradient echo short axis image (A) showing right ventricular hypertrophy and systolic flattening of the inter-ventricular septum in a 64 year old patient with pulmonary arterial hypertension. Corresponding tagged image (B) and graph (C) show reduced magnitude and delayed RV free wall peak shortening (red curve 1) compared to the septum (green curve 2) and LV lateral wall (blue curve 3).