Utility of magnetic resonance imaging in the evaluation of left ventricular thickening

Fig. 1. Illustration showing the various types of left ventricular thickening. In a normal heart, the LV wall thickness, septal/lateral wall ratio, LV mass, LV volume, relative wall mass and ejection fraction are normal; in concentric hypertrophy, the wall thickness, LV mass and relative wall mass are increased. While septal/lateral wall ratio is normal, the LV volume is normal or increased and ejection fraction is normal or decreased; in asymmetric hypertrophy, the wall thickness, LV mass and relative wall mass are increased, but the septal/lateral wall ratio is increased. In eccentric hypertrophy, the wall thickness and septal/lateral wall ratio are normal, but LV mass and LV volume are increased, while ejection fraction and relative wall mass are decreased. In concentric remodelling, the relative wall mass is increased, the LV volume is decreased, but septal/lateral wall ratio, wall thickness, LV mass and ejection fraction are normal. In asymmetric remodelling, the relative wall mass is increased and LV volume is decreased. While septal/lateral wall ratio is increased, wall thickness, LV mass and EF are normal

Fig. 2. Flow chart showing the differentiation of various causes of LV thickening

Fig. 3. a Short axis cine-SSFP image in a patient with hypertension shows severe concentric LV hypertrophy with maximal thickness of 2.2 cm in the mid septum in end diastole. b 4-chamber cine SSFP image in another patient with HT shows severe concentric LV hypertrophy. c Coronal T1-weighted image through the upper abdomen after gadolinium administration shows an intensely enhancing mass in the upper abdomen (arrow), consistent with a pheochromocytoma

Fig. 4. a Short axis cine SSFP image through the aortic valve shows thickening of the valve leaflets (arrow) and restricted systolic opening. The valve area was measured to be 0.5 cm2, consistent with severe aortic stenosis. b 3-chamber cine SSFP sequence in the same patient shows restricted systolic opening of the aortic valve and flow acceleration through the aortic valve (straight arrow), consistent with aortic stenosis. Concentric LV hypertrophy is also seen (curved arrow). c Short axis cine SSFP image through the aortic valve shows a unicuspid aortic valve with thickened leaflets (arrows) and restricted opening consistent with aortic stenosis

Fig. 5. a Sagittal volume rendered 3D image in a patient with concentric LV thickening shows severe coarctation of the aortic arch (straight arrow) and multiple collateral vessels(curved arrows). b Velocity encoded phase contrast image in the sagittal plane in another patient shows flow acceleration through the aortic arch at the site of coarctation, which was quantified and the pressure gradient was estimated to be 20 mm Hg

Fig. 6. 3-chamber cine SSFP image shows concentric LV thickening. There is flow acceleration in the LVOT below the level of the aortic valve (straight arrow). There is a linear discrete membrane at the LVOT (curved arrow), which is responsible for the flow acceleration, consistent with a subaortic membrane

Fig. 7. a 4-chamber SSFP image in a patient with cardiac amyloidosis shows concentric LV thickening (straight arrow). There is also thickening of the interatrial septum (curved arrow). b Post contrast T1-w inversion recovery gradient echo image shows diffuse sub-endocardial to mid myocardial LGE of the ventricles (straight arrow), interatrial septum (curved arrow) and the atrial walls (arrowhead). c Short-axis TI scout (Look Locker sequence image) at the level of mid-ventricular septum in a patient with cardiac amyloidosis. At an inversion time of 150 milliseconds, both the blood pool (LV) and myocardium (M) are dark. This is due to diffuse myocardial infiltration with amyloid, which takes up gadolinium and results in T1 shortening

Fig. 8. Short-axis post contrast T1-w inversion recovery gradient echo MRI sequence shows patchy mid myocardial LGE in the basal lateral (straight arrow) in a patient with Anderson Fabry’s disease

Fig. 9. Short-axis post-contrast T1-w inversion recovery gradient echo image shows patchy mid myocardial LGE (arrows) of severely thickened myocardium in a patient with Danon disease

Fig. 10. 3-chamber post contrast T1-w inversion recovery image shows a triple layered pattern of enhancement with an inner layer of dark thrombus (arrowhead), middle layer of LGE due to enhancing fibrous tissue (straight arrow) and an outer layer of dark normal myocardium (curved arrow)

Fig. 11. Short-axis multi-echo gradient echo T2 weighted images obtained at different TEs, shows that the myocardium gets progressively darker with increasing TEs, with complete darkness at TE of 14.2 milliseconds, indicating significant iron deposition

Fig. 12. Short-axis post-contrast T1-w inversion recovery gradient echo image shows mild concentric LV thickening and patchy areas of mid myocardial and subepicardial LGE (arrows) in a patient with cardiac sarcoidosis