Validation of in vivo myocardial strain measurement by magnetic resonance tagging with sonomicrometry.

OBJECTIVES: This study was designed to validate strain measurements obtained using magnetic resonance tagging with spatial modulation of magnetization (SPAMM). We compared circumferential segment shortening measurements (%S) obtained using SPAMM to sonomicrometry %S in a canine model with (n = 28) and without (n = 3) coronary artery ligation. BACKGROUND: Magnetic resonance tagging enables noninvasive measurement of myocardial strain, but such strain measurements have not yet been validated in vivo. METHODS: Circumferential sonomicrometry crystal pairs were placed in apical myocardium at ischemic risk in ligation studies and in adjacent and remote myocardium. The %S was obtained from closely juxtaposed sonomicrometry and SPAMM sites. RESULTS: Paired data were available from 19 of 31 studies. Both methods distinguished remote from ischemic function effectively (p = 0.014 for SPAMM and p = 0.002 for sonomicrometry). SPAMM %S was similar to sonomicrometry %S in ischemic myocardium (2 +/- 3 vs. 0 +/- 3 p = 0.067) but was slightly higher than sonomicrometry %S in remote myocardium (11 +/- 10 vs. 7 +/- 5, p = 0.033). End-systolic (n = 30) and late systolic (n = 34) SPAMM %S correlated well with sonomicrometry %S (r = 0.84, p < 0.0001 and r = 0.88, p < 0.0001). CONCLUSIONS: Magnetic resonance tagging using SPAMM can quantitate myocardial strain in ischemic and remote myocardium. This study validates its application in scientific investigation and clinical assessment of patients with myocardial ischemia.

Intramural myocardial shortening in hypertensive left ventricular hypertrophy with normal pump function.

BACKGROUND: In hypertensive left ventricular hypertrophy (LVH), intrinsic myocardial systolic function may be normal or depressed. Magnetic resonance tagging can depict intramural myocardial shortening in vivo. METHODS AND RESULTS: Tagged left ventricular magnetic resonance images were obtained in 30 hypertensive subjects with LVH (mean LV mass index, 142 +/- 41 g/m) and normal ejection fraction (mean, 64 +/- 9%) using spatial modulation of magnetization. In 26 subjects, circumferential myocardial shortening (%S) was compared with results obtained in 10 normal subjects at endocardium, midwall, and epicardium on up to 4 short-axis slices each. Similarly, in 10 subjects, midwall long-axis shortening at basal, midventricular, and apical sites was compared with results obtained in 12 normal volunteers. Circumferential %S was reduced in hypertensive subjects. Mean shortening was 29 +/- 6% at the endocardium in hypertensive subjects versus 44 +/- 6% in normal subjects (P = .0001); 20 +/- 6% at the midwall versus 30 +/- 6% (P = .0001); and 13 +/- 5% at the epicardium versus 21 +/- 5% (P = .0002). However, the transmural gradient in percent shortening from endocardium to epicardium in hypertensive subjects paralleled that in normal subjects. The normal base-to-apex gradient in circumferential %S was absent in LVH. In contrast to normal subjects, circumferential %S showed regional heterogeneity in hypertensive subjects, being maximal in the lateral wall and least in the inferior wall. Longitudinal shortening was also uniformly depressed in hypertensive subjects: 10 +/- 9% at the base versus 21 +/- 6% in normal subjects (P = .0001); 14 +/- 8% at the midventricle versus 18 +/- 3% (P = .03); and 14 +/- 8% at the apex versus 18 +/- 4% (P = .04). CONCLUSIONS: In hypertensive LVH with normal pump function, intramural circumferential and longitudinal myocardial shortening are depressed.