Background: Bone marrow fat increases when bone mass decreases, which could be attributed to the fact that adipogenesis competes with osteogenesis. Bone marrow fat has the potential to predict abnormal bone density and osteoporosis. Purpose: To investigate the predictive value of using vertebral bone marrow fat fraction(BMFF) obtained from modified Dixon(mDixon) Quant in the determination of abnormal bone density and osteoporosis. Study type: Prospective. Population: 257 subjects (age: 20-79 years old; BMI: 16.6-32.9 kg/m 2 ;181 females,76 males) without known spinal tumor, history of trauma, dysplasia, spinal surgery or hormone therapy. Field strength/sequence: 3.0T/mDixon. Assessment: BMFF was measured at the L1, L2 and L3 vertebral body on fat fraction maps of the lumbar spine. Bone mineral density (BMD) was obtained using quantitative computed tomography, which served as the reference standard. Statistical tests: The BMFF between the three groups (normal bone density, osteopenia and osteoporosis) was tested using one-way analysis of variance in SPSS. The correlation and partial correlation of BMFF and BMD were analyzed before and after controlling for age, sex and BMI. Logistic regression analysis using independent training and validation data was conducted to evaluate the performance of predicting abnormal BMD or osteoporosis using BMFF. Results: There was a significant difference in vertebral BMFF between the three groups (P < 0.001). Moderate inverse correlation was found between vertebral BMFF and BMD after controlling age, sex and BMI (r = -0.529; P < 0.001). The mean area under the curve, sensitivity, specificity and negative predictive value (NPV) for predicting abnormal bone density were 0.940, 0.877, 0.896, and 0.890, respectively. The corresponding results for predicting subjects with osteoporosis were 0.896, 0.848, 0.853, and 0.969, respectively. Data conclusion: mDixon Quant is a fast, simple, noninvasive and nonionizing method to access vertebral BMFF and has a high predictive power for identifying abnormal bone density and osteoporosis. Level of Evidence: 1 Technical Efficacy: Stage 2
Extracellular recording and stimulation techniques have been used to demonstrate that the effective refractory period of epicardial ventricular cells is significantly influenced by the sequence of activation. Whether myocardial fiber orientation is also important in determining the repolarization process is unclear. To determine the importance of fiber orientation on the repolarization process, we studied 12 blocks of pig right ventricular tissue in vitro. The size of each tissue block was 30 x 30 x 2 mm. Transmembrane action potentials were recorded, and effective refractory periods were measured from the preparation's epicardial surface, which showed nearly uniform fiber orientation. Tissues were paced at 500- and 1,000-ms cycle lengths. Sequential recordings were made at 1, 4, 7, 10, 13, and 16 mm from the stimulation site along and across the fibers. The results show that propagation of depolarization was much slower in the transverse direction than in the longitudinal direction. In the transverse direction, action potential duration was longest at the closest observation point, i.e., 1 mm from the stimulation, site (188 +/- 14 and 267 +/- 18 ms for 500- and 1,000-ms pacing cycle lengths, respectively). Action potential duration progressively shortened as the recording site was moved farther from the stimulation site (P < 0.001). The action potential duration 16 mm from the stimulation site was 165 +/- 11 and 247 +/- 12 ms for 500- and 1,000-ms pacing cycle lengths, respectively. In contrast, the action potential duration in the longitudinal direction did not change as the distance between the recording site and stimulation site increased. We conclude that, at physiological temperature and pacing cycle lengths, sequence of activation significantly influenced action potential duration when the propagation of activation was transverse to myocardial fiber orientation. When activation propagated parallel to fiber orientation, there was little or no change of action potential duration as distance increased.
This study was designed to test the hypothesis that protective zones appear recurrently at the initiation of ventricular fibrillation (VF) and that when shocks are delivered during protective zones, there can be a decrease in the defibrillation energy requirement. A total of 12 open-chest dogs were studied. Six dogs were included in protocol 1. After eight baseline pacing stimuli (S1) with cycle lengths of 300 ms, a strong premature stimulus (S2) (73 +/- 10 mA) was given to induce VF. In subsequent episodes, a second strong premature stimulus (S3) was given at progressively longer S2-S3 intervals in 20-ms increments. In protocol 2, we delivered unsuccessful defibrillation shocks via a transvenous defibrillation electrode placed in the right ventricular apex of six dogs. A second shock was then delivered to patch electrodes on the right ventricular outflow tract and the posterior wall of the left ventricle. The results of protocol 1 showed that the S3 terminated reentry and prevented VF only when it occurred at specific time intervals after the S2 (the protective zones). These protective zones appear recurrently up to 375 ms after the onset of VF. The results of protocol 2 showed that the total energy required for successful defibrillation was dependent on the interval between the first and second shocks. Intervals favoring effective defibrillation (protective zones) appeared recurrently for up to 280 ms after the first shock. When the second shock was delivered during a protective zone, the defibrillation energy requirement was decreased by up to 23% (from 13.1 +/- 2.0 to 10.1 +/- 1.8 J, P < 0.003). However, when the shock was delivered outside the protective zone, a significant increase in the defibrillation energy requirement was observed. We conclude that protective zones appear recurrently at the onset of VF and after unsuccessful defibrillation shocks.
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