Spatial modulation (tagging) of the longitudinal magnetization allows diffusive displacements to be measured over times approximately as long as T 1 and over correspondingly long distances. Magnetization tagging is used here with hyperpolarized 3 He gas in canine lungs with unilateral elastase-induced emphysema. A new scheme for analyzing images subsequent to tagging determines the spatially-resolved fractional modulation and its decay rate, using a sliding window. The free diffusivity D o of 3 He, dilute in air or N 2 , is exceptionally large at 0.88 cm 2 /s. Thus, the root mean square (RMS) free displacement of a typical 3 He atom during several milliseconds is larger than the diameter of the acinar airways, with the result that the apparent diffusivity measured over such times is restricted by collisions with airway walls and is near 0.2 cm 2 /s in healthy lung (1-4). Airway expansion and destruction of airway and alveolar walls in emphysema (5) result in reduced restriction of diffusion (D Ϸ 0.55 cm 2 /s in a group of severely diseased subjects) (3). Nearly all of the work to date has measured D msec , taken from the decay of transverse magnetization measured at two b-values (that is, with and without a pulsed, diffusion-sensitizing field gradient) (3,4,6 -8). The experiment is sensitive to displacements during the gradient waveform that is typically several milliseconds in duration, corresponding to displacements of a few hundred microns. This time is limited by the short T* 2 of 3 He in lung (about 20 ms in 1.5 T) (9,10). The small length scale associated with this method limits the motion to individual acinar airways where 95% of the gas resides; the time is not sufficient for many of the atoms to move from one airway to the next. Multi-b-value measurements of the decay of transverse magnetization over times of milliseconds have been understood in terms of anisotropic diffusion, with different values longitudinal and transverse to the airways (D L and D T ) (1). Diffusion values so measured are sensitive indicators of the changes in localized lung morphology that accompany emphysema.However, by probing gas diffusion over longer times, one can examine the structure of the airway network over longer length scales. In the canonical description of lung (11), there are 24 levels of branching airways, where the trachea is Z ϭ 0 and the alveolar sacs are Z ϭ 23. The acinar units are the primary regions of gas exchange and comprise the highest-numbered eight airway levels. The mean linear size of an acinar unit is about 7 mm, with individual acinar airways having lengths of approximately 1 mm (11). Because the average acinar-airway length is small, and the acini contain the vast majority of gas in the lung, diffusion between arbitrary points that are centimeter(s) apart requires that atoms must travel from one acinus to another, connecting via a common conducting airway node. From the alveolar sacs, for example, this is a path through eight or more airway levels. The diffusion coefficient measured over such long ...

-Long-range diffusivity of hyperpolarized 3 He gas was measured from the decay rate of sinusoidally modulated longitudinal nuclear magnetization in three normal donor and nine severely emphysematous explanted human lungs. This (long-range) diffusivity, which we call D sec, is measured over seconds and centimeters and is ϳ10 times smaller in healthy lungs (0.022 cm 2 /s) than the more traditionally measured Dmsec, which is measured over milliseconds and submillimeters. The increased restriction of D sec reflects the complex, tortuous paths required to navigate long distances through the maze of branching peripheral airways. In emphysematous lungs, D sec is substantially increased, with some regions showing nearly the unrestricted value of the self-diffusion coefficient (0.88 cm 2 /s for dilute 3 He in air, a 40-fold increase). This suggests the presence of large collateral pathways opened by alveolar destruction that bypass the airways proper. This destruction was confirmed by comparison with histology in seven lungs and by removal of trapped gas via holes in the pleural surface in five lungs. emphysema; diffusivity; airways; transplant surgery; alveolar destruction IN RECENT YEARS,3 He magnetic resonance imaging has been shown to be an effective tool for characterizing lung ventilation and microstructure. Maps of 3 He spin density have been used to identify ventilation defects in a variety of lung diseases (11,15), and measurements of restricted diffusion over millisecond time scales have been a powerful probe of emphysema (3,4,20,21,29). Air space expansion and tissue destruction due to emphysema result in fewer and larger air spaces; alveolar walls, which normally restrict gas diffusion, are absent, giving rise to an increase in gas diffusivity (19,25). During a typical experimental diffusion time of 2 ms, most 3 He atoms cannot diffuse from one acinar airway (e.g., an alveolar duct) to its neighbor; thus the results are sensitive only to the size and geometry of alveoli and individual alveolar-lined airways within the acinus (8, 29).Measurements of 3 He diffusion over longer times and distances are possible with spatially modulated longitudinal magnetization, because the time constant for relaxation of longitudinal magnetization (T 1 ) is much longer than the time constant for transverse magnetization (T * 2 ): in humans at 1.5 T, T 1 of 3 He in lung is Ն20 s and T * 2 is 20 ms (11). Spatial modulation of longitudinal magnetization has been used to monitor cardiac or thoracic motion (1, 7, 17); in the air spaces of lungs as used here, the motion of 3 He is stochastic (diffusive) and results in attenuation of the spatial modulation (16). Diffusion averages across the spatially modulated magnetization, so the diffusivity may be determined from the decay rate of the amplitude of the modulation. Recently, experiments of 3 He diffusion over seconds and centimeters via magnetization tagging have shown that the long-range diffusivity (D sec ) is very restricted in healthy human and canine lungs: 0.015-0.02 cm 2 /s (...

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There have been several reports of a malpositioned pacemaker lead as a complication in pacemaker implantation. Herein we report a rare case of a malpositioned pacemaker lead in the left ventricle, which could occur in patients with cardiac structural abnormalities. A 70-year-old woman, who had undergone implantation of a pacemaker at the left subclavian position for complete atrioventricular block five years previously, was evaluated because of dyspnea and low grade fever. Echocardiography revealed a congenital atrial septal defect through which the lead was placed into the left ventricle. Whereas percuteneous lead removal seemed to be full of risk with concerns of thromboembolic events and infective endocarditis, the patient was referred to our hospital for surgical removal of the wire and closure of the defect. The lead was a screw-in type and removed and was extracted in the theatre using radiography. Intraoperatively it was found that the lead was positioned in the left ventricle apex after perforating the posterior mitral leaflet. Repair of the mitral valve perforation and closure of the septal defect and epicardial pacemaker lead implantation was performed. This case demonstrated the possibility of malposition of the pacemaker lead to the left ventricle in a transvenous pacemaker implantation procedure, which may lead to thromboembolic complication or infective endocarditis, and the pre-eminent role of echocardiography in the diagnosis of cardiac structural abnormalities. A malpositioned pacemaker lead in the left ventricle is a rare complication that can occur in patients with cardiac structural abnormalities. Lateral chest roentgenogram and echocardiography is efficient in preventing this complication. The removal of the lead in concerns of thromboembolic events and infection is preferable.