Purpose To examine how left ventricular (LV) volume and function affect flow dynamics by analyzing 3D intra‐LV vortex features using 4D‐Flow. Materials and Methods Twenty‐one patients with preserved (LVEF > 60%) and 14 with impaired LV function (LVEF < 40%) underwent 4D‐Flow (at 3T). Results In patients with preserved LV function, the intra‐LV vortices developed in both the early and late diastolic phases. The shift of inflow vectors at the basal LV toward the posterior‐lateral side of the LV and the mid‐ventricular turn of inflow vectors toward the LV outflow could explain clearer vortex formation in the late diastolic phase. In patients with impaired LV function, the intra‐LV vortices during the diastolic phase located at the more apical LV were larger and more spherically shaped. Both the distance to the vortex core and the vortex area correlated significantly with LV end‐diastolic volume (r = 0.66 and 0.73), LVEF (r = –0.74 and –0.68), LV sphericity index (r = –0.60 and –0.65), and peak filling rate (r = –0.61 and –0.64), respectively (P < 0.01). The intra‐LV vortices developed during the systolic phase in 10 cases. In those, some of the particles at the apical LV rotated within the LV, whereas in patients with preserved LV function, all of the particles were directed straight to the ascending aorta with accelerated flow velocity (256.8 ± 120.2 cm/s vs. 414.3 ± 88.2 cm/s, P < 0.01). Conclusion Vortex formation during the diastolic phase may be critical for both LV filling and ejection. 4D‐Flow showed the 3D alterations of intra‐LV flow dynamics by LV dilatation and dysfunction in a noninvasive and comprehensive manner. J. Magn. Reson. Imaging 2016;44:1493–1503.

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Implantation of a cardiac resynchronization therapy (CRT) device is usually scheduled in the compensated phase of heart failure; however, procedural safety may be sometimes disturbed in the decompensated phase. We report a case of a successful semi-urgent implantation of a CRT device temporary assisted with Impella in a patient with the decompensated phase of severe heart failure dependent on inotropic agents and who cannot maintain the supine position. Impella assistance with left ventricular (LV) unloading and maintenance of end-organ perfusion contributed to early recovery from acute heart failure. Furthermore, an acute effect of mechanical resynchronization by biventricular pacing plays an important role in weaning from the mechanical support or inotropic dependence. These mutual effects of mechanical support and CRT might contribute to a decrease in LV end-diastolic pressure and to a remarkable early recovery from a severely decompensated condition.

IntroductionTramadol, a weak opioid anesthetic, is used for pain management in patients with cancer, but the effects of tramadol on cancer via µ-opioid receptor are still unknown. We assessed the effects of tramadol on pancreatic ductal adenocarcinoma using transgenic mice (LSL-KrasG12D/+; Trp53flox/flox; Pdx-1cre/+).MethodsSix-week-old transgenic mice were orally administered 10 mg/kg/day tramadol (n=12), 10 mg/kg/day tramadol and 1 mg/kg/day naltrexone (n=9), or vehicle water (n=14) until the humane endpoint. Cancer-related pain and plasma cytokine levels were assessed by the mouse grimace scale and cytokine array, respectively. Tumor status was determined histopathologically. Tramadol’s effects on proliferation and invasion in pancreatic ductal adenocarcinoma cell lines were studied in vitro.ResultsTramadol with/without naltrexone improved mouse grimace scale scores while decreasing inflammatory cytokines such as tumor necrosis factor-α and interleukin-6. Proliferative Ki-67 and cyclins decreased by tramadol, while local M1-like tumor-associated macrophages increased by tramadol, which was blocked by naltrexone. Meanwhile, tramadol with/without naltrexone reduced juxta-tumoral cancer-associated fibroblasts and M2-like tumor-associated macrophages. Tumor-associated neutrophils, natural killers, and cytotoxic T cells were not altered. Tramadol decreased the proliferative and invasive potentials of pancreatic ductal adenocarcinoma cell lines via decreasing cyclins/cyclin-dependent kinases, which was partially reversed by naltrexone.ConclusionsThese findings imply that tramadol might be a useful anesthetic for pancreatic ductal adenocarcinoma: inhibiting the proliferation and invasion along with increasing antitumor M1-like tumor-associated macrophages via the µ-opioid receptor, while improving cancer-associated pain possibly through the antitumor effects with the decrease of inflammatory cytokines.