| 1.
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Imaizumi, Tadaatsu ; Mori, Fumiaki ; Yagihashi, Norito ; Kitamura, Hideo ; Sashinami, Hiroshi ; Suzuki, Koichi ; Yamashita, Koji ; Taima, Kageaki ; Kubota, Kosei ; Tanji, Kunikazu ; Sakaki, Hirotaka ; Matsumiya, Tomoh ; Yoshida, Hidemi ; Mariya, Yasushi ; Nakane, Hajime ; Tanaka, Hiroshi ; Takanashi, Shingo ; Wakabayashi, Koichi ; Yagihashi, Soroku ; Nakane, Akio ; Ito, Etsuro ; Okumura, Ken ; Kimura, Hiroto ; Satoh, Kei
概要:
Retinoic acid-inducible gene-I （RIG-I） is a cytoplasmic protein regarded as putative RNA helicase.Immunohistochemical st
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udies revealed high levels of RIG-I expression in epidermic cells in psoriasis, in macrophagesin atherosclerotic lesions and in glomeruli of lupus nephritis. RIG-I expression was also demonstrated in macrophagesand vascular endothelial cells in experimental animals with Listeria or Hanta virus infection. In vitro studies using cellcultures revealed the expression of RIG-I, in various cells including endothelial cells, macrophages and astroglial cells, inresponse to the stimulation with cytokines, lipopolysaccharide, double-stranded RNA, Listeria monocytogenes, etc. Thestudies employing the overexpression or RNA interference suggested that RIG-I is involved in the regulation of cytokineexpression including CXCL10/IP-10 and CCL5/RANTES. These results suggest that RIG-I constitutes a part of theintracellular pathway for the regulation of infl ammatory and immune responses.
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| 2.
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Ashitate, Toshihiro ; Osanai, Tomohiro ; Tanaka, Makoto ; Magota, Koji ; Echizen, Takashi ; Tomita, Hirofumi ; Okumura, Ken
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We showed that endogenous prostacyclin inhibitor coupling factor 6 （CF6） is released from vascularendothelial cells and
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its release is stimulated by tumor necrosis factor-α, which is related to congestive heart failure（CHF）. We also showed that CF6 increases the gene expression related to CHF. To investigate the role of CF6 inthe genesis of CHF, we generated CF6-overexpressing transgenic（ TG） mice, and characterized the phenotype. DNAfragment consisting of human elongation factor 1α promoter, and human calcitonin/CF6 fused gene was injected intothe embryo of C57BL/6J mouse, and homozygous TG mice were generated. In TG mice, CF6 gene was overexpressedby two fold in overall tissues compared with wild type（ WT） mice. Under normal salt diet, blood pressure, heart rate,and the expression of energy metabolism-related genes were similar between TG and WT mice. When the mice werefed with 8% -salt diet for 35 weeks, the mortality of TG mice was higher than that of WT mice（ survival rate; 50% inTG versus 92% in WT, p<0.05 by log-rank test）. This preliminary report indicates that further examination, especiallyanalysis of the cardiac function, is needed to clarify the cause of high mortality of TG mice under high salt intake.
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| 3.
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Kato, Chisato ; Osanai, Tomohiro ; Shibutani, Shuji ; Hanada, Kenji ; Okumura, Ken
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Insulin-like growth factor （IGF）-1 is known to exert benefi cial eff ects on the heart, but its source andfunction under
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hypoxia are unknown. We investigated the eff ect of hypoxia on IGF-1 expression and its role in theregeneration in the heart. Cardiac myocytes and fi broblasts obtained from neonate mice heart were cultured andexposed to hypoxia. mRNA of IGF-1, IGF-binding protein 3 （IGFBP3）, and vascular endothelial growth factor-A（VEGF-A） was measured by real-time PCR. In cardiac myocytes, IGF-1 mRNA was increased by 3.5±1.1 fold at 3hours after hypoxia concomitantly with the increase in IGFBP3 and VEGF-A mRNA, and returned to the baseline at24 hours. In contrast, IGF-1 mRNA in cardiac fi broblasts was unchanged by hypoxia, although VEGF-A mRNA wasincreased. To investigate the role of IGF-1 in the heart regeneration, we measured the gene expressions of stromalcell-derived factor-1（ SDF-1）, its receptor CXCR4, and matrix metalloproteinase（ MMP）-14 related to cell homing. Incardiac myocytes, SDF-1 and MMP-14 mRNA were increased at 3 hours after hypoxia and tended to be positivelycorrelated with IGF-1 mRNA. These suggest that hypoxia increases IGF-1 expression in cardiac myocytes, and thisendogenous IGF-1 may exert benefi cial eff ects on regeneration in the heart.
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| 4.
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Horiuchi, Daisuke ; Osanai, Tomohiro ; Echizen, Takashi ; Ashitate, Toshihiro ; Kato, Chisato ; Yokoyama, Hiroaki ; Hanada, Kenji ; Shibutani, Shuji ; Itoh, Taihei ; Okumura, Ken
概要:
Structural remodeling occurs in diverse heart diseases and affects their clinical courses. We reportedthat amiodarone su
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ppresses both electrical and structural remodeling in a canine persistent atrial fi brillation model.As a mechanism for amiodarone’s effect on structural remodeling, we suggested its inhibitory effect on matrixmetalloproteinase（ MMP） activity. To elucidate it, we investigated the eff ect of amiodarone on MMP activity in a ratmyocardial infarction model created by left coronary artery（ LCA） ligation. Adult Sprague-Dawley rats were dividedinto sham-operated （Sham）, sham-operated with amiodarone （Sham+AMD）, LCA-ligated without amiodarone （MI）and LCA-ligated with amiodarone rats （MI+AMD）. Amiodarone （20 mg/kg/day） was administered for 2 weeksbefore and for 4 weeks after operation. The hearts were excised at 4 weeks after operation. MMP-2 activity wasmeasured by gelatin zymography. At 4 weeks after surgery, left ventricular fractional shortening was decreased inMI but not in MI+AMD rats. There was no diff erence in the infarct size between MI and MI+AMD rats （P=NS）.As compared with Sham, MMP-2 activity was increased in MI （P<0.01）, but not in MI+AMD （P=NS versus Sham;P<0.05 versus MI）. MMP-2 activity was not increased in Sham+AMD（ P=NS）. Thus, amiodarone exerts an inhibitoryeff ect on MMP activity. This may be related to the improvement left ventricular function in MI rats.
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| 5.
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Hasegawa, Kazushi ; Oikawa, Koichi ; Yoshida, Ikko ; Ishizaka, Hiroshi ; Osanai, Tomohiro ; Motomura, Shigeru ; Okumura, Ken
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To examine the effect of chronic hypertension on endothelium-derived hyperpolarizing factor（ EDHF）responses, the hearts
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of Wistar-Kyoto rats（ WKY） and spontaneously hypertensive rats（ SHR） were isolated andperfused using Langendorff system with constant perfusion pressure. Bradykinin increased coronary fl ow（ CF） dosedependentlyand this was not aff ected by NG-nitro-L-arginine methyl ester or indomethacin, indicating that bradykinin’seff ect on CF was not mediated by nitric oxide or prostacyclin but by EDHF. Bradykinin-induced CF increase was smallerin SHR than in WKY. Tetrabutylammonium（ a non-specific KCa channel blocker） abolished bradykinin-induced CFincrease in both rats. 1-Ethyl-2-benzimedazolinone（ 1-EBIO, an agonist of intermediate conductance KCa channel）-inducedincrease in CF was smaller in SHR than in WKY. 1,3-Dihydro-1-[2-hydroxy-5（- trifl uoromethyl） phenyl]-5（- trifl uoromethyl）-2H-benzimidazol-2-one（ NS1619, an agonist of large conductance KCa channel）-induced increase in CF did not differbetween SHR and WKY. In early stage of hypertension, there was no signifi cant diff erence between SHR and WKY inbradykinin- and 1-EBIO-induced increases in CF. In conclusion, EDHF response in coronary microcirculation is impairedin SHR due to dysfunction of intermediate-conductance calcium-activated potassium channels.
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| 6.
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Yoshida, Ikko ; Ishizaka, Hiroshi ; Hasegawa, Kazushi ; Satoh, Kiyohiko ; Osanai, Tomohiro ; Motomura, Shigeru ; Okumura, Ken
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Objectives The purpose of this study was to test the hypothesis that adenosine-induced coronarymicrovascular dilation is
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blunted in the animals with diabetes mellitus（ DM） through the impairment of KATP channelfunction. Background Adenosine-induced coronary vasodilation is demonstrated to be mediated by activation of ATPsensitivepotassium（ KATP） channels and nitric oxide（ NO）. Methods The hearts of Otsuka Long-Evans Tokushima fatty rats （OLETF, type 2 DM rats）, and control Long-Evans Tokushima fatty rats（ LETO） at the ages of 32 and 8 weeks were perfused using a Langendorff system withconstant perfusion pressure （80 mmHg）. Changes in coronary fl ow to adenosine, pinacidil and sodium nitroprusside（SNP） were examined before and after administration of glibenclamide（ 10-7 M）, or NG-nitro-L-arginine methyl ester（L-NAME, 10-4 M）. Results At the age of 32 weeks, adenosine- and pinacidil-induced increases in coronary fl ow were blunted in OLETFas compared with those in LETO （both p<0.05）. Glibenclamide attenuated adenosine-induced increase in coronaryfl ow in LETO （p<0.05）, but not in OLETF. In contrast, L-NAME attenuated adenosine-induced increase in coronaryflow in OLETF （p<0.05）, but not in LETO. SNP-induced increases in coronary flow in LETO and OLETF werecomparable and were not aff ected by glibenclamide. In 8-week-old OLETF and LETO, no diff erence was observed inadenosine-, pinacidil- and SNP-induced increases in coronary fl ow between OLETF and LETO. Conclusions In this type 2 DM model, KATP channel function in coronary microcirculation is impaired. Adenosineinducedincrease in coronary fl ow is mediated mainly by NO mechanism.
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| 7.
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Yokoyama, Hiroaki ; Saito, Shin ; Higuma, Takumi ; Hanada, Hiroyuki ; Osanai, Tomohiro ; Daitoku, Kazuyuki ; Fukuda, Ikuo ; Okumura, Ken
概要:
Adipose tissue secretes various bioactive molecules （adipokines）, and apelin is one kind of adipokines.Recently, it was
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shown that plasma apelin level is decreased in patients with chronic heart failure, and apelin mightplay an important role in the pathogenesis of cardiovascular disease. However, plasma apelin level in coronary arterydisease（ CAD） or other heart disease such as valvular heart disease（ VHD） has not been elucidated. We enrolled 31patients with CAD and 14 patients with VHD who underwent elective cardiac surgery. We also examined plasmaapelin level in 20 healthy subjects （Control）. Blood samples were obtained before the surgery. Paired samples ofvisceral and subcutaneous adipose tissues were harvested during surgery. Plasma apelin level was lower in both CADand VHD than in Control. When compared between CAD and VHD, it was lower in CAD than in VHD, and was notaff ected by treatment with HMG-CoA reductase inhibitors （statins） which was shown to increase adiponectin level.Left ventricular ejection fraction（ LVEF） was lower in CAD than in VHD. There was no correlation between plasmaapelin level and LVEF. Gene expression of apelin in visceral adipose tissue was higher than that in subcutaneousadipose tissue, but it was similar between two groups. These suggest that plasma apelin level was decreased inpatients with cardiac diseases, especially in those with CAD. Its role in the pathophysiology of CAD remains to beelucidated.
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| 8.
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Hanada, Kenji ; Osanai, Tomohiro ; Sukekawa, Takanori ; Ohya, Fumie ; Izumiyama, Kei ; Sagara, Shigeki ; Itoh, Taihei ; Yamamoto, Yuko ; Shibutani, Shuji ; Tomita, Hirofumi ; Okumura, Ken
概要:
Background: P38 mitogen-activated protein kinase（MAP kinase）plays on important role for progression of pathological card
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iac hypertrophy. However, the role of p38 MAP kinase in cardiac hypertrophy induced by pressure overload remains unclear. We investigated the effect of chronic treatment with p38 MAP kinase inhibitor on the development of heart failure induced by transverse aortic constriction（TAC）in mice. Methods and Results: TAC increased left ventricular septal wall thickness（LVSWT）and cross-sectional area（CSA）of cardiomyocyte, and decreased LV fractional shortening（FS）compared with sham operation after 6 weeks. TAC also increased phosphorylation of p38 MAP kinase, whereas other hypertrophic signals were unchanged. In another experiment, TAC mice and sham operated mice were treated with subcutaneous injection of p38 MAP kinase inhibitor SB202190（5mg/kg/day）or placebo five times a week for six weeks. Treatment with p38 MAP kinase inhibitor attenuated the increase in LVSWT and CSA, and the decrease in FS in mice with TAC.Conclusions: Inhibition of p38 MAP kinase attenuated left ventricular hypertrophy and inhibited progression of systolic dysfunction in pressure overload-induced cardiac hypertrophy. These results suggest that inhibition of p38 MAP kinase has a protective effect for development of heart failure induced by pressure overload.
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| 9.
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Shibutani, Shuji ; Osanai, Tomohiro ; Ohya, Fumie ; Sagara, Shigeki ; Izumiyama, Kei ; Yamamoto, Yuko ; Hanada, Kenji ; Tomita, Hirofumi ; Okumura, Ken
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Coronary artery spasm plays an important role in the etiology of coronary spastic angina（CSA）and other acute coronary sy
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ndromes. Mice with a targeted disruption of the ATP-binding cassette transporter C9‒ABCC9 gene were developed as an animal model of CSA. Thus, the ABCC9 may be involved in the regulation of coronary artery vasomotility. The aim of this study was to investigate whether mutation in the coding region of the ABCC9 gene is detected in Japanese patients with CSA. The study included 9 Japanese patients with CSA （6 men and 3 women with a mean age of 51±13 years）. Genomic DNA was extracted from the whole blood, and Mutation analysis of the coding region of ABCC9 was performed by direct sequencing. In one CSA patient, we found a single base substitution（G to A）at nucleotide position 126 in exon 21 of the coding region, which was heterozygous and did not cause amino acid substitution（T878T, silent mutation）.In the remaining 8 patients, no base substitution wasdetected in the coding region of the ABCC9 gene. The results indicate that the mutation of the ABCC9 gene may not be involved in the genetic pathogenesis of CSA in humans.
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| 10.
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Mikuniya, Megumi ; Nakamura, Kunihiko ; Okudera, Koichi ; Takanashi, Shingo ; Hayashi, Akihito ; Morimoto, Takeshi ; Taima, Kageaki ; Dempoya, Junichi ; Tanaka, Yoshihito ; Okumura, Ken
概要:
Few studies have reported the time spent outdoors in patients undergoing long-term oxygen therapy（LTOT）. Also, few have
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determined whether time spent outdoors was influenced by psychological impairments. Theaim of the present study was to examine the usage of oxygen cylinders to assess the time spent outdoors of patientsreceiving LTOT, and to evaluate the prevalence of dementia and depressive states and determine the correlationbetween these disorders and time spent outdoors. Fifty-four LTOT patients were enrolled in the present study,and dementia and depressive states were investigated using specific questionnaires. Among them, 23 patients werereassessed one year after the initial evaluation. There was a large variation in time spent outdoors among LTOTpatients, and the median number was one hour per day. Measured by the Hasegawa Dementia Scale-Revised（ HDS-R）,dementia was observed in 41% of the patients. Depressive state, measured by the Self-Rating Depression Scale（ SDS）,was observed in 24%. There were no correlations between time spent outdoors and psychological impairments. Thepercentage of patients in depressive states was statistically higher in the 2nd assessment. More attention must begiven to LTOT patients’ usage of oxygen cylinders, and dementia and depressive state should be periodically assessed.
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Nakamura, Kunihiko ; Mikuniya, Megumi ; Takanashi, Shingo ; Hayashi, Akihito ; Morimoto, Takeshi ; Taima, Kageaki ; Dempoya, Junichi ; Okumura, Ken
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Introduction: Although analysis of bronchoalveolar lavage fluid （BALF） is a useful examination to assess airway inflamma
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tion, it is an invasive technique with limitation and risk of complications.Objectives: The aim of this study was to examine molecules in exhaled breath condensate（ EBC） in comparison with BALF, and to clarify the clinical usability of EBC.Methods: EBC was collected from sixteen subjects suspected to have sarcoidosis just before BAL. The 40 different inflammatory molecules in EBC and BALF were analyzed by protein array.Results: BALF levels of 6 molecules including soluble tumor necrosis factor receptor type II （sTNF-RII） and regulated upon activation, normal T cell expressed and secreted （RANTES）, and EBC levels of 13 molecules including sTNF-RII and RANTES were significantly correlated with percentage of lymphocyte in BALF （%Lym）. We found significant correlations between levels of EBC and BALF in 16 out of 40 molecules. Levels of macrophage colony-stimulating factor（ M-CSF）, RANTES, TNF-α and sTNF-RII in EBC were significantly correlated with BALF. Their levels in EBC and BALF also were correlated with %Lym.Conclusion: Protein array, a highly sensitive approach allowed us to detect inflammatory molecules in EBC. Comprehensive analysis of EBC might be an equivalent to that of BALF.
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Narumi, Shunji ; Murakami, Reiichi ; Hatakeyama, Shingo ; Fujita, Tadashi ; Koie, Takuya ; Yoneyama, Takahiro ; Kudo, Shigemasa ; Kamimura, Noritaka ; Mori, Kazuyuki ; Shimada, Michiko ; Nakamura, Norio ; Umehara, Minoru ; Saito, Hisao ; Okumura, Ken ; Hakamada, Kenichi ; Ohyama, Chikara
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Introduction Kidney transplantation has been widely accepted as a definitive therapy for patients with renal failure. Th
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e Hirosaki Kidney Transplant Unit was organized in June 2006 in conjunction with the Departments of Urology, Cardiology, Respiratory Medicine and Nephrology, and Gastrointestinal Surgery, from the Hirosaki University School of Medicine. Herein, we introduce our current results and discuss our future strategies. Patients and Methods From June 2006 to December 2011, 36 kidney transplants were performed with 31 living donors and 5 deceased donors. Immunosuppression therapy included an inductor treatment of anti-CD25 antibody andtriple therapy with calcineurin inhibitor, mycophenolate mofetil, and steroids. Results Recipients included 25 males and 11 females. The patients’ average age was 41.8 years. Nine living–pairs were ABO incompatible. Deceased donors were performed at Oyokyo Hospital. Median follow-up period was 27.6 months. Acute cellular rejection occurred in 8.3% of patients. Positive antigenemia for cytomegalovirus happened in 16.7% of patients, but none developed invasive diseases. All recipients are currently surviving. Graft survival rates at 1, 3, and 5 years are 100%, 94.7%, and 94.7%, respectively. Conclusion Successful kidney transplantations have been performed by a multidisciplinary unit at Hirosaki University. Our next step is a promotion to increase organ donation.
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Fujita, Takeshi ; Narita, Ikuyo ; Shimada, Michiko ; Nakamura, Norio ; Osawa, Hiroshi ; Yamabe, Hideaki ; Okumura, Ken ; Murakami, Reiichi ; Narumi, Shunji ; Ohyama, Chikara
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Although graft survival rates in kidney transplant recipients have improved over the years. Cardiovascular disease remai
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ns the major cause of death after kidney transplantation. Therefore, relevant control of dyslipidemia is important for both the prevention of cardiovascular disease and protection of graft function. We retrospectively analyzed 28 patients who underwent kidney transplantation from June 2006 to February 2011 at Hirosaki University Hospital, of which 6 were excluded because of insufficient data. We applied the following diagnostic criteria for dyslipidemia established by the Japan Atherosclerosis Society: （1） low-density lipoprotein cholesterol levels ≥ 140 mg/dl, （2） triglyceride levels ≥ 150 mg/dl, and （3） high-density lipoprotein cholesterol levels < 40 mg/dl. Serum samples were obtained after overnight fasting. Five patients had dyslipidemia before kidney transplantation, and 4 patients developed new-onset dyslipidemia after kidney transplantation. Although 13 patients had normal lipid levels, 5 of them received prophylactic medication for dyslipidemia. We analyzed the 3 groups of patients to determine risk factors for dyslipidemia related kidney transplantation. Our data suggested that high trough levels of tacrolimus （Tac） tended to correlate with new-onset dyslipidemia after kidney transplantation（ P=0.06）.
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| 14.
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Suzuki, Akiko ; Osanai, Tomohiro ; Tanaka, Makoto ; Endo, Tomohide ; Murakami, Kazuo ; Tomita, Hirofumi ; Okumura, Ken
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Abstract Objectives: Vascular endothelial cells are exposed to an acidic pH, but its influence on chemokine receptors ex
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pressed in the vascular endothelial cells is unclear. We investigated the role of coupling factor 6 (CF6), a novel stimulator of proton importer, in the regulation of chemokine receptors in the vascular endothelial cells.Methods and Results: In microarray analysis, there were the increased expression of CC chemokine receptor 9 (CCR9) and CX3C chemokine receptor 1 (CX3CR1) and the decreased expression of CXC chemokine receptor 4 (CXCR4) in the human umbilical vascular endothelial cells (HUVEC) that were exposed to CF6. The ratio of CXCR4 to GAPDH mRNA was decreased in HUVEC that were exposed to either CF6 at 10-7M or hypoxia to a similar degree. Apoptotic cells, measured by annexin-V propidium iodide kit, were increased in HUVEC that were exposed to CF6 for 24 hours in normoxia.Conclusions: CF6 influences the expression of chemokine receptors and induces apoptosis in the vascular endothelial cells.
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Tanaka, Yoshihito ; Takanashi, Shingo ; Morimoto, Takeshi ; Taima, Kageaki ; Nakamura, Kunihiko ; Tanaka, Hisashi ; Okumura, Ken
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Abstract Background: Bronchial asthma in children often resolves as they grow. In persons with resolved asthma, spiromet
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ry measurements such as FEV1 and FEV1/FVC show almost normal values. The forced oscillation technique (FOT) is a new index of pulmonary function, and seems to be useful in detecting small changes that are not seen on spirometry. This study aimed to compare spirometry, exhaled nitric oxide fraction (FeNO), and FOT between the subjects with resolved asthma and normal subjects.Methods: We recruited 484 subjects from our university (mean age, 18.5; male, 257). A questionnaire about past history including bronchial asthma and other allergic diseases, spirometry, FeNO measurement, and FOT were completed by 119 resolved asthma patients and 365 normal subjects.Results: FEV1/FVC was significantly lower and FeNO was higher in resolved asthma patients than in controls. There were significant differences between resolved asthma patients and controls in X5, Fres, and ALX as reactance parameters. There were, however, no differences in the resistance parameters such as R5, R20.Conclusions: There is a group of patients whose childhood asthma has resolved with respiratory impairment. Further study will be required to determine whether spirometry, FeNO, and FOT are useful in making an early diagnosis of asthma relapse.
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Murakami, Kazuo ; Osanai, Tomohiro ; Tanaka, Makoto ; Kinjo, Takahiko ; Tanno, Tomohiro ; Narita, Ikuyo ; Kawai, Misato ; Tomita, Hirofumi ; Okumura, Ken
概要:
Background: We reported that enhanced phospholipase C （PLC）-δ1, which was detected in patients with coronary spasm, caus
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ed coronary spasm in mice. We investigated the role of protein kinase C（ PKC） in acetylcholine （ACh）-induced Ca2+ influx under enhanced PLC-δ1 using human embryonic kidney（ HEK）-293 cells. Methods and Results: Intracellular free Ca2+ concentration （[Ca2+]i） was measured by fura-2, and Ca2+ influx was evaluated by the increase in [Ca2+]i after addition of extracellular Ca2+. ACh-induced Ca2+ influx（ nM） in HEK-293 cells was 21±2 in control HEK-293 cells, 52±6 in the cells with PLC-δ1 overexpression, and 75±9 in those with PLC-δ1 overexpression and PKC down-regulation （all p<0.05 among 3 groups）. Ca2+ influx under treatment with nifedipine at 10-5M was 2.9±0.1 times higher in the cells with PLC-δ1 overexpression and 5.6±0.2 times higher in those with PLC-δ1 overexpression and PKC down-regulation compared with the control cells（ all p<0.05 among 3 groups）. Conclusions: ACh-induced Ca2+ influx was enhanced by PLC-δ1 overexpression, but was attenuated by PKC activation. PKC plays an important role in Ca2+ influx under enhanced PLC-δ1 in a negative feedback fashion.
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| 17.
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Shoji, Yoshihiro ; Sasaki, Shingo ; Toyama, Yuichi ; Nishizaki, Kimitaka ; Kinjo, Takahiko ; Ishida, Yuji ; Endo, Tomohide ; Nishizaki, Fumie ; Itoh, Taihei ; Yokota, Takashi ; Yokoyama, Hiroaki ; Yamada, Masahiro ; Horiuchi, Daisuke ; Kimura, Masaomi ; Higuma, Takumi ; Okumura, Ken ; Tomita, Hirofumi
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Wearable cardioverter-defibrillator （WCD） is an external device capable of automatic detection and treatment of ventric
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ular tachycardia（VT）/ventricular fibrillation（ VF）. We examined whether WCD use for patients at high risk for VT/VF is associated with shortening the length of stay in the intensive care unit （ICU） and safemanagement in the general ward until implantable cardioverter-defibrillator（ ICD） implantation. From June 2012 to May 2014, ICD was implanted in 44 patients for secondary prevention of VT/VF （control group）. From June 2014 to May 2016, WCD was prescribed in 50 patients for secondary prevention, of which 29 patients had ICD implantation（ WCD group）. The median length（ 25th–75th percentiles） of the ICU stay was 3（ 1–7）days in the control and 0（ 0–1.5） days in the WCD group（ p<0.05）. The period until ICD implantation in the general ward was 0（ 0–3） days in the control and 10（ 5–19） days in the WCD group（ p<0.05）. No sudden cardiac death and no readmission to the ICU were reported in both groups before ICD implantation. In patients with indication for ICD implantation for secondary prevention, WCD use can shorten the length of ICU stay and provide a safe management in a general ward.
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