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Background: The mobile cloud electrocardiography (C-ECG) system is useful for reducing door-to-balloon (DTB) time in patients with acute coronary syndrome (ACS), but few studies have reported the usefulness of the C-ECG system across a wide provincial prefecture, such as Oita, in Japan. MethodsâandâResults: On 17 April 2017, the C-ECG system was integrated into the Oita remote image transmission system, in 10 ambulances of 10 respective fire departments in Oita Prefecture. During 6 months, 162 ECG indicating suspected ACS were transmitted to 18 hospitals using the C-ECG system. Of 162 patients, 17 who received emergency percutaneous coronary intervention (PCI) were assigned to the cloud group (mean age, 71±11 years). The control group consisted of 29 consecutive ACS patients who were transported to Oita University Hospital without using the C-ECG system (mean age, 66±12 years). Another 40 consecutive patients were diagnosed with ACS before transportation to Oita University Hospital, and were assigned to the diagnosed group (mean age, 70±14 years). DTB time (70±26 min vs. 96±24 min, P<0.005) and door-to-catheterization laboratory time (33±20 min vs. 53±22 min, P<0.0001) were shorter in the cloud group than in the control group, respectively. Conclusions: C-ECG system integration in Oita Prefecture was useful to appropriately transfer ACS patients to hospital and to facilitate earlier PCI than in the conventional diagnostic system.
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[This corrects the article DOI: 10.1253/circrep.CR-19-0020.].
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BACKGROUND: Spleen reserves monocytes, which deploy to inflammatory sites. Monocytosis is known to be observed in chronic low-grade inflammatory state, including chronic heart failure (CHF). CHF also induces splenomegaly. We tested the hypotheses that the number of peripheral blood monocytes and size of spleen at baseline could be related to the response to cardiac resynchronization therapy (CRT). METHODS: From 2010, a total of 49 consecutive patients implanted with CRT device were evaluated at baseline and 6-8 months later. The size of spleen was evaluated at baseline by computed tomography. Blood monocyte counts (BMCs) were examined by blood test apparatus. RESULTS: Patients were categorized as responders (13 female, mean age 69.0±7.9 years, n=34) and nonresponders (2 female, mean age 72.0±8.8 years, n=15) according to echocardiographic findings. In non-responders, spleen index was also greater in non-responders than in responders (4504±1338mm2 vs. 3240±1115mm2; mean±SE, p<0.01). Median baseline BMCs were significantly smaller in responders than non-responders (537±211/µl vs. 336±107/µl, p<0.01). In addition, BMC is positively correlated with the spleen index (R2=0.179, p=0.02). Based on the receiver-operating characteristic curve, low BMC was set at <400/µl. Kaplan-Meier survival analysis demonstrated that the low BMC patients had lower prevalence of new hospitalization due to HF progression (log rank 5.35, p=0.02). CONCLUSIONS: Our results demonstrated that BMC and the size of spleen might be important factors for response to CRT.
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Terapia de Ressincronização Cardíaca , Insuficiência Cardíaca/patologia , Insuficiência Cardíaca/terapia , Leucócitos Mononucleares/metabolismo , Baço/patologia , Idoso , Idoso de 80 Anos ou mais , Doença Crônica , Progressão da Doença , Ecocardiografia , Feminino , Insuficiência Cardíaca/mortalidade , Hospitalização , Humanos , Estimativa de Kaplan-Meier , Contagem de Leucócitos , Masculino , Pessoa de Meia-Idade , Tamanho do Órgão , Curva ROC , Baço/citologia , Esplenomegalia/etiologia , Esplenomegalia/patologia , Fatores de Tempo , Resultado do TratamentoRESUMO
BACKGROUND: Obesity, characterized by systemic low-grade inflammation, is considered a well-known risk for atrial fibrillation. In fact, IL-10 (interleukin 10), which is a potent anti-inflammatory cytokine, has been reported to decrease in obese and diabetic patients. We tested the hypotheses forwarding that genetic deletion of IL-10 exacerbates high-fat diet (HFD)-induced obesity-caused atrial inflammation, lipidosis, fibrosis, and fibrillation and that IL-10 therapy inhibits this pathology. METHODS: Eight- to 10-week-old male CL57/B6 (wild-type) mice and IL-10 knockout mice were divided into a 12-week HFD group and a 12-week normal-fat diet (NFD) group, respectively. In addition, the effect of IL-10 administration was also investigated. RESULTS: HFD-induced obesity for 12 weeks significantly depressed serum levels of IL-10 but were found to increase several proinflammatory cytokines in wild-type mice. Adverse atrial remodeling, including atrial inflammation, lipidosis, and fibrosis, was induced in both wild-type and IL-10 knockout mice by HFD. Vulnerability to atrial fibrillation was also significantly enhanced by HFD. With regard to epicardial and pericardial adipose tissue, the total amount of epicardial adipose tissue+pericardial adipose tissue volume was increased by HFD. Besides, proinflammatory and profibrotic cytokines of epicardial adipose tissue+pericardial adipose tissue were also upregulated. In contrast, the protein level of adiponectin was downregulated by HFD. These HFD-induced obesity-caused adverse effects were further exaggerated in IL-10 knockout mice in comparison to wild-type mice. Systemic IL-10 administration markedly ameliorated HFD-induced obesity-caused left atrial remodeling and vulnerability to atrial fibrillation, in addition to improving the quality of epicardial adipose tissue+pericardial adipose tissue. CONCLUSIONS: Our results highlight IL-10 treatment as a potential therapeutic approach to limit the progression of HFD-induced obesity-caused atrial fibrillation.