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Left ventricular dysfunction was found in DM2. In this research, we compared the left ventricular dysfunction of coronary artery disease (CAD) patients with and without type 2 diabetes mellitus as well as normal controls using the volume-time curve of cardiac magnetic resonance (CMR). Sixty-one CAD patients (28 with DM2 and 33 without DM2) and 18 normal individuals were enrolled in this study. Left ventricular function parameters, including the end-diastolic and end-systolic volumes (EDV, ESV), stroke volume (SV) and ejection fraction (EF), and morphologic dimension parameters (end diastolic and systolic diameter (EDD and ESD), were measured and compared. Volume-time curve parameters, including the peak ejection rate (PER), peak ejection time (PET), peak filling rate (PFR), peak filling time from ES (PFT), peak ejection rate normalized to EDV (PER\u002FEDV), and peak filling rate normalized to EDV (PFR\u002FEDV), were derived automatically and compared. LVEF in the diabetic CAD group was markedly reduced when compared to the normal and CAD without DM2 groups (all p \u003C 0.05). LVEDD of the diabetic CAD group was significantly enlarged compared to the normal and non-diabetic CAD groups (all p \u003C 0.05). More importantly, the lowest parameters of the left ventricle volume time curve (i.e., PER, PFR, PER\u002FEDV and PFR\u002FEDV) were obtained in diabetic CAD patients (all p \u003C 0.05). In diabetic CAD patients, logistic regression analysis indicated that PET, PFT and PFR\u002FEDV were independent predictors of left ventricular dysfunction (odds ratio [OR]: 1.1208, 1.0161, and 0.0139, respectively). The sensitivity and specificity of PET were 81.2 and 90%, respectively, when the threshold value was greater than 164.4 msec; for PFT, the sensitivity and specificity were 87.5 and 95.0%, respectively (criterion >166.0 msec). Higher sensitivity (87.5%) and specificity (100.0%) were obtained for PFR\u002FEDV (criterion ≤3.7EDV\u002Fs). Parameters that are derived from the volume-time curve on CMR, including PET, PFT and PFR\u002FEDV, allow clinicians to predict left ventricular dysfunction in diabetic CAD subjects with a high degree of sensitivity and specificity.",{"EN":178},"Volume-time curve of cardiac magnetic resonance assessed left ventricular dysfunction in coronary artery disease patients with type 2 diabetes mellitus",{"VOID":180},"[\"15085084405180358598\"]",{"VOID":182},"10.1186\u002Fs12872-017-0583-5","PUBLICATION","VERIFIED","2024-05-01T06:48:49.553+00:00","Auto 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Left ventricular diastolic function in type 2 diabetes mellitus and the association with coronary artery calcium score: a cardiac MRI study. AJR. 2014;202:1207–14.",{"doi":371},{"id":367,"text":415,"url":369,"identifiers":416},"Montalescot G, Sechtem U, Achenbach S, et al. 2013 ESC guidelines on the management of stable coronary artery disease: the task force on the management of stable coronary artery disease of the European Society of Cardiology. Eur Heart J. 2013;34:2949–3003.",{"doi":371},{"id":20,"text":418,"url":419,"identifiers":420},"International Diabetes Federation. Global guideline for type 2 diabetes. https:\u002F\u002Fwww.idf.org\u002Fe-library\u002Fguidelines.html.","https:\u002F\u002Fwww.idf.org\u002Fe-library\u002Fguidelines.html",{},{"id":422,"text":423,"url":424,"identifiers":425},"6e2113cb-6f67-48d5-bb92-efa9e56c6136","van der Wall EE, Reiber JH. Assessment of left ventricular function: visual or quantitative? Int J Cardiovasc Imaging. 2011;27(4):573–7.","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs10554-010-9735-8",{"doi":426},"10.1007\u002Fs10554-010-9735-8",{"id":428,"text":429,"url":430,"identifiers":431},"1284a000-eea7-4f62-99fb-b15b579d7568","Hedeer F, Palmer J, Arheden H, Ugander M. Gated myocardial perfusion SPECT underestimates left ventricular volumes and shows high variability compared to cardiac magnetic resonance imaging -- a comparison of four different commercial automated software packages. BMC Med Imaging. 2010;10:10.","https:\u002F\u002Fbmcmedimaging.biomedcentral.com\u002Farticles\u002F10.1186\u002F1471-2342-10-10",{"doi":432},"10.1186\u002F1471-2342-10-10",{"id":367,"text":434,"url":369,"identifiers":435},"Ioannidis JP, Trikalinos TA, Danias PG. Electrocardiogram-gated single-photon emission computed tomography versus cardiac magnetic resonance imaging for the assessment of left ventricular volumes and ejection fraction: a meta-analysis. J Am Coll Cardiol. 2002;39(12):2059–68.",{"doi":371},{"id":367,"text":437,"url":369,"identifiers":438},"Chen X, Hu H, Qian Y, Shu J. Relation of late gadolinium enhancement in cardiac magnetic resonance on the diastolic volume recovery of left ventricle with hypertrophic cardiomyopathy. J Thorac Dis. 2014;6:988–94.",{"doi":371},{"id":440,"text":441,"url":442,"identifiers":443},"6aea5358-ef19-4a8d-987d-e413a5efaf34","Zeidan Z, Erbel R, Barkhausen J, Hunold P, Bartel T, Buck T. Analysis of global systolic and diastolic left ventricular performance using volume-time curves by real-time three-dimensional echocardiography. J Am Soc Echocardiogr. 2003;16:29–37.","https:\u002F\u002Fwww.sciencedirect.com\u002Fscience\u002Farticle\u002Fpii\u002FS0894731702744702",{"doi":444},"10.1067\u002Fmje.2003.40",{"id":367,"text":446,"url":369,"identifiers":447},"Cosson S, Kevorkian JP. Left ventricular diastolic dysfunction: an early sign of diabetic cardiomyopathy. Diabetes Metab. 2003;29:455–66.",{"doi":371},{"id":367,"text":449,"url":369,"identifiers":450},"Avogaro A, Fadini G, de Kreutzenberg SV, Tiengo A. Coronary heart disease in diabetes. Int Congr Ser. 2007;1303:70–3.",{"doi":371},{"id":367,"text":452,"url":369,"identifiers":453},"Chiha M, Njeim M, Chedrawy EG. Diabetes and coronary heart disease: a risk factor for the global epidemic. Int J Hypertens. 2012;2012:697240.",{"doi":371},{"id":367,"text":455,"url":369,"identifiers":456},"From AM, Scott CG, Chen HH. Changes in diastolic dysfunction in diabetes mellitus over time. Am J Cardiol. 2009;103:1463–6.",{"doi":371},{"id":367,"text":458,"url":369,"identifiers":459},"Haffner SM, Lehto S, Ronnemaa T, Pyorala K, Laakso M. Mortality from coronary heart disease in subjects with type 2 diabetes and in nondiabetic subjects with and without prior myocardial infarction. New Engl J Med. 1998;339:229–34.",{"doi":371},{"id":367,"text":461,"url":369,"identifiers":462},"Naito R, Kasai T. Coronary artery disease in type 2 diabetes mellitus: recent treatment strategies and future perspectives. World J Cardiol. 2015;7(3):119–24.",{"doi":371},{"id":367,"text":464,"url":369,"identifiers":465},"Boxt LM. Cardiac MR imaging: a guide for the beginner. Radiographics. 1999;19:1009–25.",{"doi":371},{"id":467,"text":468,"url":469,"identifiers":470},"e3cfabe9-73b3-44cb-90b2-d05bba7df2c4","Fei H, He Y, Hou Y, Xu Y, Huang X, Feng B. Preliminary clinical study of real-time three-dimensional echocardiographic volume-time curve in evaluating left ventricular diastolic function. J Huazhong Univ Sci Technolog Med Sci. 2007;27:475–8.","http:\u002F\u002Flink.springer.com\u002F10.1007\u002Fs11596-007-0433-2",{"doi":471},"10.1007\u002Fs11596-007-0433-2",false,{"id":474,"createTime":475,"updateTime":476,"relativeEntities":477,"slug":478,"properties":479,"entityType":183,"verifyStatus":184,"verifyTime":488,"verifyNote":186,"languages":20,"translateLanguages":20,"viewCount":21,"primaryUrl":489,"fullTextUrl":20,"authors":490,"publicationType":311,"publisherRelationship":599,"citationCount":646,"citationInfo":647,"publishDate":650,"publishYear":648,"citationAnalyzeStatus":363,"lastCitationAnalyze":651,"indexDatabases":652,"openAccess":20,"references":653,"isForceReanalyzing":472},"fa5b717a-71bd-4446-8045-76612f254d2e","2024-01-04T04:56:32.348+00:00","2026-08-19T02:43:38.837+00:00",[],"Estimated-plasma-volume-status-ePVS-is-a-predictor-for-acute-myocardial-infarction-in-hospital-mortality-analysis-based-on-MIMIC-III-database",{"abstract":480,"title":482,"gsPaper":484,"doi":486},{"EN":481},"Estimated plasma volume status (ePVS) has been reported that associated with poor prognosis in heart failure patients. However, no researchinvestigated the association of ePVS and prognosis in patients with acute myocardial infarction (AMI). Therefore, we aimed to determine the association between ePVS and in-hospital mortality in AMI patients. We extracted AMI patients data from MIMIC-III database. A generalized additive model and logistic regression model were used to demonstrate the association between ePVS levels and in-hospital mortality in AMI patients. Kaplan–Meier survival analysis was used to pooled the in-hospital mortality between the various group. ROC curve analysis were used to assessed the discrimination of ePVS for predicting in-hospital mortality. 1534 eligible subjects (1004 males and 530 females) with an average age of 67.36 ± 0.36 years old were included in our study finally. 136 patients (73 males and 63 females) died in hospital, with the prevalence of in-hospital mortality was 8.9%. The result of the Kaplan–Meier analysis showed that the high-ePVS group (ePVS ≥ 5.28 mL\u002Fg) had significant lower survival possibility in-hospital admission compared with the low-ePVS group (ePVS \u003C 5.28 mL\u002Fg). In the unadjusted model, high-level of ePVS was associated with higher OR (1.09; 95% CI 1.06–1.12; P \u003C 0.001) compared with low-level of ePVS. After adjusted the vital signs data, laboratory data, and treatment, high-level of ePVS were also associated with increased OR of in-hospital mortality, 1.06 (95% CI 1.03–1.09; P \u003C 0.001), 1.05 (95% CI 1.01–1.08; P = 0.009), 1.04 (95% CI 1.01–1.07; P = 0.023), respectively. The ROC curve indicated that ePVS has acceptable discrimination for predicting in-hospital mortality. The AUC value was found to be 0.667 (95% CI 0.653–0.681). Higher ePVS values, calculated simply from Duarte’s formula (based on hemoglobin\u002Fhematocrit) was associated with poor prognosis in AMI patients. EPVS is a predictor for predicting in-hospital mortality of AMI, and could help refine risk stratification.",{"EN":483},"Estimated plasma volume status (ePVS) is a predictor for acute myocardial infarction in-hospital mortality: analysis based on MIMIC-III 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B, James S, Agewall S, Antunes MJ, Bucciarelli-Ducci C, Bueno H, Caforio ALP, Crea F, Goudevenos JA, Halvorsen S, Hindricks G, Kastrati A, Lenzen MJ, Prescott E, Roffi M, Valgimigli M, Varenhorst C, Vranckx P, Widimský P; ESC Scientific Document Group. 2017 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation: The Task Force for the management of acute myocardial infarction in patients presenting with ST-segment elevation of the European Society of Cardiology (ESC). Eur Heart J. 2018;39(2):119–77",{},{"id":367,"text":658,"url":369,"identifiers":659},"Jneid H, Addison D, Bhatt DL, Fonarow GC, Gokak S, Grady KL, Green LA, Heidenreich PA, Ho PM, Jurgens CY, King ML, Kumbhani DJ, Pancholy S. 2017 AHA\u002FACC clinical performance and quality measures for adults with ST-elevation and non-ST-elevation myocardial infarction: a report of the American College of Cardiology\u002FAmerican Heart Association Task Force on Performance Measures. J Am Coll Cardiol. 2017;70(16):2048–90.",{"doi":371},{"id":367,"text":661,"url":369,"identifiers":662},"Yamamoto T, Yoshida N, Takayama M, Tokyo CCU Network. Temporal trends in acute myocardial infarction incidence and mortality between 2006 and 2016 in Tokyo-report from the Tokyo CCU Network. Circ J. 2019;83(6):1405–9",{"doi":371},{"id":367,"text":664,"url":369,"identifiers":665},"Fudim M, Miller WL. Calculated estimates of plasma volume in patients with chronic heart failure-comparison with measured volumes. J Card Fail. 2018;24(9):553–60.",{"doi":371},{"id":367,"text":667,"url":369,"identifiers":668},"Movilli E, Cancarini GC, Cassamali S, Camerini C, Brunori G, Maffei C, Maiorca R. Inter-dialytic variations in blood volume and total body water in uraemic patients treated by dialysis. Nephrol Dial Transplant. 2004;19(1):185–9.",{"doi":371},{"id":367,"text":670,"url":369,"identifiers":671},"Duarte K, Monnez JM, Albuisson E, Pitt B, Zannad F, Rossignol P. Prognostic value of estimated plasma volume in heart failure. JACC Heart Fail. 2015;3:886–93.",{"doi":371},{"id":367,"text":673,"url":369,"identifiers":674},"Dekkers CCJ, Sjostrom CD, Greasley PJ, Cain V, Boulton DW, Heerspink HJL. Effects of the sodium-glucose cotransporter-2 inhibitor dapagliflozin on estimated plasma volume in patients with type 2 diabetes. Diabetes Obes Metab. 2019;21(12):2667–73.",{"doi":371},{"id":676,"text":677,"url":678,"identifiers":679},"847e7a34-4f4a-4d96-9da9-a24d64ea495a","Kobayashi M, Huttin O, Donal E, Duarte K, Hubert A, Le Breton H, Galli E, Fournet M, Mabo P, Schnell F, Leclercq C, Rossignol P, Girerd N. Association of estimated plasma volume status with hemodynamic and echocardiographic parameters. Clin Res Cardiol. 2020;109(8):1060–9.","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs00392-020-01599-9",{"doi":680},"10.1007\u002Fs00392-020-01599-9",{"id":367,"text":682,"url":369,"identifiers":683},"Johnson AE, Pollard TJ, Shen L, Lehman LW, Feng M, Ghassemi M, Moody B, Szolovits P, Celi LA, Mark RG. MIMIC-III, a freely accessible critical care database. Sci Data. 2016;24(3):160035.",{"doi":371},{"id":367,"text":685,"url":369,"identifiers":686},"Anderson JL, Morrow DA. Acute myocardial infarction. N Engl J Med. 2017;376(21):2053–64.",{"doi":371},{"id":367,"text":688,"url":369,"identifiers":689},"Le Gall JR, Lemeshow S, Saulnier F. A new simplified acute physiology score (SAPS II) based on a European\u002FNorth American multicenter study. JAMA. 1993;270(24):2957–63.",{"doi":371},{"id":20,"text":691,"url":20,"identifiers":692},"Raith EP, Udy AA, Bailey M, McGloughlin S, MacIsaac C, Bellomo R, Pilcher DV, Australian, New Zealand Intensive Care Society Centre for O, Resource E. Prognostic accuracy of the SOFA score, SIRS criteria, and qSOFA score for in-hospital mortality among adults with suspected infection admitted to the intensive care unit. JAMA. 2017;317(3):290–300",{},{"id":694,"text":695,"url":696,"identifiers":697},"06f73ba2-c6df-4686-a42f-d307d38adc97","Kobayashi M, Girerd N, Duarte K, Chouihed T, Chikamori T, Pitt B, Zannad F, Rossignol P. Estimated plasma volume status in heart failure: clinical implications and future directions. Clin Res Cardiol. 2021. https:\u002F\u002Fdoi.org\u002F10.1007\u002Fs00392-020-01794-8.","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs00392-020-01794-8",{"doi":698},"10.1007\u002Fs00392-020-01794-8",{"id":367,"text":700,"url":369,"identifiers":701},"Pedersen AB, Mikkelsen EM, Cronin-Fenton D, Kristensen NR, Pham TM, Pedersen L, Petersen I. Missing data and multiple imputation in clinical epidemiological research. Clin Epidemiol. 2017;9:157–66.",{"doi":371},{"id":20,"text":703,"url":20,"identifiers":704},"Agoritsas T, Merglen A, Shah ND, O’Donnell M, Guyatt GH. Adjusted analyses in studies addressing therapy and harm: users’ guides to the medical literature. JAMA. 2017;317(7):748–59.",{},{"id":367,"text":706,"url":369,"identifiers":707},"Grodin JL, Philips S, Mullens W, Nijst P, Martens P, Fang JC, Drazner MH, Tang WHW, Pandey A. Prognostic implications of plasma volume status estimates in heart failure with preserved ejection fraction: insights from TOPCAT. Eur J Heart Fail. 2019;21(5):634–42.",{"doi":371},{"id":709,"text":710,"url":711,"identifiers":712},"04b25619-0eda-4ef5-8a15-c549d430ebc7","Kobayashi M, Rossignol P, Ferreira JP, Aragão I, Paku Y, Iwasaki Y, Watanabe M, Fudim M, Duarte K, Zannad F, Girerd N. Prognostic value of estimated plasma volume in acute heart failure in three cohort studies. Clin Res Cardiol. 2019;108(5):549–61.","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs00392-018-1385-1",{"doi":713},"10.1007\u002Fs00392-018-1385-1",{"id":367,"text":715,"url":369,"identifiers":716},"Ling HZ, Flint J, Damgaard M, Bonfils PK, Cheng AS, Aggarwal S, Velmurugan S, Mendonca M, Rashid M, Kang S, Papalia F, Weissert S, Coats CJ, Thomas M, Kuskowski M, Cohn JN, Woldman S, Anand IS, Okonko DO. Calculated plasma volume status and prognosis in chronic heart failure. Eur J Heart Fail. 2015;17(1):35–43.",{"doi":371},{"id":367,"text":718,"url":369,"identifiers":719},"Fudim M, Lerman JB, Page C, Alhanti B, Califf RM, Ezekowitz JA, Girerd N, Grodin JL, Miller WL, Pandey A, et al. Plasma volume status and its association with in-hospital and postdischarge outcomes in decompensated heart failure. J Card Fail. 2021;27(3):297–308.",{"doi":371},{"id":367,"text":721,"url":369,"identifiers":722},"Lin Y, Xue Y, Liu J, Wang X, Wei L, Bai L, Ma A. Prognostic value of estimated plasma volume in patients with chronic systolic heart failure. J Investig Med. 2021;69(2):338–44.",{"doi":371},{"id":367,"text":724,"url":369,"identifiers":725},"Turcato G, Zaboli A, Ciccariello L, Pfeifer N. Estimated plasma volume status (ePVS) could be an easy-to-use clinical tool to determine the risk of sepsis or death in patients with fever. 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However, the role of omentin-1, a novel adipocytokine, in structural remodeling remains unknown. Hematoxylin and eosin (H&E) and Masson’s trichrome stains were used to investigate the histology of EAT and right atrial appendages. The expression levels of adipocytokines in these human samples were determined by immunohistochemical assay and western blotting. Models of transforming growth factor (TGF)-β1-induced activation of cardiac fibroblasts (CFs) and TGF-β1-induced endothelial-mesenchymal transition (EndMT) of human umbilical vein endothelial cell (HUVEC) were established to explore roles of omentin-1 in these processes. To determine changes in adipocytokines secretion under hypoxia conditions, adipocytes were treated with 5% O2 and 95% N2, and then CFs and HUVECs were co-cultured with the conditioned medium of adipocytes to determine the effects of hypoxia-treated adipocytes on these cells. Expression of omentin-1 was downregulated in the EAT and right atrial appendages from patients with AF compared to samples from patients without AF, while the TGF-β1 level was upregulated in EAT from patients with AF. EAT from patients with AF exhibited adipocyte hypertrophy and severe interstitial fibrosis. Omentin-1 inhibited TGF-β1-induced CF activation and reversed TGF-β1-induced HUVEC EndMT. Adipocytes treated with hypoxia exhibited downregulation of omentin-1 and partly activated CFs. This study demonstrated that omentin-1 was an antifibrotic adipocytokine and was downregulated in patients with AF, which was partly mediated by hypoxia.",{"EN":766},"Omentin-1 is associated with atrial fibrillation in patients with cardiac valve disease",{"VOID":768},"[\"13377372562372092596\"]",{"VOID":770},"citation_journal_title=Circulation; citation_title=Worldwide epidemiology of atrial fibrillation: a global burden of disease 2010 study; citation_author=SS Chugh, R Havmoeller, K Narayanan, D Singh, M Rienstra, EJ Benjamin, RF Gillum, YH Kim, JH McAnulty, ZJ Zheng; citation_volume=129; citation_issue=8; citation_publication_date=2014; citation_pages=837-847; citation_doi=10.1161\u002FCIRCULATIONAHA.113.005119; citation_id=CR1\ncitation_journal_title=J Am Coll Cardiol; citation_title=Atrial fibrosis: mechanisms and clinical relevance in atrial fibrillation; citation_author=B Burstein, S Nattel; citation_volume=51; citation_issue=8; citation_publication_date=2008; 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decreases total body water and improves the alveolar to arterial oxygen gradient. The aims of the study were to investigate the efficacy and safety of early ultrafiltration in acute decompensated heart failure (ADHF) patients. 100 patients with ADHF within 24 h of admission were randomly assigned into early ultrafiltration (n = 40) or torasemide plus tolvaptan (n = 60) groups. The primary outcomes were weight loss and an increase in urine output on days 4 and 8 of treatment. Patients who received early ultrafiltration for 3 days achieved a greater weight loss (kg) (− 2.94 ± 3.76 vs − 0.64 ± 0.91, P \u003C 0.001) and urine increase (mL) (198.00 ± 170.70 vs 61.77 ± 4.67, P \u003C 0.001) than the torasemide plus tolvaptan group on day 4. From days 4 to 7, patients in the early ultrafiltration group received sequential therapy of torasemide and tolvaptan. Better control of volume was reflected in a greater weight loss (− 3.72 ± 3.81 vs − 1.34 ± 1.32, P \u003C 0.001) and urine increase (373.80 ± 120.90 vs 79.5 ± 52.35, P \u003C 0.001), greater reduction of B-type natriuretic peptide (BNP) (pg\u002FmL) (− 1144 ± 1435 vs − 654.02 ± 889.65, P = 0.037), NYHA (New York Heart Association) functional class (− 1.45 ± 0.50 vs − 1.17 ± 0.62, P = 0.018), jugular venous pulse (JVP) score (points) (− 1.9 ± 1.13 vs − 0.78 ± 0.69, P \u003C 0.001), inferior vena cava (IVC) diameter (mm) (− 15.35 ± 11.03 vs − 4.98 ± 6.00, P \u003C 0.001) and an increase in the dyspnea score (points) (4.08 ± 3.44 vs 2.77 ± 2.03, P = 0.035) in the early ultrafiltration group on day 8. No significant differences were found in the readmission and mortality rates in the 2 patient groups at the 1-month and 3-month follow-ups. Both groups had a similar stable renal profile. Early ultrafiltration is superior to diuretics for volume overload treatment initiation of ADHF patients. Trial registration Chinese Clinical Trial Registry, ChiCTR2000030696, Registered 10 March 2020—Retrospectively registered, \n                  https:\u002F\u002Fwww.chictr.org.cn\u002Fshowproj.aspx?proj=29099\n                  \n                .",{"EN":938},"Efficacy and safety of early ultrafiltration in patients with acute decompensated heart failure with volume overload: a prospective, randomized, controlled clinical trial",{"VOID":940},"[\"12292130293622899934\"]",{"VOID":942},"Farmakis D, Parissis J, Lekakis J, Filippatos G. Acute heart failure: epidemiology, risk factors, and prevention. Rev Esp Cardiol (Engl Ed). 2015;68(3):245–8.\nAdams KF, Fonarow GC, Emerman CL, LeJemtel TH, Costanzo MR, Abraham WT, et al. Characteristics and outcomes of patients hospitalized for heart failure in the United States: Rationale, design, and preliminary observations from the first 100,000 cases in the Acute Decompensated Heart Failure National Registry (ADHERE). Am Heart J. 2005;149(2):209–16.\nGheorghiade M, Follath F, Ponikowski P, Barsuk JH, Blair JEA, Cleland JG, et al. Assessing and grading congestion in acute heart failure: a scientific statement from the Acute Heart Failure Committee of the Heart Failure Association of the European Society of Cardiology and endorsed by the European Society of Intensive Care Medicine. Eur J Heart Fail. 2010;12(5):423–33.\nGheorghiade M, Filippatos G, De Luca L, Burnett J. Congestion in acute heart failure syndromes: an essential target of evaluation and treatment. Am J Med. 2006;119(12):S3–10.\nTestani JM, Chen J, McCauley BD, Kimmel SE, Shannon RP. Potential effects of aggressive decongestion during the treatment of decompensated heart failure on renal function and survival. Circulation. 2010;122(3):265–72.\nPonikowski P, Voors AA, Anker SD, Bueno H, Cleland JG, Coats AJ, et al. ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure: the Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC). Developed with the special contribution of the Heart Failure Association (HFA) of the ESC. Eur J Heart Fail. 2016;18(8):891–975.\nChiong JR, Cheung RJ. Loop diuretic therapy in heart failure: the need for solid evidence on a fluid issue. Clin Cardiol. 2010;33(6):345–52.\nFonarow GC, Adams KF Jr, Abraham WT, Yancy CW, Boscardin WJ. Risk stratification for in-hospital mortality in acutely decompensated heart failure: classification and regression tree analysis. JAMA. 2005;293(5):572–80.\nFonarow GC. Epidemiology and risk stratification in acute heart failure. Am Heart J. 2008;155(2):200–7.\nKrumholz HM, Parent EM, Tu N, Vaccarino V, Wang Y, Radford MJ, et al. Readmission after hospitalization for congestive heart failure among Medicare beneficiaries. Arch Intern Med. 1997;157(1):99–104.\nKo DT, Alter DA, Austin PC, You JJ, Lee DS, Qiu F, et al. Life expectancy after an index hospitalization for patients with heart failure: a population-based study. Am Heart J. 2008;155(2):324–31.\nGoh CY, Vizzi G, De Cal M, Ronco C. Cardiorenal syndrome: a complex series of combined heart\u002Fkidney disorders. Contrib Nephrol. 2011;174:33–45.\nShchekochikhin D, Al Ammary F, Lindenfeld JA, Schrier R. Role of diuretics and ultrafiltration in congestive heart failure. Pharmaceuticals (Basel). 2013;6(7):851–66.\nLu R, Muciño-Bermejo MJ, Ribeiro LC, Tonini E, Estremadoyro C, Samoni S, et al. Peritoneal dialysis in patients with refractory congestive heart failure: a systematic review. Cardiorenal Med. 2015;5(2):145–56.\nRonco C, Ricci Z, Bellomo R, Bedogni F. Extracorporeal ultrafiltration for the treatment of overhydration and congestive heart failure. Cardiology. 2001;96(3–4):155–68.\nBart BA, Boyle A, Bank AJ, Anand I, Olivari MT, Kraemer M, et al. Ultrafiltration versus usual care for hospitalized patients with heart failure: the Relief for Acutely Fluid-Overloaded Patients With Decompensated Congestive Heart Failure (RAPID-CHF) trial. J Am Coll Cardiol. 2005;46(11):2043–6.\nCostanzo MR, Guglin ME, Saltzberg MT, Jessup ML, Bart BA, Teerlink JR, et al. Ultrafiltration versus intravenous diuretics for patients hospitalized for acute decompensated heart failure. J Am Coll Cardiol. 2007;49(6):675–83.\nHanna MA, Tang WH, Teo BW, O’Neill JO, Weinstein DM, Lau SM, et al. Extracorporeal ultrafiltration vs. conventional diuretic therapy in advanced decompensated heart failure. Congest Heart Fail. 2012;18(1):54–63.\nSiddiqui WJ, Kohut AR, Hasni SF, Goldman JM, Silverman B, Kelepouris E, et al. Readmission rate after ultrafiltration in acute decompensated heart failure: a systematic review and meta-analysis. Heart Fail Rev. 2017;22(6):685–98.\nChung ES, O’Brien TM, Menon S, Bartone C, Mazur W, Kereiakes DJ. A pilot study of target weight guided treatment in acute heart failure using ultrafiltration or usual care: effect on sodium removal. Korean Circ J. 2014;44(3):156–61.\nGrodin JL, Carter S, Bart BA, Goldsmith SR, Drazner MH, Tang WHW. Direct comparison of ultrafiltration to pharmacological decongestion in heart failure: a per-protocol analysis of CARRESS-HF. Eur J Heart Fail. 2018;20(7):1148–56.\nBart BA, Goldsmith SR, Lee KL, Givertz MM, O’Connor CM, Bull DA, et al. Ultrafiltration in decompensated heart failure with cardiorenal syndrome. N Engl J Med. 2012;367(24):2296–304.\nCostanzo MR, Saltzberg MT, Jessup M, Teerlink JR, Sobotka PA. Ultrafiltration is associated with fewer rehospitalizations than continuous diuretic infusion in patients with decompensated heart failure: results from UNLOAD. J Card Fail. 2010;16(4):277–84.\nJaski BE, Ha J, Denys BG, Lamba S, Trupp RJ, Abraham WT. Peripherally inserted veno-venous ultrafiltration for rapid treatment of volume overloaded patients. J Card Fail. 2003;9(3):227–31.\nCostanzo MR, Saltzberg M, O’Sullivan J, Sobotka P. Early ultrafiltration in patients with decompensated heart failure and diuretic resistance. J Am Coll Cardiol. 2005;46(11):2047–51.\nBart BA, Boyle A, Bank AJ, Anand I, Olivari MT, Kraemer M, et al. Randomized controlled trial of ultrafiltration versus usual care for hospitalized patients with heart failure: preliminary report of the rapid trial. J Cardiac Fail. 2004;10(4):S23.\nYancy CW, Jessup M, Bozkurt B, Butler J, Casey DE Jr, Colvin MM, et al. 2017 ACC\u002FAHA\u002FHFSA focused update of the 2013 ACCF\u002FAHA guideline for the management of heart failure: a report of the American College of Cardiology\u002FAmerican Heart Association Task Force on Clinical Practice Guidelines and the Heart Failure Society of America. Circulation. 2017;136(6):e137–61.\nSinger M, Deutschman CS, Seymour CW, Shankar-Hari M, Annane D, Bauer M, et al. The third international consensus definitions for sepsis and septic shock (Sepsis-3). JAMA. 2016;315(8):801–10.\nPang PS, Cleland JG, Teerlink JR, Collins SP, Lindsell CJ, Sopko G, et al. A proposal to standardize dyspnoea measurement in clinical trials of acute heart failure syndromes: the need for a uniform approach. Eur Heart J. 2008;29(6):816–24.\nDao Q, Krishnaswamy P, Kazanegra R, Harrison A, Amirnovin R, Lenert L, et al. Utility of B-type natriuretic peptide in the diagnosis of congestive heart failure in an urgent-care setting. J Am Coll Cardiol. 2001;37(2):379–85.\nTeo LY, Lim CP, Neo CL, Teo LW, Ng SL, Chan LL, et al. Ultrafiltration in patients with decompensated heart failure and diuretic resistance: an Asian centre’s experience. Singapore Med J. 2016;57(7):378–83.\nAgostoni P, Marenzi G, Lauri G, Perego G, Schianni M, Sganzerla P, et al. Sustained improvement in functional capacity after removal of body fluid with isolated ultrafiltration in chronic cardiac insufficiency: failure of furosemide to provide the same result. Am J Med. 1994;96(3):191–9.\nEllison DH. Diuretic therapy and resistance in congestive heart failure. Cardiology. 2001;96(3–4):132–43.\nBart BA. Treatment of congestion in congestive heart failure: ultrafiltration is the only rational initial treatment of volume overload in decompensated heart failure. Circ Heart Fail. 2009;2(5):499–504.\nFelker GM, Mentz RJ. Diuretics and ultrafiltration in acute decompensated heart failure. J Am Coll Cardiol. 2012;59(24):2145–53.\nLibetta C, Sepe V, Zucchi M, Campana C, Dal Canton A. Standard hemodiafiltration improves diuretic responsiveness in advanced congestive heart failure. Cardiology. 2006;105(2):122–3.\nNakagawa O, Ogawa Y, Itoh H, Suga S, Komatsu Y, Kishimoto I, et al. Rapid transcriptional activation and early mRNA turnover of brain natriuretic peptide in cardiocyte hypertrophy. Evidence for brain natriuretic peptide as an “emergency” cardiac hormone against ventricular overload. J Clin Investig. 1995;96(3):1280–7.\nDickstein K. Natriuretic peptides in detection of heart failure. Lancet. 1998;351(9095):4.\nMaeda K, Tsutamoto T, Wada A, Hisanaga T, Kinoshita M. Plasma brain natriuretic peptide as a biochemical marker of high left ventricular end-diastolic pressure in patients with symptomatic left ventricular dysfunction. Am Heart J. 1998;135(5 Pt 1):825–32.\nClerico A, Iervasi G, Del Chicca MG, Emdin M, Maffei S, Nannipieri M, et al. Circulating levels of cardiac natriuretic peptides (ANP and BNP) measured by highly sensitive and specific immunoradiometric assays in normal subjects and in patients with different degrees of heart failure. J Endocrinol Invest. 1998;21(3):170–9.\nKorhan E, Selçuk S, Bülent U. Early ultrafiltration therapy in a patient with decompansated heart failure and acute pulmonary edema in the setting of diuretic resistance. Ann Med Res. 2007;14(2):111–3.\nDahle TG, Blake D, Ali SS, Olinger CC, Bunte MC, Boyle AJ. Large volume ultrafiltration for acute decompensated heart failure using standard peripheral intravenous catheters. J Card Fail. 2006;12(5):349–52.\nGiglioli C, Landi D, Cecchi E, Chiostri M, Gensini GF, Valente S, et al. Effects of ULTRAfiltration vs. DIureticS on clinical, biohumoral and haemodynamic variables in patients with deCOmpensated heart failure: the ULTRADISCO study. Eur J Heart Fail. 2011;13(3):337–46.\nPang PS, Gheorghiade M, Dihu J, Swedberg K, Khan S, Maggioni AP, et al. Effects of tolvaptan on physician-assessed symptoms and signs in patients hospitalized with acute heart failure syndromes: analysis from the efficacy of vasopressin antagonism in heart failure outcome study with tolvaptan (EVEREST) trials. Am Heart J. 2011;161(6):1067–72.\nPang PS, Konstam MA, Krasa HB, Swedberg K, Zannad F, Blair JEA, et al. Effects of tolvaptan on dyspnoea relief from the EVEREST trials. Eur Heart J. 2009;30(18):2233–40.\nFelker GM, Mentz RJ, Cole RT, Adams KF, Egnaczyk GF, Fiuzat M, et al. Efficacy and safety of tolvaptan in patients hospitalized with acute heart failure. J Am Coll Cardiol. 2017;69(11):1399–406.\nHeart Failure Professional Committee of Chinese Medical Docter Association, Editorial Board of Chinses Jourol of Heart Failure and Cardiomyopathy. Expert recommendation on the voume control in heart failure management. Chin J Heart Fail Cardiomyopathy. 2018;2(1):8–16.\nAssociation CSoCoCM, Cardiology EBoCJo. Guidelines for the diagnosis and management of chronic heart failure. Chin J Cardiol. 2007;35(12):1076–95.",{"VOID":944},"10.1186\u002Fs12872-020-01733-5","2024-05-13T07:19:41.504+00:00","https:\u002F\u002Fbmccardiovascdisord.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs12872-020-01733-5",[948,963,976,989,1004,1017,1029],{"id":949,"sortIndex":21,"researcher":20,"roles":950,"affiliations":951,"properties":960,"displayName":962,"givenName":20,"familyName":20},"c02f2746-ed07-488e-a0d7-9e89e5b98fb7",[192],[952],{"id":953,"sortIndex":21,"affiliation":954,"properties":20},"65b65040-7702-4a46-b5ab-6eb4c53fb755",{"id":953,"createTime":20,"updateTime":20,"relativeEntities":955,"slug":20,"properties":956,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":959,"statistic":20},[],{"title":957},{"VI":958},"Department of Critical Care Medicine (Specialty of Heart Failure), Tongren Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 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progenitor cells (EPC) are involved in neovascularization and endothelial integrity. They might be protective in atherosclerosis. Optical coherence tomography (OCT) is a precise intracoronary imaging modality that allows assessment of subintimal plaque development. We evaluated the influence of EPC on coronary plaque burden in stable disease and implemented a novel computational plaque analysis algorithm using OCT. Forty-three patients (69.8% males, 69.6 ± 7.7 years) were investigated by OCT during re-angiography 6 months after elective stent implantation. Different subpopulations of EPCs were identified by flow cytometry according to their co-expression of antigens (CD34+, CD133+, kinase domain receptor, KDR+). An algorithm was applied to calculate the underlying total plaque burden of the stented segments from OCT images. Plaque morphology was assessed according to international consensus in OCT imaging. A cumulative sub-strut plaque volume of 10.87 ± 12.7 mm3 and a sub-stent plaque area of 16.23 ± 17.0 mm2 were found within the stented vessel segments with no significant differences between different stent types. All EPC subpopulations (mean of EPC levels: CD34+\u002FCD133+: 2.66 ± 2.0%; CD34+\u002FKDR+: 7.50 ± 5.0%; CD34+\u002FCD133+\u002FKDR+: 1.12 ± 1.0%) inversely correlated with the identified underlying total plaque volume and plaque area (p ≤ 0.012). This novel analysis algorithm allows for the first time comprehensive quantification of coronary plaque burden by OCT and illustration as spread out vessel charts. Increased EPC levels are associated with less sub-stent coronary plaque burden which adds to previous findings of their protective role in atherosclerosis.",{"EN":1104},"Endothelial progenitor cells and plaque burden in stented coronary artery segments: an optical coherence tomography study six months after elective PCI",{"VOID":1106},"[\"4343782011744404640\"]",{"VOID":1108},"Walter DH, Dimmeler S. Endothelial progenitor cells: regulation and contribution to adult neovascularization. Herz. 2002;27(7):579–88.\nKong D, Melo LG, Gnecchi M, Zhang L, Mostoslavsky G, Liew CC, Pratt RE, Dzau VJ. Cytokine-induced mobilization of circulating endothelial progenitor cells enhances repair of injured arteries. Circulation. 2004;110(14):2039–46.\nWerner N, Junk S, Laufs U, Link A, Walenta K, Bohm M, Nickenig G. Intravenous transfusion of endothelial progenitor cells reduces neointima formation after vascular injury. Circ Res. 2003;93(2):e17–24.\nAsahara T, Masuda H, Takahashi T, Kalka C, Pastore C, Silver M, Kearne M, Magner M, Isner JM. Bone marrow origin of endothelial progenitor cells responsible for postnatal vasculogenesis in physiological and pathological neovascularization. Circ Res. 1999;85(3):221–8.\nWerner N, Kosiol S, Schiegl T, Ahlers P, Walenta K, Link A, Bohm M, Nickenig G. Circulating endothelial progenitor cells and cardiovascular outcomes. N Engl J Med. 2005;353(10):999–1007.\nSchmidt-Lucke C, Rossig L, Fichtlscherer S, Vasa M, Britten M, Kamper U, Dimmeler S, Zeiher AM. Reduced number of circulating endothelial progenitor cells predicts future cardiovascular events: proof of concept for the clinical importance of endogenous vascular repair. Circulation. 2005;111(22):2981–7.\nHill JM, Zalos G, Halcox JP, Schenke WH, Waclawiw MA, Quyyumi AA, Finkel T. Circulating endothelial progenitor cells, vascular function, and cardiovascular risk. N Engl J Med. 2003;348(7):593–600.\nGeorge J, Herz I, Goldstein E, Abashidze S, Deutch V, Finkelstein A, Michowitz Y, Miller H, Keren G. Number and adhesive properties of circulating endothelial progenitor cells in patients with in-stent restenosis. Arterioscler Thromb Vasc Biol. 2003;23(12):e57–60.\nJung C, Rafnsson A, Shemyakin A, Bohm F, Pernow J. Different subpopulations of endothelial progenitor cells and circulating apoptotic progenitor cells in patients with vascular disease and diabetes. Int J Cardiol. 2010;143(3):368–72. doi:10.1016\u002Fj.ijcard.2009.03.075.\nLaufs U, Wassmann S, Czech T, Munzel T, Eisenhauer M, Bohm M, Nickenig G. Physical inactivity increases oxidative stress, endothelial dysfunction, and atherosclerosis. Arterioscler Thromb Vasc Biol. 2005;25(4):809–14.\nChen JZ, Zhang FR, Tao QM, Wang XX, Zhu JH, Zhu JH. Number and activity of endothelial progenitor cells from peripheral blood in patients with hypercholesterolaemia. Clin Sci (Lond). 2004;107(3):273–80.\nWang X, Zhu J, Chen J, Shang Y. Effects of nicotine on the number and activity of circulating endothelial progenitor cells. J Clin Pharmacol. 2004;44(8):881–9.\nZhu JH, Tao QM, Chen JZ, Wang XX, Zhu JH, Shang YP. Statins contribute to enhancement of the number and the function of endothelial progenitor cells from peripheral blood. Sheng Li Xue Bao. 2004;56(3):357–64.\nPellegatta F, Bragheri M, Grigore L, Raselli S, Maggi FM, Brambilla C, Reduzzi A, Pirillo A, Norata GD, Catapano AL. In vitro isolation of circulating endothelial progenitor cells is related to the high density lipoprotein plasma levels. Int J Mol Med. 2006;17(2):203–8.\nIannaccone M, D'Ascenzo F, Templin C, Omede P, Montefusco A, Guagliumi G, Serruys PW, Di Mario C, Kochman J, Quadri G, et al. Optical coherence tomography evaluation of intermediate-term healing of different stent types: systemic review and meta-analysis. Eur Heart J Cardiovasc Imaging. 2017;18(2):159–66. doi:10.1093\u002Fehjci\u002Fjew070.\nIannaccone M, Quadri G, Taha S, D'Ascenzo F, Montefusco A, Omede P, Jang IK, Niccoli G, Souteyrand G, Yundai C, et al. Prevalence and predictors of culprit plaque rupture at OCT in patients with coronary artery disease: a meta-analysis. Eur Heart J Cardiovasc Imaging. 2016;17(10):1128–37.\nPrati F, Regar E, Mintz GS, Arbustini E, Di Mario C, Jang IK, Akasaka T, Costa M, Guagliumi G, Grube E, et al. Expert review document on methodology, terminology, and clinical applications of optical coherence tomography: physical principles, methodology of image acquisition, and clinical application for assessment of coronary arteries and atherosclerosis. Eur Heart J. 2010;31(4):401–15.\nPrati F, Guagliumi G, Mintz GS, Costa M, Regar E, Akasaka T, Barlis P, Tearney GJ, Jang IK, Arbustini E, et al. Expert review document part 2: methodology, terminology and clinical applications of optical coherence tomography for the assessment of interventional procedures. Eur Heart J. 2012;33(20):2513–20.\nTearney GJ, Regar E, Akasaka T, Adriaenssens T, Barlis P, Bezerra HG, Bouma B, Bruining N, Cho JM, Chowdhary S, et al. Consensus standards for acquisition, measurement, and reporting of intravascular optical coherence tomography studies: a report from the International Working Group for Intravascular Optical Coherence Tomography Standardization and Validation. J Am Coll Cardiol. 2012;59(12):1058–72.\nOtto S, Gassdorf J, Nitsche K, Gutiérrez-Chico J, Kryvanos A, Goebel B, Schulze PC, Figulla HR, Poerner TC. Time Course of Vascular Response after an A Priori Strategy of Bare Metal Stent Implantation Post-Dilated with a Paclitaxel-coated Balloon: Implementation of a Three Dimensional Analysis Algorithm with Optical Coherence Tomography. Cardiol J. 2016;23(3):296–306. doi:10.5603\u002FCJ.a2016.0018.\nPoerner TC, Otto S, Gassdorf J, Janiak F, Danzer C, Ferrari M, Figulla HR. A prospective randomised study using optical coherence tomography to assess endothelial coverage and neointimal proliferation at 6-months after implantation of a coronary everolimus-eluting stent compared with a bare metal stent postdilated with a paclitaxel-eluting balloon (OCTOPUS Trial): rationale, design and methods. EuroIntervention. 2011;7(Suppl K):K93–9.\nPoerner TC, Otto S, Gassdorf J, Nitsche K, Janiak F, Scheller B, Goebel B, Jung C, Figulla HR. Stent coverage and neointimal proliferation in bare metal stents postdilated with a Paclitaxel-eluting balloon versus everolimus-eluting stents: prospective randomized study using optical coherence tomography at 6-month follow-up. Circ Cardiovasc Interv. 2014;7(6):760–7.\nBraden B. The Surveyor's Area Formula. 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CCR5 facilitates endothelial progenitor cell recruitment and promotes the stabilization of atherosclerotic plaques in ApoE−\u002F− mice. Stem Cell Res Ther. 2015;6:36.\nLiu Y, Hao F, Zhang H, Cao D, Lu X, Li X. Panax notoginseng saponins promote endothelial progenitor cell mobilization and attenuate atherosclerotic lesions in apolipoprotein E knockout mice. Cell Physiol Biochem. 2013;32(4):814–26.\nHerlea-Pana O, Yao L, Heuser-Baker J, Wang Q, Wang Q, Georgescu C, Zou MH, Barlic-Dicen J. Chemokine receptors CXCR2 and CX3CR1 differentially regulate functional responses of bone-marrow endothelial progenitors during atherosclerotic plaque regression. Cardiovasc Res. 2015;106(2):324–37.\nKeymel S, Kalka C, Rassaf T, Yeghiazarians Y, Kelm M, Heiss C. Impaired endothelial progenitor cell function predicts age-dependent carotid intimal thickening. Basic Res Cardiol. 2008;103(6):582–6.\nMoon JH, Chae MK, Kim KJ, Kim HM, Cha BS, Lee HC, Kim YJ, Lee BW. Decreased endothelial progenitor cells and increased serum glycated albumin are independently correlated with plaque-forming carotid artery atherosclerosis in type 2 diabetes patients without documented ischemic disease. Circ J. 2012;76(9):2273–9.\nLau KK, Chan YH, Yiu KH, Li SW, Tam S, Lau CP, Kwong YL, Tse HF. Burden of carotid atherosclerosis in patients with stroke: relationships with circulating endothelial progenitor cells and hypertension. J Hum Hypertens. 2007;21(6):445–51.\nGeorge J, Afek A, Abashidze A, Shmilovich H, Deutsch V, Kopolovich J, Miller H, Keren G. Transfer of endothelial progenitor and bone marrow cells influences atherosclerotic plaque size and composition in apolipoprotein E knockout mice. Arterioscler Thromb Vasc Biol. 2005;25(12):2636–41.\nHagensen MK, Shim J, Thim T, Falk E, Bentzon JF. Circulating endothelial progenitor cells do not contribute to plaque endothelium in murine atherosclerosis. Circulation. 2010;121(7):898–905.\nSilvestre JS, Gojova A, Brun V, Potteaux S, Esposito B, Duriez M, Clergue M, Le Ricousse-Roussanne S, Barateau V, Merval R, et al. Transplantation of bone marrow-derived mononuclear cells in ischemic apolipoprotein E-knockout mice accelerates atherosclerosis without altering plaque composition. Circulation. 2003;108(23):2839–42.\nPeichev M, Naiyer AJ, Pereira D, Zhu Z, Lane WJ, Williams M, Oz MC, Hicklin DJ, Witte L, Moore MA, et al. Expression of VEGFR-2 and AC133 by circulating human CD34(+) cells identifies a population of functional endothelial precursors. Blood. 2000;95(3):952–8.\nHaude M, Lee SW, Worthley SG, Silber S, Verheye S, Erbs S, Rosli MA, Botelho R, Meredith I, Sim KH, et al. The REMEDEE trial: a randomized comparison of a combination sirolimus-eluting endothelial progenitor cell capture stent with a paclitaxel-eluting stent. 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Frequency and predictor of coronary thin-cap fibroatheroma in patients with acute myocardial infarction and stable angina pectoris a 3-vessel optical coherence tomography study. J Am Coll Cardiol. 2008;52(9):787–8.\nWang L, Parodi G, Maehara A, Valenti R, Migliorini A, Vergara R, Carrabba N, Mintz GS, Antoniucci D. Variable underlying morphology of culprit plaques associated with ST-elevation myocardial infarction: an optical coherence tomography analysis from the SMART trial. Eur Heart J Cardiovasc Imaging. 2015;16(12):1381–9.\nYonetsu T, Kato K, Uemura S, Kim BK, Jang Y, Kang SJ, Park SJ, Lee S, Kim SJ, Jia H, et al. Features of coronary plaque in patients with metabolic syndrome and diabetes mellitus assessed by 3-vessel optical coherence tomography. Circ Cardiovasc Imaging. 2013;6(5):665–73.",{"VOID":1110},"10.1186\u002Fs12872-017-0534-1","2024-08-30T21:29:35.136+00:00","https:\u002F\u002Fbmccardiovascdisord.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs12872-017-0534-1",[1114,1129,1142,1159,1174,1191,1204,1219,1232,1246,1260],{"id":1115,"sortIndex":21,"researcher":20,"roles":1116,"affiliations":1117,"properties":1126,"displayName":1128,"givenName":20,"familyName":20},"73394b6c-a330-46c1-b935-7f6839fd075b",[192],[1118],{"id":1119,"sortIndex":21,"affiliation":1120,"properties":20},"1a589c5f-f9ce-40a7-8d2b-336925fa13c8",{"id":1119,"createTime":20,"updateTime":20,"relativeEntities":1121,"slug":20,"properties":1122,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1125,"statistic":20},[],{"title":1123},{"VI":1124},"Department of Internal Medicine I, Division of Cardiology, Angiology, Pneumology and Intensive Medical Care, University Hospital Jena Friedrich-Schiller-University Jena, Jena, Germany",[],{"title":1127},{"VI":1128},"Sylvia Otto",{"id":1130,"sortIndex":207,"researcher":20,"roles":1131,"affiliations":1132,"properties":1139,"displayName":1141,"givenName":20,"familyName":20},"80fa8359-9c1b-46b1-9aa5-372931dbd5ba",[192],[1133],{"id":1119,"sortIndex":21,"affiliation":1134,"properties":20},{"id":1119,"createTime":20,"updateTime":20,"relativeEntities":1135,"slug":20,"properties":1136,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1138,"statistic":20},[],{"title":1137},{"VI":1124},[],{"title":1140},{"VI":1141},"Kristina 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The study aims to characterize plaque morphology and intimal hyperplasia of the RA in patients with ACS, using optical coherence tomography (OCT). In this retrospective study involving 239 ACS patients underwent RA OCT without guidewire shadow, 3 groups were divided according to the following criteria: radial artery plaque (RAP) group included patients with fibrous, lipid or calcified plaque; patients without RAP were further classified into radial intimal hyperplasia (RIH) group (intima media thickness ratio [IMR] ≥ 1) or normal group (IMR \u003C 1). The presence and characteristics of RAP and its related risk factors were identified. The RAP, RIH and normal groups included 76 (31.8%), 69 (28.9%) and 94 (39.3%) patients, respectively. Patients in RAP group were the oldest, compared with those in the RIH and normal groups (p \u003C 0.001), and more frequently had triple vessel disease (p = 0.004). The percentage of plaque rupture (72.4% vs. 56.4%, p = 0.018) and calcification (42.1% vs. 27.6%, p = 0.026) at culprit lesion were significantly higher in patients with RAP than those without RAP. A total of 148 RAP were revealed by OCT, including fibrous (72, 48.6%), lipid (50, 33.8%) and calcified plaques (26, 17.6%). The microvessels were also frequently observed in the RAP group than that in RIH and normal groups (59.2% vs. 8.7% vs. 9.6%, p \u003C 0.001). Multivariate logistic regression analysis showed that age, diabetes, and smoking history (all p \u003C 0.05) were independent risk factors for RAP. In terms of insights gained from OCT, RA atherosclerosis is not uncommon in ACS patients by OCT, sharing several morphological characters with early coronary atherosclerosis. Aging, diabetes, and smoking are risk factors for RAP.",{"EN":1334},"Assessment of radial artery atherosclerosis in acute coronary syndrome patients: an in vivo study using optical coherence tomography",{"VOID":1336},"[\"11070154586176247942\"]",{"VOID":1338},"Libby P, Buring JE, Badimon L, Hansson GK, Deanfield J, Bittencourt MS, Tokgozoglu L, Lewis EF. Atherosclerosis. Nat Rev Dis Primers. 2019;5(1):56.\nEklund C, Omerovic E, Haraldsson I, Friberg P, Gan LM. Radial artery intima-media thickness predicts major cardiovascular events in patients with suspected coronary artery disease. Eur Heart J Cardiovasc Imaging. 2014;15(7):769–75.\nXu M, Zhang M, Xu J, Zhu M, Zhang C, Zhang P, Zhang Y. The independent and add-on values of radial intima thickness measured by ultrasound biomicroscopy for diagnosis of coronary artery disease. Eur Heart J Cardiovasc Imaging. 2019;20(8):889–96.\nMyredal A, Osika W, Li Ming G, Friberg P, Johansson M. Increased intima thickness of the radial artery in patients with coronary heart disease. Vasc Med. 2010;15(1):33–7.\nEklund C, Friberg P, Gan LM. High-resolution radial artery intima-media thickness and cardiovascular risk factors in patients with suspected coronary artery disease—comparison with common carotid artery intima-media thickness. Atherosclerosis. 2012;221(1):118–23.\nChowdhury UK, Airan B, Mishra PK, Kothari SS, Subramaniam GK, Ray R, Singh R, Venugopal P. Histopathology and morphometry of radial artery conduits: basic study and clinical application. Ann Thorac Surg. 2004;78(5):1614–21.\nKaufer E, Factor SM, Frame R, Brodman RF. Pathology of the radial and internal thoracic arteries used as coronary artery bypass grafts. Ann Thorac Surg. 1997;63(4):1118–22.\nNicolosi AC, Pohl LL, Parsons P, Cambria RA, Olinger GN. Increased incidence of radial artery calcification in patients with diabetes mellitus. J Surg Res. 2002;102(1):1–5.\nRuengsakulrach P, Brooks M, Sinclair R, Hare D, Gordon I, Buxton B. Prevalence and prediction of calcification and plaques in radial artery grafts by ultrasound. J Thorac Cardiovasc Surg. 2001;122(2):398–9.\nMoon KW, Kim JH, Yoo KD, Oh SS, Kim DB, Kim CM. Evaluation of radial artery atherosclerosis by intravascular ultrasound. Angiology. 2013;64(1):73–9.\nJang I-K, Bouma BE, Kang D-H, Park S-J, Park S-W, Seung K-B, Choi K-B, Shishkov M, Schlendorf K, Pomerantsev E, et al. Visualization of coronary atherosclerotic plaques in patients using optical coherence tomography: comparison with intravascular ultrasound. J Am Coll Cardiol. 2002;39(4):604–9.\nPrati F, Guagliumi G, Mintz GS, Costa M, Regar E, Akasaka T, Barlis P, Tearney GJ, Jang IK, Arbustini E, et al. Expert review document part 2: methodology, terminology and clinical applications of optical coherence tomography for the assessment of interventional procedures. Eur Heart J. 2012;33(20):2513–20.\nYonetsu T, Kakuta T, Lee T, Takayama K, Kakita K, Iwamoto T, Kawaguchi N, Takahashi K, Yamamoto G, Iesaka Y, et al. Assessment of acute injuries and chronic intimal thickening of the radial artery after transradial coronary intervention by optical coherence tomography. Eur Heart J. 2010;31(13):1608–15.\nRuengsakulrach P, Sinclair R, Komeda M, Raman J, Gordon I, Buxton B. Comparative histopathology of radial artery versus internal thoracic artery and risk factors for development of intimal hyperplasia and atherosclerosis. Circulation. 1999;100(19 Suppl):II139-144.\nTearney GJ, Regar E, Akasaka T, Adriaenssens T, Barlis P, Bezerra HG, Bouma B, Bruining N, Cho JM, Chowdhary S, et al. Consensus standards for acquisition, measurement, and reporting of intravascular optical coherence tomography studies: a report from the International Working Group for Intravascular Optical Coherence Tomography Standardization and Validation. J Am Coll Cardiol. 2012;59(12):1058–72.\nYabushita H, Bouma BE, Houser SL, Aretz HT, Jang IK, Schlendorf KH, Kauffman CR, Shishkov M, Kang DH, Halpern EF, et al. Characterization of human atherosclerosis by optical coherence tomography. Circulation. 2002;106(13):1640–5.\nOtsuka F, Joner M, Prati F, Virmani R, Narula J. Clinical classification of plaque morphology in coronary disease. Nat Rev Cardiol. 2014;11(7):379–89.\nVink A, Schoneveld AH, Poppen M, de Kleijn DP, Borst C, Pasterkamp G. Morphometric and immunohistochemical characterization of the intimal layer throughout the arterial system of elderly humans. J Anat. 2002;200(Pt 1):97–103.\nBrzezinski M, Luisetti T, London MJ. Radial artery cannulation: a comprehensive review of recent anatomic and physiologic investigations. Anesth Analg. 2009;109(6):1763–81.\nBurris N, Schwartz K, Tang CM, Jafri MS, Schmitt J, Kwon MH, Toshinaga O, Gu J, Brown J, Brown E, et al. Catheter-based infrared light scanner as a tool to assess conduit quality in coronary artery bypass surgery. J Thorac Cardiovasc Surg. 2007;133(2):419–27.\nDi Vito L, Porto I, Burzotta F, Trani C, Pirozzolo G, Niccoli G, Leone AM, Crea F. Radial artery intima-media ratio predicts presence of coronary thin-cap fibroatheroma: a frequency domain-optical coherence tomography study. Int J Cardiol. 2013;168(3):1917–22.\nBrown EN, Burris NS, Gu J, Kon ZN, Laird P, Kallam S, Tang CM, Schmitt JM, Poston RS. Thinking inside the graft: applications of optical coherence tomography in coronary artery bypass grafting. J Biomed Opt. 2007;12(5):051704.\nNiccoli G, Montone RA, Di Vito L, Gramegna M, Refaat H, Scalone G, Leone AM, Trani C, Burzotta F, Porto I, et al. Plaque rupture and intact fibrous cap assessed by optical coherence tomography portend different outcomes in patients with acute coronary syndrome. Eur Heart J. 2015;36(22):1377–84.\nHoshino M, Yonetsu T, Usui E, Kanaji Y, Ohya H, Sumino Y, Yamaguchi M, Hada M, Hamaya R, Kanno Y, et al. Clinical significance of the presence or absence of lipid-rich plaque underneath intact fibrous cap plaque in acute coronary syndrome. J Am Heart Assoc. 2019;8(9):e011820.\nMueed I, Zhang Y, Aziz T, Chu V, Janssen LJ. Structural and electrophysiological changes in atherosclerotic radial artery grafts account for impairment of vessel reactivity. Atherosclerosis. 2009;206(2):405–10.\nZhang Y, Janssen L, Chu FV. Atherosclerosis of radial arterial graft may increase the potential of vessel spasm in coronary bypass surgery. J Thorac Cardiovasc Surg. 2005;130(5):1477–8.\nBrown EN, Burris NS, Kon ZN, Grant MC, Brazio PS, Xu C, Laird P, Gu J, Kallam S, Desai P, et al. Intraoperative detection of intimal lipid in the radial artery predicts degree of postoperative spasm. Atherosclerosis. 2009;205(2):466–71.\nArroyo-Úcar E, Torres Saura F, Vazquiánez R, Pizarro Sánchez G, Moreno R, Ibañez B. Calcified plaques in the radial artery: OCT insight. REC Interv Cardiol (Engl Edn) 2021.\nOwusu J, Barrett E. Early microvascular dysfunction: is the vasa vasorum a “missing link” in insulin resistance and atherosclerosis. Int J Mol Sci. 2021;22(14):7574.\nvan Son JA, Smedts F, Vincent JG, van Lier HJ, Kubat K. Comparative anatomic studies of various arterial conduits for myocardial revascularization. J Thorac Cardiovasc Surg. 1990;99(4):703–7.\nBoren J, Chapman MJ, Krauss RM, Packard CJ, Bentzon JF, Binder CJ, Daemen MJ, Demer LL, Hegele RA, Nicholls SJ, et al. Low-density lipoproteins cause atherosclerotic cardiovascular disease: pathophysiological, genetic, and therapeutic insights: a consensus statement from the European Atherosclerosis Society Consensus Panel. Eur Heart J. 2020;41(24):2313–30.\nSubbotin VM. Excessive intimal hyperplasia in human coronary arteries before intimal lipid depositions is the initiation of coronary atherosclerosis and constitutes a therapeutic target. Drug Discov Today. 2016;21(10):1578–95.\nGuerri-Guttenberg R, Castilla R, Cao G, Azzato F, Ambrosio G, Milei J. Coronary intimal thickening begins in fetuses and progresses in pediatric population and adolescents to atherosclerosis. Angiology. 2020;71(1):62–9.\nNakagawa K, Nakashima Y. Pathologic intimal thickening in human atherosclerosis is formed by extracellular accumulation of plasma-derived lipids and dispersion of intimal smooth muscle cells. Atherosclerosis. 2018;274:235–42.\nMcGovern E, Hosking MCK, Balbacid E, Voss C, Berger F, Schubert S, Harris KC. Optical coherence tomography for the early detection of coronary vascular changes in children and adolescents after cardiac transplantation: findings from the International Pediatric OCT Registry. J Am Coll Cardiol Imaging. 2019;12(12):2492–501.\nStary HC, Blankenhorn DH, Chandler AB, Glagov S, Insull W Jr, Richardson M, Rosenfeld ME, Schaffer SA, Schwartz CJ, Wagner WD, et al. A definition of the intima of human arteries and of its atherosclerosis-prone regions. A report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association. Circulation. 1992;85(1):391–405.\nThijssen DH, Carter SE, Green DJ. Arterial structure and function in vascular ageing: are you as old as your arteries? J Physiol. 2016;594(8):2275–84.\nKim YO, Song HC, Yoon SA, Yang CW, Kim NI, Choi YJ, Lee EJ, Kim WY, Chang YS, Bang BK. Preexisting intimal hyperplasia of radial artery is associated with early failure of radiocephalic arteriovenous fistula in hemodialysis patients. Am J Kidney Dis. 2003;41(2):422–8.\nChoudhary BP, Antoniades C, Brading AF, Galione A, Channon K, Taggart DP. Diabetes mellitus as a predictor for radial artery vasoreactivity in patients undergoing coronary artery bypass grafting. J Am Coll Cardiol. 2007;50(11):1047–53.\nMuller-Schweinitzer E, Muller SE, Reineke DC, Kern T, Carrel TP, Eckstein FS, Grapow MT. Reactive oxygen species mediate functional differences in human radial and internal thoracic arteries from smokers. J Vasc Surg. 2010;51(2):438–44.\nNeumann FJ, Sousa-Uva M, Ahlsson A, Alfonso F, Banning AP, Benedetto U, Byrne RA, Collet JP, Falk V, Head SJ, et al. 2018 ESC\u002FEACTS guidelines on myocardial revascularization. Eur Heart J. 2019;40(2):87–165.\nGaudino M, Benedetto U, Fremes S, Ballman K, Biondi-Zoccai G, Sedrakyan A, Nasso G, Raman J, Buxton B, Hayward PA, et al. Association of Radial Artery Graft vs saphenous vein graft with long-term cardiovascular outcomes among patients undergoing coronary artery bypass grafting: a systematic review and meta-analysis. JAMA. 2020;324(2):179–87.\nGaudino M, Di Franco A, Bhatt DL, Alexander JH, Abbate A, Azzalini L, Sandner S, Sharma G, Rao SV, Crea F, et al. The association between coronary graft patency and clinical status in patients with coronary artery disease. Eur Heart J. 2021;42(14):1433–41.\nWakeyama T, Ogawa H, Iida H, Takaki A, Iwami T, Mochizuki M, Tanaka T. Intima-media thickening of the radial artery after transradial intervention. An intravascular ultrasound study. J Am Coll Cardiol. 2003;41(7):1109–14.",{"VOID":1340},"10.1186\u002Fs12872-022-02561-5","2024-06-24T20:49:46.447+00:00","https:\u002F\u002Fbmccardiovascdisord.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs12872-022-02561-5",[1344,1359,1374,1387,1400,1413,1426,1439],{"id":1345,"sortIndex":21,"researcher":20,"roles":1346,"affiliations":1347,"properties":1356,"displayName":1358,"givenName":20,"familyName":20},"8197e063-0601-4c12-b28e-40401f21d0fc",[192],[1348],{"id":1349,"sortIndex":21,"affiliation":1350,"properties":20},"906ba016-7c14-4ca5-aa91-e41f08ef670c",{"id":1349,"createTime":20,"updateTime":20,"relativeEntities":1351,"slug":20,"properties":1352,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1355,"statistic":20},[],{"title":1353},{"VI":1354},"Department of Cardiology, Beijing Luhe Hospital, Capital Medical University, Beijing, China",[],{"title":1357},{"VI":1358},"Zixuan 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with chronic kidney disease (CKD) experience abnormality of intracardiac blood flow status during early-stages of disease. Left ventricular energy loss (EL) derived from vector flow mapping (VFM) represents fluid energy lost as heat in left ventricle and had been used to detect intracardiac blood flow efficiency. We aimed to evaluate the left ventricular EL in stage 1–3 CKD patients, and explored whether hypertension, a main cardiovascular risk, deteriorate the abnormality of intracardiac blood flow status. Transthoracic echocardiography was performed in 41 controls and 48 patients with stages 1–3 CKD. CKD patients consisted a subgroup with no hypertension, a subgroup with well-controlled hypertension and a subgroup with poorly controlled hypertension. The EL were calculated in the left ventricle using VFM analysis from the apical 3-chamber view. Furthermore, the correlation and stepwise multiple regression analysis were used to explore the potential independent predictors of left ventricular EL. Compared with controls, stage 1–3 CKD patients showed increased left ventricular EL during total diastole, late diastole, total systole, isovolumic contraction and ejection. CKD patients with poorly controlled hypertension had higher left ventricular EL compared to the other CKD subgroups. Additionally, the ratio of mitral early filling wave peak velocity and early mitral annular peak velocity on septal side, mitral early filling wave peak velocity, and left ventricular mass index were independent predictors of the diastolic EL; whereas systolic blood pressure and left ventricular mass index were independent predictors of the systolic EL. Left ventricular EL was a useful echocardiographic parameter to evaluate the impaired intracardiac blood flow efficiency in patients with stages 1–3 CKD. Hypertension was a crucial contributor for intracardiac blood flow abnormality. This study might provide valuable clinical data to discern cardiac dysfunction and reduce the cardiovascular risk in early-stage CKD.",{"EN":1513},"Assessment of left ventricular energy loss using vector flow mapping in patients with stages 1–3 chronic kidney 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Cardiovasc Diabetol. 2019;18:45.","https:\u002F\u002Fcardiab.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs12933-019-0849-6",{"doi":1681},"10.1186\u002Fs12933-019-0849-6",{"id":1683,"text":1684,"url":1685,"identifiers":1686},"c997d5d1-93f4-4fc5-a169-7669246ee589","Sengupta PP, Pedrizzetti G, Kilner PJ, Kheradvar A, Ebbers T, Tonti G, et al. Emerging trends in CV flow visualization. J Am Coll Cardiol Img. 2012;5:305–16.","https:\u002F\u002Fwww.sciencedirect.com\u002Fscience\u002Farticle\u002Fpii\u002FS1936878X12000125",{"doi":1687},"10.1016\u002Fj.jcmg.2012.01.003",{"id":367,"text":1689,"url":369,"identifiers":1690},"Itatani K, Okada T, Uejima T, Tanaka T, Ono M, Miyaji K, et al. Intraventricular flow velocity vector visualization based on the continuity equation and measurements of vorticity and wall shear stress. 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J Ultrasound Med. 2013;32:2063–71.",{"doi":371},{"id":367,"text":1704,"url":369,"identifiers":1705},"Hayashi T, Itatani K, Inuzuka R, Shimizu N, Shindo T, Hirata Y, et al. Dissipative energy loss within the left ventricle detected by vector flow mapping in children: Normal values and effects of age and heart rate. J Cardiol. 2015;66:403–10.",{"doi":371},{"id":367,"text":1707,"url":369,"identifiers":1708},"Wang Y, Ma R, Ding G, Hou D, Li Z, Yin L, et al. Left ventricular energy loss assessed by vector flow mapping in patients with prediabetes and type 2 diabetes mellitus. Ultrasound Med Biol. 2016;42:1730–40.",{"doi":371},{"id":1710,"text":1711,"url":1712,"identifiers":1713},"04d2cfda-dc47-4d4a-9fc9-cb2d93b7e357","Li CM, Bai WJ, Liu YT, Tang H, Rao L. Dissipative energy loss within the left ventricle detected by vector flow mapping in diabetic patients with controlled and uncontrolled blood glucose levels. 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Evaluation of left ventricular diastolic function based on flow energetic parameters in chronic kidney disease with diastolic dysfunction. Echocardiography (Mount Kisco, NY). 2019;36:567–76.",{"doi":371},{"id":367,"text":1764,"url":369,"identifiers":1765},"Bermejo J, Benito Y, Alhama M, Yotti R, Martínez-Legazpi P, Del Villar CP, et al. Intraventricular vortex properties in nonischemic dilated cardiomyopathy. Am J Physiol Heart Circ Physiol. 2014;306:H718–29.",{"doi":371},{"id":367,"text":1767,"url":369,"identifiers":1768},"Rodríguez Muñoz D, Moya Mur JL, Fernández-Golfín C, Becker Filho DC, González Gómez A, Fernández Santos S, et al. Left ventricular vortices as observed by vector flow mapping: main determinants and their relation to left ventricular filling. Echocardiography (Mount Kisco, NY). 2015;32:96–105.",{"doi":371},{"id":367,"text":1770,"url":369,"identifiers":1771},"Chen R, Zhao BW, Wang B, Tang HL, Li P, Pan M, et al. Assessment of left ventricular hemodynamics and function of patients with uremia by vortex formation using vector flow mapping. Echocardiography (Mount Kisco, NY). 2012;29:1081–90.",{"doi":371},{"id":367,"text":1773,"url":369,"identifiers":1774},"Wikstrand J. Left ventricular function in early primary hypertension. Functional consequences of cardiovascular structural changes. Hypertension. 1984;6:Iii108–16.",{"doi":371},{"id":367,"text":1776,"url":369,"identifiers":1777},"Xu L, Sun C, Zhu X, Liu W, Ta S, Zhao D, et al. Characterization of left ventricle energy loss in healthy adults using vector flow mapping: preliminary results. Echocardiography (Mount Kisco, NY). 2017;34:700–8.",{"doi":371},{"id":20,"text":1779,"url":20,"identifiers":1780},"Thomas G, Xie D, Chen HY, Anderson AH, Appel LJ, Bodana S, et al. Prevalence and prognostic significance of apparent treatment resistant hypertension in chronic kidney disease: report from the chronic renal insufficiency cohort study. 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Please see the retraction notice for more detail: https:\u002F\u002Fdoi.org\u002F10.1186\u002Fs12872-020-01688-7.",{"EN":1791},"Retraction Note: Prognostic value of heart failure in hemodialysis-dependent end-stage renal disease patients with myocardial fibrosis quantification by extracellular volume on cardiac magnetic resonance imaging",{"VOID":1793},"[]",{"EN":1795},"",{"VOID":1797},"Xu H, Yang Z, Zhang Y, et al. Prognostic value of heart failure in hemodialysis-dependent end-stage renal disease patients with myocardial fibrosis quantification by extracellular volume on cardiac magnetic resonance imaging. BMC Cardiovasc Disord. 2020;20:12. https:\u002F\u002Fdoi.org\u002F10.1186\u002Fs12872-019-01313-2.\nPrchal D, Holmes DT, Levin A. Nephrogenic systemic fibrosis: the story unfolds. 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coronary events (CE) and ischemic stroke share many risk factors, there are also some important differences. The aim of this paper was to assess the association of risk factors in relation to incident CE and ischemic stroke and to evaluate the heterogeneity in patterns of risk factors between the two outcomes.\n Traditional risk factors and inflammatory markers associated with coronary events and ischemic stroke were measured in the Malmö Diet and Cancer Cohort (MDCS, n = 26 519), where a total of 2270 incident ischemic stroke and 3087 incident CE occurred during a mean follow up time 19 ± 6 years, and in relation to inflammatory markers in the cardiovascular sub-cohort (MDC-CV, n = 4795). Cox regression analysis was used to obtain hazard ratios. A modified Lunn-McNeil competing risk analysis was conducted to assess the significance of any differences in risk profiles of these outcomes. Most cardiovascular risk factors were associated both with incident CE and ischemic stroke. However, current smoking, ApoB, low ApoA1, male sex and education level of ≤ 9 years of schooling were preferentially associated with CE compared to ischemic stroke. Conversely, age showed a stronger association with ischemic stroke than with CE. CE and ischemic stroke have broadly similar risk factors profiles. However, there are some important differential associations, as well as substantial differences in the magnitude of the association. These could reflect the distinct biology of atherogenesis in different vascular beds. 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Ann Intern Med. 2005;143(11):785–92.",{"doi":371},{"id":367,"text":2360,"url":369,"identifiers":2361},"Jackson CA, Hutchison A, Dennis MS, Wardlaw JM, Lindgren A, Norrving B, Anderson CS, Hankey GJ, Jamrozik K, Appelros P, et al. Differing risk factor profiles of ischemic stroke subtypes: evidence for a distinct lacunar arteriopathy? Stroke. 2010;41(4):624–9.",{"doi":371},{"id":20,"text":2363,"url":20,"identifiers":2364},"Leppala JM, Virtamo J, Fogelholm R, Albanes D, Heinonen OP. Different risk factors for different stroke subtypes: association of blood pressure, cholesterol, and antioxidants. Stroke. 1999;30(12):2535–40.",{},{"id":367,"text":2366,"url":369,"identifiers":2367},"Perneger TV. What’s wrong with Bonferroni adjustments. BMJ. 1998;316(7139):1236–8.",{"doi":371},{"id":367,"text":2369,"url":369,"identifiers":2370},"Rothman KJ. No adjustments are needed for multiple comparisons. Epidemiology. 1990;1(1):43–6.",{"doi":371},{"id":2372,"createTime":2373,"updateTime":2374,"relativeEntities":2375,"slug":2376,"properties":2377,"entityType":183,"verifyStatus":184,"verifyTime":2388,"verifyNote":186,"languages":20,"translateLanguages":20,"viewCount":21,"primaryUrl":2389,"fullTextUrl":20,"authors":2390,"publicationType":311,"publisherRelationship":2483,"citationCount":2234,"citationInfo":2529,"publishDate":2532,"publishYear":2530,"citationAnalyzeStatus":1091,"lastCitationAnalyze":2533,"indexDatabases":2534,"openAccess":20,"references":20,"isForceReanalyzing":472},"b822fcca-22a7-4650-813c-dd525040becd","2024-01-17T18:58:28.157+00:00","2026-07-23T20:46:17.525+00:00",[],"The-feasibility-and-safety-of-a-through-and-through-wire-technique-for-central-venous-occlusion-in-dialysis-patients",{"abstract":2378,"title":2380,"gsPaper":2382,"references":2384,"doi":2386},{"EN":2379},"To retrospectively compare the operation time, success rate and efficacy between unidirectional and bidirectional procedures in the treatment of central venous occlusion diseases (CVOD), assess the advantages of the bidirectional approach, and determine the characteristics of CVOD appropriate for the bidirectional approach treatment. A total of 49 patients who underwent endovascular interventions with all relevant data between January 2011 and December 2015 at the First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China, were included in this retrospective study, and were categorized into two groups: the 19 patients in group 1 had undergone percutaneous transluminal venoplasty (PTV) via a conventional technique (unidirectional procedure from the vein distal or proximal to the obstructive lesion), and the 30 in group 2 had undergone flossing wire technique (bidirectional procedure from femoral vein and the vein distal to obstructive lesion and using a flossing wire technique). The technical success rate, the fluoroscopy time in the procedure, perioperative complications, and patency were evaluated retrospectively. Compared with group 1, group 2 had a higher initial technical success rate (83.33% vs. 47.36%, p = 0.012) but a shorter fluoroscopy time (82.6 ± 26.1 vs. 116.1 ± 42.1, p = 0.048). Receiver operating characteristic (ROC) analysis indicated that a lesion with a length of 6.5 cm was the best predictor of technique success (p = 0.02) in group 1, but no cut-off value was identified for group 2. There were no significant differences in perioperative complications between these two groups. The complication rates were 31.58% (6\u002F19) in group 1 and 6.67% (2\u002F30) in group 2, (p = 0.043), respectively. No significant difference was observed between these two groups with respect to the stent patency rate. Compared with the conventional technique, the flossing wire technique has a higher success rate, shorter fluoroscopy time, fewer complications and similar patency rate. It is a feasible treatment for CVOD, especially for long obstructive lesions.",{"EN":2381},"The feasibility and safety of a through-and-through wire technique for central venous occlusion in dialysis patients",{"VOID":2383},"[\"10388912750985153404\"]",{"VOID":2385},"Modabber M, Kundu S. Central venous disease in hemodialysis patients: an update. Cardiovasc Intervent Radiol. 2013;36(4):898–903.\nAsif A, Salman L, Carrillo RG, Garisto JD, Lopera G, Barakat U, Lenz O, Yevzlin A, Agarwal A, Gadalean F, et al. Patency rates for angioplasty in the treatment of pacemaker-induced central venous stenosis in hemodialysis patients: results of a multi-center study. Semin Dial. 2009;22(6):671–6.\nKotoda A, Akimoto T, Kato M, Kanazawa H, Nakata M, Sugase T, Ogura M, Ito C, Sugimoto H, Muto S, et al. Central venous stenosis among hemodialysis patients is often not associated with previous central venous catheters. ASAIO J. 2011;57(5):439–43.\nMorosetti M, Meloni C, Gandini R, Galderisi C, Pampana E, Nicoletti M, Gallucci MT, Simonetti G, Casciani CU. Late symptomatic venous stenosis in three hemodialysis patients without previous central venous catheters. Artif Organs. 2000;24(12):929–31.\nTordoir JH, Bode AS, Peppelenbosch N, van der Sande FM, de Haan MW. Surgical or endovascular repair of thrombosed dialysis vascular access: is there any evidence? J Vasc Surg. 2009;50(4):953–6.\nBakken AM, Protack CD, Saad WE, Lee DE, Waldman DL, Davies MG. Long-term outcomes of primary angioplasty and primary stenting of central venous stenosis in hemodialysis patients. J Vasc Surg. 2007;45(4):776–83.\nMaya ID, Saddekni S, Allon M. Treatment of refractory central vein stenosis in hemodialysis patients with stents. Semin Dial. 2007;20(1):78–82.\nAnaya-Ayala JE, Smolock CJ, Colvard BD, Naoum JJ, Bismuth J, Lumsden AB, Davies MG, Peden EK. Efficacy of covered stent placement for central venous occlusive disease in hemodialysis patients. J Vasc Surg. 2011;54(3):754–9.\nHaskal ZJ, Trerotola S, Dolmatch B, Schuman E, Altman S, Mietling S, Berman S, McLennan G, Trimmer C, Ross J, et al. Stent graft versus balloon angioplasty for failing dialysis-access grafts. N Engl J Med. 2010;362(6):494–503.\nMaskova J, Komarkova J, Kivanek J, Danes J, Slavikova M. Endovascular treatment of central vein stenoses and\u002For occlusions in hemodialysis patients. Cardiovasc Intervent Radiol. 2003;26(1):27–30.\nOzyer U, Harman A, Yildirim E, Aytekin C, Karakayali F, Boyvat F. Long-term results of angioplasty and stent placement for treatment of central venous obstruction in 126 hemodialysis patients: a 10-year single-center experience. AJR Am J Roentgenol. 2009;193(6):1672–9.\nKim YC, Won JY, Choi SY, Ko HK, Lee KH, Lee do Y, Kang BC, Kim SJ. Percutaneous treatment of central venous stenosis in hemodialysis patients: long-term outcomes. Cardiovasc Intervent Radiol. 2009;32(2):271–8.\nVerstandig AG, Bloom AI, Sasson T, Haviv YS, Rubinger D. Shortening and migration of Wallstents after stenting of central venous stenoses in hemodialysis patients. Cardiovasc Intervent Radiol. 2003;26(1):58–64.\nChen CY, Liang HL, Pan HB, Chung HM, Chen WL, Fang HC, Lo A, Chen CK, Lai PH, Yang CF. Metallic stenting for treatment of central venous obstruction in hemodialysis patients. J Chin Med Assoc. 2003;66(3):166–72.\nde Graaf R, van Laanen J, Sailer A, Tordoir J. Long segment recanalization and dedicated central venous stenting in an ultimate attempt to restore vascular access central vein outflow. J Vasc Access. 2014;15 Suppl 7:S109–113.\nKrycinska R, Trznadel A, Kuchalska P, Lis M, Dolega-Kozierowski B, Dys K, Drelichowski S, Witkiewicz W. Brachiocephalic Vein Stenting and Body-Floss Technique as a Treatment of CVD in Dialysis-Dependent Patient - Case Report and Literature Review. Pol J Radiol. 2015;80:247–51.\nFoundation NK. KDOQI Clinical Practice Guidelines and Clinical Practice Recommendations for 2006 Updates. Am J Kidney Dis. 2006;48(July 2006):S1–S322.\nSection II. Haemodialysis adequacy. Nephrol Dial Transplant. 2002;17 Suppl 7:16–31.\nLevit RD, Cohen RM, Kwak A, Shlansky-Goldberg RD, Clark TW, Patel AA, Stavropoulos SW, Mondschein JI, Solomon JA, Tuite CM, et al. Asymptomatic central venous stenosis in hemodialysis patients. Radiology. 2006;238(3):1051–6.\nThwaites SE, Robless PA. Central vein stenosis in an Asian hemodialysis population. Asian Cardiovasc Thorac Ann. 2012;20(5):560–5.\nShi YX, Ye M, Liang W, Zhang H, Zhao YP, Zhang JW. Endovascular treatment of central venous stenosis and obstruction in hemodialysis patients. Chin Med J. 2013;126(3):426–30.\nSidawy AN, Gray R, Besarab A, Henry M, Ascher E, Silva Jr M, Miller A, Scher L, Trerotola S, Gregory RT, et al. Recommended standards for reports dealing with arteriovenous hemodialysis accesses. J Vasc Surg. 2002;35(3):603–10.\nDuvnjak S, Andersen P. Endovascular treatment of superior vena cava syndrome. Int Angiol. 2011;30(5):458–61.\nRajan DK, Saluja JS. Use of nitinol stents following recanalization of central venous occlusions in hemodialysis patients. Cardiovasc Intervent Radiol. 2007;30(4):662–7.\nKundu S, Modabber M, You JM, Tam P, Nagai G, Ting R. Use of PTFE stent grafts for hemodialysis-related central venous occlusions: intermediate-term results. Cardiovasc Intervent Radiol. 2011;34(5):949–57.\nFerral H, Bjarnason H, Wholey M, Lopera J, Maynar M, Castaneda-Zuniga WR. Recanalization of occluded veins to provide access for central catheter placement. J Vasc Interv Radiol. 1996;7(5):681–5.\nMatsushita J, Morita S, Suzuki K, Inoue H, Yokomizo H, Yoshimatsu K, Aoshima H, Mae M, Ueno E. Pull-through technique with pincer tactics for stent placement in severe superior vena cava syndrome. Annals of vascular surgery. 2012;26(3):421. e411-425.\nClark TW. Endovascular stenting in superior vena cava syndrome: utility of a through-and-through guidewire technique. Can Assoc Radiol J. 2000;51(4):254–9.\nMalgor RD, Wood EA, Gasparis AP, Hashisho M. Endovascular strategy for recanalization of long-segment central vein occlusion with concomitant arteriovenous fistula creation. Annals of vascular surgery. 2012;26(7):1012. e1017-1020.\nMassmann A, Rostam A, Fries P, Buecker A. A wire transposition technique for recanalization of chronic complex central venous occlusions. Phlebology. 2016;31(1):57–60.\nHaage P, Vorwerk D, Piroth W, Schuermann K, Guenther RW. Treatment of hemodialysis-related central venous stenosis or occlusion: results of primary Wallstent placement and follow-up in 50 patients. Radiology. 1999;212(1):175–80.\nMaeda K, Furukawa A, Yamasaki M, Murata K. Percutaneous transluminal angioplasty for Brescia-Cimino hemodialysis fistula dysfunction: technical success rate, patency rate and factors that influence the results. Eur J Radiol. 2005;54(3):426–30.\nYamamoto K, Komori K, Narita H, Morimae H, Tokuda Y, Araki Y, Oshima H, Usui A. A 'through-and-through bowing technique' for antegrade thoracic endovascular aneurysm repair with total arch debranching: a technical note and the initial results. Eur J Cardiothorac Surg. 2015.\nRamponi F, Vallely MP, Stephen MS, Bannon PG, Bayfield MS, White GH. Transapical wire-assisted endovascular repair of thoracic aortic dissection. J Endovasc Ther. 2011;18(3):350–4.\nDayama A, Riesenman PJ, Cheek RA, Kasirajan K. Endovascular management of aortic arch vessel occlusion: successful revascularization of innominate and left subclavian arteries. Vasc Endovasc Surg. 2012;46(3):273–6.\nvan Loon MM, Kessels AG, van der Sande FM, Tordoir JH. Cannulation practice patterns in haemodialysis vascular access: predictors for unsuccessful cannulation. J Ren Care. 2009;35(2):82–9.\nKovalik EC, Newman GE, Suhocki P, Knelson M, Schwab SJ. Correction of central venous stenoses: use of angioplasty and vascular Wallstents. Kidney Int. 1994;45(4):1177–81.",{"VOID":2387},"10.1186\u002Fs12872-016-0411-3","2024-08-30T13:47:02.111+00:00","https:\u002F\u002Fbmccardiovascdisord.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs12872-016-0411-3",[2391,2406,2419,2432,2445,2457,2470],{"id":2392,"sortIndex":21,"researcher":20,"roles":2393,"affiliations":2394,"properties":2403,"displayName":2405,"givenName":20,"familyName":20},"041b5c93-eb69-4296-bb47-fdddba2852d9",[192],[2395],{"id":2396,"sortIndex":21,"affiliation":2397,"properties":20},"6c0d9b67-8e3e-4260-84fa-0752ef014206",{"id":2396,"createTime":20,"updateTime":20,"relativeEntities":2398,"slug":20,"properties":2399,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":2402,"statistic":20},[],{"title":2400},{"VI":2401},"The Department of Interventional Radiology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China",[],{"title":2404},{"VI":2405},"Yonghui Huang",{"id":2407,"sortIndex":207,"researcher":20,"roles":2408,"affiliations":2409,"properties":2416,"displayName":2418,"givenName":20,"familyName":20},"45ea5215-aba4-4638-985d-ad726d52c9cb",[192],[2410],{"id":2396,"sortIndex":21,"affiliation":2411,"properties":20},{"id":2396,"createTime":20,"updateTime":20,"relativeEntities":2412,"slug":20,"properties":2413,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":2415,"statistic":20},[],{"title":2414},{"VI":2401},[],{"title":2417},{"VI":2418},"Bing 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