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The study group consisted of 41 RA patients. The following parameters were assessed at subsequent visits [initial (T0), follow-up after 6 years (T6)]: traditional CV risk factors, carotid intima media thickness (cIMT), QTc duration, serum concentration of amino-terminal pro-brain natriuretic peptide (NT-proBNP). A comparative cIMT assessment was performed on 23 healthy controls of comparable age. The mean (SD) cIMT value in RA patients was significantly higher at T6 than at T0 [0.87 (0.21) vs 0.76 (0.15) mm, p \u003C 0.001], the increase in patients with atherosclerotic plaques was noted. Patients with plaques were significantly older, had higher inflammatory parameters. The mean cIMT was significantly higher in RA patients than in controls at both T6, T0 visits. Certain traditional CV risk factors exacerbated during follow up. Unfavorable metabolic parameters and significantly higher cIMT were found in male patients than in female patients at T6. During follow-up, no significant differences in NT-proBNP, QTc were found. There were no significant relationships between cIMT, NT-proBNP, QTc and parameters of disease activity at T6. During the 6-year course of established RA, significant exacerbation of atherosclerosis was found, revealed by higher cIMT. A careful monitoring should be applied to patients with atherosclerotic plaques and of male gender due to higher burden of CV risk. In long-standing disease, traditional CV risk factors seem to play a key role, beyond the inflammatory activity.",{"EN":180},"Prospective assessment of cardiovascular risk parameters in patients with rheumatoid arthritis",{"VOID":182},"[\"330000126527581040\"]",{"VOID":184},"Corrales A, Dessein PH, Tsang L, Pina T, Blanco R, Gonzalez-Juanatey C, et al. Carotid artery plaque in women with rheumatoid arthritis and low estimated cardiovascular disease risk: a cross-sectional study. Arthritis Res Ther. 2015;17:55.\nProvan SA, Angel K, Odegård S, Mowinckel P, Atar D, Kvien TK. The association between disease activity and NT-proBNP in 238 patients with rheumatoid arthritis: a 10-year longitudinal study. Arthritis Res Ther. 2008;10:R70.\nPope JE, Nevskaya T, Barra L, Parraga G. Carotid artery atherosclerosis in patients with active rheumatoid arthritis: predictors of plaque occurrence and progression over 24 weeks. Open Rheumatol J. 2016;10:49–59.\nLazzerini PE, Capecchi PL, Acampa M, Galeazzi M, Laghi-Pasini F. Arrhythmic risk in rheumatoid arthritis: the driving role of systemic inflammation. Autoimmun Rev. 2014;13:936–44.\nProvan S, Angel K, Semb AG, Atar D, Kvien TK. NT-proBNP predicts mortality in patients with rheumatoid arthritis: results from 10-year follow-up of the EURIDISS study. Ann Rheum Dis. 2010;69:1946–50.\nZhang J, Chen L, Delzell E, Muntner P, Hillegass WB, Safford MM, et al. The association between inflammatory markers, serum lipids and the risk of cardiovascular events in patients with rheumatoid arthritis. Ann Rheum Dis. 2014;73:1301–8.\nNavarro-Millán I, Yang S, DuVall SL, Chen L, Baddley J, Cannon GW, et al. Association of hyperlipidaemia, inflammation and serological status and coronary heart disease among patients with rheumatoid arthritis: data from the National Veterans Health Administration. Ann Rheum Dis. 2016;75:341–7.\nAmbrosino P, Lupoli R, Di Minno A, Tasso M, Peluso R, Di Minno MN. Subclinical atherosclerosis in patients with rheumatoid arthritis. A meta-analysis of literature studies. Thromb Haemost. 2015;113:916–30.\nWang P, Guan SY, Xu SZ, Li HM, Leng RX, Li XP, et al. Increased carotid intima-media thickness in rheumatoid arthritis: an update meta-analysis. Clin Rheumatol. 2016;35:315–23.\nTargońska-Stępniak B, Drelich-Zbroja A, Majdan M. The relationship between carotid intima-media thickness and the activity of rheumatoid arthritis. J Clin Rheumatol. 2011;17:249–55.\nSödergren A, Karp K, Bengtsson C, Möller B, Rantapää-Dahlqvist S, Wållberg-Jonsson S. The extent of subclinical atherosclerosis is partially predicted by the inflammatory load: a prospective study over 5 years in patients with rheumatoid arthritis and matched controls. J Rheumatol. 2015;42:935–42.\nMirjafari H, Welsh P, Verstappen SM, Wilson P, Marshall T, Edlin H, et al. N-terminal pro-brain-type natriuretic peptide (NT-pro-BNP) and mortality risk in early inflammatory polyarthritis: results from the Norfolk arthritis registry (NOAR). Ann Rheum Dis. 2014;73:684–90.\nTargońska-Stępniak B, Majdan M. Amino-terminal pro-brain natriuretic peptide as a prognostic marker in patients with rheumatoid arthritis. Clin Rheumatol. 2011;30:61–9.\nAvouac J, Meune C, Chenevier-Gobeaux C, Dieudé P, Borderie D, Lefevre G, et al. Inflammation and disease activity are associated with high circulating cardiac markers in rheumatoid arthritis independently of traditional cardiovascular risk factors. J Rheumatol. 2014;41:248–55.\nLazzerini PE, Capecchi PL, Laghi-Pasini F. Systemic inflammation and arrhythmic risk: lessons from rheumatoid arthritis. Eur Heart J. 2017;38:1717–27.\nAletaha D, Neogi T, Silman AJ, Funovits J, Felson DT, Bingham CO 3rd, et al. 2010 Rheumatoid arthritis classification criteria: an American College of Rheumatology\u002FEuropean League Against Rheumatism collaborative initiative. Arthritis Rheum. 2010;62:2569–81.\nPrevoo ML, van’t Hof MA, Kuper HH, van Leeuwen AN, van de Putte LB, van Riel PL. Modified disease activity scores that include twenty-eight-joint counts: development and validation in a prospective longitudinal study of patients with rheumatoid arthritis. Arthritis Rheum. 1995;38:44–8.\nPincus T, Sokka T, Kautiainen H. Further development of a physical function scale on a MDHAQ [corrected] for standard care of patients with rheumatic diseases. J Rheumatol. 2005;32:1432–9.\nPopa CD, Arts E, Fransen J, van Riel PLCM. Atherogenic Index and high-density lipoprotein cholesterol as cardiovascular risk determinants in Rheumatoid Arthritis: The Impact of Therapy with Biologicals. Mediators Inflamm. 2012;2012:785946.\nPeters MJL, Symmons DPM, McCarey D, Dijkmans BAC, Nicola P, Kvien TK, et al. EULAR evidence-based recommendations for cardiovascular risk management in patients with rheumatoid arthritis and other forms of inflammatory arthritis. Ann Rheum Dis. 2010;69:325–31.\nGonzalez-Gay MA, Gonzalez-Juanatey C, Vazquez-Rodriguez TR, Martin J, Llorca J. Endothelial dysfunction, carotid intima-media thickness and accelerated atherosclerosis in rheumatoid arthritis. Semin Arthritis Rheum. 2008;38:67–70.\nGonzalez-Juanatey C, Llorca J, Martin J, Gonzalez-Gay MA. Carotid intima-media thickness predicts the development of cardiovascular events in patients with rheumatoid arthritis. Semin Arthritis Rheum. 2009;38:366–71.\nGoldenberg I, Moss AJ, Zareba W. QT interval: how to measure it and what is “normal”. J Cardiovasc Electrophysiol. 2006;17:333–6.\nVan Sijl AM, Van Den Hurk K, Peters MJ, Van Halm VP, Nijpels G, Stehouwer CDA, et al. Different type of carotid Arterial Wall remodeling in rheumatoid arthritis compared with healthy subjects: a case-control study. J Rheumatol. 2012;39:2261–6.\nGiles JT, Post WS, Blumenthal RS, Polak J, Petri M, Gelber AC, et al. Longitudinal predictors of progression of carotid atherosclerosis in rheumatoid arthritis. Arthritis Rheum. 2011;63:3216–25.\nEvans MR, Escalante A, Battafarano DF, Freeman GL, O’Leary DH, del Rincón I. Carotid atherosclerosis predicts incident acute coronary syndromes in rheumatoid arthritis. Arthritis Rheum. 2011;63:1211–20.\nSemb AG, Rollefstad S, Provan SA, Kvien TK, Stranden E, Olsen IC, et al. Carotid plaque characteristics and disease activity in rheumatoid arthritis. J Rheumatol. 2013;40:359–68.\nJansen H, Willenborg C, Lieb W, Zeng L, Ferrario PG, Loley C, et al. Rheumatoid arthritis and coronary artery disease: genetic analyses do not support a causal relation. J Rheumatol. 2017;44:4–10.\nBaghdadi LR, Woodman RJ, Shanahan EM, Mangoni AA. The impact of traditional cardiovascular risk factors on cardiovascular outcomes in patients with rheumatoid arthritis: a systematic review and meta-analysis. PLoS One. 2015;10:e0117952.\nKitas GD, Gabriel SE. Cardiovascular disease in rheumatoid arthritis: state of the art and future perspectives. Ann Rheum Dis. 2011;70:8–14.\nDalbeni A, Giollo A, Tagetti A, Atanasio S, Orsolini G, Cioffi G, et al. Traditional cardiovascular risk factors or inflammation: which factors accelerate atherosclerosis in arthritis patients? Int J Cardiol. 2017;236:488–92.\nRoman MJ, Naqvi TZ, Gardin JM, et al. American society of echocardiography report. Clinical application of noninvasive vascular ultrasound in cardiovascular risk stratification: a report from the American Society of Echocardiography and the society for vascular medicine and biology. Vasc Med. 2006;11:201–11.\nKim HJ, Kim MJ, Lee CK, Hong YH. Effects of methotrexate on carotid intima-media thickness in patients with rheumatoid arthritis. J Korean Med Sci. 2015;30:1589–96.\nDel Porto F, Laganà B, Lai S, Nofroni I, Tinti F, Vitale M, et al. Response to anti-tumour necrosis factor alpha blockade is associated with reduction of carotid intima-media thickness in patients with active rheumatoid arthritis. Rheumatology (Oxford). 2007;46:1111–5.\nPeters MJ, Welsh P, McInnes IB, Wolbink G, Dijkmans BA, Sattar N, et al. Tumour necrosis factor {alpha} blockade reduces circulating N-terminal pro-brain natriuretic peptide levels in patients with active rheumatoid arthritis: results from a prospective cohort study. Ann Rheum Dis. 2010;69:1281–5.",{"VOID":186},"10.1186\u002Fs12947-018-0136-9","PUBLICATION","VERIFIED","2024-06-24T02:09:53.807+00:00","Auto Verify","https:\u002F\u002Fcardiovascularultrasound.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs12947-018-0136-9",[193,211,224,237,252],{"id":194,"sortIndex":21,"researcher":20,"roles":195,"affiliations":197,"properties":206,"displayName":208,"givenName":20,"familyName":20},"1cb8469c-7d10-48db-b3be-ce65c4ddd931",[196],"AUTHOR",[198],{"id":199,"sortIndex":21,"affiliation":200,"properties":20},"24120e2a-ce35-4d57-acf8-2b66e59ec005",{"id":199,"createTime":20,"updateTime":20,"relativeEntities":201,"slug":20,"properties":202,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":205,"statistic":20},[],{"title":203},{"VI":204},"Department of Rheumatology and Connective Tissue Diseases, Medical University of Lublin, Lublin, 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5-7 months of physical inactivity during hibernation, brown bears (Ursus arctos) are able to cope with physiological conditions that would be detrimental to humans. During hibernation, the tissue metabolic demands fall to 25% of the active state. Our objective was to assess cardiac function associated with metabolic depression in the hibernating vs. active states in free-ranging Scandinavian brown bears. We performed echocardiography on seven free-ranging brown bears in Dalarna, Sweden, anesthetized with medetomidine-zolazepam-tiletamine-ketamine during winter hibernation in February 2013 and with medetomidine-zolazepam-tiletamine during active state in June 2013. We measured cardiac output noninvasively using estimates of hemodynamics obtained by pulsed wave Doppler echocardiography and 2D imaging. Comparisons were made using paired T-tests. During hibernation, all hemodynamic indices were significantly decreased (hibernating vs. active state): mean heart rate was 26.0 (standard deviation (SD): 5.6) beats per min vs. 75.0 (SD: 17.1) per min (P = 0.002), mean stroke volume 32.3 (SD: 5.2) ml vs. 47.1 (SD: 7.9) ml (P = 0.008), mean cardiac output 0.86 (SD: 0.31) l\u002Fmin vs. 3.54 (SD: 1.04) l\u002Fmin (P = 0.003), and mean cardiac index 0.63 (SD: 0.21) l\u002Fmin\u002Fkg vs. 2.45 (SD: 0.52) l\u002Fmin\u002F m2 (P \u003C 0.001). Spontaneous echo contrast was present in all cardiac chambers in all seven bears during hibernation, despite the absence of atrial arrhythmias and valvular disease. Free-ranging brown bears demonstrate hemodynamics comparable to humans during active state, whereas during hibernation, we documented extremely low-flow hemodynamics. Understanding these physiological changes in bears may help to gain insight into the mechanisms of cardiogenic shock and heart failure in humans.",{"EN":340},"Low cardiac output as physiological phenomenon in hibernating, free-ranging Scandinavian brown bears (Ursus arctos) – an observational 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S, Swenson J: Denning behaviour of Scandinavian brown bears Ursus arctos. Wildl Biol. 2005, 11: 125-132.","https:\u002F\u002Flink.springer.com\u002F10.1007\u002Fs10440-022-00541-7",{"doi":525},"10.1007\u002Fs10440-022-00541-7",{"id":527,"text":528,"url":529,"identifiers":530},"0de8b2c1-f8b5-4cd9-a6a1-af9bab5795cf","Shavlakadze T, Grounds M: Of bears, frogs, meat, mice and men: complexity of factors affecting skeletal muscle mass and fat. BioEssays. 2006, 28: 994-1009. 10.1002\u002Fbies.20479.","https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1002\u002Fbies.20479",{"doi":531},"10.1002\u002Fbies.20479",{"id":533,"text":534,"url":535,"identifiers":536},"0306289e-71f9-47a0-96be-e9de296e7a31","Donahue SW, Galley SA, Vaughan MR, Patterson-Buckendahl P, Demers LM, Vance JL, McGee ME: Parathyroid hormone may maintain bone formation in hibernating black bears (Ursus americanus) to prevent disuse osteoporosis. J Exp Biol. 2006, 209: 1630-1638. 10.1242\u002Fjeb.02185.","https:\u002F\u002Fjournals.biologists.com\u002Fjeb\u002Farticle\u002F209\u002F9\u002F1630\u002F16954\u002FParathyroid-hormone-may-maintain-bone-formation-in",{"doi":537},"10.1242\u002Fjeb.02185",{"id":521,"text":539,"url":523,"identifiers":540},"Vestergaard P, Støen O-G, Swenson JE, Mosekilde L, Heickendorff L, Fröbert O: Vitamin D status and bone and connective tissue turnover in brown bears (Ursus arctos) during hibernation and the active state. PLoS One. 2011, 6: e21483-10.1371\u002Fjournal.pone.0021483.",{"doi":525},{"id":542,"text":543,"url":544,"identifiers":545},"57582eee-ff26-4196-8e3c-b771bbaf9690","Fink T, Rasmussen JG, Emmersen J, Pilgaard L, Fahlman Å, Brunberg S, Josefsson J, Arnemo JM, Zachar V, Swenson JE, Fröbert O: Adipose-derived stem cells from the brown bear (Ursus arctos) spontaneously undergo chondrogenic and osteogenic differentiation in vitro. Stem Cell Res. 2011, 7: 89-95. 10.1016\u002Fj.scr.2011.03.003.","https:\u002F\u002Flinkinghub.elsevier.com\u002Fretrieve\u002Fpii\u002FS1873506111000286",{"doi":546},"10.1016\u002Fj.scr.2011.03.003",{"id":548,"text":549,"url":550,"identifiers":551},"9f01d4ff-ccb0-49ec-9511-b54c85f78e54","Nelson OL, McEwen M-M, Robbins CT, Felicetti L, Christensen WF: Evaluation of cardiac function in active and hibernating grizzly bears. J Am Vet Med Assoc. 2003, 223: 1170-1175. 10.2460\u002Fjavma.2003.223.1170.","https:\u002F\u002Favmajournals.avma.org\u002Fview\u002Fjournals\u002Fjavma\u002F223\u002F8\u002Fjavma.2003.223.1170.xml",{"doi":552},"10.2460\u002Fjavma.2003.223.1170",{"id":521,"text":554,"url":523,"identifiers":555},"Nelson OL, Robbins CT, Wu Y, Granzier H: Titin isoform switching is a major cardiac adaptive response in hibernating grizzly bears. 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J Am Coll Cardiol. 1991, 18: 398-404. 10.1016\u002F0735-1097(91)90592-W.","https:\u002F\u002Fwww.sciencedirect.com\u002Fscience\u002Farticle\u002Fpii\u002F073510979190592W",{"doi":597},"10.1016\u002F0735-1097(91)90592-w",{"id":599,"text":600,"url":601,"identifiers":602},"614bbefc-4553-4256-9623-2781dd84c68a","Leung DYC, Black IW, Cranney GB, Hopkins AP, Walsh WF: Prognostic implications of left artial spontaneous echo contrast in nonvalvular atrial fibrillation. J Am Coll Cardiol. 1994, 24: 755-762. 10.1016\u002F0735-1097(94)90025-6.","https:\u002F\u002Fwww.sciencedirect.com\u002Fscience\u002Farticle\u002Fpii\u002F0735109794900256",{"doi":603},"10.1016\u002F0735-1097(94)90025-6",{"id":605,"text":606,"url":607,"identifiers":608},"6b2614e4-e3cd-41bd-9b2b-aaad9f693aae","Iliceto S, Antonelli G, Sorino M, Biasco G, Rizzon P: Dynamic intracavitary left atrial echoes in mitral stenosis. Am J Cardiol. 1985, 55: 603-606. 10.1016\u002F0002-9149(85)90267-X.","https:\u002F\u002Flinkinghub.elsevier.com\u002Fretrieve\u002Fpii\u002F000291498590267X",{"doi":609},"10.1016\u002F0002-9149(85)90267-x",{"id":521,"text":611,"url":523,"identifiers":612},"Kim M-K, Park D-G: Correlation between stroke and spontaneous echo contrast by tissue harmonic imaging in patients with dilated cardiomyopathy. J Cardiovasc Ultrasound. 2009, 17: 10-10.4250\u002Fjcu.2009.17.1.10.",{"doi":525},{"id":614,"text":615,"url":616,"identifiers":617},"b3e27f84-5d8a-4db0-a7f9-b26e4bc13998","Shen WF, Tribouilloy C, Rida Z, Peltier M, Choquet D, Rey JL, Lesbre JP: Clinical significance of intracavitary spontaneous echo contrast in patients with dilated cardiomyopathy. Cardiology. 1996, 87: 141-146. 10.1159\u002F000177077.","https:\u002F\u002Fkarger.com\u002FCRD\u002Farticle\u002Fdoi\u002F10.1159\u002F000177077",{"doi":618},"10.1159\u002F000177077",{"id":20,"text":620,"url":20,"identifiers":621},"Hissa R: Physiology of the European brown bear (Ursus arctos arctos). Ann Zool Fenn. 1997, 34: 267-287.",{},{"id":521,"text":623,"url":523,"identifiers":624},"Evans AL, Sahlén V, Støen O-G, Fahlman Å, Brunberg S, Madslien K, Fröbert O, Swenson JE, Arnemo JM: Capture, anesthesia, and disturbance of free-ranging brown bears (Ursus arctos) during hibernation. PLoS One. 2012, 7: e40520-10.1371\u002Fjournal.pone.0040520.",{"doi":525},{"id":626,"text":627,"url":628,"identifiers":629},"dfbf1c14-9d2c-41e8-8cc1-d2cc3dc2addb","Hill RC, Scott KC: Energy requirements and body surface area of cats and dogs. J Am Vet Med Assoc. 2004, 225: 689-694. 10.2460\u002Fjavma.2004.225.689.","https:\u002F\u002Favmajournals.avma.org\u002Fview\u002Fjournals\u002Fjavma\u002F225\u002F5\u002Fjavma.2004.225.689.xml",{"doi":630},"10.2460\u002Fjavma.2004.225.689",{"id":20,"text":632,"url":20,"identifiers":633},"Reynolds HR, Hochman JS: Cardiogenic shock current concepts and improving outcomes. Circulation. 2008, 117: 686-697. 10.1161\u002FCIRCULATIONAHA.106.613596.",{"doi":634},"10.1161\u002FCIRCULATIONAHA.106.613596",{"id":636,"text":637,"url":638,"identifiers":639},"82764479-f08b-4287-8b2a-22d1211172a5","Campos J-M, Paniagua P: Hypothermia during cardiac surgery. Best Pract Res Clin Anaesthesiol. 2008, 22: 695-709. 10.1016\u002Fj.bpa.2008.03.001.","https:\u002F\u002Flinkinghub.elsevier.com\u002Fretrieve\u002Fpii\u002FS1521689608000256",{"doi":640},"10.1016\u002Fj.bpa.2008.03.001",{"id":642,"text":643,"url":644,"identifiers":645},"85337e08-c9e1-4f02-b5b6-8bb43fb6c532","Espinoza A, Kerans V, Opdahl A, Skulstad H, Halvorsen PS, Bugge JF, Fosse E, Edvardsen T: Effects of therapeutic hypothermia on left ventricular function assessed by ultrasound imaging. J Am Soc Echocardiogr. 2013, 26: 1353-1363. 10.1016\u002Fj.echo.2013.06.021.","https:\u002F\u002Fwww.sciencedirect.com\u002Fscience\u002Farticle\u002Fpii\u002FS0894731713004914",{"doi":646},"10.1016\u002Fj.echo.2013.06.021",{"id":648,"text":649,"url":650,"identifiers":651},"c8a6f7b7-383f-42aa-96e6-01955cf4be4f","Dawe AR, Spurrier WA: Hibernation induced in ground squirrels by blood transfusion. Science. 1969, 163: 298-299. 10.1126\u002Fscience.163.3864.298.","https:\u002F\u002Fwww.science.org\u002Fdoi\u002F10.1126\u002Fscience.163.3864.298",{"doi":652},"10.1126\u002Fscience.163.3864.298",{"id":654,"text":655,"url":656,"identifiers":657},"d012488b-5134-497e-80aa-a50b0555abe0","Swan H, Schätte C: Antimetabolic extract from the brain of the hibernating ground squirrel citellus tridecemlineatus. Science. 1977, 195: 84-85. 10.1126\u002Fscience.831261.","https:\u002F\u002Fwww.science.org\u002Fdoi\u002F10.1126\u002Fscience.831261",{"doi":658},"10.1126\u002Fscience.831261",{"id":521,"text":660,"url":523,"identifiers":661},"Bolling SF, Benedict MB, Tramontini NL, Kilgore KS, Harlow HH, Su T-P, Oeltgen PR: Hibernation triggers and myocardial protection. Circulation. 1998, 98 (19 Suppl): II220-II223.",{"doi":525},{"id":663,"text":664,"url":665,"identifiers":666},"5216695c-f197-4328-9a5f-31c2f29c3604","Blackstone E: H2S induces a suspended animation-like state in mice. Science. 2005, 308: 518-518. 10.1126\u002Fscience.1108581.","https:\u002F\u002Fwww.science.org\u002Fdoi\u002F10.1126\u002Fscience.1108581",{"doi":667},"10.1126\u002Fscience.1108581",{"id":20,"text":669,"url":20,"identifiers":670},"Volpato GPMD, Searles RBA, Yu BPD, Scherrer-Crosbie MMD, Bloch KDMD, Ichinose FMD, Zapol WMMD: Inhaled hydrogen sulfide: a rapidly reversible inhibitor of cardiac and metabolic function in the mouse. Anesthesiol. 2008, 108: 659-668. 10.1097\u002FALN.0b013e318167af0d.",{"doi":671},"10.1097\u002FALN.0b013e318167af0d",{"id":673,"text":674,"url":675,"identifiers":676},"91ef3306-ef09-445c-9121-def2556c2572","Beppu S, Nimura Y, Sakakibara H, Nagata S, Park Y-D, Izumi S: Smoke-like echo in the left atrial cavity in mitral valve disease: its features and significance. J Am Coll Cardiol. 1985, 6: 744-749. 10.1016\u002FS0735-1097(85)80476-9.","https:\u002F\u002Fwww.sciencedirect.com\u002Fscience\u002Farticle\u002Fpii\u002FS0735109785804769",{"doi":677},"10.1016\u002Fs0735-1097(85)80476-9",{"id":679,"text":680,"url":681,"identifiers":682},"88633e13-c55e-4d8b-a606-9c0f92720556","Mikell FL, Asinger RW, Elsperger KJ, Anderson WR, Hodges M: Regional stasis of blood in the dysfunctional left ventricle: echocardiographic detection and differentiation from early thrombosis. Circulation. 1982, 66: 755-763. 10.1161\u002F01.CIR.66.4.755.","https:\u002F\u002Fwww.ahajournals.org\u002Fdoi\u002F10.1161\u002F01.CIR.66.4.755",{"doi":683},"10.1161\u002F01.cir.66.4.755",{"id":521,"text":685,"url":523,"identifiers":686},"Barth E, Albuszies G, Baumgart K, Matejovic M, Wachter U, Vogt J, Radermacher P, Calzia E: Glucose metabolism and catecholamines. Crit Care Med. 2007, 35 (9 Suppl): S508-S518.",{"doi":525},{"id":688,"createTime":689,"updateTime":690,"relativeEntities":691,"slug":692,"properties":693,"entityType":187,"verifyStatus":188,"verifyTime":704,"verifyNote":190,"languages":705,"translateLanguages":20,"viewCount":21,"primaryUrl":707,"fullTextUrl":20,"authors":708,"publicationType":266,"publisherRelationship":786,"citationCount":20,"citationInfo":20,"publishDate":836,"publishYear":837,"citationAnalyzeStatus":838,"lastCitationAnalyze":690,"indexDatabases":839,"openAccess":20,"references":840,"isForceReanalyzing":329},"50968b00-3d7a-4725-813d-b91f3020c8f8","2024-04-11T09:59:06.995+00:00","2026-06-27T00:03:46.254+00:00",[],"The-effects-of-beta-blockers-on-dobutamine-atropine-stress-echocardiography-early-protocol-versus-standard-protocol",{"abstract":694,"title":696,"gsPaper":698,"keywords":700,"doi":702},{"EN":695},"To study the effects of Beta-blockers during Dobutamine Stress Echocardiography (DSE) comparing the hemodynamic benefits of an early administration of atropine in patients taking or not Beta-blockers. One hundred and twenty-one patients were submitted to dobutamine stress echocardiography for the investigation of myocardial ischemia. The administration of atropine was randomized into two groups: A or B (early protocol when atropine was administered at 10 and 20 mcg\u002Fkg\u002Fmin of dobutamine, respectively) and C (standard protocol with atropine at 40 mcg\u002Fkg\u002Fmin of dobutamine). Analysis of the effects of Beta-blockers was done regarding the behavior pattern of heart rate and blood pressure, test time, number of conclusive and inconclusive (negative sub-maximum test) results, total doses of atropine and dobutamine, and general complications. Beta-blocked patients who received early atropine (Group A&B) had a significantly lower double product (p = 0.008), a higher mean test time (p = 0.010) and required a higher dose of atropine (p = 0.0005) when compared to the patients in this group who were not Beta-blocked. The same findings occurred in the standard protocol (Group C), however the early administration of atropine reduced test time both in the presence and absence of this therapy (p = 0.0001). The patients with Beta-blockers in Group A&B had a lower rate of inconclusive tests (26%) compared to those in Group C (40%). Complications were similar in both groups. The chronotropic response during dobutamine stress echocardiography was significantly reduced with the use of Beta-blockers. The early administration of atropine optimized the hemodynamic response, reduced test time in patients with or without Beta-blockers and reduced the number of inconclusive tests in the early protocol.",{"EN":697},"The effects of beta-blockers on dobutamine-atropine stress echocardiography: early protocol versus standard 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RD: Miller's Anesthesia. Churchill Livingstone Inc; 2000.",{"id":20,"text":844,"url":20,"identifiers":20},"Batlouni M, Ramires JF: Farmacologia e terapêutica cardiovascular. Atheneu 1st edition. 1999.",{"id":20,"text":846,"url":20,"identifiers":20},"McNeill AJ, Fioretti PM, el-Said SM, Salustri A, Forster T, Roelandt JR: Enhanced sensitivity for detection of coronary artery disease by addition of atropine to dobutamine stress echocardiography. Am J Cardiol. 1992, 70: 41-46. 10.1016\u002F0002-9149(92)91387-J",{"id":20,"text":848,"url":20,"identifiers":20},"Severi S, Underwood R, Mohiaddin , Boyd H, Paterni M, Camici PG: Dobutamine stress: Effects on regional myocardial blood flow and wall motion. J Am Coll Cardiol. 1995, 26: 1187-1195. 10.1016\u002F0735-1097(95)00319-3",{"id":20,"text":850,"url":20,"identifiers":20},"Smart SC, Knickelbine T, Stoiber TR, Carlos M, Wynsen JC, Sagar KB: Safety and accuracy of dobutamine-atropine stress echocardiography for the detection of residual stenosis of the infarct-related artery and multivessel disease during the first week after acute myocardial infarction. Circulation. 1997, 95: 1394-1401.",{"id":20,"text":852,"url":20,"identifiers":20},"Pingitore A, Picano E, Colosso MQ, Reisenhofer B, Gigli G, Lucarini AR, Petix N, Previtali M, Bigi R, Chiaranda G, Minardi G, de Alcantara M, Lowenstein J, Sclavo MG, Palmieri C, Galati A, Seveso G, Heyman J, Mathias W, Casazza F, Sicari R, Raciti M, Landi P, Marzilli M: The atropine factor in pharmacologic stress echocardiography. J Am Coll Cardiol. 1996, 27: 1164-1170. 10.1016\u002F0735-1097(95)00586-2",{"id":20,"text":854,"url":20,"identifiers":20},"Fioretti PM, Poldermans D, Salustri A, Forster T, Bellotti P, Boersma E, McNeill AJ, el-Said ES, Roelandt JR: Atropine increases the accuracy of dobutamine stress echocardiography in patients taking beta-blockers. Eur Heart J. 1994, 15: 355-360.",{"id":20,"text":856,"url":20,"identifiers":20},"Tomoike H, Ross JJ, Franklin D, Crozatier B, McKown D, Kemper WS: Improvement by propranolol of regional myocardial dysfunction and abnormal coronary flow pattern in conscious dogs with coronary narrowing. Am J Cardiol. 1978, 41: 689-696. 10.1016\u002F0002-9149(78)90819-6",{"id":20,"text":858,"url":20,"identifiers":20},"Weissman NJ, Levangie MW, Newell JB, Guerrero JL, Weyman AE, Picard MH: Effect of beta-adrenergic receptor blockade on the physiologic response to dobutamine stress echocardiography. Am Heart J. 1995, 130: 248-253. 10.1016\u002F0002-8703(95)90436-0",{"id":20,"text":860,"url":20,"identifiers":20},"Daly AL, Linares OA, Smith MJ, Starling MR, Supiano MA: Dobutamine pharmacokinetics during dobutamine stress echocardiography. Am J Cardiol. 1997, 79: 1381-1386. 10.1016\u002FS0002-9149(97)00144-6",{"id":20,"text":862,"url":20,"identifiers":20},"Camarozano AC, Siqueira-Filho AG, Weitzel LH, Resende P, Noe R: The effects of early administration of atropine during dobutamine stress echocardiography: advantages and disadvantages of early dobutamine-atropine protocol. Cardiov Ultras. 2006, 4: 17-24. 10.1186\u002F1476-7120-4-17. 10.1186\u002F1476-7120-4-17",{"id":20,"text":864,"url":20,"identifiers":20},"Schiller NB, Shah PM, Crawford M: Recommendation for quantitation of the left ventricle by two-dimensional echocardiography. J Am Soc Echocardiogr. 1989, 2: 358-367.",{"id":20,"text":866,"url":20,"identifiers":20},"Hepner AM, Bach DS, Armstrong WF: Early chronotropic incompetence predicts the need for atropine during dobutamine stress echocardiography. Am J Cardiol. 1997, 79: 365-366. 10.1016\u002FS0002-9149(96)00764-3",{"id":20,"text":868,"url":20,"identifiers":20},"Brofferio A, Alaeddini J, Oommen R, DiBitetto T, Shalomoff Y, Ilercil A, Shirani J: Effect of early administration of atropine on paradoxic sinus deceleration during dobutamine stress echocardiography. Am J Cardiol. 2002, 89: 645-647. 10.1016\u002FS0002-9149(01)02318-9",{"id":20,"text":870,"url":20,"identifiers":20},"Mark AL: The Bezold-Jarisch reflex revisited: clinical implications of inhibitory reflexes originating in the heart. J Am Coll Cardiol. 1983, 1: 90-102.",{"id":20,"text":872,"url":20,"identifiers":20},"Attenhofer CH, Pellikka PA, McCully RB, Roger VL, Seward JB: Paradoxical sinus deceleration during dobutamine stress echocardiography description and angiographic correlation. J Am Coll Cardiol. 1997, 29: 994-999. 10.1016\u002FS0735-1097(97)00030-2",{"id":20,"text":874,"url":20,"identifiers":20},"Sawada SG, Segar DS, Ryan T, Brown SE, Dohan AM, Williams R, Fineberg NS, Armstrong WF, Feigenbaum H: Echocardiographic detection of coronary artery disease during dobutamine infusion. Circulation. 1991, 83: 1605-1614.",{"id":20,"text":876,"url":20,"identifiers":20},"Ghaleh B, Bea ML, Dubois-Rnade JL, Giudicelli JF, Hittinger L, Berdeaux A: Endothelial modulation of β-adrenergic dilation of large coronary arteries in conscious dogs. Circulation. 1995, 92: 2627-2635.",{"id":20,"text":878,"url":20,"identifiers":20},"Chen L, Ma L, de Prada VA, Chen M, Feng YJ, Waters D, Gillam L, Chen C: Effects of beta-blockade and atropine on ischemic responses in left ventricular regions subtending coronary stenosis during dobutamine stress echocardiography. J Am Coll Cardiol. 1996, 28: 1866-1876. 10.1016\u002FS0735-1097(96)00384-1",{"id":20,"text":880,"url":20,"identifiers":20},"Ling LH, Pellikka PA, Mahoney DW, Oh JK, McCully RB, Roger VL, Seward JB: Atropine augmentation in dobutamine stress echocardiography: role and incremental value in a clinical practice setting. J Am Coll Cardiol. 1996, 28: 551-557. 10.1016\u002F0735-1097(96)00195-7",{"id":20,"text":882,"url":20,"identifiers":20},"Lattanzi F, Picano E, Bolognese L, Piccinino C, Sarasso G, Orlandini A, L'Abbate A: Inhibition of dipyridamole-induced ischemia by antianginal therapy in humans. Circulation. 1991, 83: 1256-1262.",{"id":20,"text":884,"url":20,"identifiers":20},"Vatner SF, Mcritchie RJ, Braunwald E: Effects of dobutamine on left ventricular performance, coronary dynamics, and distribution of cardiac output in conscious dogs. J Clin Invest. 1974, 53: 1265-1273.",{"id":20,"text":886,"url":20,"identifiers":20},"Poldermans D, Sozzi FB, Bax JJ, Boersma E, Duncker DJ, Vourvouri E, Elhendy A, Valkema R, Roelandt JR: Influence of continuation of beta blockers during dobutamine stress echocardiography for the assessment of myocardial viability in patients with severe ischemic left ventricular dysfunction. Am J Cardiol. 2001, 88 (A7): 68-70. 10.1016\u002FS0002-9149(01)01591-0. 10.1016\u002FS0002-9149(01)01591-0",{"id":20,"text":888,"url":20,"identifiers":20},"Poldermans D, Fioretti PM, Boersma E, Bax JJ, Thomson IR, Roelandt JR, Simoons ML: Long-term prognostic value of dobutamine-atropine stress echocardiography in 1737 patients with known or suspected coronary artery disease: A single-center experience. Circulation. 1998, 99: 757-762.",{"id":20,"text":890,"url":20,"identifiers":20},"Lewandowski TH, Armstrong WF, Bac DS: Reduced test time by early identification of patients requiring atropine during dobutamine stress echocardiography. J Am Soc Echocardiogr. 1998, 11 (3): 236-243. 10.1016\u002FS0894-7317(98)70085-9",{"id":20,"text":892,"url":20,"identifiers":20},"Tsuitui JM, Lario FC, Fernandes DR, Kowatsch I, Sbano JC, Franchini Ramires JA, Mathias W: Safety and cardiac chronotropic responsiveness to the early injection of atropine during dobutamine stress echocardiography in the elderly. Heart. 2005, 91 (12): 1563-1567. 10.1136\u002Fhrt.2004.054445",{"id":894,"createTime":895,"updateTime":896,"relativeEntities":897,"slug":898,"properties":899,"entityType":187,"verifyStatus":188,"verifyTime":909,"verifyNote":190,"languages":20,"translateLanguages":20,"viewCount":21,"primaryUrl":910,"fullTextUrl":20,"authors":911,"publicationType":266,"publisherRelationship":1024,"citationCount":20,"citationInfo":20,"publishDate":1079,"publishYear":1080,"citationAnalyzeStatus":838,"lastCitationAnalyze":1081,"indexDatabases":1082,"openAccess":20,"references":20,"isForceReanalyzing":329},"4b0eb0a8-45b8-4e4b-813e-0f4372d1a78d","2023-12-31T06:23:48.238+00:00","2026-06-25T11:19:50.537+00:00",[],"Preoperative-single-ventricle-function-determines-early-outcome-after-second-stage-palliation-of-single-ventricle-heart",{"abstract":900,"title":902,"gsPaper":904,"references":905,"doi":907},{"EN":901},"Second-stage palliation with hemi-Fontan or bidirectional Glenn procedures has improved the outcomes of patients treated for single-ventricle heart disease. The aim of this study was to retrospectively analyze risk factors for death after second-stage palliation of single-ventricle heart and to compare therapeutic results achieved with the hemi-Fontan and bidirectional Glenn procedures. We analyzed 60 patients who had undergone second-stage palliation for single-ventricle heart. Group HF consisted of 23 (38.3%) children who had been operated with the hemi-Fontan method; Group BDG consisted of 37 (61.7%) who had been operated with the bidirectional Glenn method. The analysis focused on 30-day postoperative mortality rates, clinical and echocardiographic data, and early complications. The patients’ ages at the time of repair was 33 ± 11.2 weeks; weight was 6.7 ± 1.2 kg. The most common anatomic subtype was hypoplastic left heart syndrome, in 36 (60%) patients. The early mortality rate was 13.3%. Significant preoperative atrioventricular valve regurgitation, single-ventricle heart dysfunction, pneumonia\u002Fsepsis, and arrhythmias were associated with higher mortality rates after second-stage palliation. Multivariate analysis identified significant preoperative single-ventricle heart dysfunction as an independent predictor of early death after second-stage palliation. No differences were found in the analyzed variables after bidirectional Glenn compared with hemi-Fontan procedures. Significant preoperative atrioventricular valve regurgitation, arrhythmias and pneumonia\u002Fsepsis are closely correlated with mortality in patients with single-ventricle heart after second-stage palliation. Preoperative significant single-ventricle heart dysfunction is an independent mortality predictor in this group of patients. There are no differences in clinical, echocardiographic data, or outcomes in patients treated with the hemi-Fontan compared with bidirectional Glenn procedures.",{"EN":903},"Preoperative single ventricle function determines early outcome after second-stage palliation of single ventricle heart",{"VOID":699},{"VOID":906},"Seliem MA, Baffa JM, Vetter JM, Chen SL, Chin AJ, Norwood WI Jr. Changes in right ventricular geometry and heart rate early after hemi-Fontan procedure. Ann Thorac Surg. 1993;55:1508–12.\nFogel MA, Weinberg PM, Chin AJ, Fellows KE, Hoffman EA. Late ventricular geometry and performance changes of functional single-ventricle throughout staged Fontan reconstruction assessed by magnetic resonance imaging. J Am Coll Cardiol. 1996;28:212–21.\nJacobs ML, Rychik J, Rome JJ, Apoustopoulou S, Pizarro C, Murphy ID, et al. Early reduction of the volume work of the single-ventricle: the hemi fontan operation. Ann Thorac Surg. 1996;62:456–62.\nDeal BJ, Mavroudis C, Backer CL. Arrhythmia Management in the Fontan Patient. Pediatric Cardiology November. 2007;28:448–56.\nPekkan K, Dasi LP, de Zélicourt D, Sundareswaran KS, Fogel MA, Kanter KR, Yoganathan AP. Hemodynamic performance of stage-2 univentricular reconstruction: Glenn vs. hemi-Fontan templates. Ann Biomed Eng. 2009;37:50–63.\nScholl FG, Boucek MM, Chan KC, Valdes-Cruz L, Perryman R. Preliminary experience with cardiac reconstruction using decellularized porcine extracellular matrix scaffold: human applications in congenital heart disease. World J Pediatr Congenit Heart Surg. 2010;1:132–6.\nQuarti A, Nardone S, Colaneri M, Santoro G, Pozzi M. Preliminary experience in the use of an extracellular matrix to repair congenital heart diseases. Interact Cardiovasc Thorac Surg. 2011;13:569–72.\nWong DJ, Iyengar AJ, Wheaton GR, Ramsay JM, Grigg LE, Horton S, Konstantinov IE, Brizard CP, d’Udekem Y. Long-term outcomes after atrioventricular valve operations in patients undergoing single-ventricle palliation. Ann Thorac Surg. 2012;94:606–13.\nTomkiewicz-Pająk L, Hoffman P, Trojnarska O, Bednarek J, Płazak W, Pająk JW, Olszowska M, Komar M, Podolec PS. Long-term follow-up in adult patients after Fontan operation. Polish Journal of Thoracic and Cardiovascular Surgery. 2013;10:357–63.\nLee TM, Aiyagari R, Hirsch JC, Ohye RG, Bove EL, Devaney EJ. Risk factor analysis for second-stage palliation of single-ventricle anatomy. Ann Thorac Surg. 2012;93:614–8.\nSano S, Ishino K, Kawada M, Arai S, Kasahara S, Asai T, Masuda Z, Takeuchi M, Ohtsuki S. Right ventricle-pulmonary artery shunt in first-stage palliation of hypoplastic left heart syndrome. J Thorac Cardiovasc Surg. 2003;126:504–9.\nScheurer MA, Hill EG, Vasuki N, Maurer S, Graham EM, Bandisode V, Shirali GS, Atz AM, Bradley SM. Survival after bidirectional cavopulmonary anastomosis: analysis of preoperative risk factors. J Thorac Cardiovasc Surg. 2007;134:82–9.\nOwens GE, Gomez-Fifer C, Gelehrter S, Owens ST. Outcomes for patients with unbalanced atrioventricular septal defects. Pediatr Cardiol. 2009;30:431–5.\nBharucha T, Khan R, Mertens L, Friedberg MK. Right ventricular mechanical dyssynchrony and asymmetric contraction in hypoplastic heart syndrome are associated with tricuspid regurgitation. J Am Soc Echocardiogr. 2013;2610:1214–20.\nReichlin A, Prêtre R, Dave H, Hug MI, Gass M. Balmer C postoperative arrhythmia in patients with bidirectional cavopulmonary anastomosis. Eur J Cardiothorac Surg. 2014;45:620–4.\nTrivedi B, Smith PB, Barker PC, Jaggers J, Lodge AJ, Kanter RJ. Arrhythmias in patients with hypoplastic left heart syndrome. Am Heart J. 2011;161:138–44.\nLove BA, Collins KK, Walsh EP, Triedman JK. Electroanatomic characterization of conduction barriers in sinus\u002Fatrially paced rhythm and association with intra-atrial reentrant tachycardia circuits following congenital heart disease surgery. J Cardiovasc Electrophysiol. 2001;12:17–25.\nHibino N, McConnell P, Shinoka T, Malik M, Galantowicz M. Preliminary experience in the use of an extracellular matrix (CorMatrix) as a tube graft: word of caution. Semin Thorac Cardiovasc Surg. 2015;27:288–95.",{"VOID":908},"10.1186\u002Fs12947-017-0114-7","2024-07-19T10:39:12.452+00:00","https:\u002F\u002Fcardiovascularultrasound.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs12947-017-0114-7",[912,927,940,955,968,981,996,1009],{"id":913,"sortIndex":21,"researcher":20,"roles":914,"affiliations":915,"properties":924,"displayName":926,"givenName":20,"familyName":20},"ab7c1421-e594-407e-8ddc-91a40e220147",[196],[916],{"id":917,"sortIndex":21,"affiliation":918,"properties":20},"93104435-01f9-41fa-b6b8-1faa01cf7d40",{"id":917,"createTime":20,"updateTime":20,"relativeEntities":919,"slug":20,"properties":920,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":923,"statistic":20},[],{"title":921},{"VI":922},"Pediatric Heart Surgery and General Pediatric Surgery Department, Medical University of Warsaw, Warszawa, Poland",[],{"title":925},{"VI":926},"Jacek 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fistulas (AAF) are rare but important pathophysiologic conditions of the aorta and have varied presentations such as acute pulmonary edema, chronic heart failure and incidental detection of the fistula. A variety of mechanisms such as aortic dissection, endocarditis with pseudoaneurysm formation, post surgical scenarios or trauma may precipitate the fistula formation. With increasing survival of patients, particularly following complex aortic reconstructive surgeries and redo valve surgeries, recognition of this complication, its clinical features and echocardiographic diagnosis is important. Since physical exam in this condition may be misleading, echocardiography serves as the cornerstone for diagnosis. The case below illustrates aorto-left atrial fistula formation following redo aortic valve surgery with slowly progressive symptoms of heart failure. A brief review of the existing literature of this entity is presented including emphasis on echocardiographic diagnosis and treatment.",{"EN":1093},"Clinical and echocardiographic features of aorto-atrial fistulas",{"VOID":699},{"EN":701},{"VOID":1097},"Boyd LJ: A study of four thousand cases of aneurysm of the thoracic aorta. Am J Med Sci. 1924, 168: 654-68.\nOliveira JSM, Bestetti RB, Marin-Neto JA, Costa RS, Carneiro JJ: Ruptured aortic dissection into the left atrium: A rare case of congestive heart failure. Am Heart J. 1991, 121: 936-8.\nArnett EN, Roberts WC: Valve ring abscess in active infective endocarditis; frequency, location and clues to clinical diagnosis from study of 95 necropsy patients. Circulation. 1976, 54: 140-5.\nSakakibara S, Konno S: Congenital aneurysms of sinus of Valsalva. A clinical study. Am Heart J. 1962, 63: 708-19.\nLindsay J: Aortocameral fistula: a rare complication of aortic dissection. Am Heart J. 1993, 126: 441-3.\nTopocuoglu MS, Salih OK, San M, Kayhan C, Ulus T: Aorto-Left Atrial Fistula with Bicuspid Aortic Valve and Coronary Artery Origin Anomaly. Ann Thorac Surg. 1997, 63: 854-6.\nArcher TP, Mabee SW, Baker PB, Orsinelli DA, Leier CV: Aorto-Left Atrial fistula: A Reversible Cause of Acute Refractory Heart Failure. CHEST. 1997, 111: 828-31.\nCaruso A, Iarussi D, Materazzi C, Dialetto G, Covino F, Bossone E, Cotrufo M: Aortic Dissection with Fistula to Left Atrium: Diagnosis by Transesophageal Echocardiography with Successful Repair. J Am Soc Echocardiogr. 2000, 13: 69-72.\nAnanthasubramaniam K, Karthikeyan V: Aortic ring abscess with Aorto-atrial fistula complicating Fulminant Prosthetic Valve Endocarditis due to Proteus mirabilis. J Ultrasound Med. 2000, 19: 63-66.\nPatsouras D, Argyri O, Siminilakis S, Michalis L, Sideris D: Aortic Dissection with Aorto-Left Atrial Fistula Formation Soon After Aortic Valve Replacement: A Lethal Complication Diagnosed By Transthoracic and Transesophageal Echcoardiography. J Am Soc Echocardiogr. 2002, 15: 1409-11.\nShanewise JS, Martin RP: Assessment of endocarditis and associated complications with transesophageal echocardiography. Crit Care Clin. 1996, 12 (2): 411-27.\nTamms MA, Guyssenhoven EJ, Bos E, de Jaegere P, Roelandt JR, Sutherland GR, Bom N: Enhanced morphological diagnosis in endocarditis by transesophageal echocardiography. Br Heart J. 1990, 63: 109-",{"VOID":1099},"10.1186\u002F1476-7120-3-1","2024-05-30T11:19:23.186+00:00","https:\u002F\u002Fcardiovascularultrasound.biomedcentral.com\u002Farticles\u002F10.1186\u002F1476-7120-3-1",[1103],{"id":1104,"sortIndex":21,"researcher":20,"roles":1105,"affiliations":1106,"properties":1115,"displayName":1117,"givenName":20,"familyName":20},"36a859d5-e0b8-463e-8034-e5c4ef938ec8",[196],[1107],{"id":1108,"sortIndex":21,"affiliation":1109,"properties":20},"05d95187-18cd-4bcd-8ac3-fbebdc64a2b7",{"id":1108,"createTime":20,"updateTime":20,"relativeEntities":1110,"slug":20,"properties":1111,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1114,"statistic":20},[],{"title":1112},{"VI":1113},"Henry Ford Heart and Vascular Institute, Detroit, USA",[],{"title":1116},{"VI":1117},"Karthik 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effect of age on common carotid artery diameter is unclear for varying atherosclerosis risk levels. Cross-sectional data from the Atherosclerosis Risk in Communities Limited Access Data set were used to estimate the association of age with B-mode ultrasound common carotid artery diameter for three atherosclerosis risk levels. Based on information from clinical examinations, B-mode ultrasounds, questionnaires, blood and other tests, participants were categorized into three groups: pre-existing disease (prevalent stroke and\u002For coronary heart disease), high risk group (no pre-existing disease, but prevalent diabetes, hypertension, plaques\u002Fshadowing, body mass index >= 30, current smoking, or hyperlipidemia), and a low risk group (no pre-existing disease, no plaques\u002Fshadowing, and no major elevated risk factors). Multivariable linear regression analyses modeled the common carotid artery diameter relationship with age. Age was positively and significantly associated with common carotid artery diameter after risk factor adjustment in the overall sample, but age had a larger effect among persons with evidence of atherosclerosis (interaction p \u003C 0.05). Each year of older age was associated with 0.03 mm larger diameter\u002Fyear among persons with pre-existing disease, with 0.027 mm larger diameter\u002Fyear in the high risk group, but only 0.017 mm\u002Fyear among the low risk group. Results were qualitatively similar using plaques\u002Fshadowing status to indicate atherosclerosis severity. The significant impact of age on common carotid artery diameter among low risk, middle-aged, black and white men and women suggests arterial remodelling may occur in the absence of identified risk factors. The significantly larger impact of age among persons with, compared to persons without identified atherosclerosis or its risk factors, suggests that arterial remodelling may be an indicator of exposure duration.",{"EN":1182},"Common carotid arterial interadventitial distance (diameter) as an indicator of the damaging effects of age and atherosclerosis, a cross-sectional study of the Atherosclerosis Risk in Community Cohort Limited Access Data (ARICLAD), 1987–89",{"VOID":699},{"VOID":1185},"Chambless LE, Heiss G, Folsom AR, Rosamond W, Szklo M, Sharrett AR, Clegg LX: Association of coronary heart disease incidence with carotid arterial wall thickness and major risk factors: the Atherosclerosis Risk in Communities (ARIC) Study, 1987-1993. Am J Epidemiol. 1997, 146: 483-494.\nBots ML, Evans GW, Riley WA, Grobbee DE: Carotid intima-media thickness measurements in intervention studies--design options, progression rates, and sample size considerations: a point of view. Stroke. 2003, 34: 2985-2994.\nHodis HN, Mack WJ, LaBree L, Selzer RH, Liu C, Liu C, Azen SP: The role of carotid artery intima-media thickness in predicting clinical coronary events. Ann Intern Med. 1998, 128: 262-269.\nLu X, Zhao JB, Wang GR, Gregersen H, Kassab GS: Remodeling of the zero-stress state of femoral arteries in response to flow overload. Am J Physiol Heart Circ Physiol. 2001, 280: H1547-H1559.\nJiang Y, Kohara K, Hiwada K: Association between risk factors for atherosclerosis and mechanical forces in carotid artery. Stroke. 2000, 31: 2319-2324.\nMiyashiro JK, Poppa V, Berk BC: Flow-induced vascular remodeling in the rat carotid artery diminishes with age. Circ Res. 1997, 81: 311-319.\nPolak JF, Kronmal RA, Tell GS, O'Leary DH, Savage PJ, Gardin JM, Rutan GH, Borhani NO: Compensatory increase in common carotid artery diameter: relation to blood pressure and artery intima-media thickness in older adults. Stroke. 1996, 27: 2012-2015.\nBurke AP, Kolodgie FD, Farb A, Weber D, Virmani R: Morphological predictors of arterial remodeling in coronary atherosclerosis. Circulation. 2002, 105: 297-303.\nMoreno PR, Purushothaman KR, Fuster V, O'Connor WN: Intimomedial interface damage and adventitial inflammation is increased beneath disrupted atherosclerosis in the aorta: implications for plaque vulnerability. Circulation. 2002, 105: 2504-2511.\nNaghavi M, Libby P, Falk E, Casscells W, Litovsky S, Rumberger J, Badimon JJ, Stefanadi C, Moreno P, Pasterkamp G, Fayad ZA, Stone PH, Waxman S, Willerson JT: From vulnerable plaque to vulnerable patient, a call for new definitions and risk assessment strategies: Part I. Circulation. 2003, 108: 1664-1672.\nKiechl S, Willeit J: The natural course of atherosclerosis. Part II: vascular remodeling. Bruneck Study Group. Arterioscler Thromb Vasc Biol. 1999, 19: 1491-1498.\nKiechl S, Willeit J: The natural course of atherosclerosis: Part I: incidence and progression. Arterioscler Thromb Vasc Biol. 1999, 19: 1484-1490.\nSchmidt-Trucksass A, Grathwohl D, Schmid A, Boragk R, Upmeier C, Keul J, Huonker M: Structural, functional, and hemodynamic changes of the common carotid artery with age in male subjects. Arterioscler Thromb Vasc Biol. 1999, 19: 1091-1097.\nVarnava AM, Mills PG, Davies MJ: Relationship between coronary artery remodeling and plaque vulnerability. Circulation. 2002, 105: 939-943.\nLemne C, Jogestrand T, de Faire U: Carotid intima-media thickness and plaque in borderline hypertension. Stroke. 1995, 26: 34-39.\nKapuku GK, Treiber FA, Hartley B, Ludwig DA: Gender influences endothelial-dependent arterial dilatation via arterial size in youth. Am J Med Sci. 2004, 327: 305-309.\nSilber HA, Bluemke DA, Ouyang P, Du YP, Post WS, Lima JAC: The relationship between vascular wall shear stress and flow-mediated dilation: endothelial function assessed by phase-contrast magnetic resonance angiography. J Am Coll Cardiol. 2001, 38: 1859-1865.\nCrouse JR, Craven TE, Hagaman AP, Bond MG: Association of coronary disease with segment-specific intimal-medial thickening of the extracranial carotid artery. Circulation. 1995, 92: 1141-1147.\nCrouse JR, Goldbourt U, Evans G, Pinsky J, Sharrett AR, Sorlie P, Riley W, Heiss G: Arterial enlargement in the Atherosclerosis Risk in Communities (ARIC) cohort. In vivo quantification of carotid arterial enlargement. The ARIC Investigators. Stroke. 1994, 25: 1354-1359.\nBonithon-Kopp C, Touboul PJ, Berr C, Magne C, Ducimetiere P: Factors of carotid arterial enlargement in a population aged 59 to 71 years: the EVA study. Stroke. 1996, 27: 654-660.\nGlagov S, Zarins C, Giddens DP, Ku DN: Hemodynamics and atherosclerosis. Insights and perspectives gained from studies of human arteries. Arch Pathol Lab Med. 1988, 112: 1018-1031.\nLabropoulos N, Zarge J, Mansour MA, Kang SS, Baker WH: Compensatory arterial enlargement is a common pathobiologic response in early atherosclerosis. Am J Surg. 1998, 176: 140-143.\nPasterkamp G, Galis ZS, Kleijn DPV: Expansive arterial remodeling: location, location, location. Arterioscl Thromb Vasc Biol. 2004, 24: 650-657.\n, : The Atherosclerosis Risk in Communities (ARIC) Study: design and objectives. Am J Epidemiol. 1989, 129: 687-702.\nNational Heart LBI: http:\u002F\u002Fwww.nhlbi.nih.gov\u002Fresources\u002Fdeca\u002Fpolicy.htm.\nFolsom AR, Peacock JM, Nieto FJ, Rosamond W, Eigenbrodt ML, Davis CE, Wu KK: Plasma fibrinogen and incident hypertension in the Atherosclerosis Risk in Communities (ARIC) Study. J Hypertens. 1998, 16: 1579-1583.\nNational Heart LBI: Atherosclerosis Risk in Communities (ARIC) Study. Operations manual no. 6A:ultrasound assessment--part A, ultrasound scanning, Version 1.0. Chapel Hill, NC, ARIC Coordinating Center, School of Public Health University of North Carolina\nLi R, Duncan BB, Metcalf PA, Crouse JR, Sharrett AR, Tyroler HA, Barnes R, Heiss G: B-mode-detected carotid artery plaque in a general population. Atherosclerosis Risk in Communities (ARIC) Study Investigators. Stroke. 1994, 25: 2377-2383.\nCrouse JR, Goldbourt U, Evans G, Pinsky J, Sharrett AR, Sorlie P, Riley W, Heiss G: Risk factors and segment-specific carotid arterial enlargement in the Atherosclerosis Risk in Communities (ARIC) cohort. Stroke. 1996, 27: 69-75.\nEigenbrodt ML, Rose KM, Couper DJ, Arnett DK, Smith R, Jones D: Orthostatic hypotension as a risk factor for stroke. The Atherosclerosis Risk in Communities (ARIC) Study, 1987-1996. Stroke. 2000, 31: 2307-2313.\nToole JF, Lefkowitz DS, Chambless LE, Wijnberg L, Paton CC, Heiss G: Self-reported transient ischemic attack and stroke symptoms: methods and baseline prevalence. The ARIC Study, 1987-1989. Am J Epidemiol. 1996, 144: 849-856.\nGlagov S, Weisenberg E, Zarins CK, Stankunavicius R, Kolettis GJ: Compensatory enlargement of human atherosclerotic coronary arteries. N Eng J Med. 1987, 316: 1371-1375.\nChobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo JL, Jones DW, Materson BJ, Oparil S, Wright JT, Roccella EJ: The seventh report of the joint national committee on prevention, detection, evaluation, and treatment of high blood pressure. JAMA. 2003, 289: 2560-2572.\nIannuzzi A, Licenziati MR, Acampora C, Salvatore V, Auriemma L, Romano ML, Panico S, Rubba P, Trevisan M: Increased carotid intima media thickness and stiffness in obese children. Diabetes Care. 2004, 27: 2506-2508.\nMcGill HC, McMahan CA, Herderick EE, Zieske AW, Malcom GT, Tracy RE, Strong JP: Obesity accelerates the progression of coronary atherosclerosis in young men. Circulation. 2002, 105: 2712-2718.\nWildman RP, Mackey RH, Bostom A, Thompson T, Sutton-Tyrrell K: Measures of obesity are associated with vascular stiffness in young and older adults. Hypertension. 2003, 42: 468-473.",{"VOID":1187},"10.1186\u002F1476-7120-4-1","2024-05-27T23:28:54.592+00:00","https:\u002F\u002Fcardiovascularultrasound.biomedcentral.com\u002Farticles\u002F10.1186\u002F1476-7120-4-1",[1191,1206,1221,1236,1251,1266,1281,1296],{"id":1192,"sortIndex":21,"researcher":20,"roles":1193,"affiliations":1194,"properties":1203,"displayName":1205,"givenName":20,"familyName":20},"b6e09d3e-a206-471b-925f-62ae14501412",[196],[1195],{"id":1196,"sortIndex":21,"affiliation":1197,"properties":20},"cc88a613-ddee-4cd8-8264-fcfd174cf087",{"id":1196,"createTime":20,"updateTime":20,"relativeEntities":1198,"slug":20,"properties":1199,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1202,"statistic":20},[],{"title":1200},{"VI":1201},"Department of Epidemiology, Fay W. Boozman College of Public Health, University of Arkansas for Medical Sciences, Little Rock, USA",[],{"title":1204},{"VI":1205},"Marsha L Eigenbrodt",{"id":1207,"sortIndex":144,"researcher":20,"roles":1208,"affiliations":1209,"properties":1218,"displayName":1220,"givenName":20,"familyName":20},"07e1afa3-b0d7-41ed-975f-adb532e8ba97",[196],[1210],{"id":1211,"sortIndex":21,"affiliation":1212,"properties":20},"3b999b69-02a7-42e6-8c39-cb1bb555816e",{"id":1211,"createTime":20,"updateTime":20,"relativeEntities":1213,"slug":20,"properties":1214,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":1217,"statistic":20},[],{"title":1215},{"VI":1216},"Department of Biostatistics, Fay W. 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cardioprotective effects of certain alcoholic beverages are partly related to their polyphenol content, which may improve the vasodilatory reactivity of arteries. Effect of cognac on coronary circulation, however, remains unknown. The purpose of this randomized controlled cross-over study was to determine whether moderate doses of cognac improve coronary reactivity as assessed with cold pressor testing (CPT) and coronary flow reserve (CFR) measument. Study group consisted of 23 subjects. Coronary flow velocity and epicardial diameter was assessed using transthoracic echocardiography at rest, during CPT and adenosine infusion-derived CFR measurements before drinking, after a moderate (1.2 ± 0.1 dl) and an escalating high dose (total amount 2.4 ± 0.3 dl) of cognac. To explore the bioavailability of antioxidants, the antioxidant contents of cognac was measured and the absorption from the digestive tract was verified by plasma antioxidant capacity determination. Serum alcohol levels increased to 1.2 ± 0.2‰ and plasma antioxidant capacity from 301 ± 43.9 μmol\u002Fl to 320 ± 25.0 μmol\u002Fl by 7.6 ± 11.8%, (p = 0.01) after high doses of cognac. There was no significant change in flow velocity during CPT after cognac ingestion compared to control day. CFR was 4.4 ± 0.8, 4.1 ± 0.9 (p = NS), and 4.5 ± 1.2 (p = NS) before drinking and after moderate and high doses on cognac day, and 4.5 ± 1.4, and 4.0 ± 1.2 (p = NS) on control day. Cognac increased plasma antioxidant capacity, but it had no effect on coronary circulation in healthy young men. NCT00330213","Các tác dụng bảo vệ tim mạch của một số loại đồ uống có cồn phần nào liên quan đến hàm lượng polyphenol của chúng, có thể cải thiện sự phản ứng giãn mạch của các động mạch. Tuy nhiên, tác động của cognac đến tuần hoàn vành vẫn chưa được biết đến. Mục đích của nghiên cứu đối chứng ngẫu nhiên chéo này là xác định xem liệu liều lượng vừa phải của cognac có cải thiện phản ứng vành như đo bằng thử nghiệm lạnh (CPT) và đo trữ lượng dòng vành (CFR) hay không. Nhóm nghiên cứu gồm 23 người tham gia. Tốc độ dòng chảy và đường kính màng ngoài tim được đánh giá bằng siêu âm tim qua thành ngực trong trạng thái nghỉ, trong quá trình CPT và các phép đo CFR từ việc truyền adenosine trước khi uống, sau liều vừa (1.2 ± 0.1 dl) và một liều cao đang tăng (tổng cộng 2.4 ± 0.3 dl) của cognac. Để khám phá khả năng sinh khả dụng của các chất chống oxy hóa, hàm lượng các chất chống oxy hóa trong cognac được đo và sự hấp thu từ đường tiêu hóa được xác minh bằng việc xác định khả năng chống oxy hóa huyết plasma. Nồng độ ethanol trong huyết thanh tăng lên 1.2 ± 0.2‰ và khả năng chống oxy hóa huyết plasma từ 301 ± 43.9 μmol\u002Fl đến 320 ± 25.0 μmol\u002Fl với tỷ lệ 7.6 ± 11.8% (p = 0.01) sau khi uống liều cao của cognac. Không có sự thay đổi đáng kể nào ở tốc độ dòng chảy trong quá trình CPT sau khi uống cognac so với ngày kiểm soát. CFR là 4.4 ± 0.8, 4.1 ± 0.9 (p = NS), và 4.5 ± 1.2 (p = NS) trước khi uống và sau khi dùng liều vừa và cao vào ngày uống cognac, và 4.5 ± 1.4, và 4.0 ± 1.2 (p = NS) vào ngày kiểm soát. 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Ann Intern Med. 2000, 133: 411-9.",{"doi":525},{"id":20,"text":1622,"url":1623,"identifiers":1624},"Klatsky AL, Friedman GD, Armstrong MA, Kipp H: Wine, liquor, beer, and mortality. Am J Epidemiol. 2003, 158: 585-95. 10.1093\u002Faje\u002Fkwg184","https:\u002F\u002Fdoi.org\u002F10.1093\u002Faje\u002Fkwg184",{"mag":1625,"openalex":1626,"pm":1627,"doi":1628},"2165565317","W2165565317","12965884","10.1093\u002Faje\u002Fkwg184",{"id":521,"text":1630,"url":523,"identifiers":1631},"Shimada K, Watanabe H, Hosoda K, Takeuchi K, Yoshikawa J: Effect of red wine on coronary flow-velocity reserve. Lancet. 1999, 354: 1002- 10.1016\u002FS0140-6736(99)03478-9",{"doi":525},{"id":20,"text":1633,"url":1634,"identifiers":1635},"Agewall S, Wright S, Doughty RN, Whalley GA, Duxbury M, Sharpe N: Does a glass of red wine improve endothelial function?. Eur Heart J. 2000, 21: 74-8. 10.1053\u002Feuhj.1999.1759","https:\u002F\u002Fdoi.org\u002F10.1053\u002Feuhj.1999.1759",{"mag":1636,"openalex":1637,"pm":1638,"doi":1639},"2105039169","W2105039169","10610747","10.1053\u002Feuhj.1999.1759",{"id":1641,"text":1642,"url":1643,"identifiers":1644},"7c2e944a-b4a1-4eee-be99-f6c9851b4b05","Kiviniemi TO, Saraste A, Toikka JO, Saraste M, Raitakari OT, Pärkkä JP, Lehtimäki T, Hartiala JJ, Viikari J, Koskenvuo JW: A moderate dose of red wine, but not de-alcoholized red wine increases coronary flow reserve. Atherosclerosis. 2007, 195: e176-81. 10.1016\u002Fj.atherosclerosis.2007.06.004","https:\u002F\u002Fwww.sciencedirect.com\u002Fscience\u002Farticle\u002Fpii\u002FS0021915007003899",{"doi":1645},"10.1016\u002Fj.atherosclerosis.2007.06.004",{"id":521,"text":1647,"url":523,"identifiers":1648},"Venkov CD, Myers PR, Tanner MA, Su M, Vaughan DE: Ethanol increases endothelial nitric oxide production through modulation of nitric oxide synthase expression. Thromb Haemost. 1999, 81: 638-42.",{"doi":525},{"id":521,"text":1650,"url":523,"identifiers":1651},"Zenebe W, Pechanova O, Andriantsitohaina R: Red wine polyphenols induce vasorelaxation by increased nitric oxide bioactivity. Physiological Research. 2003, 52: 425-32.",{"doi":525},{"id":20,"text":1653,"url":1654,"identifiers":1655},"Ranaivo HR, Diebolt M, Schott C, Andriantsitohaina R: Polyphenolic compounds from Cognac induce vasorelaxation in vitro and decrease post-ischaemic cardiac infarction after an oral administration. Fundam Clin Pharmacol. 2004, 18: 331-8. 10.1111\u002Fj.1472-8206.2004.00243.x","https:\u002F\u002Fdoi.org\u002F10.1111\u002Fj.1472-8206.2004.00243.x",{"mag":1656,"openalex":1657,"pm":1658,"doi":1659},"1997070355","W1997070355","15147285","10.1111\u002Fj.1472-8206.2004.00243.x",{"id":20,"text":1661,"url":1662,"identifiers":1663},"Kiviniemi TO: Assessment of coronary blood flow and the reactivity of the microcirculation non-invasively with transthoracic echocardiography. Clin Physiol Funct Imaging. 2008, 28: 145-155. 10.1111\u002Fj.1475-097X.2008.00794.x","https:\u002F\u002Fdoi.org\u002F10.1111\u002Fj.1475-097x.2008.00794.x",{"mag":1664,"openalex":1665,"pm":1666,"doi":1667},"2087904796","W2087904796","18312446","10.1111\u002Fj.1475-097x.2008.00794.x",{"id":1669,"text":1670,"url":1671,"identifiers":1672},"0d890945-356d-433a-bc2b-ac2adde6861d","Rigo F: Coronary flow reserve in stress-echo lab. From pathophysiologic toy to diagnostic tool. Cardiovasc Ultrasound. 2005, 3: 8- 10.1186\u002F1476-7120-3-8","https:\u002F\u002Fcardiovascularultrasound.biomedcentral.com\u002Farticles\u002F10.1186\u002F1476-7120-3-8",{"doi":1673},"10.1186\u002F1476-7120-3-8",{"id":1675,"text":1676,"url":1677,"identifiers":1678},"f40b09cf-f98a-4caf-b6c5-336813b43667","Rigo F, Murer B, Ossena G, Favaretto E: Transthoracic echocardiographic imaging of coronary arteries: tips, traps, and pitfalls. Cardiovasc Ultrasound. 2008, 6: 7- 10.1186\u002F1476-7120-6-7","https:\u002F\u002Fcardiovascularultrasound.biomedcentral.com\u002Farticles\u002F10.1186\u002F1476-7120-6-7",{"doi":1679},"10.1186\u002F1476-7120-6-7",{"id":521,"text":1681,"url":523,"identifiers":1682},"Antony I, Nitenberg A: Coronary endothelial dysfunction in hypertension. Arch Mal Coeur Vaiss. 1997, 90: 21-7.",{"doi":525},{"id":20,"text":1684,"url":1685,"identifiers":1686},"Nitenberg A, Ledoux S, Valensi P, Sachs R, Attali JR, Antony I: Impairment of coronary microvascular dilation in response to cold pressor – induced sympathetic stimulation in type 2 diabetic patients with abnormal stress thallium imaging. Diabetes. 2001, 50: 1180-5. 10.2337\u002Fdiabetes.50.5.1180","https:\u002F\u002Fdoi.org\u002F10.2337\u002Fdiabetes.50.5.1180",{"mag":1687,"openalex":1688,"pm":1689,"doi":1690},"2131835655","W2131835655","11334424","10.2337\u002Fdiabetes.50.5.1180",{"id":20,"text":1692,"url":1693,"identifiers":1694},"Pitkänen OP, Raitakari OT, Niinikoski H, Nuutila P, Iida H, Voipio-Pulkki LM, Härkönen R, Wegelius U, Rönnemaa T, Viikari J, Knuuti J: Coronary flow reserve is impaired in young men with familial hypercholesterolemia. J Am Coll Cardiol. 1996, 28: 1705-11. 10.1016\u002FS0735-1097(96)00376-2","https:\u002F\u002Fdoi.org\u002F10.1016\u002Fs0735-1097(96)00376-2",{"mag":1695,"openalex":1696,"pm":1697,"doi":1698},"2017992707","W2017992707","8962555","10.1016\u002Fs0735-1097(96)00376-2",{"id":521,"text":1700,"url":523,"identifiers":1701},"Zeiher AM, Schachinger V, Weitzel SH, Wollschlager H, Just H: Intracoronary Thrombus Formation Causes Focal Vasoconstriction of Epicardial Arteries in Patients with Coronary-Artery Disease. Circulation. 1991, 83: 1519-25.",{"doi":525},{"id":20,"text":1703,"url":1704,"identifiers":1705},"Kiviniemi TO, Snapir A, Saraste M, Toikka JO, Raitakari OT, Ahotupa M, Hartiala JJ, Scheinin M, Koskenvuo JW: Determinants of coronary flow velocity reserve in healthy young men. Am J Physiol Heart Circ Physiol. 2006, 291: H564-9. 10.1152\u002Fajpheart.00915.2005","https:\u002F\u002Fdoi.org\u002F10.1152\u002Fajpheart.00915.2005",{"mag":1706,"openalex":1707,"pm":1708,"doi":1709},"2158024604","W2158024604","16501023","10.1152\u002Fajpheart.00915.2005",{"id":20,"text":1711,"url":20,"identifiers":20},", : Folin-Ciocalteau-Index. Official Journal of European Communities. 1992, 178-9.",{"id":20,"text":1713,"url":1714,"identifiers":1715},"Kähkönen MP, Heinonen M: Antioxidant activity of anthocyanins and their aglycons. J Agric Food Chem. 2003, 51: 628-33. 10.1021\u002Fjf025551i","https:\u002F\u002Fdoi.org\u002F10.1021\u002Fjf025551i",{"mag":1716,"openalex":1717,"pm":1718,"doi":1719},"2122088022","W2122088022","12537433","10.1021\u002Fjf025551i",{"id":20,"text":1721,"url":1722,"identifiers":1723},"Saraste M, Koskenvuo JW, Knuuti J, Toikka JO, Laine H, Niemi P, Sakuma H, Hartiala JJ: Coronary flow reserve: measurement with transthoracic Doppler echocardiography is reproducible and comparable with positron emission tomography. Clin Physiol. 2001, 21: 114-22. 10.1046\u002Fj.1365-2281.2001.00296.x","https:\u002F\u002Fdoi.org\u002F10.1046\u002Fj.1365-2281.2001.00296.x",{"mag":1724,"openalex":1725,"pm":1726,"doi":1727},"1990402962","W1990402962","11168305","10.1046\u002Fj.1365-2281.2001.00296.x",{"id":521,"text":1729,"url":523,"identifiers":1730},"Kiviniemi TO, Saraste M, Koskenvuo JW, Airaksinen KEJ, Toikka JO, Saraste A, Pärkkä JP, Hartiala JJ: Coronary artery diameter can be assessed reliably with transthoracic echocardiography. Am J Physiol Heart Circ Physiol. 2004, 286: H1515-20. 10.1152\u002Fajpheart.00819.2003",{"doi":525},{"id":20,"text":1732,"url":1733,"identifiers":1734},"Kiviniemi TO, Toikka JO, Koskenvuo JW, Saraste A, Saraste M, Pärkkä JP, Raitakari OT, Hartiala JJ: Vasodilation of epicardial coronary artery can be measured with transthoracic echocardiography. Ultrasound Med Biol. 2007, 33: 362-70. 10.1016\u002Fj.ultrasmedbio.2006.08.012","https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.ultrasmedbio.2006.08.012",{"mag":1735,"openalex":1736,"pm":1737,"doi":1738},"2050752808","W2050752808","17188799","10.1016\u002Fj.ultrasmedbio.2006.08.012",{"id":20,"text":1740,"url":1741,"identifiers":1742},"Goldberg DM, Hoffman B, Yang J, Soleas GJ: Phenolic constituents, furans, and total antioxidant status of distilled spirits. J Agric Food Chem. 1999, 47: 3978-85. 10.1021\u002Fjf9811626","https:\u002F\u002Fdoi.org\u002F10.1021\u002Fjf9811626",{"mag":1743,"openalex":1744,"pm":1745,"doi":1746},"1994720540","W1994720540","10552753","10.1021\u002Fjf9811626",{"id":521,"text":1748,"url":523,"identifiers":1749},"Diallo A, Sarr M, Mostefai H, Carusio N, Pricci M, Andiantsitohaina R: Cognac polyphenolic compounds increase bradykinin-induced nitric oxide production in endothelial cells. Physiol Res. 2007",{"doi":525},{"id":20,"text":1751,"url":20,"identifiers":1752},"Corder R, Mullen W, Khan NQ, Marks SC, Wood EG, Carrier MJ, Crozier A: Oenology: red wine procyanidins and vascular health. Nature. 2006, 444: 566- 10.1038\u002F444566a",{"doi":1753},"566-10.1038\u002F444566a",{"id":521,"text":1755,"url":523,"identifiers":1756},"Szmitko PE, Verma S: Antiatherogenic potential of red wine: clinician update. Am J Physiol Heart Circ Physiol. 2005, 288: H2023-30. 10.1152\u002Fajpheart.00868.2004",{"doi":525},{"id":20,"text":1758,"url":1759,"identifiers":1760},"Puddey IB, Zilkens RR, Croft KD, Beilin LJ: Alcohol and endothelial function: A brief review. Clin Exp Pharmacol Physiol. 2001, 28 (12): 1020-4. 10.1046\u002Fj.1440-1681.2001.03572.x","https:\u002F\u002Fdoi.org\u002F10.1046\u002Fj.1440-1681.2001.03572.x",{"mag":1761,"openalex":1762,"pm":1763,"doi":1764},"1977303456","W1977303456","11903307","10.1046\u002Fj.1440-1681.2001.03572.x",{"id":521,"text":1766,"url":523,"identifiers":1767},"Macho P, Hintze TH, Vatner SF: Regulation of Large Coronary-Arteries by Increases in Myocardial Metabolic Demands in Conscious Dogs. Circ Res. 1981, 49: 594-9.",{"doi":525},{"id":521,"text":1769,"url":523,"identifiers":1770},"Nabel EG, Ganz P, Gordon JB, Alexander RW, Selwyn AP: Dilation of normal and constriction of atherosclerotic coronary arteries caused by the cold pressor test. Circulation. 1988, 77: 43-52.",{"doi":525},{"id":521,"text":1772,"url":523,"identifiers":1773},"Robertson D, Johnson GA, Robertson RM, Nies AS, Shand DG, Oates JA: Comparative-Assessment of Stimuli That Release Neuronal and Adrenomedullary Catecholamines in Man. Circulation. 1979, 59: 637-43.",{"doi":525},{"id":521,"text":1775,"url":523,"identifiers":1776},"Furchgott RF, Carvalho MH, Khan MT, Matsunaga K: Evidence for Endothelium-Dependent Vasodilation of Resistance Vessels by Acetylcholine. Blood Vessels. 1987, 24: 145-9.",{"doi":525},{"id":20,"text":1778,"url":20,"identifiers":1779},"Caiati C, Montaldo C, Zedda N, Montisci R, Ruscazio M, Lai G, Cadeddu M, Meloni L, Iliceto S: Validation of a new noninvasive method (contrast-enhanced transthoracic second harmonic echo Doppler) for the evaluation of coronary flow reserve: comparison with intracoronary Doppler flow wire. J Am Coll Cardiol. 1999, 34: 1193-200. 10.1016\u002FS0735-1097(99)00342-3",{"doi":1780},"10.1016\u002FS0735-1097(99)00342-3",{"id":1782,"createTime":1783,"updateTime":1784,"relativeEntities":1785,"slug":1786,"properties":1787,"entityType":187,"verifyStatus":188,"verifyTime":1796,"verifyNote":190,"languages":20,"translateLanguages":20,"viewCount":21,"primaryUrl":1797,"fullTextUrl":20,"authors":1798,"publicationType":266,"publisherRelationship":1844,"citationCount":1897,"citationInfo":1898,"publishDate":1904,"publishYear":1613,"citationAnalyzeStatus":19,"lastCitationAnalyze":1784,"indexDatabases":1905,"openAccess":20,"references":1906,"isForceReanalyzing":329},"5896ef0b-a14f-4ef9-8002-bbf4de4b163f","2024-01-13T00:20:18.328+00:00","2026-05-08T08:43:29.226+00:00",[],"The-diagnostic-accuracy-of-pharmacological-stress-echocardiography-for-the-assessment-of-coronary-artery-disease-a-meta-analysis",{"abstract":1788,"title":1790,"gsPaper":1792,"doi":1794},{"EN":1789},"Recent American Heart Association\u002FAmerican College of Cardiology guidelines state that \"dobutamine stress echo has substantially higher sensitivity than vasodilator stress echo for detection of coronary artery stenosis\" while the European Society of Cardiology guidelines and the European Association of Echocardiography recommendations conclude that \"the two tests have very similar applications\". Who is right? To evaluate the diagnostic accuracy of dobutamine versus dipyridamole stress echocardiography through an evidence-based approach. From PubMed search, we identified all papers with coronary angiographic verification and head-to-head comparison of dobutamine stress echo (40 mcg\u002Fkg\u002Fmin ± atropine) versus dipyridamole stress echo performed with state-of-the art protocols (either 0.84 mg\u002Fkg in 10' plus atropine, or 0.84 mg\u002Fkg in 6' without atropine). A total of 5 papers have been found. Pooled weight meta-analysis was performed. the 5 analyzed papers recruited 435 patients, 299 with and 136 without angiographically assessed coronary artery disease (quantitatively assessed stenosis > 50%). Dipyridamole and dobutamine showed similar accuracy (87%, 95% confidence intervals, CI, 83–90, vs. 84%, CI, 80–88, p = 0.48), sensitivity (85%, CI 80–89, vs. 86%, CI 78–91, p = 0.81) and specificity (89%, CI 82–94 vs. 86%, CI 75–89, p = 0.15). When state-of-the art protocols are considered, dipyridamole and dobutamine stress echo have similar accuracy, specificity and – most importantly – sensitivity for detection of CAD. European recommendations concluding that \"dobutamine and vasodilators (at appropriately high doses) are equally potent ischemic stressors for inducing wall motion abnormalities in presence of a critical coronary artery stenosis\" are evidence-based.",{"EN":1791},"The diagnostic accuracy of pharmacological stress echocardiography for the assessment of coronary artery disease: a 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Heart. 1996, 75: 240-6. 10.1136\u002Fhrt.75.3.240","https:\u002F\u002Fdoi.org\u002F10.1136\u002Fhrt.75.3.240",{"mag":2224,"pmc":2225,"openalex":2226,"pm":2227,"doi":2228},"1983734203","484279","W1983734203","8800985","10.1136\u002Fhrt.75.3.240",{"id":20,"text":2230,"url":2231,"identifiers":2232},"Sicari R, Nihyoannopoulos P, Evangelista A, Karspzak J, Lancelotti P, Poldermans D, Voigt JU, Zamorano JL: Stress echocardiography expert consensus statement of European Association of Echocardiography. Eur J Echocardiography. 2008, 9: 415-37. 10.1093\u002Fejechocard\u002Fjen175. 10.1093\u002Fejechocard\u002Fjen175","10.1093\u002Fejechocard\u002Fjen175.10.1093\u002Fejechocard\u002Fjen175",{"doi":2231},{"id":2234,"createTime":2235,"updateTime":2236,"relativeEntities":2237,"slug":2238,"properties":2239,"entityType":187,"verifyStatus":188,"verifyTime":2256,"verifyNote":190,"languages":2257,"translateLanguages":20,"viewCount":21,"primaryUrl":2258,"fullTextUrl":20,"authors":2259,"publicationType":266,"publisherRelationship":2339,"citationCount":1545,"citationInfo":2394,"publishDate":2396,"publishYear":1169,"citationAnalyzeStatus":19,"lastCitationAnalyze":2397,"indexDatabases":2398,"openAccess":20,"references":2399,"isForceReanalyzing":329},"41361ef6-8786-487f-810e-e0042ef5db3f","2024-04-17T10:21:37.206+00:00","2026-05-03T09:45:32.505+00:00",[],"Left-ventricular-apical-thrombus-after-systemic-thrombolysis-with-recombinant-tissue-plasminogen-activator-in-a-patient-with-acute-ischemic-stroke",{"mag":2240,"gsPaper":2242,"pmc":2244,"openalex":2246,"abstract":2248,"title":2250,"pm":2252,"doi":2254},{"VOID":2241},"2130384898",{"VOID":2243},"[\"827764623780358543\"]",{"VOID":2245},"1156922",{"VOID":2247},"W2130384898",{"EN":2249},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\n          \u003Cjats:sec>\n            \u003Cjats:title>Background\u003C\u002Fjats:title>\n            \u003Cjats:p>Thrombolysis with recombinant tissue plasminogen activator (rtPA) is an established treatment in acute stroke. To prevent rethrombosis after rtPA therapy, secondary anticoagulation with heparin is commonly performed. However, the recommended time-point and extent of heparin treatment vary and are not well investigated.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>\n          \u003Cjats:sec>\n            \u003Cjats:title>Case presentation\u003C\u002Fjats:title>\n            \u003Cjats:p>We report a 61-year-old man who developed an acute global aphasia and right-sided hemiparesis. Cranial CT was normal and systemic thrombolytic therapy with tPA was started 120 minutes after symptom onset. Low-dose subcutaneous heparin treatment was initiated 24 hours later. Transthoracic echocardiography (TTE) 12 hours after admission showed slightly reduced left ventricular ejection fraction (LVEF) but was otherwise normal. 48 hours later the patient suddenly deteriorated with clinical signs of dyspnea and tachycardia. TTE revelead a large left ventricular apical thrombus as well as a reduction of LVEF to 20 %. Serial further TTE investigations demonstrated a complete resolution of the thrombus and normalisation of LVEF within two days.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>\n          \u003Cjats:sec>\n            \u003Cjats:title>Conclusion\u003C\u002Fjats:title>\n            \u003Cjats:p>Our case demonstrates an intracardiac thrombus formation following rtPA treatment of acute stroke, probably caused by secondary hypercoagulability. Rethrombosis or new thrombus formation might be an underestimated complication of rtPA therapy and potentially explain cases of secondary stroke progression.\u003C\u002Fjats:p>\n          \u003C\u002Fjats:sec>",{"EN":2251},"Left ventricular apical thrombus after systemic thrombolysis with recombinant tissue plasminogen activator in a patient with acute ischemic stroke",{"VOID":2253},"15918893",{"VOID":2255},"10.1186\u002F1476-7120-3-14","2024-06-24T15:17:17.531+00:00",[706],"https:\u002F\u002Fcardiovascularultrasound.biomedcentral.com\u002Farticles\u002F10.1186\u002F1476-7120-3-14",[2260,2277,2294,2309,2324],{"id":2261,"sortIndex":21,"researcher":20,"roles":2262,"affiliations":2263,"properties":2272,"displayName":2274,"givenName":20,"familyName":20},"a7784314-955f-4a5e-b90a-e99cf3b78131",[],[2264],{"id":2265,"sortIndex":21,"affiliation":2266,"properties":20},"411dee30-f2e4-48e7-ad37-47467d6772f0",{"id":2265,"createTime":20,"updateTime":20,"relativeEntities":2267,"slug":20,"properties":2268,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":2271,"statistic":20},[],{"title":2269},{"VI":2270},"Department of Neurology, University Hospital Charité, Berlin, Germany",[],{"title":2273,"openalex":2275},{"EN":2274},"Florian Doepp",{"VOID":2276},"A5004611600",{"id":2278,"sortIndex":144,"researcher":20,"roles":2279,"affiliations":2280,"properties":2289,"displayName":2291,"givenName":20,"familyName":20},"412d72ad-d65a-4ba0-ac5e-05d4becd3c5c",[],[2281],{"id":2282,"sortIndex":21,"affiliation":2283,"properties":20},"1c96932f-6050-48ab-9033-aef5c3a172e6",{"id":2282,"createTime":20,"updateTime":20,"relativeEntities":2284,"slug":20,"properties":2285,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":2288,"statistic":20},[],{"title":2286},{"EN":2287},"Department of Cardiology, University Hospital Charité, Berlin, Germany",[],{"title":2290,"openalex":2292},{"EN":2291},"Wasiem Sanad",{"VOID":2293},"A5048928693",{"id":2295,"sortIndex":106,"researcher":20,"roles":2296,"affiliations":2297,"properties":2304,"displayName":2306,"givenName":20,"familyName":20},"c3821c19-4285-4c39-b10e-8d80672d182c",[],[2298],{"id":2265,"sortIndex":21,"affiliation":2299,"properties":20},{"id":2265,"createTime":20,"updateTime":20,"relativeEntities":2300,"slug":20,"properties":2301,"entityType":20,"verifyStatus":20,"verifyTime":20,"verifyNote":20,"languages":20,"translateLanguages":20,"viewCount":20,"url":20,"parentIds":2303,"statistic":20},[],{"title":2302},{"VI":2270},[],{"title":2305,"openalex":2307},{"EN":2306},"Stephan J. 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N Engl J Med 1995, 333: 1581-1587. 10.1056\u002FNEJM199512143332401",{"doi":2403},"10.1056\u002FNEJM199512143332401",{"id":20,"text":2405,"url":20,"identifiers":2406},"Hacke W, Kaste M, Fieschi C, Toni D, Lesaffre E, von Kummer R, Boysen G, Bluhmki E, Hoxter G, Mahagne MH, for the ECASS Group: Intravenous thrombolysis with recombinant tissue plasminogen activator for acute hemispheric stroke: The European Cooperative Acute Stroke Study. JAMA 1995, 274: 1017-1025. 10.1001\u002Fjama.274.13.1017",{"doi":2407},"10.1001\u002Fjama.1995.03530130023023",{"id":20,"text":2409,"url":20,"identifiers":2410},"Fassbender K, Dempfle CE, Mielke O, Schwartz A, Daffertshofer M, Eschenfelder C, Dollman M, Hennerici M: Changes in Coagulation and fibrinolysis markers in acute ischemic stroke treated with recombinant plasminogen activator. 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Stroke 2005, 36: 916-921. 10.1161\u002F01.STR.0000163257.66207.2d",{"doi":2430},"10.1161\u002F01.STR.0000163257.66207.2d",{"id":20,"text":2432,"url":20,"identifiers":2433},"Schenkel J, Weimar C, Knoll T, Haberl RL, Busse O, Hamann GF, Koennecke HC, Diener HC: R1-Systemic Thrombolysis in German Stroke Units. The experience from the German Stroke Data Bank. J Neurol 2003, 250: 320-324. 10.1007\u002Fs00415-003-1004-5",{"doi":2434},"10.1007\u002Fs00415-003-1004-5",{"id":20,"text":2436,"url":20,"identifiers":2437},"Trouillas P, Nighoghossian N, Derex L, Adeleine P, Honnorat J, Neuschwander P, Riche G, Getenet JC, Li W, Froment JC, Turjman F, Malicier D, Fournier G, Gabry AL, Ledoux X, Berthezene Y, Ffrench P, Dechavanne M: Thrombolysis with intravenous rtPA in a series of 100 cases of acute carotid territory stroke. Determination of etiological, topographic, and radiological outcome factors. Stroke 1998, 29: 2529-2540.",{"doi":2438},"10.1161\u002F01.STR.29.12.2529",{"id":20,"text":2440,"url":20,"identifiers":2441},"Kilic E, Bähr M, Hermann DM: Effect of recombinant tissue plasminogen activator after intraluminal thread occlusion in mice. Role of hemodynamic alterations. Stroke 2001, 32: 2641-2647.",{"doi":2442},"10.1161\u002Fhs1101.097381",{"id":20,"text":2444,"url":20,"identifiers":2445},"Maki A, Shirato C, Ohguchi M, Aoki N, Ochiai I, Ishikawa K: Mechanism of re-thrombosis after thrombolytic therapy: angiographic findings and investigation of the coagulation system in dogs. Angiology 1998, 49: 447-453.",{"doi":2446},"10.1177\u002F000331979804900605",{"id":20,"text":2448,"url":20,"identifiers":2449},"Nilsen DW, Goransson L, Larsen AI, Hetland O, Kierulf P: Systemic thrombin generation and activity resistant to low molecular weight heparin administered prior to streptokinase in patients with acute myocardial infarction. 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Am J Cardiol 1997, 80: 442-448. 10.1016\u002FS0002-9149(97)00392-5",{"doi":2458},"10.1016\u002FS0002-9149(97)00392-5",{"id":20,"text":2460,"url":20,"identifiers":2461},"Vaitkus PT, Barnathan ES: Embolic potential, prevention and management of mural thrombus complicating anterior myocardial infarction: a meta-analysis. J Am Coll Cardiol 1993, 22: 1004-1009.",{"doi":2462},"10.1016\u002F0735-1097(93)90409-T",{"id":20,"text":2464,"url":20,"identifiers":2465},"Kono , et al.: Left ventricular wall motion abnormalities in patients with subarachnoid hemorrhage: neurogenic stunned myocardium. J Am Coll Cardiol 1994, 24: 636-640.",{"doi":2466},"10.1016\u002F0735-1097(94)90008-6",{"id":20,"text":2468,"url":20,"identifiers":2469},"Robert , et al.: Evidence of stunned myocardium in humans: a 2001 update. Coron Artery Dis 2001, 12: 349-356. 10.1097\u002F00019501-200108000-00003",{"doi":2470},"10.1097\u002F00019501-200108000-00003",{"id":20,"text":2472,"url":20,"identifiers":2473},"Bulsara , et al.: Use of the peak troponin value to differentiate myocardial infarction from reversible neurogenic ventricular dysfunction associated with aneurysmal subarachnoid hemorrhage. J Neurosurg 2003, 98: 524-528.",{"doi":2474},"10.3171\u002Fjns.2003.98.3.0524",{"id":20,"text":2476,"url":20,"identifiers":2477},"Jain , et al.: Management of patients with stunned myocardium associated with subarachnoid hemorrhage. Am J Neuroradiol 2004, 25: 126-129.",{},{"id":20,"text":2479,"url":20,"identifiers":2480},"Ohtsuka , et al.: Neurogenic stunned myocardium. Circulation 2000, 101: 2122-2124.",{"doi":2481},"10.1161\u002F01.CIR.101.17.2122",{"id":20,"text":2483,"url":20,"identifiers":2484},"Bernstein R, Mayer SA, Magnano A: Neurogenic stunned myocardium in Guillaine-Barre syndrome. Neurology 2000, 54: 759-762.",{"doi":2485},"10.1212\u002FWNL.54.3.759",{"id":2487,"createTime":2488,"updateTime":2489,"relativeEntities":2490,"slug":2491,"properties":2492,"entityType":187,"verifyStatus":188,"verifyTime":2501,"verifyNote":190,"languages":20,"translateLanguages":20,"viewCount":21,"primaryUrl":2502,"fullTextUrl":20,"authors":2503,"publicationType":266,"publisherRelationship":2701,"citationCount":1900,"citationInfo":2756,"publishDate":2759,"publishYear":2757,"citationAnalyzeStatus":19,"lastCitationAnalyze":2489,"indexDatabases":2760,"openAccess":20,"references":2761,"isForceReanalyzing":329},"500b78b0-d01b-4a10-802d-d2f607087a22","2024-02-13T06:32:56.747+00:00","2026-04-26T16:12:34.871+00:00",[],"One-two-and-three-dimensional-ultrasound-measurements-of-carotid-atherosclerosis-before-and-after-cardiac-rehabilitation-preliminary-results-of-a-randomized-controlled-trial",{"abstract":2493,"title":2495,"gsPaper":2497,"doi":2499},{"EN":2494},"It is still not known how patients who are post-transient ischemic attack (TIA) or post-stroke might benefit from prospectively planned comprehensive cardiac rehabilitation (CCR). In this pilot evaluation of a larger ongoing randomized-controlled-trial, we evaluated ultrasound (US) measurements of carotid atherosclerosis in subjects following TIA or mild non-disabling stroke and their relationship with risk factors before and after 6-months of CCR. Carotid ultrasound (US) measurements of one-dimensional intima-media-thickness (IMT), two-dimensional total-plaque-area (TPA), three-dimensional total-plaque-volume (TPV) and vessel-wall-volume (VWV) were acquired before and after 6-months CCR for 39 subjects who had previously experienced a TIA and provided written informed consent to participate in this randomized controlled trial. We maintained blinding for this ongoing study by representing treatment and control groups as A or B, although we did not identify which of A or B was treatment or control. Carotid IMT, TPA, TPV and VWV were measured before and after CCR as were changes in body mass index (BMI), total cholesterol (TC), high-density lipoprotein (HDL), low-density lipoprotein (LDL), triglycerides (TG), systolic blood pressure (SBP) and diastolic blood pressure (DBP). There were no significant differences in US measurements or risk factors between groups A and B. There was no significant change in carotid ultrasound measurements for group A (IMT, p = .728; TPA, p = .629; TPV, p = .674; VWV, p = .507) or B (IMT, p = .054; TPA, p = .567; TPV, p = .773; VWV, p = .431) at the end of CCR. There were significant but weak-to-moderate correlations between IMT and VWV (r = 0.25, p = .01), IMT and TPV (r = 0.21, p = .01), TPV and TPA (r = 0.60, p \u003C .0001) and VWV and TPV (r = 0.22, p = .02). Subjects with improved TC\u002FHDL ratios showed improved carotid VWV although, this was not statistically significant. In this preliminary evaluation, there were no significant differences in carotid US measurements in the control or CCR group; a larger sample size and\u002For longer duration is required to detect significant changes in US or other risk factor measurements.",{"EN":2496},"One, two and three-dimensional ultrasound measurements of carotid atherosclerosis before and after cardiac rehabilitation: preliminary results of a randomized controlled 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