期刊论文详细信息
BMC Cardiovascular Disorders
Influence of glycemic control on gain in VO2 peak, in patients with type 2 diabetes enrolled in cardiac rehabilitation after an acute coronary syndrome. The prospective DARE study
Michel Fischbach4  Bogdan Catargi5  Hervé Douard3  Jean-Michel Feige1  Jean-Henri Bertrand1  Isabelle Simoneau-Robin2  Marie-Christine Iliou6  Bénédicte Patois-Vergès7  Bruno Vergès2 
[1] Unité de réadaptation cardiaque, Clinique du Lavarin, Avignon, France;Service endocrinologie, diabétologie, CHU Le Bocage, Dijon, 21000, France;Service réadaptation cardiaque, Hôpital du Haut Lévêque, Pessac, France;URCA, Bordeaux, France;Service endocrinologie, diabétologie, Hôpital du Haut Lévêque, Pessac, France;Service réadaptation cardiaque, Hôpital Corentin Celton, Issy les Moulineaux, France;Unité de réadaptation cardiaque, Clinique Les Rosiers, Dijon, France
关键词: Hyperglycemia;    Myocardial infarction;    Cardiac rehabilitation;    Diabetes;   
Others  :  1217883
DOI  :  10.1186/s12872-015-0055-8
 received in 2015-01-21, accepted in 2015-06-10,  发布年份 2015
PDF
【 摘 要 】

Background

Gain in VO2 peak after cardiac rehabilitation (CR) following an acute coronary syndrome (ACS), is associated with reduced mortality and morbidity. We have previously shown in CR, that gain in VO2 peak is reduced in Type 2 diabetic patients and that response to CR is impaired by hyperglycemia.

Methods

We set up a prospective multicenter study (DARE) whose primary objective was to determine whether good glycemic control during CR may improve the gain in VO2 peak. Sixty four type 2 diabetic patients, referred to CR after a recent ACS, were randomized to insulin intensive therapy or a control group with continuation of the pre-CR antidiabetic treatment. The primary objective was to study the effect of glycemic control during CR on the improvement of peak VO2 by comparing first the 2 treatment groups (insulin intensive vs. control) and second, 2 pre-specified glycemic control groups according to the final fructosamine level (below and above the median).

Results

At the end of the CR program, the gain in VO2 peak and the final fructosamine level (assessing glycemic level during CR) were not different between the 2 treatment groups. However, patients who had final fructosamine level below the median value, assessing good glycemic control during CR, showed significantly higher gain in VO2 peak (3.5 ± 2.4 vs. 1.7 ± 2.4 ml/kg/min,p = 0.014) and ventilatory threshold (2.7 ± 2.5 vs. 1.2 ± 1.9 ml/kg/min,p = 0.04) and a higher proportion of good CR-responders (relative gain in VO2 peak ≥ 16 %): 66 % vs. 36 %, p = 0.011. In multivariate analysis, gain in VO2 peak was associated with final fructosamine level (p = 0.010) but not with age, gender, duration of diabetes, type of ACS, insulin treatment or basal fructosamine.

Conclusions

The DARE study shows that, in type 2 diabetes, good glycemic control during CR is an independent factor associated with gain in VO2 peak. This emphasizes the need for good glycemic control in CR for type 2 diabetic patients.

Trial registration

Trial registered as NCT00354237 (19 July 2006).

【 授权许可】

   
2015 Vergès et al.

【 预 览 】
附件列表
Files Size Format View
20150709015132278.pdf 478KB PDF download
Fig. 1. 16KB Image download
【 图 表 】

Fig. 1.

【 参考文献 】
  • [1]Belardinelli R, Paolini I, Cianci G, Piva R, Georgiou D, Purcaro A: Exercise training intervention after coronary angioplasty: the ETICA trial. J Am Coll Cardiol 2001, 37(7):1891-900.
  • [2]Goel K, Lennon RJ, Tilbury RT, Squires RW, Thomas RJ: Impact of cardiac rehabilitation on mortality and cardiovascular events after percutaneous coronary intervention in the community. Circulation 2011, 123(21):2344-52.
  • [3]O’Connor GT, Buring JE, Yusuf S, Goldhaber SZ, Olmstead EM, Paffenbarger RS Jr, et al.: An overview of randomized trials of rehabilitation with exercise after myocardial infarction. Circulation 1989, 80(2):234-44.
  • [4]Oldridge NB, Guyatt GH, Fischer ME, Rimm AA: Cardiac rehabilitation after myocardial infarction. Combined experience of randomized clinical trials JAMA 1988, 260(7):945-50.
  • [5]Taylor RS, Brown A, Ebrahim S, Jolliffe J, Noorani H, Rees K, et al.: Exercise-based rehabilitation for patients with coronary heart disease: systematic review and meta-analysis of randomized controlled trials. Am J Med 2004, 116(10):682-92.
  • [6]Oldridge N: Exercise-based cardiac rehabilitation in patients with coronary heart disease: meta-analysis outcomes revisited. Future Cardiol 2012, 8(5):729-51.
  • [7]Clark AM, Hartling L, Vandermeer B, McAlister FA: Meta-analysis: secondary prevention programs for patients with coronary artery disease. Ann Intern Med 2005, 143(9):659-72.
  • [8]Heran BS, Chen JM, Ebrahim S, Moxham T, Oldridge N, Rees K, et al.: Exercise-based cardiac rehabilitation for coronary heart disease. Cochrane Database Syst Rev 2011, 7:CD001800.
  • [9]Dunlay SM, Pack QR, Thomas RJ, Killian JM, Roger VL: Participation in cardiac rehabilitation, readmissions, and death after acute myocardial infarction. Am J Med 2014, 127(6):538-46.
  • [10]Hedbäck B, Perk J, Wodlin P: Long-term reduction of cardiac mortality after myocardial infarction: 10-year results of a comprehensive rehabilitation programme. Eur Heart J 1993, 14(6):831-5.
  • [11]Fletcher GF, Ades PA, Kligfield P, Arena R, Balady GJ, Bittner VA, et al.: Exercise standards for testing and training: a scientific statement from the American Heart Association. Circulation 2013, 128(8):873-934.
  • [12]Piepoli MF, Corrà U, Benzer W, Bjarnason-Wehrens B, Dendale P, Gaita D, et al.: Secondary prevention through cardiac rehabilitation: from knowledge to implementation. A position paper from the Cardiac Rehabilitation Section of the European Association of Cardiovascular Prevention and Rehabilitation. Eur J Cardiovasc Prev Rehabil 2010, 17(1):1-17.
  • [13]Perk J, De Backer G, Gohlke H, Graham I, Reiner Z, Verschuren M, et al.: European Guidelines on cardiovascular disease prevention in clinical practice (version 2012). The Fifth Joint Task Force of the European Society of Cardiology and Other Societies on Cardiovascular Disease Prevention in Clinical Practice (constituted by representatives of nine societies and by invited experts). Eur Heart J 2012, 33(13):1635-701.
  • [14]Pavy B, Iliou M-C, Vergès-Patois B, Brion R, Monpère C, Carré F, et al.: French Society of Cardiology guidelines for cardiac rehabilitation in adults. Arch Cardiovasc Dis 2012, 105(5):309-28.
  • [15]Antman EM, Anbe DT, Armstrong PW, Bates ER, Green LA, Hand M, et al.: ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction–executive summary. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to revise the 1999 guidelines for the management of patients with acute myocardial infarction). J Am Coll Cardiol 2004, 44(3):671-719.
  • [16]Myers J, Prakash M, Froelicher V, Do D, Partington S, Atwood JE: Exercise capacity and mortality among men referred for exercise testing. N Engl J Med 2002, 346(11):793-801.
  • [17]Kavanagh T, Mertens DJ, Hamm LF, Beyene J, Kennedy J, Corey P, et al.: Prediction of long-term prognosis in 12 169 men referred for cardiac rehabilitation. Circulation 2002, 106(6):666-71.
  • [18]Vanhees L, Fagard R, Thijs L, Amery A: Prognostic value of training-induced change in peak exercise capacity in patients with myocardial infarcts and patients with coronary bypass surgery. Am J Cardiol 1995, 76(14):1014-9.
  • [19]Emerging Risk Factors CollaborationSRK Seshasai: Kaptoge S, Thompson A, Di Angelantonio E, Gao P, et al. Diabetes mellitus, fasting glucose, and risk of cause-specific death N Engl J Med 2011, 364(9):829-41.
  • [20]Krempf M, Parhofer KG, Steg PG, Bhatt DL, Ohman EM, Röther J, et al.: Cardiovascular Event Rates in Diabetic and Nondiabetic Individuals With and Without Established Atherothrombosis (from the REduction of Atherothrombosis for Continued Health [REACH] Registry). Am J Cardiol 2010, 105(5):667-71.
  • [21]Suresh V, Harrison RA, Houghton P, Naqvi N: Standard cardiac rehabilitation is less effective for diabetics. Int J Clin Pract 2001, 55(7):445-8.
  • [22]Soleimani A, Abbasi K, Nejatian M, Movahhedi N, Hajizaynali MA, Salehiomran A, et al.: Effect of gender and type 2 diabetes mellitus on heart rate recovery in patients with coronary artery disease after cardiac rehabilitation. Minerva Endocrinol 2010, 35(1):1-7.
  • [23]Savage PD, Antkowiak M, Ades PA: Failure to improve cardiopulmonary fitness in cardiac rehabilitation. J Cardiopulm Rehabil Prev 2009, 29(5):284-91.
  • [24]Vergès B, Patois-Vergès B, Cohen M, Lucas B, Galland-Jos C, Casillas JM: Effects of cardiac rehabilitation on exercise capacity in Type 2 diabetic patients with coronary artery disease. Diabet Med 2004, 21(8):889-95.
  • [25]Holman RR, Turner RC: Insulin therapy in type II diabetes. Diabetes Res Clin Pract 1995, 28(Suppl):S179-84.
  • [26]Turner RC, Holman RR: Insulin use in NIDDM. Rationale based on pathophysiology of disease Diabetes Care 1990, 13(9):1011-20.
  • [27]Riddle MC, Rosenstock J, Gerich J: Insulin Glargine 4002 Study Investigators. The treat-to-target trial: randomized addition of glargine or human NPH insulin to oral therapy of type 2 diabetic patients. Diabetes Care 2003, 26(11):3080-6.
  • [28]European Diabetes Policy Group. A desktop guide to Type 2 diabetes mellitus. European Diabetes Policy Group 1999. Diabet Med. 1999 Sep;16(9):716–30.
  • [29]Wasserman K, Hansen J, Sue D, Casaburi R, Whipp B: Principles of exercise testing and interpretation. 3rd edition. Lippincott, Williams & Wilkins, Philadelphia, Pa, USA; 1999.
  • [30]Wasserman K, Whipp BJ, Koyl SN, Beaver WL: Anaerobic threshold and respiratory gas exchange during exercise. J Appl Physiol 1973, 35(2):236-43.
  • [31]Mampuya WM: Cardiac rehabilitation past, present and future: an overview. Cardiovasc Diagn Ther 2012, 2(1):38-49.
  • [32]Armbruster DA: Fructosamine: structure, analysis, and clinical usefulness. Clin Chem 1987, 33(12):2153-63.
  • [33]Banzer JA, Maguire TE, Kennedy CM, O’Malley CJ, Balady GJ: Results of cardiac rehabilitation in patients with diabetes mellitus. Am J Cardiol 2004, 93(1):81-4.
  • [34]Yohannes AM, Yalfani A, Doherty P, Bundy C: Predictors of drop-out from an outpatient cardiac rehabilitation programme. Clin Rehabil 2007, 21(3):222-9.
  • [35]Wittmer M, Volpatti M, Piazzalonga S, Hoffmann A: Expectation, satisfaction, and predictors of dropout in cardiac rehabilitation. Eur J Prev Cardiol 2012, 19(5):1082-8.
  • [36]Milani RV, Lavie CJ: Behavioral differences and effects of cardiac rehabilitation in diabetic patients following cardiac events. Am J Med 1996, 100(5):517-23.
  • [37]Nishitani M, Shimada K, Masaki M, Sunayama S, Kume A, Fukao K, et al.: Effect of cardiac rehabilitation on muscle mass, muscle strength, and exercise tolerance in diabetic patients after coronary artery bypass grafting. J Cardiol 2013, 61(3):216-21.
  • [38]Fang ZY, Sharman J, Prins JB, Marwick TH: Determinants of exercise capacity in patients with type 2 diabetes. Diabetes Care 2005, 28(7):1643-8.
  • [39]Younce CW, Wang K, Kolattukudy PE: Hyperglycaemia-induced cardiomyocyte death is mediated via MCP-1 production and induction of a novel zinc-finger protein MCPIP. Cardiovasc Res 2010, 87(4):665-74.
  • [40]Rajamani U, Essop MF: Hyperglycemia-mediated activation of the hexosamine biosynthetic pathway results in myocardial apoptosis. Am J Physiol Cell Physiol 2010, 299(1):C139-47.
  • [41]Su H, Ji L, Xing W, Zhang W, Zhou H, Qian X, et al.: Acute hyperglycaemia enhances oxidative stress and aggravates myocardial ischaemia/reperfusion injury: role of thioredoxin-interacting protein. J Cell Mol Med 2013, 17(1):181-91.
  • [42]Groenendyk J, Sreenivasaiah PK, Kim DH, Agellon LB, Michalak M: Biology of endoplasmic reticulum stress in the heart. Circ Res 2010, 107(10):1185-97.
  • [43]Lakshmanan AP, Harima M, Suzuki K, Soetikno V, Nagata M, Nakamura T, et al.: The hyperglycemia stimulated myocardial endoplasmic reticulum (ER) stress contributes to diabetic cardiomyopathy in the transgenic non-obese type 2 diabetic rats: a differential role of unfolded protein response (UPR) signaling proteins. Int J Biochem Cell Biol 2013, 45(2):438-47.
  • [44]Ren J, Gintant GA, Miller RE, Davidoff AJ: High extracellular glucose impairs cardiac E-C coupling in a glycosylation-dependent manner. Am J Physiol 1997, 273(6 Pt 2):H2876-83.
  • [45]Pang Y, Hunton DL, Bounelis P, Marchase RB: Hyperglycemia inhibits capacitative calcium entry and hypertrophy in neonatal cardiomyocytes. Diabetes 2002, 51(12):3461-7.
  • [46]Clark RJ, McDonough PM, Swanson E, Trost SU, Suzuki M, Fukuda M, et al.: Diabetes and the accompanying hyperglycemia impairs cardiomyocyte calcium cycling through increased nuclear O-GlcNAcylation. J Biol Chem 2003, 278(45):44230-7.
  • [47]Kobayashi S, Mao K, Zheng H, Wang X, Patterson C, O’Connell TD, et al.: Diminished GATA4 protein levels contribute to hyperglycemia-induced cardiomyocyte injury. J Biol Chem 2007, 282(30):21945-52.
  • [48]Lei S, Li H, Xu J, Liu Y, Gao X, Wang J, et al.: Hyperglycemia-induced protein kinase C β2 activation induces diastolic cardiac dysfunction in diabetic rats by impairing caveolin-3 expression and Akt/eNOS signaling. Diabetes 2013, 62(7):2318-28.
  • [49]Liao Y, Takashima S, Zhao H, Asano Y, Shintani Y, Minamino T, et al.: Control of plasma glucose with alpha-glucosidase inhibitor attenuates oxidative stress and slows the progression of heart failure in mice. Cardiovasc Res 2006, 70(1):107-16.
  • [50]Kelley DE, He J, Menshikova EV, Ritov VB: Dysfunction of mitochondria in human skeletal muscle in type 2 diabetes. Diabetes 2002, 51(10):2944-50.
  • [51]Tagougui S, Leclair E, Fontaine P, Matran R, Marais G, Aucouturier J, et al.: Muscle Oxygen Supply Impairment during Exercise in Poorly Controlled Type 1 Diabetes. Med Sci Sports Exerc 2015, 47(2):231-9.
  • [52]DeFronzo RA, Eldor R, Abdul-Ghani M: Pathophysiologic approach to therapy in patients with newly diagnosed type 2 diabetes. Diabetes Care 2013, 36(Suppl 2):S127-38.
  文献评价指标  
  下载次数:6次 浏览次数:5次