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• W2100810368 abstract "HomeCirculationVol. 119, No. 25Exercise Training for Type 2 Diabetes Mellitus Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissionsDownload Articles + Supplements ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toSupplemental MaterialFree AccessReview ArticlePDF/EPUBExercise Training for Type 2 Diabetes MellitusImpact on Cardiovascular Risk: A Scientific Statement From the American Heart Association Thomas H. Marwick, MD, PhD, Chair, Matthew D. Hordern, PhD, Todd Miller, MD, FAHA, Deborah A. Chyun, RN, PhD, FAHA, Alain G. Bertoni, MD, MPH, FAHA, Roger S. Blumenthal, MD, FAHA, George Philippides, MD, Albert Rocchini, MD, FAHA and Thomas H. MarwickThomas H. Marwick Search for more papers by this author , Matthew D. HordernMatthew D. Hordern Search for more papers by this author , Todd MillerTodd Miller Search for more papers by this author , Deborah A. ChyunDeborah A. Chyun Search for more papers by this author , Alain G. BertoniAlain G. Bertoni Search for more papers by this author , Roger S. BlumenthalRoger S. Blumenthal Search for more papers by this author , George PhilippidesGeorge Philippides Search for more papers by this author , Albert RocchiniAlbert Rocchini Search for more papers by this author and Search for more papers by this author and on behalf of the American Heart Association Exercise, Cardiac Rehabilitation, and Prevention Committee of the Council on Clinical Cardiology; Council on Cardiovascular Disease in the Young; Council on Cardiovascular Nursing; Council on Nutrition, Physical Activity, and Metabolism; and the Interdisciplinary Council on Quality of Care and Outcomes Research Originally published8 Jun 2009https://doi.org/10.1161/CIRCULATIONAHA.109.192521Circulation. 2009;119:3244–3262Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: June 8, 2009: Previous Version 1 Introduction …3244Beneficial Effects of Exercise in T2DM…3245 Glycemic Control…3245 Body Composition…3248 Risk Factors…3248 Vascular Effects…3248 Myocardial Function…3248 Development of CVD…3248Cardiac Risks of Exercise Training in T2DM…3249 Generic Cardiac Risks of Training…3249 Screening for Coronary Artery Disease…3249 Prior Studies of CAD Screening…3249 Guidelines/Position Statements…3250Noncardiac Risks of Exercise Training in T2DM…3251 Hypoglycemia…3251 Peripheral Arterial Disease and Foot Care…3251 Microvascular Disease…3252Exercise Training Guidelines…3252 Preparation for Exercise…3253 Frequency…3253 Intensity…3253 Duration…3254 Session Duration…3254 Program Duration…3254 Type…3254 Aerobic…3254 Resistance…3254Approaches to Adherence…3254 Health Behavior…3254 Counseling…3255 Long-Term Efficacy…3255Special/Minority Groups…3255Conclusions…3256References…32571. IntroductionThe increasing prevalence of overweight and obesity has led to an unprecedented epidemic of type 2 diabetes mellitus (T2DM)1–4 and is likely to be followed by an epidemic of patients with complications of T2DM.5 Given the observed increases in the prevalence of T2DM in adults over the past few decades in developed countries,1,2,6 population-based efforts to reduce the cardiovascular complications of T2DM are as critical as the measures to prevent the problem.4,7 T2DM is the sixth-leading cause of death,8 with most deaths attributed to cardiovascular disease (CVD; nearly 70%) and with ischemic heart disease being responsible for nearly 50% of these deaths.9 The economic cost of T2DM has been estimated to be $172 billion in 2007 in the United States alone3 (up from $132 billion in 2002)10 and is likely to be greater when the other indirect costs of its associated complications are included.11 These complications are due to atherosclerotic vascular disease4 but also reflect a susceptibility of patients with T2DM to heart failure,12,13 perhaps mediated by direct effects on the myocardium.14,15 Pharmaceutical intervention for glycemic control has shown beneficial results for microvascular complications in patients with T2DM; however, whether this therapy has beneficial effects on macrovascular complications and cardiovascular events remains unclear, with recent work suggesting some benefit,16 although previous studies report conflicting results.17–20Exercise, which is often viewed in relation to glycemic control, has important effects on the development of cardiovascular complications in T2DM. For the purpose of this statement, exercise is defined as planned and structured activity that is aimed at improving cardiovascular health and metabolic control. The goals of this scientific statement are to document the mechanisms whereby exercise is important in T2DM management, analyze the existing evidence regarding exercise interventions, and provide practical guidelines about preparation for exercise training programs and safety issues, as well as specific exercise training guidelines that can be used to initiate an exercise program. The recommendations are based on data available from previous investigations; unfortunately, only a few large-scale, randomized, controlled trials are available, and more are needed to confirm this position. The recommendations provided have been classified according to Table 1. Throughout this statement, the classifications and levels of evidence are shown in abbreviated form as class (level of evidence) (eg, [I(A)] for Class I, Level of Evidence A). Table 1. Classification of Recommendations and Level of EvidenceDescriptionThroughout the document, these are listed as [class (level)]; for example, class I, level of evidence A is listed as [I (A)].Classification of recommendation Class IConditions for which there is evidence and/or general agreement that a given procedure or treatment is beneficial, useful, and effective Class IIConditions for which there is conflicting evidence and/or a divergence of opinion about the usefulness/efficacy of a procedure or treatment Class IIaWeight of evidence/opinion is in favor of usefulness/efficacy Class IIbUsefulness/efficacy is less well established by evidence/opinion Class IIIConditions for which there is evidence and/or general agreement that a procedure/ treatment is not useful/effective and in some cases may be harmfulLevel of evidence Level of evidence AData derived from multiple randomized clinical trials or meta-analyses Level of evidence BData derived from a single randomized trial or from nonrandomized studies Level of evidence CConsensus opinion of experts2. Beneficial Effects of Exercise in T2DMThe overall beneficial effects of exercise in T2DM are well documented with regard to glucose control and multiple CVD risk factors. Table 2 outlines the exercise prescription and general effect of randomized, controlled trials that have assessed the effect of exercise training on glycemic control and other CVD risk factors in patients with T2DM.21–45 Searches of PubMed for exercise training intervention studies using the terms exercise and diabetes were performed. Criteria for the inclusion of studies in Table 2 were as follows: (1) The study was written in English; (2) it was published in August 2008 or earlier; (3) it included patients with T2DM only; (4) the study design included a nonexercise control group that did not receive intensive dietary therapy; (5) details of the randomized, controlled design were included; and (6) changes in glycemic control were assessed. Studies that included a separate or combined dietary component to the intervention were included; however, focus was placed on the exercise prescription of these studies. Improvements in glycemic control included improvements in hemoglobin (Hb) A1c, blood glucose, insulin sensitivity, and glucose area under the curve during an oral glucose tolerance test, among others. Table 3 similarly outlines the exercise prescription and effects of randomized, controlled trials that have assessed the effect of exercise training on endothelial function and vascular structure and distensibility in patients with T2DM.46–48 Searches for these studies were identical to those performed for glycemic control, except that studies were selected that included vascular structure and function as outcome measures. Changes in vascular function included changes in endothelial function (eg, flow-mediated dilation), carotid artery intima-media thickness, and arterial distensibility. Tables 2 and 3 also report changes in body composition, body mass index, and V̇o2max when data are available. Briefly, exercise has favorable metabolic effects (glycemic control, weight loss), effects on other risk factors (lipids, hypertension), and direct vascular effects. However, despite a number of studies suggesting favorable effects on metabolic control and CVD risk factors, the net effect of these on clinical outcomes in T2DM is yet to be defined. Table 2. Randomized, Controlled Exercise Training Intervention Studies in Patients With T2DM and Their Effect on Metabolic ControlFirst Author of StudyYearPatientsExercise PrescriptionEffectFrequencyIntensityDurationPeriodTypeWing21198825 T2DM3 d/wk3 mph60 min/d81/2 moAerobic• No improvement in glycemic control• No improvement in BMI30 T2DM4 d/wk3 mph60 min/d141/2 moAerobic• No improvement in glycemic control• Greater reduction in medication• Reduction in BMIKhan22199539 Sedentary T2DM5 d/wk40%–60% V̇o2max50 min/d15 wkAerobic• No improvement in glycemic control• Reduction in body fat• Increase in V̇o2maxAgurs-Collins23199764 Black T2DM3 d/wkUnspecified30 min/d6 moAerobic• Improvement in glycemic control• Reduction in body weight• Maintained BPDunstan24199755 Sedentary T2DM3 d/wk55%–65% V̇o2max45 min/d8 wkAerobic• Prevented a deterioration in glycemic control• Reduction in body weight• Increase in V̇o2maxHonkola25199738 Sedentary T2DM2 d/wk12–15 RMUnspecified5 moResistance• Improvement in glycemic control• Improvement in blood lipid profileMourier26199724 T2DM3 d/wk75% V̇o2max45 min/d8 wkAerobic & interval• Increase in insulin sensitivity50%–58% V̇o2max• Increase in V̇o2max• Decrease in abdominal fatDunstan27199821 T2DM3 d/wk50%–55% 1RM60 min/d8 wkCircuit resistance• Improvement in glycemic control• Reduction in BMITessier28200039 Elderly T2DM3 d/wk60%–79% HRmax60 min/d16 wkAerobic & resistance• Improvement in glycemic control• Increase in exercise capacityCastaneda29200262 T2DM3 d/wk60%–80% 1RM45 min/d16 wkResistance• Improvement in glycemic control• Increase muscle glycogen stores• Reduction in T2DM medications• No reduction in body weight• No reduction in whole-body fat mass• Reduction in trunk fat massDunstan30200236 Sedentary older T2DM3 d/wk75%–85% 1RM45 min/d6 moResistance• Improvement in glycemic control• Increase in muscular strength• Increase in lean massMaiorana31200216 T2DM3 d/wk70%–80% HRmax (aerobic)60 min/d8 wkAerobic & resistance• Improvement in glycemic control55%–65% 1RM• Reduction in body fat and waist-to-hip ratio• Increase in exercise capacityTsujiuchi32200226 T2DMUnspecifiedUnspecified120 min/d4 moThai Chi• Improvement in glycemic controlBaldi33200318 T2DM3 d/wk12 RMUnspecified10 wkResistance• Improvement in blood glucose and insulin• Increase in fat free mass• Prevent increase in fat mass• Increase in muscular strengthCuff34200328 Obese T2DM women3 d/wk60%–75% HRR, 12 RM75 min/d16 wkAerobic & resistance• Increase in insulin sensitivity• Reduction in body weight, abdominal obesity• Increase in V̇o2max3 d/wk60%–75% HRR75 min/d16 wkAerobic• Reduction in body weight, abdominal obesity• Increase in V̇o2max(Continued)Table 2. ContinuedFirst Author of StudyYearPatientsExercise PrescriptionEffectFrequencyIntensityDurationPeriodTypeBMI indicates body mass index; V̇o2max, maximal cardiorespiratory fitness; BP, blood pressure; RM, repetition maximum; 1RM, 1 repetition maximum; HRmax, maximum heart rate; HRR, heart rate reserve; and MET, metabolic equivalents.Di Loreto352003340 T2DMUnspecified>10 MET.h/wk2 y• Improvement in glycemic control• Reduction in BMIDunstan36200536 Sedentary older T2DM3 d/wk75%–85% 1RM45 min/d6 mo (1st Period)Resistance• Improvement in glycemic control• Increase in muscular strength• Increase in lean mass3 d/wk75%–85% 1RM45 min/d6 mo (2nd Period)Resistance• Failure to maintain improvement in glycemic control• Maintained strength gainsKadoglou37200795 T2DM4 d/wk50%–80% V̇o2max45–60 min/d8 moAerobic• Improvement in glycemic control• Increased V̇o2maxKadoglou38200760 Overweight T2DM4 d/wk50%–75% V̇o2max45–60 min/d6 moAerobic• Improvement in glycemic control• Reduction in insulin resistance• Improvement in antiinflammatory markers• Improvement in blood lipid profile• Increase in V̇o2max• No change in body compositionPi-Sunyer3920075145 T2DMWeekly to monthlyModerate175 min/wk12 moAerobic• Improvement in glycemic control• Decrease in BP• Improvement in blood lipid profileSigal402007251 T2DM3 d/wk75% HRmax45 min/d6 moAerobic• Improvement in glycemic control• Reduction in BMI, waist circumference, fat mass• Increase in muscle mass• Improvement in glycemic control3 d/wk7–9 RM45 min/d6 moResistance• Reduction in subcutaneous fat• Increase in muscle mass3 d/wk75% HRmax, 7–9 RM90 min/d6 moAerobic & resistance• Greater improvement in glycemic controlBrun41200825 T2DM2 d/wkVentilatory threshold30–45 min/d12 moAerobic• Increase in insulin sensitivity• No change in body composition• Maintained V̇o2maxKrousel-Wood42200876 Sedentary T2DM5 d/wk3–6 METS30 min/d3 moAerobic & resistance• No improvement in glycemic control• Trend towards improvement in BMI and quality of lifeNojima432008134 T2DM3 d/wk50% V̇o2max30 min/d12 moAerobic• Improvement in glycemic control• Reduction in oxidative stress• Improvement in body composition• Reduction in BPTsang44200838 T2DM2 d/wkLight60 min/d16 wkThai Chi• No improvement in glycemic control• No effect on body compositionWinnick45200813 T2DM women7 d/wk60%–70% V̇o2max50–60 min/d7 dAerobic• Improvement in whole-body insulin sensitivity but not hepatic insulin sensitivityTable 3. Randomized, Controlled Exercise Training Intervention Studies in Patients With T2DM and the Effect on Vascular Structure and FunctionFirst Author of StudyYearPatientsExercise PrescriptionEffectFrequencyIntensityDurationPeriodTypeMaiorana46200116 T2DM3 d/wk70%–80% HRmax (aerobic), 55%–65% 1RM60 min/d8 wkAerobic and resistance• Improvement in endothelial function• Improvement in glycemic control• Increase in V̇o2maxKim47200658 T2DM150 min/wk6 moAerobic• Attenuated progression of carotid intima-media thickness• Improvement in glycemic control, BP, body massMiddlebrooke48200659 T2DM3 d/wk70%–80% HRmax30 min/d6 mo• No improvement in microvascular function• No improvement in glycemic control, V̇o2max, or CVD risk factorsGlycemic ControlThe effects of exercise on metabolic control have been an important focus of exercise prescription.49 Previous studies have reported that exercise leads to improvements in metabolic control, measured by HbA1c, blood glucose, or insulin sensitivity (Table 2) [I (A)]. Generally, studies that failed to elicit this benefit have utilized interventions of low intensity21,22 or low volume41 or have reported poor adherence to the intervention.42 Importantly, the definitive study on this to date, a randomized, controlled trial in 251 T2DM patients, reported improvements ranging from −0.38 to −0.97 percentage points in HbA1c from exercise training that ranged from ≈135 to 270 minutes of exercise per week for 6 months.40 Quantification of effects across trials reveals that the overall beneficial effect of exercise on HbA1c levels is modest (average HbA1c reduction −0.8%, 90% confidence interval [CI] −1.3% to −0.2%)50; however, even these small improvements have been reported to be clinically significant in terms of the effects on an aggregate composite of macrovascular, microvascular, and nonvascular end points, similar to what is produced from an intensive pharmaceutical intervention.17In addition, previous research has reported improved insulin sensitivity/resistance and reductions in hyperglycemia-related medications as a result of exercise training.34,51 These changes typically have been reported in obese subjects with T2DM,39,52–55 which suggests that there is a good relationship between loss of body fat and improved glycemic control.56 However, improvement in glycemic control may be independent of fat loss.51 Moreover, patients with greater metabolic disturbances have shown the greatest improvement in glycemic control.57 Other potential mechanisms for better glucose control include improvement in insulin sensitivity58,59 and effects on glucose transporters (eg, GLUT4).60–64 Muscle contractions can elicit movement of glucose transporters (GLUT4) to the plasma membrane independently of insulin,65–67 and it is further speculated that muscle hypertrophy30,40,51,68 and blood flow69 are also contributing mechanisms.Body CompositionExercise improves and maintains cardiorespiratory fitness, muscular strength, endurance, and body composition (Table 2) [I (A)]. Again, quantification of effects across trials shows modest reductions in body mass (average −5.1%, 90% CI −7.6% to −2.5%) and body fat (average −15%, 90% CI −26% to −2%).50 Moreover, improvements in body composition may not be a precondition for the beneficial effect of endurance training, most likely because this reduces visceral fat.26 Indeed, loss in body fat alone, achieved through liposuction, fails to improve T2DM and other risk parameters, which emphasizes mediation of the benefits of weight loss through the metabolic effects of exercise,70 because liposuction would not alter visceral adiposity. Because weight loss is related to energy expenditure, aerobic exercise training has greater potential to yield results than resistance training, although studies have reported beneficial effects on weight loss and body composition from both modes of training.30,33,40 However, although there are studies that have reported these benefits as a result of exercise training, not all of the studies have shown improvements in body composition. This may be due to the different methods used to assess body composition (eg, body mass index, weight, or fat mass), different training regimens (ie, aerobic versus resistance), and potentially the inclusion or lack of a dietary component to accompany the intervention.Risk FactorsExercise has a favorable effect on cardiovascular risk factors. In particular, it has specific beneficial effects on the reduction of hypertension, hyperlipidemia, and obesity and the improvement in blood lipid profile,71,72 even when combined with a rigorous calorie-restricted diet in obese patients with T2DM [II (A)].39 Many trials have shown the reduction in systolic (average −5.6 mm Hg, 90% CI −9.3 to −1.8 mm Hg) and diastolic (average −5.5 mm Hg, 90% CI −9.9 to −1.1 mm Hg) blood pressure to be in the range associated with prognostic benefit.73 Modest reductions in triglycerides (average −26.6 mg/dL [−0.3 mmol/L], 90% CI −124.0 to 70.9 mg/dL) and small increases in high-density lipoprotein (average 5.0 mg/dL [0.13 mmol/L], 90% CI 2.7 to 7.7 mg/dL)72 are less clearly associated with prognostic benefit.Vascular EffectsThe effects of exercise training on abnormal vascular structure and function (including endothelial dysfunction and vascular distensibility) associated with T2DM are yet to be fully understood. Table 3 summarizes recent human studies, some of which show beneficial effects. Furthermore, another study, without a nonexercise control group, showed no effect on endothelial function in T2DM patients with severe chronic heart failure, in whom the intervention lasted for only 4 weeks.74 However, in this same investigation, the authors reported improvements in exercise capacity, left ventricular ejection fraction, and left ventricular stroke volume over the training period.Myocardial FunctionTo date, the effect of exercise training on myocardial function generally has been limited to animal models of T2DM. Most of these involve 5 days per week of exercise over an 8- to 10-week period and involve treadmill training at 20 to 30 m/min. These studies have uniformly shown that exercise training restores myocardial structure and performance, with increasing resistance to ischemia and favorable metabolic effects.75–84 A recent study showed that weight loss in patients enrolled in an exercise program may have a beneficial effect on myocardial function, but the relative roles of exercise and weight loss require further definition.85Development of CVDInactivity is associated with reduced survival in T2DM, irrespective of weight level86 and other risk factors.87 The inverse association of moderate-intensity physical activity with the development of coronary atherosclerosis, as evidenced by coronary calcification, has been demonstrated in patients without T2DM.88 The combined effects of exercise on metabolism, risk factors, and vascular function have been proposed to be beneficial in T2DM,89 but it is unclear to what extent this can be expected to reduce the prevalence of atherosclerotic CVD.3. Cardiac Risks of Exercise Training in T2DMGeneric Cardiac Risks of TrainingThe risk of a major cardiac event during exercise is small,90 and even in heart failure patients, who are recognized as being at high risk, no deaths have been reported during exercise in the course of an exercise training study (>80 000 patient-hours).91 The overall balance of benefit of exercise substantially exceeds its risk in unselected subjects,92 although this balance has not been defined in patients with T2DM. The major concern relates to whether exercise may be either limited or hazardous because of occult coronary artery disease. Whether exercise limitation due to undiagnosed left ventricular dysfunction may be improved by exercise training remains undefined.Screening for Coronary Artery DiseaseThe office attendance of a patient with T2DM for advice regarding exercise is an opportunity for lifestyle modification and general health screening. These patients should undergo a thorough history and physical examination before pursuing an exercise program. Patients with symptoms suggestive of coronary artery disease (CAD) should be evaluated appropriately, irrespective of T2DM status.93,94The investigation of asymptomatic patients for CAD is a vexing topic. The use of screening before an exercise program might be justifiable on 2 grounds but remains unproven. First, the identification of occult CAD might identify patients who are at risk from exercise, but the risks of exercise are minimal. Second, CAD is more prevalent, cardiovascular event rates are higher, and myocardial ischemia is more often silent in patients with rather than those without T2DM.95 Patients with advanced CAD may derive prognostic benefit from coronary revascularization, but this is unproven in subjects with T2DM, in whom revascularization targets may be suboptimal. Several arguments have been proposed in favor of and against such a program (Table 4).96–103 Perhaps the least favorable aspect is that screening for CAD represents an additional barrier to exercise in an overweight and deconditioned group among whom barriers to exercise need to be reduced. Table 4. Features in Favor of and Against Screening for CAD in Patients With T2DM Before Exercise TrainingForAgainstMI indicates myocardial infarction; DIAD, Detection of Ischemia in Asymptomatic Diabetics.Detection of some patients with severe (left main and/or 3-vessel) CADPatients with silent CAD may include those with prognostically important CAD who are candidates for revascularization therapyNo published data demonstrating that screening for CAD in asymptomatic diabetic patients results in improved outcomes in this population and 1 randomized trial demonstrating no effect on clinical outcomes (DIAD)96Identification of more minor CADRecognition of CAD could lead to more intensive treatment of risk factorsExisting recommendations in T2DM already recommend more aggressive treatment of hypertension and lipids simply on the basis of T2DM status and do not require the demonstration of CAD97,98Identification of low riskAvailable stress imaging modalities can risk-stratify symptomatic and asymptomatic patients with T2DMIdentification of a truly low-risk subset with T2DM is difficult.99 Annual rates of cardiovascular death and MI or total mortality with normal or low-risk images are 2% to 6% in retrospective studies.100–102Use in exercise prescriptionIdentification of patients with myocardial ischemia may be of value in instructing these patients to keep their target heart rate below their ischemic thresholdCost-effectiveness80% of the 18 million diabetic patients in the United States do not have established CAD,103 which leads to many negative test resultsPrior Studies of CAD ScreeningA number of studies with standard exercise (treadmill or cycle ergometry) testing, nuclear or echocardiographic stress imaging, and, more recently, computed tomography for detection of coronary artery calcification (CAC) have given a range of results for screening for CAD in asymptomatic T2DM patients. Many of these studies had methodological limitations, including small numbers of patients, enrollment of highly selected patients, retrospective design, or poorly described or outdated stress testing techniques (eg, planar thallium imaging). Many studies have been performed with pharmacological stress, which is less potent than exercise stress and may provide less prognostic information than obtained with exercise testing. However, the biggest problem is a probabilistic one: The limited return of studies in low-risk patients is well exemplified by the Milan Study on Atherosclerosis and Diabetes (MiSAD), which identified only 3 fatal myocardial infarctions and 20 nonfatal myocardial infarctions in a follow-up study of a subset of 735 of these patients over 5 years.104The published studies of stress imaging that involved 500 or more asymptomatic patients with T2DM but without known CAD are summarized in Table 5.96,102,105–107 Two retrospectively designed studies, which included patients with abnormal resting electrocardiograms (ECGs), reported abnormal stress single-photon emission computed tomography images in 39%105 and 58%102 of patients, respectively, and suggested that this test was useful for risk stratification. In contrast, in the prospectively designed Detection of Ischemia in Asymptomatic Diabetics (DIAD) study, which excluded patients with abnormal resting ECGs,96 the yield of abnormal studies was only 22% (16% with perfusion abnormalities and 6% with stress ECG or ventricular function abnormalities). Myocardial contrast echocardiography was abnormal in 60% of patients in a large, prospectively designed echocardiographic study106 that excluded patients with abnormal resting ECGs; 65% of these had significant anatomic CAD (stenoses >50%) at angiography. Table 5. Results of Stress SPECT and Stress Echocardiographic Screening for CAD in Patients With T2DMFirst AuthorYearDesignPatientsAge, yMen, %Diabetes Duration, yAbnormal ECG ExcludedType of StressResultsSPECT indicates single-photon emission computed tomography; MiSAD, Milan Study on Atherosclerosis and Diabetes; and T1-201, thallium 201.MiSAD Group1071997Prospective asymptomatic92554±6647.4±6.0Yes (if echocardiographic confirmation)Exercise ECG followed by exercise planar Tl-201 if equivocal or positiveExercise test abnormal 12% (112/925); exercise Tl-201 abnormal in 53% (59/112)Zellweger1052004Retrospective symptomatic/ asymptomatic82665±1257…NoExercise SPECT 54%; adenosine SPECT 46%Abnormal 39%Rajagopalan1022005Retrospective asymptomatic142760±147010 (Median)No (ECG Q wave 9%, ST-T abnormality 34%)Exercise SPECT 52%; SPECT 48%Abnormal 58%; high-risk 18%Wackers (DIAD)962004Prospective asymptomatic52261±7538.1±7.1YesLow-level exercise adenosine SPECTAbnormal 22%; 16% abnormal SPECTScognamiglio1062006Prospective asymptomatic189952±7679±6YesDipyridamole myocardial contrast echocardiogramAbnormal 59%The limited number of studies that have examined the value of computed tomography for detection of CAC in asymptomatic T2DM patients have shown that a majority of the population had at least some CAC (Table 6).108–111 The percentages of patients with Agatston CAC scores >100 were 31% to 53%, and CAC scores >400 were found in 12% to 27%. In a prospectively designed study that used a sequential imaging strategy of computed tomography in all patients followed by stress single-photon emission computed tomography in those with CAC >100 (27% of the population), Anand et al111 reported that 39% had mild to moderate perfusion abnormalities. Race clearly has an effect on the prevalence of subclinical abnormalities in CAC. In a Multiethnic Study of Atherosclerosis substudy of 204 white, 387 black, 311 Hispanic, and 126 Chinese individuals with T2DM in which the overall prevalence of CAC was 62%, the highest prevalence of measurable CAC was in whites (78%), followed by Chinese (68%), Hispanics (58%), and blacks (54%). High scores (CAC >400, 17% of the total) followed a similar pattern of prevalence, with 24%, 20%, 15%, and 14% of white, Chinese, Hispanic, and black participants, respectively, having high scores.112 In 2 studies that collected follow-up data,110,111 the CAC score was associated with patient outcome; however, a smaller study (n=269) reported that CAC scores were not predictive of outcome in T2DM.113Table 6. Results of Electron Beam Computed Tomography Screening for CAD in Patients With T2DMFirst AuthorYearDesignPatientsAge, yMen, %Diabetes Duration, yAbnormal ECG ExcludedType of ExaminationResultsPREDICT indicates Prospective Evaluation of Diabetic Ischemic Heart Disease by Computed Tomography; EBCT, electron" @default.
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• W2100810368 title "Exercise Training for Type 2 Diabetes Mellitus" @default.
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