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- W2156830771 abstract "HomeCirculationVol. 113, No. 4Stress Testing in Patients With Diabetes Mellitus Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessReview ArticlePDF/EPUBStress Testing in Patients With Diabetes MellitusDiagnostic and Prognostic Value Anne R. Albers, Marc Z. Krichavsky and Gary J. Balady Anne R. AlbersAnne R. Albers From the Department of Medicine and the Section of Cardiology, Boston Medical Center, Boston University School of Medicine, Boston, Mass. Search for more papers by this author , Marc Z. KrichavskyMarc Z. Krichavsky From the Department of Medicine and the Section of Cardiology, Boston Medical Center, Boston University School of Medicine, Boston, Mass. Search for more papers by this author and Gary J. BaladyGary J. Balady From the Department of Medicine and the Section of Cardiology, Boston Medical Center, Boston University School of Medicine, Boston, Mass. Search for more papers by this author Originally published31 Jan 2006https://doi.org/10.1161/CIRCULATIONAHA.105.584524Circulation. 2006;113:583–592Exercise ECG and stress imaging tests are used for diagnostic and prognostic purposes and to monitor the effects of therapeutic interventions.1,2 Such testing is most often applied to individuals with known or suspected coronary artery disease (CAD), and its value has been well studied.1 CAD is more severe, more prevalent, and occurs at a younger age in patients with diabetes mellitus (DM). Diabetic patients without known CAD have similar rates of subsequent myocardial infarction (MI) compared with nondiabetic patients with a previous MI.3 Accordingly, DM is considered a risk equivalent to established CAD, and national guidelines for treatment of cardiac risk factors recommend similar goals for diabetic patients and those with known CAD.4–8 Diabetic patients have significantly higher rates of silent ischemia than the general population, and it has been postulated that this contributes to more advanced CAD on initial presentation and worse outcomes in diabetic patients.9 Because of this altered natural history, investigators have evaluated stress testing and its diagnostic and prognostic value among patients with DM. In particular, the utility of stress testing among asymptomatic diabetic patients remains an area of active study.The following article seeks to review the diagnostic and prognostic value of exercise ECG and stress imaging tests in symptomatic and asymptomatic patients with DM. Additionally, it aims to identify gaps in the current literature and summarize what recommendations can be made from the available data. PubMed and Medline 1966 through June 2005 databases were searched to identify all studies that addressed stress testing primarily among patients with DM using the following keywords: diabetes mellitus, stress testing, coronary arteriosclerosis, myocardial infarction or ischemia, exercise test, predictive value of tests, or electrocardiography. References within each article were evaluated for inclusion as well. Studies that comprised >50 patients were included for review. Studies in which stress testing was used primarily to assess perioperative cardiovascular risk were excluded.Diabetes and Cardiovascular DiseaseIt is estimated that there are 18.2 million people with the diagnosis of DM in the United States.10 In 2001, the prevalence of DM was 7.9% in the United States, but it has increased 61% since 1990.11 A total of 1.3 million new cases of DM and 798 000 new cases of type 2 DM (T2DM) occur each year.10 Impaired glucose tolerance (fasting glucose >100 mg/dL and <126 mg/dL) is estimated to be present in 35% of the elderly US population, and its prevalence is on the rise in overweight adolescents.7,12 DM is the fifth-leading cause of death in the United States and is associated with a 2- to 8-fold higher prevalence of, incidence of, and mortality from cardiovascular disease.7 Remarkably, 65% to 75% of patients with DM die of cardiovascular disease.13,14 By age 55 years, 35% of patients with type 1 DM (T1DM) have died of CAD.13 Direct and indirect healthcare costs of DM totaled $132 billion in 2002 and are expected to rise to $192 billion dollars by the year 2020.10,11,15The association between DM and CAD is becoming increasingly better understood. Endothelial dysfunction is heightened in DM and may represent a common pathophysiologic pathway for CVD. Vascular endothelium plays a key role in regulating vascular tone, leukocyte attraction, vascular smooth muscle growth, nutrient delivery and waste removal, inflammation, coagulation, and thrombosis.16 Nitric oxide (NO) has been shown to be a key regulatory factor of endothelial function, and hyperglycemia in DM is thought to decrease NO bioavailability. Increased endothelial cell matrix metalloproteinase is produced, which decreases vascular smooth muscle cell collagen in the fibrous caps of atheromas and increases the risk of plaque rupture and thrombosis. Plasminogen activator inhibitor type 1 (PAI-1) levels are elevated in DM, which inhibits fibrinolysis. These alterations in vasoconstriction, inflammation, and thrombosis collectively create a dysfunctional endothelium and contribute to the microvascular and macrovascular sequelae seen in DM.17Silent Ischemia and DiabetesThere are as many as 12.5 million diabetic patients with asymptomatic CAD.18 The reported prevalence varies widely in the literature (4% to 75%),19,20 which likely reflects variation in the cohort studied and in the definition of silent ischemia itself (eg, the absence of angina with an abnormal ECG, stress test, or angiogram). Diabetic patients mostly have been shown to have a higher incidence of silent ischemia than nondiabetic patients.19–21 One study, however, by Falcone et al22 found equivalent rates of ischemia during exercise ECG testing in the absence of angina (58% versus 64%, P=NS). However, only patients with documented CAD by angiography were included, and those with neuropathy and retinopathy were excluded. It has been hypothesized that afferent sympathetic fibers play a key role in the sensation of angina and that these fibers may be disrupted in those with autonomic dysfunction.21 A study of T1DM patients found an association between glycemic control and silent CAD.23 The pathophysiology of silent ischemia remains controversial, and other factors may also play a role, including differences in plasma opioid receptors, ischemic damage to nerve endings, and psychological factors.22 Regardless of the cause, silent ischemia may delay or mask the diagnosis of CAD, contributing to more advanced disease when it is finally discovered.Diagnostic Utility of Stress Testing and the Issue of Verification BiasBecause of the well-established association between DM and CAD, clinicians commonly request stress tests in diabetic patients to diagnose CAD; however, the use of stress testing for diagnostic purposes has inherent limitations, as do many of the studies evaluating the diagnostic accuracy of various stress testing modalities. One flaw is that the “gold standard,” coronary angiography, has well-recognized limitations and may underestimate disease.24 Additionally, most studies evaluating the sensitivity and specificity of various stress testing modalities suffer from “verification bias,” also called “workup bias,” “posttest referral bias,” or “selection bias.” This occurs when the decision to perform the “gold standard” test is influenced by the outcome of the diagnostic test itself. Most trials investigating noninvasive stress tests are organized so that primarily patients with abnormal stress tests proceed to invasive angiography. This creates a higher-risk subgroup within the study population who undergo angiography, most likely with a higher prevalence of CAD. Accordingly, the sensitivity of the stress test is overestimated, and the specificity is underestimated.25 In a study designed to eliminate verification bias, more than 800 patients with suspected coronary disease underwent exercise ECG testing, followed by angiography regardless of the outcome.26 This study found a sensitivity of 45% and specificity of 85%, which differs significantly from the traditionally accepted 70% sensitivity and specificity for exercise ECG testing.27 Similar findings have been found for stress echocardiography and stress nuclear imaging.28,29Exercise ECG TestingDiagnostic ValueGraded exercise tests are widely used clinically to assess the ability of an individual to safely tolerate increased physical activity while ECG, hemodynamic, and symptomatic responses are monitored for the development of myocardial ischemia, electrical instability, or other exertion-related abnormalities. The exercise ECG remains an inexpensive test that has been well validated in the general population, and it can be used as the first diagnostic test for patients with an intermediate risk of having CAD. Given the differences in presentation of CAD within the diabetic population and particularly the higher incidence of silent myocardial ischemia, various groups have attempted to evaluate whether the exercise ECG has similar accuracy in a diabetic population.Lee et al30 (Table 1) retrospectively evaluated 190 diabetic patients among 1282 male veterans presenting with chest pain who underwent an exercise ECG test and coronary angiography within a 4-month period. With standard ECG criteria used to define a positive test,1 38% of diabetic patients had an abnormal exercise test, whereas 69% had CAD as defined by angiography. The sensitivity of the exercise test among diabetic patients was 47%, and the specificity was 81%, with a positive predictive value of 85% and negative predictive value of 41%. This did not differ significantly from the 1092 patients without DM (sensitivity 52%, specificity 80%, positive predictive value 78%, and negative predictive value 55%). Although the study was limited by a relatively small percentage of diabetic patients (15%) and was subject to verification bias, it suggests that exercise ECG testing offers similar diagnostic value for patients with and without DM who present with chest pain. TABLE 1. Summary of Studies Using Stress Testing in the Diagnosis of Suspected CAD in Patients With DiabetesType of TestStudyDM Subjects, nReference StandardSensitivity, %Specificity, %PPV, %NPV, %PPV indicates positive predictive value; NPV, negative predictive value; ECG, exercise ECG stress test; DSE, dobutamine stress echocardiography; and N/A, not available.ECGLee et al30190Angiography47818541DSEHennessy et al3152Angiography82548450NuclearKang et al32138Angiography8656N/AN/AExercise ECG testing has also been used to assess asymptomatic diabetic patients for CAD. Blandine et al9 (Table 2) prospectively screened 203 diabetic patients without anginal symptoms who had normal resting ECGs with exercise ECG tests (stress nuclear imaging was used if exercise ECG testing was contraindicated or inconclusive). Sixteen percent of the group had an abnormal stress test, whereas 9% had silent CAD as defined by angiography. The vast majority of patients (84%) with silent angiographic CAD had T2DM. Koistinen et al33 studied 136 asymptomatic diabetic patients who underwent exercise ECG testing and thallium imaging, with subsequent cardiac catheterization if noninvasive testing was positive. Exercise ECG testing was abnormal in 14% of these asymptomatic patients, with a positive predictive value of 94%. This result is higher than previous studies and may reflect the relatively older, male, and poorly controlled diabetic cohort (mean HgA1c 11.3%) with a higher incidence of CAD. Bacci et al34 evaluated 206 consecutive higher-risk, asymptomatic, T2DM patients with peripheral arterial disease (PAD) and at least 2 cardiovascular risk factors (CRFs); 19% had an abnormal test. Coronary angiography was performed in 71 patients (27 with a positive test and 44 randomly selected patients with a negative test). Of these, 29% had significant CAD. The positive predictive accuracy of the exercise ECG was 79%. Although relatively small in size and often subject to verification bias, these studies collectively support the notion that among higher-risk cohorts of asymptomatic patients with DM, up to nearly one third may have unrecognized CAD, and that exercise ECG testing may provide useful diagnostic information to identify these patients. TABLE 2. Summary of Studies Using Stress Testing in the Diagnosis of CAD in Asymptomatic Patients With DiabetesType of TestStudyDM Subjects, nReference StandardSensitivity, %Specificity, %PPV, %NPV, %Abbreviations as in Table 1.ECGBlandine et al998AngiographyN/AN/A90N/AECGKoistinen et al33136AngiographyN/AN/A94N/AECGBacci et al34206AngiographyN/AN/A79N/AECGPenfornis et al3556AngiographyN/AN/A60N/ADSEPenfornis et al3556AngiographyN/AN/A69N/ANuclearBlandine et al9103AngiographyN/AN/A63N/ANuclearWackers et al191123NoneN/AN/AN/AN/ANuclearRajagopalan et al201427Angiography92688960NuclearPenfornis et al3556AngiographyN/AN/A75N/APrognostic ValueAlthough the literature suggests that exercise ECG tests may identify CAD in diabetic patients, national guidelines recommend that all diabetic patients should be treated as if they have CAD with regard to blood pressure management, lipid goals, aspirin use, and other secondary preventive measures. Therefore, a key issue facing clinicians is to risk-stratify the long-term likelihood of morbidity and mortality due to CAD and to identify those patients who might benefit from more aggressive treatment strategies to mitigate these risks.In a study of 68 asymptomatic male veterans with DM, Rubler et al36 (Table 3) found that exercise ECG testing had a 50% sensitivity and 83% specificity for predicting subsequent cardiac events (cardiac death, MI, or angina) over an average of 41 months of follow-up. The Milan Study on Atherosclerosis and Diabetes (MiSAD)37 prospectively screened 735 asymptomatic diabetic patients for CAD and followed this group for cardiac events for 5 years. All patients underwent exercise ECG, with a positive test prompting stress nuclear testing and additional therapy as guided by participating cardiologists. Selection criteria favored a relatively low-risk cohort, excluding those with nephropathy (creatinine >1.5 mg/dL), retinopathy, cerebrovascular disease, or peripheral vascular disease, with a mean hemoglobin A1c of 7.3. Among the 638 subjects (87%) with a normal exercise ECG test, the incidence of cardiac events (death, MI, or angina) was 0.97/100 person-years (CI 0.66 to 1.38) compared with 3.85/100 person-years (CI 1.84 to 7.07) in those with abnormal stress testing (P<0.0001). Although these data are limited by verification bias, they suggest that asymptomatic patients with uncomplicated DM who have a negative exercise ECG test have a lower cardiac event rate and relatively favorable prognosis. The prognostic implications of a negative exercise ECG test in asymptomatic diabetic patients with higher-risk profiles, including PAD and multiple CRFs, has not been addressed in the literature to the best of our knowledge. TABLE 3. Summary of Studies Using Stress Testing to Assess Prognosis in Patients With DiabetesType of TestStudyDM Subjects, nSummaryCE indicates cardiac events; PPV, positive predictive value; NPV, negative predictive value; CV, cardiovascular; DSE, dobutamine stress echocardiography; RR, relative risk; HR, hazard ratio; and WMSI, wall motion score index.ECGRubler et al3668Exercise ECG among asymptomatic DM predicted CE over 41 months with sensitivity 50%, specificity 83%, PPV 30%, NPV 88%ECGFaglia et al37735Negative exercise ECG in relatively low-risk asymptomatic diabetes cohort provided favorable prognosis: 0.97 CE/100 person-years vs 3.85/100 person-years, P<0.0001ECGSeshadri et al3851DM was an independent predictor of an abnormal HRR (adjusted OR 2.1, P=0.04)ECGCheng et al392333DM with impaired HRR 5 minutes after exercise had highest rates of CV and overall mortality (P for trend<0.001)ECGWei et al401263Strong association among DM males between poor fitness and mortality (RR 2.1)Echocardiography Exercise, DSEMarwick et al41937Abnormal test independent predictor of mortality (HR 1.8). Inability to exercise most powerful predictor of mortality (HR 3.9) ExerciseMcCully et al42206DM (RR 1.9), prior MI (RR 2.4), and exercise-induced LV dysfunction (RR 1.6) were multivariate predictors of cardiac death or MI in cohort with good exercise capacity ExerciseElhendy et al43563Increased risk of cardiac death or MI at 5 years (23% vs 7%, P<0.0001) with abnormal test. Negative test associated with no events at 2 years, 8% at 5 years. DSEKamalesh et al44144Increased incidence of CE despite negative stress echocardiography in DM cohort (6% vs 2.9%/year). Event rate increased significantly in DM after 18 months. DSESozzi et al45396WMSI on DSE predicted CE (χ2 37 vs 18, P<0.05) and mortality (χ2 52 vs 43, P<0.05) DSE, dipyridamoleBigi et al46259Abnormal test associated with lower event-free survival (OR 2.9, P<0.001). WMSI only independent predictor of CE.NuclearRajagopalan et al201427Annual mortality rate among asymptomatic diabetic patients varies significantly based on low- (3.6%), medium- (5.0%), or high-risk (5.9%) test (P<0.001)NuclearGiri et al47929Diabetic patients had significantly more cardiac events than nondiabetics (8.6% vs 4.5%, P<0.0001)NuclearKang et al481080Increasing annual rate of cardiac death or MI with normal (1–2%), mildly abnormal (3–4%), and moderately to severely abnormal (>7%) test (χ2=36, P<0.0001)NuclearSchinkel et al49207Abnormal test conferred greater risk of cardiac death (HR 7.2, P<0.0001) in a high-risk diabetic cohort unable to exercise. No deaths in 2.5 years after a normal test.NuclearHachamovitch et al501818Presence of DM, known CAD, age, gender, and inability to exercise provided incremental prognostic information beyond the stress test result.NuclearVanzetto et al51158Ability to exercise associated with low risk of future CE, and nuclear imaging provides limited additional value. Inability to exercise associated with higher risk (OR 6.8, P=0.001), particularly with abnormal scan (OR 7.9, P<0.005).NuclearDe Lorenzo et al52180Increasing annual rates of cardiac death or MI among high-risk asymptomatic DM with no (3%), 1 (10%), and multiple (>31%) perfusion defects (P=0.0001)NuclearBerman et al531222Among diabetics, T1DM had higher annual mortality than T2DM (9% vs 5%, P<0.05); females had greater annual mortality than males (P<0.0001).Non–ST-Segment VariablesSignificant diagnostic and prognostic information beyond the ST-segment response and presence of angina can be obtained from the carefully performed exercise ECG test. Exercise capacity is well established as a predictor of cardiovascular mortality, and tools like the Duke Treadmill Exercise Score are commonly used to provide prognostic information.54 More recently, investigators have identified additional parameters that provide prognostic information in both general clinical and diabetic populations. These include heart rate recovery (HRR) after exercise and chronotropic response (percentage of heart rate reserve used). Autonomic dysfunction and alterations in sympathetic and parasympathetic tone have been hypothesized to play a role in these physiological parameters. Diabetic patients have a higher incidence of autonomic dysfunction.55 Prolonged HRR after exercise predicts mortality in the general population.56 An abnormal HRR is variably defined in the literature. In one large study from the Cleveland Clinic,57 it is defined as failure to decrease heart rate by at least 12 bpm 1 minute after peak exercise. Recent studies have applied HRR analysis to patients with DM. Seshadri et al38 found that increasing blood sugar levels correlated with decreased HRR and that the diagnosis of DM was an independent predictor of an abnormal HRR response to exercise. Cheng et al39 followed up 2333 diabetic men for 15 years after exercise ECG testing, in which the HRR was measured 5 minutes after maximal exercise. The cohort was divided into quartiles based on HRR. Both cardiovascular and all-cause mortality were highest in the patients with impaired HRR (P<0.001 for trend).A patient’s cardiorespiratory fitness level, obtained by maximal exercise testing, predicts mortality in patients with DM.40 A total of 1263 men with T2DM underwent a medical evaluation including exercise ECG testing and were prospectively followed up for 12 years. Study patients were categorized as low, moderately, or highly fit on the basis of maximal metabolic units (METs) achieved, normalized for age and gender. There was a strong association between low fitness and increased mortality in diabetic patients, with an adjusted relative risk for death of 2.1 (CI 1.5 to 2.9). Each 1-MET increase in exercise capacity was associated with a 25% (CI 17% to 32%) decrease in mortality in the multivariate analysis (P<0.001). Rubler et al36 further showed that duration of exercise on exercise ECG testing was the single predictor of cardiac events (death, MI, or angina) in a cohort of 68 diabetic patients followed up for a mean of 41 months (P<0.005).SummaryExercise ECG testing remains a well-established, inexpensive test available to assist clinicians in the diagnosis and prognosis of CAD in diabetic patients. It appears to have similar diagnostic sensitivity (&50%) and specificity (&80%) for diabetic patients presenting with angina as for nondiabetic patients. It can identify a subgroup of asymptomatic diabetic patients who have significant CAD as defined by angiography, and in lower-risk diabetic cohorts, it may offer short-term prognostic reassurance to those asymptomatic patients with negative tests. However, considerable prognostic power of the exercise ECG test lies beyond the ST-segment response and the presence of angina during exercise. Parameters including exercise capacity and HRR offer significant information, particularly in diabetic patients, who may not experience angina during exercise and who may have increased autonomic dysfunction. Chronotropic response during exercise testing has not been studied in diabetic patients. Further studies are needed to assess the value of these non–ST-segment variables and the value of the Duke Prognostic Score among patients with DM.Stress EchocardiographyDiagnostic ValueStress testing with imaging is well recognized to provide greater diagnostic accuracy than exercise ECG testing in the general clinical population.58,59 Stress echocardiography has a mean sensitivity of 86% and a specificity of 81% in the general population.58 There are limited data that specifically address the utility of stress echocardiography in patients with DM. Hennessy et al31 (Table 1) evaluated 52 patients with DM referred for cardiac assessment using dobutamine stress echocardiography (DSE). Significant CAD was defined as >50% stenosis on coronary angiography. Sensitivity, specificity, and positive and negative predictive values of DSE for CAD detection were 82%, 54%, 84%, and 50%, respectively. Although the study was limited by the small size of the cohort, it demonstrated similar diagnostic accuracy for DSE in a diabetic population. Penfornis et al35 (Table 2) compared the efficacy of DSE to exercise ECG testing and SPECT (single-photon emission computed tomography) nuclear perfusion imaging in 56 asymptomatic diabetic patients with 3 additional CRFs but normal resting ECGs. Participants underwent all forms of noninvasive stress testing, but coronary angiography was only performed if at least 1 test was abnormal (47%), which precluded the measurement of diagnostic sensitivity and specificity. Positive predictive value was 69% for DSE, 60% for exercise ECG, and 75% for thallium SPECT.Prognostic ValueSeveral studies have evaluated the prognostic value of stress echocardiography among diabetic patients. Marwick et al41 (Table 3) reported on the use of stress echocardiography to predict mortality in 937 diabetic patients with known or suspected CAD over 4 years of follow-up. Exercise echocardiography was performed in 333 patients (36%), whereas 604 (64%) underwent DSE. An abnormal test was an independent incremental predictor of mortality (hazard ratio 1.77). However, the strongest predictor of mortality was referral for pharmacological stress testing, which conferred a 4-fold higher risk compared with those who underwent exercise echocardiography. This likely reflected more severe comorbidities in those unable to exercise. However, imaging results do appear to offer incremental information in addition to exercise capacity. McCully et al42 reported the outcome of 206 diabetic and 1874 overall patients with good exercise capacity (≥5 METs in females, ≥7 METs in males) but abnormal exercise echocardiograms. After a mean follow-up of 3 years, the annual rate of cardiac death or nonfatal MI was 2%. DM, history of MI, and exercise-induced left ventricular (LV) dysfunction were multivariate predictors of adverse outcome.Elhendy et al43 studied the outcomes of 563 diabetic patients with known (30%) or suspected CAD undergoing exercise echocardiography over a median follow-up of 3 years. Patients with an abnormal stress echocardiography result had a higher event rate (cardiac death and MI) than those with a normal test at 1 year (2% versus 0%), 3 years (12% versus 2%), and 5 years (23% versus 8%). Resting LV ejection fraction and the number of ischemic segments during exercise provided independent incremental prognostic information above clinical and exercise data. Evidence of multivessel distribution of echocardiographic abnormalities conferred the worst prognosis. The event rate was poorly predicted by a prior history of angina or by stress-induced angina during the test, which reinforces the notion that the absence of symptoms does not necessarily imply low cardiac risk among diabetic patients. Notably, there were no cardiac events among patients with a normal test through 2 years of follow-up. By 5 years, the event rate had increased to 8%. Kamalesh et al44,60 reviewed multiple stress echocardiography and stress nuclear studies in diabetic cohorts and found similarly concerning late event rates (beyond 2 years) among diabetic patients with normal stress imaging results. This phenomenon is not seen in the nondiabetic population and is hypothesized to reflect the challenge of detecting diffuse small-vessel disease in diabetic patients, as well as an increased propensity for future events due to rapid progression of atherosclerosis, increased inflammation, thrombosis, and risk of plaque rupture. This has led some to suggest that a repeat stress test may be indicated after 2 years to reassess cardiac risk in diabetic patients, although to date, this strategy has not been studied prospectively in the literature.43,60Sozzi et al45 studied the incremental value of DSE for risk stratification in diabetic patients who were unable to exercise. A total of 396 patients with known limited exercise capacity underwent DSE for evaluation of known or suspected CAD and were followed up for cardiac events (cardiac death and nonfatal MI) and all-cause mortality for a median of 3 years. Clinical predictors of cardiac events were a history of congestive heart failure, previous MI, hypercholesterolemia, and resting LV ejection fraction. Quantification of ischemia using a wall-motion score index on DSE (with higher numbers reflecting increasingly abnormal wall motion at peak exercise) offered significant additional prognostic value for cardiac events (χ2 37 versus 18, P<0.05) and all-cause mortality (χ2 52 versus 43, P<0.05). Bigi et al46 also assessed the value of pharmacological stress echocardiography for risk stratification of diabetic patients with known or suspected CAD. A total of 259 patients with DM underwent dobutamine (42%) or dipyridamole (58%) stress echocardiography and were followed up for a mean of 2 years for cardiac death and nonfatal MI. Wall-motion score index was the sole independent predictor of events on multivariate analysis. A positive stress echocardiogram was associated with a 3-fold lower event-free survival.SummaryStress echocardiographic imaging provides improved sensitivity and specificity compared with exercise ECG testing. Increasing data are available to support both its diagnostic accuracy and, in particular, its prognostic ability to risk-stratify diabetic patients for future cardiac events. The presence of resting LV systolic dysfunction and stress-induced wall-motion abnormalities provides incremental prognostic information to clinical and exercise parameters in multiple studies involving both exercise and pharmacological stress echocardiography. Patients referred for pharmacological stress echocardiography demonstrate a higher risk for cardiovascular events than those referred for exercise testing, which likely reflects more severe underlying cardiovascular disease and comorbidities. Diabetic patients with normal stress echocardiograms appear to have a greater risk for subsequent cardiovascular events than nondiabetic patients, particularly beyond 2 years. The hypothesis that diabetic patients require more frequent follow-up testing merits further investigation.Stress Nuclear TestingDiagnostic ValueStress nuclear testing has a sensitivity of 88% and specificity of 74% (uncorrected for verification bias) for the detection of angiographic CAD in the general clinical population and has been found to have similar diagnostic value among diabetic cohorts.59 Among stress imaging modalities, stress nuclear testing is the most extensively studied in diabetic populations. Kang et al32 (Table 1) retrospectively evaluated 138 diabetic (12% T1DM) and 188 nondiabetic patients with susp" @default.
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- W2156830771 cites W120704691 @default.
- W2156830771 cites W1516314655 @default.
- W2156830771 cites W1602983020 @default.
- W2156830771 cites W1814644851 @default.
- W2156830771 cites W188821610 @default.
- W2156830771 cites W1974033444 @default.
- W2156830771 cites W1974424968 @default.
- W2156830771 cites W1988801247 @default.
- W2156830771 cites W1994742785 @default.
- W2156830771 cites W2002424788 @default.
- W2156830771 cites W2005247608 @default.
- W2156830771 cites W2013760808 @default.
- W2156830771 cites W2023821775 @default.
- W2156830771 cites W2034765544 @default.
- W2156830771 cites W2047049447 @default.
- W2156830771 cites W2053991755 @default.
- W2156830771 cites W2055932611 @default.
- W2156830771 cites W2059307948 @default.
- W2156830771 cites W2062986428 @default.
- W2156830771 cites W2076126377 @default.
- W2156830771 cites W2078757199 @default.
- W2156830771 cites W2081623156 @default.
- W2156830771 cites W2085550373 @default.
- W2156830771 cites W2088413028 @default.
- W2156830771 cites W2095523868 @default.
- W2156830771 cites W2100493298 @default.
- W2156830771 cites W2104247536 @default.
- W2156830771 cites W2108216546 @default.
- W2156830771 cites W2113080681 @default.
- W2156830771 cites W2117855475 @default.
- W2156830771 cites W2119130035 @default.
- W2156830771 cites W2119243222 @default.
- W2156830771 cites W2122510881 @default.
- W2156830771 cites W2132163522 @default.
- W2156830771 cites W2138674605 @default.
- W2156830771 cites W2142695863 @default.
- W2156830771 cites W2144355614 @default.
- W2156830771 cites W2153043086 @default.
- W2156830771 cites W2156121263 @default.
- W2156830771 cites W2159222156 @default.
- W2156830771 cites W2159465923 @default.
- W2156830771 cites W2165256339 @default.
- W2156830771 cites W2168536185 @default.
- W2156830771 cites W2169625790 @default.
- W2156830771 cites W2170795054 @default.
- W2156830771 cites W2171860808 @default.
- W2156830771 cites W2318588083 @default.
- W2156830771 cites W2331274940 @default.
- W2156830771 cites W2342311534 @default.
- W2156830771 cites W2909539111 @default.
- W2156830771 cites W3122152400 @default.
- W2156830771 cites W4230870013 @default.
- W2156830771 cites W4234393699 @default.
- W2156830771 cites W4246329408 @default.
- W2156830771 cites W4255078542 @default.
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