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Final Evidence Summary

Coronary Heart Disease: Screening with Electrocardiography

September 15, 2011

Recommendations made by the USPSTF are independent of the U.S. government. They should not be construed as an official position of the Agency for Healthcare Research and Quality or the U.S. Department of Health and Human Services.

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Screening Asymptomatic Adults With Resting or Exercise Electrocardiography

A Review of the Evidence for the U.S. Preventive Services Task Force

Release Date: September 2011

By Roger Chou, MD; Bhaskar Arora, MD; Tracy Dana, MLS; Rongwei Fu, PhD; Miranda Walker, MA; and Linda Humphrey, MD

The information in this article is intended to help clinicians, employers, policymakers, and others make informed decisions about the provision of health care services. This article is intended as a reference and not as a substitute for clinical judgment.

This article may be used, in whole or in part, as the basis for the development of clinical practice guidelines and other quality enhancement tools, or as a basis for reimbursement and coverage policies. AHRQ or U.S. Department of Health and Human Services endorsement of such derivative products may not be stated or implied.

This article was first published in Annals of Internal Medicine on September 20, 2011 (Ann Intern Med 2011;155:375-385; http://www.annals.org).

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Background: Coronary heart disease is the leading cause of death in adults. Screening for abnormalities by using resting or exercise electrocardiography (ECG) might help identify persons who would benefit from interventions to reduce cardiovascular risk.

Purpose: To update the 2004 U.S. Preventive Services Task Force evidence review on screening for resting or exercise ECG abnormalities in asymptomatic adults.

Data Sources: MEDLINE (2002 through January 2011), the Cochrane Library database (through the fourth quarter of 2010), and reference lists.

Study Selection: Randomized, controlled trials and prospective cohort studies.

Data Extraction: Investigators abstracted details about the study population, study design, data analysis, follow-up, and results and assessed quality by using predefined criteria.

Data Synthesis: No study evaluated clinical outcomes or use of risk-reducing therapies after screening versus no screening. No study estimated how accurately resting or exercise ECG classified participants into high-, intermediate-, or low-risk groups, compared with traditional risk factor assessment alone. Sixty-three prospective cohort studies evaluated abnormalities on resting or exercise ECG as predictors of cardiovascular events after adjustment for traditional risk factors. Abnormalities on resting ECG (ST-segment or T-wave abnormalities, left ventricular hypertrophy, bundle branch block, or left-axis deviation) or exercise ECG (ST-segment depression with exercise, chronotropic incompetence, abnormal heart rate recovery, or decreased exercise capacity) were associated with increased risk (pooled hazard ratio estimates, 1.4 to 2.1). Evidence on harms was limited, but direct harms seemed minimal (for resting ECG) or small (for exercise ECG). No study estimated harms from subsequent testing or interventions, although rates of angiography after exercise ECG ranged from 0.6% to 2.9%.

Limitation: Only English-language studies were included. Statistical heterogeneity was present in several of the pooled analyses.

Conclusion: Abnormalities on resting or exercise ECG are associated with an increased risk for subsequent cardiovascular events after adjustment for traditional risk factors, but the clinical implications of these findings are unclear.

Primary Funding Source: Agency for Healthcare Research and Quality

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Coronary heart disease (CHD) is the leading cause of death in U.S. adults1,2. Many persons do not experience symptoms before a major first CHD event, such as sudden cardiac arrest, myocardial infarction, congestive heart failure, or unstable angina3. Traditional Framingham risk factors (age, sex, blood pressure, serum total or low-density lipoprotein cholesterol concentration, high-density lipoprotein cholesterol concentration, cigarette smoking, and diabetes) can help predict future CHD events but do not explain all of the excess risk4,5. Supplementing traditional risk factor assessment with other methods, including resting or exercise electrocardiography (ECG), might help better guide use of risk-reduction therapies in asymptomatic persons without known CHD6.

In 2004, the U.S. Preventive Services Task Force (USPSTF) recommended against screening with resting or exercise ECG in adults at low risk for CHD (D recommendation) and found insufficient evidence for a recommendation in adults at increased risk (I recommendation)7. To update its recommendations, the USPSTF commissioned a new evidence review in 2009 to systematically evaluate the current evidence on screening with resting or exercise ECG. Our report differs from earlier USPSTF reviews because we focused on studies that adjusted for traditional cardiovascular risk factors, performed meta-analysis, and evaluated whether screening with ECG improves risk reclassification. The key questions, analytic framework (Appendix Figure), and scope were developed in accordance with previously published USPSTF processes and methods. The key questions were as follows:

  1. What are the benefits of screening for abnormalities on resting or exercise electrocardiography compared with no screening on coronary heart disease outcomes?
  2. How does the identification of high-risk persons via resting or exercise electrocardiography affect use of treatments to reduce cardiovascular risk?
  3. What is the accuracy of resting or exercise electrocardiography for stratifying persons into high-, intermediate-, and low-risk groups?
  4. What are the harms of screening with resting or exercise electrocardiography?
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We followed a standard protocol for this review. Detailed search strategies, selection criteria, evidence tables, quality assessments, and forest plots are available in a technical report available at the U.S. Preventive Services Task Force (USPSTF) Web site8.

Data Sources

We searched MEDLINE from 2002 through January 2011 and the Cochrane Library database through the fourth quarter of 2010 to identify relevant English-language articles. We also reviewed reference lists of relevant articles and included studies from the previous USPSTF review that met inclusion criteria.

Study Selection

We included studies that evaluated persons without symptoms of CHD, reported results separately for asymptomatic persons, or had fewer than 10% of participants with symptoms. Randomized, controlled trials and controlled observational studies were included if they evaluated the effects of screening with resting or exercise ECG versus no screening on clinical outcomes (benefits or harms) or the use of lipid-lowering therapy or aspirin (interventions for which recommended use varies by assessed cardiovascular risk). Prospective cohort studies that reported rates of cardiovascular outcomes and controlled for at least 5 of the 7 Framingham cardiovascular risk factors (male sex, age, tobacco use, diabetes, hypertension, total or low-density lipoprotein cholesterol concentration, and high-density lipoprotein cholesterol concentration) by means of restriction (such as by enrolling only male participants) or adjustment were also included. Two reviewers independently evaluated each study to determine inclusion eligibility. Only published studies were included.

Data Extraction and Quality Assessment

One investigator abstracted details about the population, study design, analysis, and duration of follow-up; the Framingham risk factors and other adjusted confounding factors; and results. A second investigator reviewed the data abstraction for accuracy. Two investigators independently applied criteria developed by the USPSTF9 to rate the quality of each study as good, fair, or poor. Discrepancies in quality ratings were resolved by consensus.

Data Synthesis and Analysis

Using methods developed by the USPSTF, we assessed the aggregate internal validity (quality) of the body of evidence for each key question as good, fair, or poor, on the basis of the number, quality, and size of the studies; consistency of results between studies; and directness of evidence9. To evaluate the benefits of screening for asymptomatic CHD, we focused on (in order of preference) death from CHD, death from cardiovascular disease, nonfatal myocardial infarction, all-cause mortality, stroke, other cardiovascular outcomes (such as congestive heart failure), and composite cardiovascular outcomes. The accuracy of screening with ECG for identifying the presence or degree of asymptomatic atherosclerosis was not evaluated because of its unclear clinical implications. Participant anxiety, labeling, and rates and consequences of subsequent tests and procedures were evaluated to assess the harms of screening. Other USPSTF reviews10,11 have evaluated adverse outcomes associated with lipid-lowering therapy and aspirin.

Several methods were used to assess the incremental value of resting or exercise ECG12. We evaluated how adding screening with ECG to traditional risk factor assessment affects reclassification of persons as being at high (10-year risk for CHD events >20%), medium (10% to 20%), or low (<10%) risk compared with classification on the basis of traditional risk factors alone13. The recent literature13-16 has emphasized understanding the frequency and accuracy by which people are reclassified into different risk categories, which can have an important effect on clinical decisions6,17. We also evaluated how adding resting or exercise ECG to traditional risk factor assessment changed the c-statistic (which measures how accurately a risk assessment method separates persons with from those without a disease or outcome18, when this was reported, and whether screening with ECG improves calibration (the degree to which predicted and observed risk estimates agree15.

Most studies did not provide sufficient data to estimate the degree and accuracy of reclassification. They instead provided an estimate of risk associated with the presence (vs. the absence) of abnormalities on ECG after adjustment for traditional risk factors. We used Stata/IC, version 11.1 (StataCorp, College Station, Texas), to conduct meta-analyses of abnormalities on ECG that were evaluated by at least 3 studies of (in order of preference) adjusted estimates of risk for CHD death, death from cardiovascular disease, nonfatal myocardial infarction, all-cause mortality, or composite cardiovascular outcomes, using the DerSimonian–Laird random-effects model19. Heterogeneity was estimated by using the I2 statistic20. If at least 5 studies evaluated an electrocardiographic abnormality, potential sources of heterogeneity were assessed by stratifying studies according to the outcome evaluated, study quality, and use of different definitions for the abnormality being evaluated. Sensitivity analyses were performed that excluded outlier studies, if present. Meta-regression was also performed on the proportion of men enrolled in the study, the number of traditional risk factors adjusted for (range, 5 to 7), and the duration of follow-up.

Role of the Funding Source

This study was funded by the Agency for Healthcare Research and Quality under a contract to support the work of the USPSTF. Staff at AHRQ and members of the USPSTF helped to develop the scope of this work and reviewed draft manuscripts. Approval from AHRQ was required before this manuscript could be submitted for publication, but the authors are solely responsible for the content and the decision to submit it for publication.

 
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The Figure shows the results of the evidence search and selection process.

Key Question 1

What are the benefits of screening for abnormalities on resting or exercise electrocardiography compared with no screening on coronary heart disease outcomes?

Similar to the previous USPSTF reviewers21, we found no randomized, controlled trials or prospective cohort studies on the effects of screening asymptomatic adults with resting or exercise ECG versus no screening on clinical outcomes.

Key Question 2

How does the identification of high-risk persons via resting or exercise electrocardiography affect use of treatments to reduce cardiovascular risk?

Like the previous USPSTF reviewers21, we identified no studies that evaluated how screening affects use of lipid-lowering therapy or aspirin.

Key Question 3

What is the accuracy of resting or exercise electrocardiography for stratifying persons into high-, intermediate-, and low-risk groups?

No study estimated how accurately resting or exercise ECG classified participants into high-, intermediate-, or low-risk groups compared with traditional risk factor assessment alone, or provided sufficient data for constructing risk-stratification tables13. One study in women22 found that adding resting ECG findings to the Framingham risk score increased the c-statistic for prediction of future CHD events from 0.69 to 0.74, but the CIs for the estimates overlapped substantially. Another study in men and women23 reported a c-statistic of 0.73 for traditional risk factor assessment by using the European Systematic Coronary Risk Evaluation (SCORE) alone versus 0.76 for SCORE plus exercise ECG variables (CIs not reported).

Twenty-seven prospective cohort studies of resting ECG, reported in 28 publications22,24-50, and 38 prospective cohort studies of exercise ECG23,24,34,51-85 evaluated abnormalities on baseline ECG and risk for subsequent cardiovascular events; 2 studies24,34 evaluated both resting and exercise ECG (Supplement Tables 1 and 2). Excluding double-counted populations, we evaluated resting ECG in 173,710 participants and exercise ECG in 91,746 participants. Duration of follow-up ranged from 3 years31,79 to 56 years27. Ten studies of resting ECG22,24,29,30,32,34,36,44,45,50 and 19 studies of exercise ECG24,34,51,52,54-58,60,63,67-69,72,75,78,80,83 were rated good-quality; the rest were rated fair-quality. The most common methodological shortcomings were no description of handling of participants with uninterpretable ECG results (43 of 62 studies), loss to follow-up (39 of 62 studies), or race in reports of baseline demographic characteristics (31 of 62 studies). Three studies70,71,79, discussed separately, only enrolled persons with diabetes mellitus or impaired fasting glucose.

Several abnormalities on resting ECG were associated with an increased risk for subsequent cardiovascular events(Table 1). The pooled adjusted hazard ratio (HR) was 1.9 (95% CI, 1.4 to 2.5; I2 = 62%) for persons with resting ST-segment abnormalities (5 studies27,29,33,36,39), 1.6 (CI, 1.3 to 1.8; I2 = 56%) for those with T-wave abnormalities (6 studies27,29,33,36,39,45), and 1.9 (CI, 1.6 to 2.4; I2 = 50%) for those with either ST-segment or T-wave abnormalities (7 studies28,31,33,41,42,49,50).

Left ventricular hypertrophy (LVH), left-axis deviation, and bundle branch block on resting ECG were each associated with a similar risk for subsequent cardiovascular events. The pooled adjusted HR was 1.6 (CI, 1.3 to 2.0; I2 = 46%) for LVH (8 studies24,25,29,35,36,39,41,50), 1.5 (CI, 1.1 to 1.9; I2 = 0%) for left-axis deviation (3 studies29,41,50), and 1.5 (CI, 0.98 to 2.3; I2 = 46%) for bundle branch block (4 studies29,39,41,42).

Six studies22,29,37,38,41,50 evaluated major or minor abnormalities on resting ECG and subsequent cardiovascular events, but the results could not be pooled because the definitions of major and minor varied (Table 2). Two studies29,41 reported an association between presence of a major abnormality on resting ECG and CHD death over 10 years (HR, 2.3 [CI, 1.5 to 3.7] and 3.1 [CI, 1.9 to 5.1], respectively), and a third22 reported an association with CHD events over 5 years (HR, 3.0 [CI, 2.0 to 4.5]). In each study, the risk estimate for minor abnormalities was weaker than the estimate for major abnormalities. For example, 1 study41 reported HRs of 1.8 (CI, 1.3 to 2.5) for minor abnormalities and subsequent CHD death and 3.1 (CI, 1.9 to 5.1) for major abnormalities. In some studies29,50, the association between minor abnormalities and subsequent CHD events did not reach statistical significance.

Other abnormalities on resting ECG have been evaluated, including prolonged QT interval, ischemic changes, atrial fibrillation, right-axis deviation, Q waves, ventricular premature contractions, and high resting heart rate26,32,34,38-40,42,46-48,86, but these were evaluated in too few studies or were too variably defined to draw firm conclusions about their usefulness as predictors. Several studies were not included in the meta-analyses because they evaluated nonpooled outcomes of electrocardiographic abnormalities. One study43 found ST-segment abnormalities (but not T-wave abnormalities or LVH) associated with increased risk for stroke over 0 to 30 years of follow-up (HR, 3.4 [CI, 2.1 to 5.4]), and another32 found an association between ST-segment or T-wave abnormalities and incident congestive heart failure (HR, 1.6 [CI, 1.3 to 2.1]). In 1 study, incomplete bundle branch block (HR, 1.4 [CI, 1.0 to 2.0]) and complete bundle branch block (HR, 1.7 [CI, 1.3 to 2.4]) were associated with greater risk for congestive heart failure than no bundle branch block30. Another study44 found new or incident LVH on 6-year follow-up ECG to be associated with increased risk for CHD death.

Several abnormalities on exercise ECG were also associated with an increased risk for subsequent cardiovascular events (Table 1). The most frequently evaluated abnormality, ST-segment depression with exercise (12 studies23,24,52,55,56,58,59,63,69,72,76,81), was associated with an adjusted pooled HR of 2.1 (CI, 1.6 to 2.9).

In 4 studies51,52,66,72, chronotropic incompetence on exercise ECG (defined as inability to reach 85% or 90% of maximum predicted heart rate) was associated with a pooled adjusted HR of 1.4 (CI, 1.3 to 1.6; I2 = 0%) for subsequent cardiovascular events. Abnormal heart rate recovery (defined as a decrease of <12 beats/min from peak heart rate 1 minute into recovery or of <42 beats/min after 2 minutes) was associated with a pooled adjusted HR for all-cause mortality of 1.5 (CI, 1.3 to 1.9; I2 = 0%) in 3 studies23,54,74. Studies that were excluded from the meta-analysis because they evaluated ECG findings as multicategory or continuous variables also found that lower maximum heart rate24,34,84 and slower return to baseline heart rate were associated with increased risk34.

Decreased exercise capacity or fitness (on the basis of metabolic equivalents or watts achieved or exercise duration) was consistently associated with increased risk for subsequent cardiovascular events or mortality in 9 studies23,53,60,61,69,77,81,82,85, but results could not be pooled because of the different methods of measurement and analysis. In 6 studies23,53,61,69,77,85, adjusted HRs for subsequent cardiovascular events or all-cause mortality ranged from 1.7 to 3.1 for lower versus higher exercise capacity categories. In 5 studies23,60,69,81,82, lower exercise capacity was also predictive when analyzed as a continuous variable.

Two studies63,72 found ventricular ectopy during or after exercise ECG to be associated with increased risk for cardiovascular events (HR, 2.5 [CI, 1.6 to 3.9] and 1.7 [CI, 1.1 to 2.6], respectively). One study each found decreased peak oxygen pulse53, lower Duke treadmill score60, and “abnormal” (undefined) exercise ECG53 associated with increased risk for cardiovascular events. Finally, 1 study71 found that having both low heart rate recovery and low metabolic equivalents was a stronger predictor of death from cardiovascular disease than having either abnormality alone.

Stratifying the studies in the meta-analyses by type of cardiovascular outcome assessed, study quality, or restriction to men resulted in estimates that were similar to the overall pooled estimates and did not reduce observed statistical heterogeneity. An exception was LVH on resting ECG, for which estimates were lower for the 4 studies rated good-quality (HR, 1.2 [CI, 0.9 to 1.7]; I2 = 31%)24,29,36,50 than for the 4 rated fair-quality (HR, 2.0 [CI, 1.6 to 2.5]; I2 = 0%; P for difference = 0.03)25,35,39,41. Variability in the proportion of men, duration of follow-up, or number of traditional risk factors adjusted for also did not explain the between-study variance in estimates. Excluding the outlier trials23,72 from the meta-analysis of ST-segment depression on exercise ECG did not reduce statistical heterogeneity or result in different estimates. In studies that stratified results by sex26,29,33,37,39,42,52,53,73,85, estimates of risk associated with various abnormalities in resting and exercise ECG were either similar for men and women or had overlapping CIs.

Two studies70,79 evaluated exercise ECG in diabetic participants. One study70 found that 1-mm ST-segment depression or elevation with exercise was associated with increased risk for CHD death (HR, 2.1 [CI, 1.3 to 3.3]). The second study79 also found that exercise-induced ST-segment depression was associated with increased risk for CHD events, but the sample size was small (86 participants) and the CI was very wide (HR, 21 [CI, 2 to 204]). One other study71 found higher fitness on exercise ECG (on the basis of maximum exercise duration and metabolic equivalents) was associated with a lower risk for all-cause mortality than low fitness (HR, about 0.65 for either moderate or high fitness) in women with impaired fasting glucose or undiagnosed diabetes.

Key Question 4

What are the harms of screening with resting or exercise electrocardiography testing?

Direct Harms

No studies reported harms directly associated with resting ECG. For exercise ECG, 1 study with 377 participants87, included in the previous USPSTF review, reported no complications as a direct result of screening. Survey data that included symptomatic participants undergoing exercise ECG reported arrhythmia in fewer than 0.2%, acute myocardial infarction in 0.04%, and sudden cardiac death in 0.01%88. The overall risk for experiencing sudden death or an event that requires hospitalization has been estimated to be 1 per 10,000 tests88.

Harms Associated With Subsequent Tests or Interventions

We identified no studies on harms associated with follow-up testing or interventions after a screening resting or exercise ECG. In 9 studies87,89-96, summarized in the previous USPSTF evidence review97, rates of subsequent angiography in primarily asymptomatic participants after an abnormal exercise ECG ranged from 0.6% to 2.9%, excluding an outlier study of hypertensive veterans94 with a 13% angiography rate. Two subsequent studies of screening exercise ECG23,55, comprising 4605 participants, found that 0.6% and 1.7% of the total sample subsequently had angiography, and 0.1% (4 of 3554) and 0.5% (5 of 1051), respectively, had a subsequent revascularization procedure.

None of these studies estimated complications associated with angiography or revascularization procedures. On the basis of large, population-based registries that include symptomatic persons98, the risk for any serious adverse event as a result of angiography is about 1.7%; this includes risk for death (0.1%), myocardial infarction (0.05%), stroke (0.07%), and arrhythmia (0.4%).

Coronary angiography, computed tomography angiography, and myocardial perfusion imaging are associated with radiation exposure that could increase cancer risk. Coronary angiography is associated with an average effective radiation dose of 7 mSv and myocardial perfusion imaging with a dose of 15.6 mSv99.

Persons who have an abnormal screening result and undergo additional testing, but do not have coronary artery disease, are subjected to potential harms without the possibility of benefit. One study included in the previous USPSTF review96 found severe coronary artery disease in 15% of participants who had angiography; another89 found that 55% of participants who underwent angiography had greater than 50% occlusion and 37% had greater than 70% occlusion in at least 1 coronary artery. A recent, large (nearly 400,000 participants) study100 of a primarily symptomatic population (70%) who had angiography found that 39% had no coronary artery disease (defined as <20% stenosis).

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Table 3 summarizes our results. Like the previous USPSTF reviewers, we found no studies that evaluated clinical outcomes or use of lipid-lowering therapy or aspirin after screening with resting or exercise ECG compared with no screening. Another critical research gap is that no studies directly evaluated the incremental value of adding screening with ECG to traditional risk factor assessment for accurately classifying persons into different risk categories. The lack of information on reclassification is critical from a clinical perspective because decisions regarding therapies for reducing cardiovascular risk are often based on whether a person is classified as having low (<10% risk over the next 10 years), intermediate, or high (>20%) risk for future CHD events. On the basis of current data, we cannot determine the degree to which resting or exercise ECG accurately moves a person from one risk category to another, rather than yielding a more precise estimate in a risk category (which is less clinically useful). For example, in populations at very low (<5%) risk for CHD events, such as most young adults, even a doubling of risk would not move a person from a lower to a higher risk category. Similarly, abnormalities on resting or exercise ECG are unlikely to change management decisions for persons who are already at high risk on the basis of traditional risk factor assessment. The greatest potential benefits of screening with ECG would be for intermediate-risk persons, because the presence of abnormalities would shift such persons into a high-risk group for whom additional interventions might be warranted. Two studies22,23 evaluated the effect on the c-statistic of adding resting or exercise ECG findings to traditional risk factor assessment compared with traditional risk factor assessment alone, but this measure is of limited clinical usefulness because it does not provide information about the actual predicted risks in an individual patient or the proportion of patients who are classified (or reclassified) as high-, intermediate-, or low-risk13.

Most of the available evidence evaluated the association between abnormalities on resting ECG (ST-segment abnormalities, T-wave abnormalities, LVH, left-axis deviation,or bundle branch block) or exercise ECG (ST-segment depression with exercise, chronotropic incompetence, impaired heart rate recovery, or decreased exercise capacity) and risk for subsequent cardiovascular events, after adjustment for traditional Framingham risk factors. The adjusted pooled HRs ranged from around 1.4 to around 2.1 for various abnormalities on resting or exercise ECG. Despite strong evidence that such abnormalities are associated with increased risk beyond that accounted for by assessment of traditional risk factors, understanding the usefulness of screening requires additional information on the reclassification that would result and on whether such reclassification would lead to clinical actions that improve patient outcomes6.

Evidence on harms associated with screening ECG is limited. However, serious direct harms seem to be minimal with resting ECG (other than possible anxiety or labeling) and small or rare with exercise ECG (for example, ischemia or injuries associated with exercise), assuming appropriate attention to contraindications to exercise testing and adherence to standard safety precautions. However, the potential downstream harms from additional testing or interventions that result from screening could be of greater concern. Some patients have angiography after a screening ECG and are therefore exposed to the potential harms related to that procedure, which include bleeding, radiation exposure, and contrast allergy or nephropathy. Patients who receive lipid-lowering therapy or aspirin because of screening ECG are exposed to the harms related to those interventions. Evidence on downstream harms associated with screening is not available, although data indicate that 0.6% to 1.7% of patients subsequently have angiography. A small proportion (<1%) of patients have revascularization with coronary artery bypass graft surgery or a percutaneous coronary intervention after screening exercise ECG, despite the risks of these interventions and their lack of benefits in asymptomatic persons23,55.

Our evidence review has limitations. We included only English-language studies, which could have resulted in language bias. A random-effects model was used to perform meta-analysis, because studies that evaluated the risk associated with various resting or exercise ECG abnormalities varied in quality and duration of follow-up, assessed different patient populations and cardiovascular outcomes, and used different methods to define the abnormalities. Although statistical heterogeneity was present in several of the meta-analyses, stratified analyses and meta-regression had little effect on estimates and conclusions. Referral bias could have resulted in underestimates of risk if identification of electrocardiographic abnormalities led to increased use of treatments effective at reducing cardiovascular risk.

Studies are needed to directly evaluate how screening with resting or exercise ECG affects clinical outcomes compared with no screening. Any screening study should also evaluate harms, including downstream harms related to additional testing and therapies. Although randomized trials would be desirable, well-conducted, nonrandomized prospective studies could also be informative. In the absence of direct evidence on the clinical effects of screening, data from future studies on risk prediction should enable estimates of reclassification, from which potential benefits of screening might be extrapolated on the basis of the known efficacy of interventions in high-risk populations. Decisions to allocate resources to update this or similar reviews on the usefulness of screening ECG might be predicated on the availability of such evidence, identified by using literature scans or other methods. Many of the studies included in our review evaluated large sample sizes over long periods, and the information needed to assess reclassification rates in these databases probably already exists. Reanalyzing preexisting databases would therefore be a more efficient method for obtaining information on reclassification than would initiating new studies.

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Source: This article was first published in Annals of Internal Medicine (Ann Intern Med 2011;155:375-385).

Acknowledgment: The authors thank AHRQ Medical Officer Tracy Wolff, MD, MPH; USPSTF Leads Susan Curry, PhD, Michael LeFevre, MD, MSPH, Joy Melnikow, MD, MPH, and Sanford (Sandy) Schwartz, MD, for their contributions to this report; and Christina Bougatsos, BS, Oregon Evidence-based Practice Center, for her assistance in preparing this report.

Grant Support: By contract number HHSA-290-2007-10057-I-EPC3, Task Order No. 3, from the Agency for Healthcare Research and Quality.

Potential Conflicts of Interest: Dr. Chou: Grant: Agency for Healthcare Research and Quality; Consultancy: Consumers Union. Dr. Arora: Support for travel to meetings for the study or other purposes: Agency for Healthcare Research and Quality. Ms. Dana, Dr. Fu, and Ms. Walker: Grant: (money to institution): Agency for Healthcare Research and Quality. Dr. Humphrey: Grant: Agency for Healthcare Research and Quality. Disclosures can also be viewed at www.acponline.org/authors/icmje/ConflictOfInterestForms.do?msNum=M11-0938.

Requests for Single Reprints: Roger Chou, MD, Oregon Health & Science University, 3181 Southwest Sam Jackson Park Road, Mailcode BICC, Portland, OR 97239; e-mail, chour@ohsu.edu.

Current author addresses and author contributions are available at http://www.annals.org.

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Select Text Description below for details

* Includes the Cochrane Central Register of Controlled Trials and the Cochrane Database of Systematic Reviews.
† Includes studies identified from reference lists or suggested by experts.

Text Description.

The Figure displays an accounting of studies reviewed for the evidence report. 979 studies were identified through searches of online databases as being potentially relevant to the evidence report. Of those, 662 were excluded at the title or abstract level for not meeting inclusion criteria. The full text of 317 studies were reviewed for inclusion in the evidence report. Of those, 252 were excluded for not meeting inclusion criteria. The remaining 65 studies were included in the final evidence report. Of those, no studies were included for Key Questions 1 and 2, 63 studies were included for Key Question 3, and 2 studies were included for Key Question 4.

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Type of ECG and Abnormality Studies (References), n Pooled Adjusted HR (95% CI) I2 Value, %
Resting ECG
   ST-segment abnormalities 527,29,33,36,39 1.9 (1.4–2.5) 62
   T-wave abnormalities 627,29,33,39,45 1.6 (1.3–1.8) 56
   ST-segment or T-wave abnormalities 728,31,33,41,42,49,50 1.9 (1.6–2.4) 50
   Left ventricular hypertrophy 824,25,29,35,36,39,41,50 1.6 (1.3–2.0 46
   Bundle branch block 429,39,41,42,67,68,69 1.5 (0.98–2.3) 46
   Left-axis deviation 329,41,50 1.5 (1.1–1.9) 0
Exercise ECG
   ST-segment depression with exercise 1223,24,52,55,56,58,59,63,69,72,76,81 2.1 (1.6–2.9) 71
   Chronotropic incompetence 451,52,66,72 1.4 (1.3–1.6) 0
   Abnormal heart rate recovery* 3[[23.54.74]] 1.5 (1.3–1.9) 0
   Decreased exercise capacity or fitness 623,53,61,69,77,85 Range, 1.7–3.1 (could not be pooled) -

ECG = electrocardiography; HR = hazard ratio.
* Estimate is for all-cause mortality; cardiovascular-specific outcomes could not be pooled.

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Study, Year (Reference) Study Name Sample Size, n Mean Age (Range), y Men, % Mean Duration of Follow-up, y Definition (Prevalence) of ECG Abnormalities HR for Events With Major or Minor ECG Abnormalities Compared With No Abnormalities (95% CI)
Major Minor
De Bacquer et al, 199829 Belgian Inter-University Research on Nutrition and Health 9954 48 (25–74) 52 10 Minnesota code 4.1, 4.2, 5.1, 5.2, 6.1, 6.2, 7.1, 7.2, 8.1, or 8.3 (29%) Minnesota code 1.3, 2.1, 2.2, 3.1, 3.2, 4.3, 5.3, or 9.1 (3.6%) CHD death: major, 2.3 (1.5-3.7); minor, 1.1 (0.77-1.7)
Denes et al, 200722 Women's Health Initiative 14,749 63 (50–79) 0 5.2 Novacode 1.4, 1.5, 1.7, 1.8, 1.9, 2.3.1, 2.3.2, 2.4, 3.1.0, 3.1.1, 3.2.0, 3.3.0, 3.3.1, 5.1, 5.2, 5.3, 5.4, 5.5, 5.6, 6.1.1, 6.1.4, 6.1.7, or 6.1.8 (6.2%) Novacode 2.1, 2.2.1, 3.4.1, 3.4.2, 4.1.1, 4.1.2, 5.7, 5.8, 6.1.0, 7.1, 8.1, 10.1, or 10.2 (28%) CHD events: major, 3.0 (2.0-4.5); minor, 1.6 (1.1-2.1)

CVD events: major, 2.3 (1.8-3.0); minor, 1.4 (1.1-1.7)
Liao et al, 198837 The Chicago Heart Association Detection Project in Industry 17,633 51 55 11.5 Minnesota code 6.1 or 6.2; 7.1, 7.2, or 7.4; 8.3; 8.1; 4.1; or 5.1 or 5.2 (11.1%) Minnesota code 1.3, 2.1 or 2.2, 3.1, 3.2, 4.3, 5.3, 6.3, or 9.1 (6%) CHD death: major, 3.7 for men and 1.9 for women; minor, 2.1 for men and 1.5 for women

CVD death: major, 3.4 for men and 2.1 for women; minor, 2.1 for men and 1.5 for women

All-cause mortality: major, 2.4 for men and 1.4 for women; minor, 1.7 for men and 1.2 for women*
Macfarlane et al, 200738 West of Scotland Coronary Prevention Study 5835 55 100 4.9 Not assessed Minnesota code 4.2, 4.3, 5.2, 5.3 (8%) CHD death or nonfatal myocardial infarction: minor, 1.7 (1.3-2.3)
All-cause mortality: minor, 2.2 (1.5-3.1)
Menotti et al, 200141, and Menotti and Seccareccia, 199742 The FINE Study 1785 Not reported
(65–84)		 100 10 Minnesota code 1.1, 4.1, 5.1, 6.8, 7.1, 7.4, or 8.3 (8%) Minnesota code 1.2, 1.3, 2.1, 4.2-4.4, 5.2-5.3, 6.4, 7.2, 7.3, or 8.1 (39%) CHD death: major, 3.1 (1.9-5.1); minor, 1.8 (1.3-2.5)†
Sutherland et al, 199350 Charleston Heart Study 993 48 (35–74) 100 30 Minnesota code 4.1, 4.2, 5.1, 5.2, 7.1, 7.2, 7.4, 8.1, or 8.3 (9%) Minnesota code 1.3, 2.1, 2.2, 3.1, 4.3, 5.3, 6.3, or 9.1 (14%) CHD death: major, 2.7 (1.5-5.0) for white men and 2.0 (0.93-4.1) for black men; minor, 1.3 (0.74-2.1) for white men and 0.58 (0.24-1.4) for black men

All-cause mortality: major, 2.1 (1.4-3.1) for white men and 1.4 (0.91-2.1) for black men; minor, 1.2 (0.92-1.7) for white men and 0.79 (0.52-1.2) for black men

CHD = coronary heart disease; CVD = cardiovascular disease; ECG = electrocardiography; FINE = Finland, Italy, and the Netherlands; HR = hazard ratio.
* No CIs were reported.
† Compared with absent or marginal abnormalities.

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Key Question Studies, n Overall Quality Rating Summary of Findings
1. What are the benefits of screening for abnormalities on resting or exercise electrocardiography compared with no screening on coronary heart disease outcomes? None – No randomized, controlled trials or controlled observational studies of screening asymptomatic adults for CHD with resting or exercise ECG versus no screening were identified.
2. How does the identification of high-risk persons via resting or exercise electrocardiography affect use of treatments to reduce cardiovascular risk? None – No studies were identified that evaluated how screening patients for CHD by using resting or exercise ECG affects use of interventions to reduce cardiovascular risk.
3. What is the accuracy of resting or exercise electrocardiography for stratifying persons into high-, intermediate- and low-risk groups? None on risk reclassification, 2 on changes in the c-statistic, and 63 on risk associated with abnormalities on ECG Fair No study estimated how accurately resting or exercise ECG plus traditional risk factor assessment classified patients into high-, intermediate-, or low-risk groups compared with classification on the basis of traditional risk factor assessment alone, or provided sufficient data for risk stratification tables to estimate risk reclassification rates. Two studies found resting or exercise ECG findings plus traditional risk factor assessment resulted in a slight increase in the c-statistic compared with traditional risk factor assessment alone. Pooled analyses showed that abnormalities on resting ECG (ST-segment or T-wave abnormalities, left ventricular hypertrophy, bundle branch block, or left-axis deviation) or exercise ECG (ST-segment depression with exercise, failure to reach maximum target heart rate, or low exercise capacity) are associated with an increased risk (pooled hazard ratio estimates from 1.4 to 2.1) for subsequent cardiovascular events, after adjustment for traditional risk factors.
4. What are the harms of screening with resting or exercise electrocardiography? 2 studies Poor No studies reported harms directly associated with screening with resting ECG. One study (included in the previous report) found no complications in 377 patients who had screening with exercise ECG. No studies reported downstream harms associated with follow-up testing or interventions after screening with resting or exercise ECG.

CHD = coronary heart disease; ECG = electrocardiography.

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Select Text Description below for details

CAD = coronary artery disease; CHD = coronary heart disease; ECG = electrocardiography; KQ = key question.

Text Description.

The Appendix Figure is an analytic framework for the key questions of this report that depicts the events that asymptomatic adults could experience while undergoing screening for coronary heart disease (CHD). The figure illustrates how consideration of known risk factors, including age at time of screening, sex, cholesterol, blood pressure, diabetic status, and smoking status can be considered to help determine who would benefit the most from screening for CHD. The figure shows how screening can be accomplished through the use of resting or exercise electrocardiography (ECG), with the potential for risk reclassification and risk-reducing treatments based on the results of ECG testing. The figure portrays the ultimate goal of screening as a reduction in CHD-based health outcomes. The figure also depicts the possibility of harms or adverse events occurring as a result of screening.

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Author, year Study name and country
Population		 Sample size and demographics ECG abnormalities evaluated: prevalence Mean
follow-up (years)		 Framingham risk factor adjusted for All-cause mortality and incident
CV events		 Quality
Bodegard et al, 200424 Study not named
Norway
Work volunteers		 n=2,014
Mean age: 50 years (range 40-59 years)
100% male
Race NR		 LVH: 5.3% 22 Age, sex, smoking, SBP, total cholesterol CHD death: 15%
All cause mortality: 37%
Acute MI: 19%
Coronary artery bypass graft
surgery: 6.0%
Stroke: 7.7%		 Good
Brown et al, 200025 Second National Health and Nutrition Examination Survey (NHANES II)
United States
General community		 n=7,924
Mean age: 49 years (range 25-74)
48% male
90% white
10% black		 LVH: 1.9% 15 Sex, smoking, diabetes, SBP, total cholesterol CHD death: 3.7%
Heart disease death: 5.3%		 Fair
Crow et al, 200326 Atherosclerosis Risk in Community (ARIC) Study
United States
General community		 n=14,696
Mean age: 54 years (range 45-64)
43% male
73% white		 QTc: Continuous variable
JTc: Continuous variable
Wide QRS complex: 3.1%		 13 Age, sex, smoking, diabetes, SBP, HDL, LDL Incident MI or fatal CHD event: 5.6% Fair
Cuddy et al, 200627

Other sources: www.mfus.ca

 The Manitoba Follow-Up Study
Canada
Royal Canadian Air Force recruits		 n=3,983
Mean age: 31 years (range 20-39)
100% male
Race NR		 Atrial fibrillation: 7%
VPCs: 23%
Atrioventricular block: 12%
Right bundle branch block: 5%
Left bundle branch block: 2%
LVH: 12%
ST and T-wave abnormalities: 22% (ST); 37% (T-wave)		 56 Age, sex (100% male), smoking, diabetes, SBP, DBP Sudden unexpected cardiac death: 4.3% Fair
Daviglus et al, 199928

Other publications: Oglesby, 1963101

 The Chicago Western Electric study
United States
Male electric company workers		 n=1,673
Mean age: 47 years (range 40-55)
100% male
Race NR		 Minor ST-T abnormalities: 10.3% 29 Age, sex (100% male), smoking, SBP, total cholesterol CHD death: 21%
MI death: 14%
CVD death: 28%
All cause mortality: 53%		 Fair
De Bacquer et al, 199829 Belgian Inter-University Research on Nutrition and Health (BIRNH) study
Belgium
General community		 n=9,954
Mean age: 48 years (range 25-74)
52% male
Race NR		 Any ECG abnormality: 29%
Major ECG abnormality: 29%
Minor ECG abnormality: 3.6%
Ischemic ECG abnormality: 10%
ST depression: 2%
Abnormal T wave: 8%
Arrhythmias: 6%
Bundle branch blocks: 1%
LVH: 0.6%
Left axis deviation: 4%		 10 Age, sex, smoking, diabetes, SBP, HDL, LDL, total cholesterol CHD death: 1.3%
CVD death: 2.4%
All cause mortality: 7.9%		 Good
Denes et al, 200722 Women's Health Initiative
United States
Clinical trial enrollees		 n=14,749
Mean age: 63 yrs (range 50-79)
0% male
84% white		 Major ECG abnormality: 6.2%
Minor ECG abnormality: 28%		 5.2 Age, sex (100% female), smoking, diabetes, hypertension, statin use CHD events: 4.0%
CVD events: 1.7%		 Good
Diercks et al, 200231 Prevention of Renal and Vascular Endstage Disease study
The Netherlands
General community		 n=7,330
Mean age: 48 years (range 28-75)
50% male
Race NR		 ST-T changes: 17% 3 Age, sex, smoking, diabetes, hypertension, total cholesterol CVD death: 0.3%
All cause mortality: 1.2%		 Fair
Dhingra et al, 200630 Framingham Heart Study
United States
General community		 n=1,759
Mean age: 70 years (SD 7)
37% male
Race NR		 QRS duration 100-119 ms (incomplete bundle branch block): 17%
QRS duration ≥120 ms (complete bundle branch block): 6%		 12.7 Age, sex, smoking, diabetes, hypertension, HDL, total cholesterol CHF: 18% (men 18%; women 19%) Good
Gottdiener et al, 200032

Other publications: Furberg et al, 1992102

 Cardiovascular Health Study
United States
General community		 n=4,652 (analyzed group with no prevalent CHD)
Mean age: 73 years (range 65-100 yrs; entire cohort, including prevalent CHD)
40% male
85% non-black		 Major Q/QS waves: 5.2%
LVH: 4.2%
Isolated major ST-T wave abnormalities: 6.3%
Atrial fibrillation: 3.2%
Atrioventricular block: 5.3%
Ventricular conduction defects: 8.7%
(Prevalences based on entire Cardiovascular Study cohort)		 6.3 Age, sex, smoking, diabetes, hypertension, HDL, LDL, total cholesterol CHF: 8.5% Good
Greenland et al, 200333 The Chicago Heart Association Detection Project in Industry
United States
Work-based		 n=17,615
Mean age: 50 years (range 40-64)
55% male
95% white		 Any ST changes: 3.6% men; 5.4% women
Minor T-wave abnormality: 1.6% men; 1.9% women
Minor ST depression: 1.2% men; 1.5% women		 22 Age, sex, smoking, blood glucose, SBP, total cholesterol CHD death: 7.1%
CVD death: 9.9%		 Fair
Jouven et al, 200534 Paris Protective Study I
France
Civil servants		 n=5,713
Mean age: 48 years (range 42-53 years)
100% male
Race not reported		 High (>75 beats per minute) resting heart rate: 8% 23 Age, sex (100% male), smoking, diabetes, SBP, cholesterol Fatal MI (sudden death): 1.4%
Fatal MI (nonsudden death): 2.3%
All-cause mortality: 27%		 Good
Kahn et al, 199635 Bronx Longitudinal Aging Study
United States
General community		 n=459
Mean age: 79 years (range 75-85)
35% male
>95% white		 LVH: 9.2% 10 Age, sex, smoking, hypertension, total cholesterol CVD death: 19%
MI death: 16%
All cause mortality: 34%
Cerebrovascular accident mortality: 3.3%
All cardiovascular disease: 56%
Fatal or non-fatal MI: 14%
Fatal or non-fatal cerebrovascular accident: 7.6%		 Fair
Larsen et al, 200236 The Copenhagen City Heart Study
Denmark
General community		 n=10,982
Mean age: 54 years (range 35-74)
45% male
>98% white		 Left ventricular hypertrophy: 11%
T-wave inversion: 3.4%
ST-T depression and T-wave inversion: 0.7%
LVH + T-wave inversion: 0.8%
LVH + ST-T depression + T-wave inversion: 0.7%		 21 Age, sex, smoking, diabetes, SBP, total cholesterol CVD death: 18%
Fatal or non-fatal MI: 10%
Fatal or non-fatal CHD events: 19%		 Good
Liao et al, 198837 The Chicago Heart Association Detection Project in Industry
United States
Work-based		 n=17,633
Mean age: 51 years
55% male
100% white		 Major abnormality: 11.1%
Minor abnormality: 6%
Any abnormality: 17.5%		 11.5 Age, sex, smoking, diabetes, DBP, total cholesterol CHD death: 2.9%
Cardiovascular death: 3.8%
All cause mortality: 7.8%		 Fair
MacFarlane et al, 200738 West of Scotland Coronary Prevention Study (WOSCOPS)
United Kingdom		 n=5,835
Mean age: 55 yrs
100% male
Race NR		 Left axis deviation
MN code 2.1: 2.7%
Right axis deviation
MN code 2.2 or 2.3: 0.5%
High voltage left ventricular leads
MN code 3.1: 5.1%
High voltage right ventricular leads
MN code 3.2: 0.06%
ST abnormalities
MN code 4.2 or 4.3: 2.3%
T-wave abnormalities
MN code 5.2 or 5.3: 7.9%
Right bundle branch block
MN code 7.2.1 or 7.8: 1%
Definite or probable LVH
MN code 3.1 + ST or T wave abnormalities: 0.6%; 0.3%
Possible LVH
MN code 3.1 or 3.3: 7.3%
Minor ECG abnormality
MN code 4.2, 4.3, 5.2, or 5.3: 7.7%
T-wave inversion
T-wave amplitude <0 mV: 2.6%		 4.9 yrs Age, sex (100% male), smoking, diabetes, hypertension, HDL, total cholesterol Definite MI: 5.4%
Suspected MI:1.5%
All-cause mortality: NR		 Fair
Machado et al, 200639

Other publications: ARIC
Investigators, 1989103

 Atherosclerosis Risk in Communities Study (ARIC)
United States
General community		 n=12,987
Mean age: 54 years (range 45-64)
43% male
74% white		 Minor Q wave: 2%
Prolonged QTc interval: 9%
LVH (Cornell): 2%
LVH (ST-T strain pattern): 2%
Major ventricular conduction defects: 2%
Major ST depression: <1%
Minor ST depression: 1%
ST elevation: 1%
Major T-wave findings: 4%
Any ECG abnormality: 18.1%		 11.6 Age, sex, smoking, diabetes, SBP, DBP, HDL, LDL Incident CHD: 5.6% Fair
Massing et al, 200640 Atherosclerosis Risk in Communities Study (ARIC)
United States
General community		 n=15,070
Mean age: 54 years (range 45-64)
45% male
74% white		 Ventricular premature contractions: 6.2% >10 (11.6 in other ARIC publications) Age, sex, smoking, diabetes, hypertension, HDL, LDL Asymptomatic population
CHD death: 1.6%
CHD events: 9.6%
All cause mortality: 10.5%		 Fair
Menotti et al, 199742

Other publications: RIFLE Research Group, 1993104

 RIsk Factors and Life Expectancy (RIFLE) study
Italy
General community		 n=22,553
Mean age: NR; 50% 50-69 years
54% male
Race NR		 Q-QS wave: 0.8%
ST-T changes: 5.7%
High R wave: 4.7%
Arrhythmia: 1.2%
Bundle branch blocks: 1.2%		 6 Age, sex, smoking, SBP, total cholesterol All-cause mortality (by subgroup)
Q-QS: 1.6%
ST-T: 1.6%
High R wave: 0.9%
Arrythmia:1.5%
Blocks: 1.3%		 Fair
Menotti et al, 200141

Other publications: Menotti et al, 199742

 The FINE Study
Finland, the Netherlands and Italy
General community		 n=1,785
Mean age: NR (range 65-84 years)
100% male
Race NR		 Q-QS wave: 6.8%
ST-T abnormality: 22%
High R wave: 15%
Left axis deviation: 13%
Arrhythmia: 8.5%
Bundle branch blocks: 7.3%
Major abnormalities: 8.3%
Minor abnormalities: 39%		 10 Age, sex (100% male), smoking, hypertension, total cholesterol CHD death: 9% Fair
Moller et al, 200743 Uppsala Longitudinal Study of Adult Men
Sweden
General community		 n=2,322
Age: 50 years (all participants were age 50 at enrollment)
100% male
Race NR		 Q/QS wave pattern: 1.3%
LVH: 1.2%
ST-segment depression: 2.3%
T-wave abnormality: 5.9%
Atrial fibrillation: 0.3%		 Mean NR; follow-up >20 with max 32 Age, sex (100% male), smoking, diabetes, hypertension, HDL, LDL Fatal and nonfatal stroke: 15%
Fatal and nonfatal ischemic stroke: 10%		 Fair
Prineas et al, 200144 Multiple Risk Factor Intervention Trial (MRFIT)
United States
Clinical trial enrollees		 n=12,866
Mean age: 46 years (range 35-57), based on entire MRFIT cohort
100% male
93% white		 New (incident) LVH on 6-year follow-up ECG based on various criteria:
Sokolow-Lyon: 6%
Cornell voltage: 1%
Cornell Product: 2%
Novacode: 5%
MN code 3.1 or 3.3 + 5.1, 5.2 or 5.3: 4%

Significant increase in LVH on 6-year follow-up ECG based on various criteria:
Sokolow-Lyon: 0.5%
Cornell voltage: 3.5%
Cornell product: 2.8%
Novacode: 1.4%
12 product (sum of peak-to-peak amplitudes of QRS complexes except lead avR, x QRS duration): 0.8%

 16 Age, sex (100% male), DBP, total cholesterol, smoking CHD death: 4.8%
CVD death: 6.6%		 Good
Prineas et al, 200245 Multiple Risk Factor Intervention Trial (MRFIT)
United States
Clinical trial enrollees		 n=12,866
Mean age: 46 years (range 35-57), based on entire MRFIT cohort
100% male
93% white		 Minor T-wave abnormalities: 7.1% 18 Age, sex (100% male), smoking, diabetes, DBP, HDL, LDL CHD death: 7.3%
CVD death: 10%
All cause mortality: 23%		 Good
Rautaharju et al, 2006a and 2006b47,48 Women's Health Initiative (WHI)
United States
Clinical trial enrollees		 n=35,715
Mean age: 62 years (range 50-79)
0% male
82% white		 QRS/T angle
STV5
TV1
TV5
QTrr
STV5 gradient
Myocardial infarction by ECG
Cornell voltage
QRS non-dipolar voltage
Ultrashort heart rate variability		 6.2 Age, sex (100% female), smoking, diabetes, SBP CHD death: 0.3%
Incident CHF: 1.0%
All cause mortality: 2.4%
Nonfatal and fatal CHD events: 1.4%		 Fair
Rautaharju et al, 2006c46 Cardiovascular Health Study
United States
General community		 n=4,085
Mean age: 73 years (inclusion criteria age ≥65 years)
37% male
85% non-black		 ST-depression: Continuous variable
ECG-Left ventricular mass: Continuous variable
QRS/T angle: Continuous variable		 9.1 Age, sex, smoking, diabetes, SBP (hypertensive status or use of antihypertensives) CHD death: 7.2%
All cause mortality: 35%		 Fair
Sigurdsson et al, 199649 The Reykjavik Study
Iceland
General community		 n=8,340
Mean age: 52 years (range 35-60 years)
100% male
Race NR		 ST-T changes: 5% 4 to 24 Age, sex (100% male), smoking, fasting blood glucose, hypertension (SBP and DBP), total cholesterol Silent ST-T segment group
Angina: 9%
MI: 5%
All cause mortality: 12%		 Fair
Sutherland et al, 199350 Charleston Heart Study
United States
General community		 n=993
Mean age: 48 years (range 35-74)
100% male
66% white		 Major ECG abnormality: 9%
Minor ECG abnormality: 14%
Left axis deviation: 8%
Early repolarization: 23%
Nonspecific ST-T changes: 16%
LVH: 4%		 30 Age, sex (100% male), smoking, diabetes, SBP, total cholesterol CHD death: 19% Good

Abbreviations: ARIC=Atherosclerosis Risk in Community, BIRNH=Belgian Inter-university Research on Nutrition and Health, CHD=Coronary heart disease, CHF=Congestive heart failure, CVD=Cardiovascular disease, DBP=Diastolic blood pressure, ECG=Electrocardiography, HDL=High-density lipoprotein, LDL=Low-density lipoprotein, LVH=Left ventricular hypertrophy, MRFIT=Multiple Risk Factor Intervention Trial, MI=Myocardial infarction, NHANES=National Health and Nutrition Examination Survey, NR=Not reported, RIFLE=Risk Factors and Life Expectancy, SBP=Systolic blood pressure, VPC=Ventricular premature complexes, WHI=Women's Health Initiative, WOSCOPS=West of Scotland Coronary Prevention Study.

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Author, year Study Name
Exercise Test
Country
Population		 Sample size Demographics Exercise ECG abnormality: Prevalence Mean follow-up (years) Framingham risk factor adjusted for All-cause mortality and incident CV events Quality
Adabag et al, 200851 Multiple Risk Factor Intervention Trial (MRFIT)
Treadmill/standard
Bruce protocol
United States
Clinical trial enrollees		 n=12,555
Mean age: 46 years (range 35 to 57 years)
100% male
7% black; other races NR		 Failure to reach target heart rate: 19% 25: CHD death and all-cause mortality
7: sudden death and fatal/nonfatal MI		 Age, sex, smoking, fasting glucose, SBP, HDL, LDL CHD death (25 years): 13%
All-cause mortality (25 years): 37% 7 yr follow-up
Sudden death: 1.2%
Fatal or nonfatal MI: 6.6%		 Good
Aktas et al, 200423 Study not named
Treadmill/primarily
Bruce or modified Bruce protocols
United States
Self-referred, consecutive adults undergoing routine executive physical		 n=3,554
Mean age: 57 years (range 50-75 years)
81% male
1.8% black; other races NR		 ST segment changes
1 to <2mm: 6%
≥2mm: 4.4%
Any change: 10.4%
Abnormal heart rate recovery: 15.4% (549/3554)		 8 Age, sex, smoking, total cholesterol, HDL, SBP, diabetes All-cause mortality: 3.2% (114/3554) Fair
Balady et al, 200452

Other publications: Framingham Study105

 Framingham Heart Study
Treadmill/standard Bruce protocol
United States
General community		 n=3,043
Mean age: 45 years (range 30-70 years)
47% male
Race NR		 ST segment depression: 4.3%
Failure to reach target heart rate: 9.0%		 18 Age, sex, smoking, diabetes, SBP, DBP, HDL, total cholesterol Any CHD event (angina, coronary insufficiency, MI, or CHD death): 10% Good
Blair et al, 199653

Other publications: Wei et al, 1999106

 Aerobics Center Longitudinal Study
Treadmill/Maximal
Balke protocol
United States
General community		 n=32,421
Mean age: 43 years (range 20-88 years)
79% male
Race NR		 Abnormal ECG (not defined): 6.8% 8.2 (8.4 men; 7.5 women) Age, sex (results stratified by gender), smoking, SBP, total cholesterol, fasting glucose CVD death: 0.8%
All cause mortality: 2.1%		 Fair
Bodegard et al, 200424 Study not named
Bicycle/Maximal
Norway
Work volunteers		 n=2,014
Mean age: 50 years (range 40-59 years)
100% male
Race NR		 ST segment depression: 14% 22 Age, sex, smoking, SBP, total cholesterol CHD death: 15%
All cause mortality: 37%
Acute MI: 19%
Coronary artery bypass graft surgery: 6.0%
Stroke: 7.7%		 Good
Cole et al, 200054 Lipid Research Clinics Prevalence Study
Treadmill/Standard or modified
Bruce protocol
United States
General population		 n=5,234
Mean age: 44 years
61% male
96% white
(other races NR)		 Heart rate recovery at 2 minutes <42 bpm: 33% 12 Age, sex, SBP, smoking, diabetes, lipid profiles (cholesterol) CVD death: 2.2%
All cause mortality: 6.2%		 Good
Cournot et al, 200655 Study not named
Exercise method not described/submaximal
France
Cardiology clinic attendees		 n=1,051
Mean age: 52 years (range 18-79 yrs)
64% male
Race NR		 ST segment depression: 5.3% 6 Age, sex, smoking, diabetes, SBP, HDL, total cholesterol CHD or CVD death: 0.6%
Any coronary event (cardiac death, sudden death, MI, and angina): 3.2%
All cause mortality: 1.7%
CHD or CVD death: 0.6%
Stable or unstable angina: 1.2%
Nonfatal MI: 1.4%		 Good
Ekelund et al, 198956 Lipid Research Clinics Coronary Primary Prevention Trial Treadmill/submaximal Bruce protocol
United States
Clinical trial enrollees		 n=3,775
Mean age: 47 years (range 35-59 years)
100% male
Race NR		 ST segment depression or elevation: 8.2% 7.4 Age, sex, smoking, diabetes, SBP, HDL, LDL CHD death: 1.8% Nonfatal MI: 7.6%
All cause mortality: 3.7%		 Good
Fleg et al, 199057 Baltimore Longitudinal Study of Aging
Treadmill/modified
Balke protocol
United States
General community		 n=407
Mean age: 60 years (range 40 years and older)
71% male
97% white		 ST segment depression: 16% 4.6 Age, sex, smoking, diabetes, hypertension, total cholesterol CVD death: 1.7%
Non-fatal MI: 3.2%
Angina: 4.9%
Any coronary event: 9.8%		 Good
Giagnoni et al, 198358 Study not named
Supine
Ergometer/submaximal Italy
Factory workers		 n=514
Age: 44% 46-65 years (range 18-65 years)
73% male
Race NR		 ST segment depression: 1.2% 6.0 Age, sex, smoking, SBP, total cholesterol Any coronary event (angina, myocardial infarction, or sudden death): 6.6%
All cause mortality: 3.1%		 Good
Gordon et al, 198659 Lipid Research Clinics Mortality Follow-Up study
Treadmill/submaximal
modified
Bruce protocol
United States
Lipid clinic attendees		 n=3,640
Age: 35% 50-79 years (range 30-79 years)
100% male
100% white		 ST segment depression or elevation: 18% 8.1 Age, sex (100% male), smoking, hyperglycemia, hypertension, HDL, LDL CHD death: 1.4%
CVD death: 1.8%
All cause mortality: 4.1%		 Fair
Gulati et al, 200361 St. James Women Take Heart
Treadmill/maximal
Bruce protocol
United States
General community		 n=5,271
Mean age: 52 years (range NR, standard deviation 11 years)
0% male
86% white		 Exercise capacity: Mean 8.0 METs 8.4 Age, sex (100% female), smoking, SBP, DBP, HDL, total cholesterol All cause mortality: 3.2% Fair
Gulati et al, 200560

Same population as Gulati et al, 200361

 St. James Women Take Heart
Treadmill/maximal
Bruce protocol
United States
General community		 n=5,636
Mean age: 52 years (range NR, standard deviation 11 years)
0% male
86% white		 Duke Treadmill Score: Mean score 8 9 Age, sex, smoking, diabetes, SBP, DBP, HDL, total cholesterol CHD death: 0.9%
All cause mortality: 3.0%		 Good
Josephson et al, 199062 Baltimore Longitudinal Study of Aging
Treadmill/submaximal
modified Balke protocol
United States
General population		 n=726
Mean age: 55 years (range 22-84 years)
63-87% male (varied by group)
Race NR		 ST segment depression: 12% on initial test, 13% on followup test 6.4-7.7 Age, sex, smoking, hypertension, cholesterol Cardiac events (angina, nonfatal MI, or cardiac death): 8.8% Fair
Jouven et al, 200063

Other publications: Filipovsky et al, 1992107

 Paris Protective Study
Bicycle/standardized graded exercise test
France
Civil servants		 n=6,101
Mean age: 48 years (range 42-52 years)
100% male
Race NR		 ST segment depression: 4.4%
Frequent premature ventricular contractions: 2.8%		 23 Age, sex (100% male), smoking, diabetes, SBP, total cholesterol CHD death: 7.1%
All cause mortality: 27%		 Good
Jouven et al, 200534 Paris Protective Study I
Bicycle/standardized graded exercise test
France
Civil servants		 n=5,713
Mean age: 48 years (range 42-53 years)
100% male
Race NR		 Abnormal (<89 beats per minute) heart rate increase during exercise: 8%
Abnormal heart rate recovery (heart rate decrease at 1 min after cessation of exercise <25 beats per minute): 6%		 23 Age, sex (100% male), smoking, diabetes, SBP, cholesterol Fatal MI (sudden death): 1.4%
Fatal MI (nonsudden death): 2.3%
All cause mortality: 27%		 Good
Kurl et al, 200364 Kuopio Ischemic Heart Disease Risk Factor Study
Bicycle/maximal symptom-limited exercise test
Finland
General population		 n=1,726
Mean age: 52 years (range 42-60 years)
100% male
Race NR		 ST segment depression: 7.1% 10 Age, sex (100% male), smoking, diabetes, SBP, LDL CHD death: 5.0%
Stroke: 4.2%		 Fair
Kurl et al, 200965 Kuopio Ischemic Heart Disease Risk Factor Study
Bicycle/maximal symptom-limited exercise test
Finland
General population		 n=1,639
Mean age: 52 years (range 42-60 years)
100% male
Race NR		 ST segment depression: 6.7% 16 Age, sex, smoking, diabetes, SBP, HDL, total cholesterol Stroke: 5.9% Fair
Lauer et al, 199666 Framingham Offspring Study
Treadmill/Submaximal
Bruce protocol
United States
Offspring and spouses of Framingham Heart Study participants		 n=1,575
Mean age: 43 years (range NR)
100% male
Race NR		 Failure to reach target heart rate: 21%
Increase in heart rate from rest to peak exercise: Continuous outcome
Ratio of heart rate to metabolic reserve used by stage 2 (7.1 METs) of exercise: Continuous outcome		 7.7 Age, sex, smoking, hypertension, diabetes, cholesterol CHD events (MI, angina, or sudden cardiac death): 6.0%
All cause mortality: 3.5%		 Fair
Laukkanen et al, 200167 Kuopio Ischemic Heart Disease Risk Factor Study
Bicycle/maximal symptom-limited exercise test
Finland
General population		 n=1,769
Mean age: 52 years (range 42-60 years)
100% male
Race NR		 ST segment depression
During exercise: 10.7%
After exercise: 3.1%		 10 Age, sex (100% male), smoking, SBP, diabetes, LDL, HDL CHD death: 3.0%
CVD death: 4.4%
Nonfatal coronary events (MI or typical angina): 9.8%		 Good
Laukkanen et al, 200668 Kuopio Ischemic Heart Disease Risk Factor Study
Bicycle/maximal symptom-limited exercise test
Finland
General population		 n=1,596
Mean age: 52 years (range 42-61 years)
100% male
Race NR		 Peak oxygen pulse (Vo2max/maximum heart beat): Continuous variable
ST segment depression: 6.8%		 14 Age, sex (100% male), smoking, diabetes, SBP, DBP, HDL, LDL CHD death: 4.2%
All cause mortality: 17%		 Good
Laukkanen et al, 200869 Kuopio Ischemic Heart Disease Risk Factor Study
Bicycle ergometer/maximal symptom-limited exercise test
Finland
General population		 n=1,639
Mean age: 52 years (range 42-60 years)
100% male
Race NR		 Exercise capacity measured as highest workload achieved during exercise test in watts: Continuous outcome, also categorized into quartiles (>230 W; 196-230 W; 162-195 W; <162 W)
Exercise-induced ST depression: horizontal or downsloping ST depression 1.0 mm 80 ms after the J-point: 6.5%		 16.6 Age, sex (100% male), smoking, diabetes, SBP, DBP, total cholesterol, HDL (Framingham risk score) or age, sex (100% male), total cholesterol, SBP, smoking (European SCORE) CVD death: 7.1%
Major CVD event: 21%
All cause mortality: 19%		 Good
Lyerly et al, 200870 Aerobics Center Longitudinal Study
Treadmill/maximal
modified Balke protocol
United States
General population (subgroup of diabetic persons)		 n=2,854
Mean age: 50 years (range 21-84 years)
100% male
Race NR		 ST segment depression or elevation ≥1 mm ≥0.08 seconds from the J-point: 11%
ST segment depression 0.5-1.0 mm at least 0.08 seconds: 11%		 16 Age, sex (all male), smoking, fasting glucose, hypertension, hypercholesterolemia CHD death: 11%
CVD death: 7.4%
All cause mortality: 15%		 Fair
Lyerly et al, 200971 Aerobic Center Longitudinal Study
Treadmill/Maximal
United States
Impaired fasting glucose or undiagnosed diabetes mellitus population		 n=3,044
Mean age: 47.4 years (range 20-79 years)
100% female
Mostly white (details NR)		 Cardiorespiratory fitness:
Low: 17% (517/3044)
Moderate: 34% (1041/3044)
High: 49% (1486/3044)		 15.6 Age, sex (all female), smoking, alcohol, hypertension, hypercholesterolemia, family history of diabetes CVD death: 1.6%
All cause mortality: 5.6%		 Fair
Mora et al, 200372 Lipid Research Clinics Prevalence Study
Treadmill/Maximal
Bruce protocol
United States
General population		 n=2,994
Mean age: 47 years
100% female
94% white (other races NR)		 ST segment depression: 37%
Ventricular premature contractions or tachycardia: 7.6%
Failure to reach target heart rate: 37%		 20.3 Age, sex (all female), smoking, diabetes, LDL, HDL, hypertension CVD death: 4.9%
All cause mortality: 14%		 Good
Mora et al, 200573 Lipid Research Clinics Prevalence Study
Treadmill/standard
Bruce protocol
United States
General population		 n=6,126
Mean age: 45 years (SD 10; range NR)
54% male
96% white; other races NR		 HRR + METs categorized into "high" or "low" based on sex-specific medians
High HRR and High METs: 28%
Low HRR or METs: 41%
Low HRR and Low METs: 31%		 20 Age, sex, smoking, total cholesterol, HDL, hypertension 10-year follow-up
CVD death: 1.3%
20-year follow-up
CVD death: 4%		 Fair
Morshedi-Meibodi et al, 200274 Framingham Offspring Study
Treadmill/Bruce protocol
United States
General population		 n=2,967
Mean age: 43 years (range NR, standard deviation 10 years)
47% male
Race NR		 Heart rate recovery: Continuous variable
Heart rate recovery at 1 minute <12 bpm: Prevalence NR
Heart rate recovery at 2 minutes <42 bpm: Prevalence NR		 15 Age, sex, smoking, diabetes, SBP, DBP, HDL, total cholesterol CHD events: 7.2%
CVD events: 10%
All cause mortality: 5.6%		 Fair
Okin et al, 199175 Framingham Offspring Study
Treadmill/standard
Bruce protocol
United States
General population		 n=3,168
Mean age: 44 years (range 17 to 70 years, standard deviation 10 years)
48% male
Race NR		 Heart rate adjusted ST segment depression index ≥1.6 µV bpm: 8.7%
Abnormal rate recovery loop: 6.0%		 4.3 Age, sex, smoking, diabetes (fasting blood glucose), hypertension (DBP), total cholesterol CHD events (angina, ischemic chest pain, fatal or nonfatal MI, sudden or nonsudden coronary death): 2.1% (65/3168) Good
Okin et al, 199676 Multiple Risk Factor Intervention Trial
Treadmill/standard
Bruce protocol
United States
Clinical trial enrollees		 n=5,940
Mean age: NR (range 35-57 years)
100% male
Race NR		 ST segment depression: 3.1%
Heart rate adjusted ST segment depression index ≥1.60 µV bpm: 12%		 7 Age, sex (100% male), DBP, total cholesterol, smoking CHD death: 1.8% (109/5940) Fair
Peters et al, 198377 Study not named
Bicycle ergometer/20-minute heart-rate-controlled graded exercise test
United States
Men employed in fire or law enforcement departments		 n=2,779
Median age: 41 years (mean NR; range 35-53 years)
100% male
Race NR		 Low physical work capacity, defined as below the median for each age group (median for entire cohort was 140 watts) 4.8 Age, sex (100% male), total cholesterol, smoking, hypertension Fatal MI: 0.2%
Nonfatal MI: 1.1%		 Fair
Rautaharju et al, 198678 Multiple Risk Factor Intervention Trial
Treadmill/standard
Bruce protocol
United States
Clinical trial enrollees		 n=6,150
Mean age: 46 years (range 35-57 years)
100% male
93% white
7% black		 ST segment depression: 12% 7 Age, sex (100% male), smoking, DBP, total cholesterol CHD death: 1.8%
CVD death: 2.1%
All cause mortality: 3.8%
Silent MI: 2.4%
Clinical MI: 3.5%		 Good
Rutter et al, 200279

Other publications: Rutter et al, 1999108

 Study not named
Treadmill
United Kingdom
Diabetes clinic patients		 n=86
Mean age: 62 years (range 45-75 years)
72% male
Race NR		 ST segment depression (>1mm horizontal or downsloping ST-segment depression at 80 ms after the J-point for 3 consecutive beats): 52% 2.8 Age, sex, smoking, hemoglobin a1c, clinic and 24 hour ambulatory blood pressure, total cholesterol (Framingham Risk Score also entered as a separate variable) Any CHD event (cardiac death, MI, or new-onset angina): 17% Fair
Rywik et al, 199880 Baltimore Longitudinal Study of Aging
Treadmill/submaximal
modified Balke protocol
United States
General population		 n=825
Mean age: 51 years (range 22-89 years)
60% male
Race NR		 ST segment depression: 18% during exercise, 7.6% during recovery 9 Age, sex, smoking, cholesterol, hypertension, diabetes (fasting glucose) Coronary events (angina, MI, or coronary death): 6.7% (55/825) Good
Rywik et al, 200281 Baltimore Longitudinal Study of Aging
Treadmill/modified
Balke protocol
United States
General population volunteers		 n=1,083
Mean age: 52 years (SD 18) 57% male
Race NR		 ≥1 mm horizontal or downsloping ST segment depression (MN code 11.1): 16%
≥1 mm horizontal or downsloping ST segment depression (MN code 11.1), 0.5-1 mm horizontal or downsloping ST segment depression (MN code 11.2), <0.5 mm ST segment depression but downsloping ST segment and ST segment or T nadir <0.5 mm below baseline (MN code 11.3), or ST segment depression <0.5 mm at rest or induced by postural shift or hyperventilation, worsened to type 11.1 response during or after		 7.9 Age, sex, total cholesterol, glucose, hypertension Any coronary event: 7%
Specific events
Angina: 3%
MI: 2%
CHD death: 2%		 Fair
Savonen et al, 200782 Kuopio Ischemic Heart Disease Risk Factor Study
Bicycle/maximal symptom-limited exercise test
Finland
General population		 n=1,314
Mean age: 52 years (range 42-61 years)
100% male
Race NR		 ST segment depression: 14% Workload (chronotropic index at heart rate 100/bpm): Continuous variable 12 Age, sex (100% male), smoking, diabetes, SBP, DBP, HDL, LDL CHD death: 2.7%
CVD death: 3.9%
All cause mortality: 10%		 Fair
Siscovick et al, 199183

Other publications: Lipid Research Clinics Program 1984109

 Lipid Research Clinics Coronary Primary Prevention Trial
Treadmill/submaximal
Bruce protocol
United States
Men with hypercholesterolemia		 n=3,617
Mean age: NR (range 35-59 years)
100% male
100% white		 ST depression or elevation ≥1mm or 10µV-sec 7.4 Age, sex (100% male), LDL, HDL, smoking, SBP Acute cardiac events (nonfatal MI and CHD death): 1.8% (51/2893) Good
Slattery et al, 198884 US Railroad Study
Treadmill/submaximal 3-minute exercise test
United States
Men employed in the US railroad industry		 n=2,431
Mean age: NR (range 22-79 years)
100% male 100% white		 Heart rate following 3-minute submaximal exercise test, categorized into quartiles NR, maximum duration 20 years Age, sex (100% male), SBP, total cholesterol, smoking CHD death: 11%
All cause mortality: 27%		 Fair
Sui et al, 200785 Aerobics Center Longitudinal Study
Treadmill/modified
Balke protocol
United States
General population		 n=26,637
Mean age: NR (range 18-83 years)
78% male
Race NR		 Fitness level, based on duration of maximal treadmill exercise test
Low: lowest quintile
Moderate: 2nd and 3rd quintiles
High: upper two quintiles		 10 Age, smoking, hypertension, diabetes, dyslipidemia Any CVD event (MI, revascularization, or stroke): 5.7%
MI: 1.8%
Revascularization: 2.8%
Stroke: 1.1%		 Fair

Abbreviations: bpm=Beats per minute, CHD=Coronary heart disease, CVD=Cardiovascular disease, DBP=Diastolic blood pressure, ECG=Electrocardiography, HDL=High-density lipoprotein, LDL=Low-density lipoprotein, LVH=Left ventricle hypertrophy, METs=Metabolic equivalents, MI=Myocardial infarction, MRFIT=Multiple Risk Factor Intervention Trial, NR=Not reported, SBP=Systolic blood pressure.

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