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BACKGROUND: The utility of exercise‐induced ST‐segment depression for diagnosing ischemic heart disease (IHD) in women is unclear. HYPOTHESIS: Based on evidence that IHD pathophysiology in women involves coronary vascular dysfunction, we hypothesized that coronary vascular dysfunction contributes to exercise electrocardiography (Ex‐ECG) ST‐depression in the absence of obstructive coronary artery disease, so‐called false positive results. We tested our hypothesis in a pilot study evaluating the relationship between peripheral vascular endothelial function and Ex‐ECG. METHODS: Twenty‐nine asymptomatic women without cardiac risk factors underwent maximal Bruce protocol exercise treadmill testing and peripheral endothelial function assessment using peripheral arterial tonometry (Itamar EndoPAT 2000) to measure reactive hyperemia index (RHI). The relationship between RHI and Ex‐ECG ST‐segment depression was evaluated using logistic regression and differences in subgroups using 2‐tailed t tests. RESULTS: Mean age was 54 ± 7 years, body mass index 25 ± 4 kg/m(2), and RHI 2.51 ± 0.66. Three women (10%) had RHI 0.05). RHI did not predict ST‐segment depression. CONCLUSIONS: Our pilot study demonstrates high prevalence of exercise‐induced ST‐segment depression in asymptomatic, middle‐aged, overweight women. Peripheral vascular endothelial dysfunction did not predict Ex‐ECG ST‐segment depression. Further work is needed to investigate the utility of vascular endothelial testing and Ex‐ECG for IHD diagnostic and management purposes in women.

Background: \ud Automated measurements of electrocardiographic (ECG) intervals by current-generation digital electrocardiographs are critical to computer-based ECG diagnostic statements, to serial comparison of ECGs, and to epidemiological studies of ECG findings in populations. A previous study demonstrated generally small but often significant systematic differences among 4 algorithms widely used for automated ECG in the United States and that measurement differences could be related to the degree of abnormality of the underlying tracing. Since that publication, some algorithms have been adjusted, whereas other large manufacturers of automated ECGs have asked to participate in an extension of this comparison.\ud \ud Methods: \ud Seven widely used automated algorithms for computer-based interpretation participated in this blinded study of 800 digitized ECGs provided by the Cardiac Safety Research Consortium. All tracings were different from the study of 4 algorithms reported in 2014, and the selected population was heavily weighted toward groups with known effects on the QT interval: included were 200 normal subjects, 200 normal subjects receiving moxifloxacin as part of an active control arm of thorough QT studies, 200 subjects with genetically proved long QT syndrome type 1 (LQT1), and 200 subjects with genetically proved long QT syndrome Type 2 (LQT2).\ud \ud Results: \ud For the entire population of 800 subjects, pairwise differences between algorithms for each mean interval value were clinically small, even where statistically significant, ranging from 0.2 to 3.6 milliseconds for the PR interval, 0.1 to 8.1 milliseconds for QRS duration, and 0.1 to 9.3 milliseconds for QT interval. The mean value of all paired differences among algorithms was higher in the long QT groups than in normals for both QRS duration and QT intervals. Differences in mean QRS duration ranged from 0.2 to 13.3 milliseconds in the LQT1 subjects and from 0.2 to 11.0 milliseconds in the LQT2 subjects. Differences in measured QT duration (not corrected for heart rate) ranged from 0.2 to 10.5 milliseconds in the LQT1 subjects and from 0.9 to 12.8 milliseconds in the LQT2 subjects.\ud \ud Conclusions: \ud Among current-generation computer-based electrocardiographs, clinically small but statistically significant differences exist between ECG interval measurements by individual algorithms. Measurement differences between algorithms for QRS duration and for QT interval are larger in long QT interval subjects than in normal subjects. Comparisons of population study norms should be aware of small systematic differences in interval measurements due to different algorithm methodologies, within-individual interval measurement comparisons should use comparable methods, and further attempts to harmonize interval measurement methodologies are warranted.

Although automated ECG analysis has been available for many years, there are some aspects which require to be re-assessed with respect to their value while newer techniques which are worthy of review are beginning to find their way into routine use. At the annual International Society of Computerized Electrocardiology conference held in April 2017, four areas in particular were debated. These were a) automated 12 lead resting ECG analysis; b) real time out of hospital ECG monitoring; c) ECG imaging; and d) single channel ECG rhythm interpretation. One speaker presented the positive aspects of each technique and another outlined the more negative aspects. Debate ensued. There were many positives set out for each technique but equally, more negative features were not in short supply, particularly for out of hospital ECG monitoring.

The electrocardiogram (ECG) is the most widely used imaging tool helping in diagnosis and initial management of patients presenting with symptoms compatible with acute coronary syndrome. Acute ischemia affects the configuration of the QRS complexes, the ST segments and the T waves. The ECG should be read along with the clinical assessment of the patient. ST segment elevation (and ST depression in leads V1 -V3 ) in patients with active symptoms usually indicates acute occlusion of an epicardial artery with ongoing transmural ischemia. These patients should be triaged for emergent reperfusion therapy per current guidelines. However, many patients have ST segment elevation secondary to nonischemic causes. ST depression in leads other than V1 -V3 usually are indicative of subendocardial ischemia secondary to subocclusion of the epicardial artery, distal embolization to small arteries or spasm supply/demand mismatch. ST depression may also be secondary to nonischemic etiologies, such as left ventricular hypertrophy, cardiomyopathies, etc. Knowing the clinical scenario, comparison to previous ECG and subsequent ECGs (in cases that there are changes in the quality or severity of symptoms) may add in the diagnosis and interpretation in difficult cases. This review addresses the different ECG patterns, typically seen in patients with active symptoms, after resolution of symptoms and the significance of such changes when seen in asymptomatic patients.

Background For many years was considered that negative T wave in ischemic heart disease represents ischemia and for many authors located in subepicardial area. Methods We performed a review based in the literature and in the experience of the authors commenting the real significance of the presence of negative T wave in patients with ischemic heart disease. Results The negative T wave may be of primary or secondary type. Negative T wave observed in ischemic heart disease are of primary origin, therefore not a consequence of abnormal repolarization pattern. The negative T wave of ischemic origin presents the following characteristics: (1) are symmetrical and of variable deepness; (2) present mirror patterns; (3) starts in the second part of repolarization; and (4) may be accompanied by positive or negative U wave. The negative T wave of ischemic origin may be seen in the following clinical settings: (1) postmyocardial infarction due to a window effect of necrotic zone and (2) as a consequence of reperfusion in case of aborted MI when the artery has opened spontaneously, or after fibrinolysis, PCI, or coronary spasm. Conclusion Acute ongoing ischemia do not cause negative T wave. This pattern appears when the ongoing ischemia is vanishing or in the chronic phase. In all these cases the cause of negative T wave is not located in the subepicardial area. Furthermore, positive exercise testing is expressed by ST depression never by isolated negative T wave. There are many circumstances that may present negative T wave outside ischemic heart disease and that have been discussed in this paper.

Background: Nonsustained ventricular tachycardia (VT), frequent in unoperated severe mitral regurgitation (MR), confers mortality risk [sudden death (SD) and cardiac death (CD)]. The prognostic value of VT after mitral valve surgery (MVS) is unknown; we aimed to define this prognostic value and to assess its modulation by left (LV) and/or right (RV) ventricular ejection fraction (EF) for mortality after MVS. Methods: In 57 patients (53% females, aged 58 ± 12 years) with severe MR prospectively followed before and after MVS, we performed 24-hour ambulatory electrocardiograms approximately annually. LVEF and RVEF were determined within 1 year after MVS by radionuclide cineangiography. Results: During 9.52 ± 3.49 endpoint-free follow-up years, late postoperative CD occurred in 11 patients (7 SD, 4 heart failures). In univariable analysis, >1 VT episode after MVS predicted SD (p < 0.01) and CD (SD or heart failure; p < 0.04). Subnormal postoperative RVEF predicted CD (p < 0.04). When adjusted for preoperative age, gender, etiology or antiarrhythmics, both postoperative VT and RVEF predicted CD (p ≤ 0.05). When postoperative VT and RVEF were both in the multivariable model, only subnormal RVEF predicted CD (p < 0.04). Among those with normal RVEF, VT >1 episode predicted SD (p = 0.03). Conclusion: Postoperative VT and subnormal RVEF predict late postoperative deaths in nonischemic MR. Their assessment may aid patient management.

A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, and the American College of Physicians, American Association for Thoracic Surgery, Preventive Cardiovascular Nurses Association, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons Published by Elsevier Inc. http://dx.doi.org/10.1016/j.jacc.2012.07.012

Background The Cardiac Safety Research Consortium (CSRC) provides both "learning" and blinded "testing" digital electrocardiographic (ECG) data sets from thorough QT (TQT) studies annotated for submission to the US Food and Drug Administration (FDA) to developers of ECG analysis technologies. This article reports the first results from a blinded testing data set that examines developer reanalysis of original sponsor-reported core laboratory data. Methods A total of 11,925 anonymized ECGs including both moxifloxacin and placebo arms of a parallel-group TQT in 181 subjects were blindly analyzed using a novel ECG analysis algorithm applying intelligent automation. Developer-measured ECG intervals were submitted to CSRC for unblinding, temporal reconstruction of the TQT exposures, and statistical comparison to core laboratory findings previously submitted to FDA by the pharmaceutical sponsor. Primary comparisons included baseline-adjusted interval measurements, baseline- and placebo-adjusted moxifloxacin QTcF changes (ddQTcF), and associated variability measures. Results Developer and sponsor-reported baseline-adjusted data were similar with average differences P Conclusion The virtually automated ECG algorithm used for this analysis produced similar yet less variable TQT results compared with the sponsor-reported study, without the use of a manual core laboratory. These findings indicate that CSRC ECG data sets can be useful for evaluating novel methods and algorithms for determining drug-induced QT/QTc prolongation. Although the results should not constitute endorsement of specific algorithms by either CSRC or FDA, the value of a public domain digital ECG warehouse to provide prospective, blinded comparisons of ECG technologies applied for QT/QTc measurement is illustrated.

TdP is an uncommon but potentially fatal arrhythmia that can be caused by drugs that cause selective prolongation of action potential durations in certain layers of the ventricular myocardium, which creates dispersion of repolarization and a long, distorted QT-U interval on the ECG. A summary of key points to remember is provided in Table 3. Table 3 Summary of Key Points For patients who receive QT-prolonging drugs in hospital units with continuous ECG monitoring, TdP should be avoidable if there is an awareness of individual risk factors and the ECG signs of drug-induced LQTS. Particularly important are the ECG risk factors for TdP, including marked QTc prolongation to >500 ms (with the exception of amiodarone- or verapamil-induced QT prolongation), marked QT-U prolongation and distortion after a pause, onset of ventricular ectopy and couplets, macroscopic T-wave alternans, or episodes of polymorphic ventricular tachycardia that are initiated with a short-long-short R-R cycle sequence (typically, PVC– compensatory pause–PVC). Recognition of these ECG harbingers of TdP allows for treatment with intravenous magnesium, removal of the offending agent, and correction of electrolyte abnormalities and other exacerbating factors, including the prevention of bradycardia and long pauses with temporary pacing if necessary.

Background: The global QT interval, emerging as a standard measurement provided by digital electrocardiographs, is defined by the earliest QRS onset and latest T-wave offset that occur in any of the standard leads. Differences between global ECG measurements and those from individual ECG leads have implications for the redefinition of normal values, for recognition of disease, and for drug safety. This study sought to quantify the differences between global QT intervals measured from 12 superimposed ECG leads with QT intervals and from single lead complexes, to examine the separate effects of QRS onset and T-wave offset on these differences, and to examine the reproducibility of these measurements. Methods: QTo intervals (Q onset to T offset) from 50 digitized ECGs sampled at 500 Hz were examined by computer assisted derivation of representative complexes from standard leads II, V2, and V3, by both baseline and tangent methods. Global QTo intervals were measured from superimposition of the representative complexes of all 12 leads. A time-coherent matrix of waveform onset and offset points allowed direct comparison of the components of the differences. Results: Global QTo and Bazett-adjusted global QTc were greater than each of the baseline and tangent measurements in representative leads II, V2, and V3, with mean differences ranging from 8 to 18 ms. QRS onset was earlier in the global complex than in each of the representative leads, with mean differences of 3–5 ms, whereas T-wave offset was significantly later in the global complex than in each of the representative leads, with mean differences of 5–11 ms. Remeasurement of all ECGs after an interval of 6 months confirmed the relative magnitudes of the global and individual lead QTo durations and small mean differences between pairs (−0.9 to 2.7 ms). Although global QTo had the largest mean difference (only 2.7 ms), it had the smallest standard deviation of the mean difference and lowest coefficient of variability (1.58%) of all measurements. Conclusion: Global QT measurements are systematically larger than measurements from representative complexes of individual leads. These differences result from the combined effects of earlier QRS onset and later T-wave offset in the global complex, with T-wave offset the more dominant component of the difference.

This statement provides a concise list of diagnostic terms for ECG interpretation that can be shared by students, teachers, and readers of electrocardiography. This effort was motivated by the existence of multiple automated diagnostic code sets containing imprecise and overlapping terms. An intended outcome of this statement list is greater uniformity of ECG diagnosis and a resultant improvement in patient care. The lexicon includes primary diagnostic statements, secondary diagnostic statements, modifiers, and statements for the comparison of ECGs. This diagnostic lexicon should be reviewed and updated periodically.

This statement examines the relation of the resting ECG to its technology. Its purpose is to foster understanding of how the modern ECG is derived and displayed and to establish standards that will improve the accuracy and usefulness of the ECG in practice. Derivation of representative waveforms and measurements based on global intervals are described. Special emphasis is placed on digital signal acquisition and computer-based signal processing, which provide automated measurements that lead to computer-generated diagnostic statements. Lead placement, recording methods, and waveform presentation are reviewed. Throughout the statement, recommendations for ECG standards are placed in context of the clinical implications of evolving ECG technology.

Background: Current guidelines do not endorse exercise electrocardiography (Ex-ECG) screening in asymptomatic adults due to poor diagnostic accuracy for clinical coronary artery disease (CAD), however Ex-ECG combined with other variables paradoxically has strong prognostic accuracy for cardiovascular mortality. Ex-ECG ST segment depression “false positive” results are common in women, who have higher rates of vascular dysfunction such as Raynaud’s and migraines compared to men. We hypothesized that ST segment depression indicates endothelial vascular dysfunction, which is known to predict an adverse prognosis. To test this hypothesis, we evaluated the relationship between Ex-ECG and peripheral endothelial vascular function in asymptomatic women. Methods: Asymptomatic women with no cardiac risk factors and normal resting ECG underwent maximal Bruce protocol Ex-ECG testing (GE Healthcare). Computer-generated Ex-ECG ST segment values were independently verified by 2 cardiologists. Based on established methods, endothelial vascular function was assessed by calculating reactive hyperemia index (RHI) using peripheral vascular testing (Endopat, Itamar). As established previously, RHI Results: Among 35 women, mean age 54±8 years and BMI 24±4, there were 5 (14%) women with abnormal RHI. Women with abnormal RHI had a greater (more abnormal) ST/HR slope, a trend toward greater peak ST depression, and achieved lower METs than women with normal RHI (Table 1). Conclusion: Among asymptomatic women, endothelial vascular dysfunction was associated with abnormal Ex-ECG results characterized by greater ST/HR slope, greater ST depression, and lower exercise capacity. These findings suggest that “false positive” ST-segment depression in the absence of clinical CAD in women may be explained by endothelial vascular dysfunction. Our study further suggests that endothelial vascular dysfunction may explain the Ex-ECG diagnostic/prognostic paradox.

Exercise testing remains the most widely accessible and relatively inexpensive method for initial evaluation of suspected coronary disease and for evaluation of its severity.1–3 Clinical usefulness has been limited, however, by poor sensitivity of standard ST-segment depression criteria for assessment of anatomic and functional coronary disease severity and for prediction of risk.1,2,4–6 Recent data make it clear that symptomatic obstructive plaques that typically result in exercise-mediated ischemia may be less relevant to infarction and sudden death than less obstructive unstable plaques.7 These limitations mandate a rethinking of the exercise ECG along 2 distinct lines: First, is it possible to improve the diagnostic value of the exercise ECG? Second, separate from its ability to diagnose obstructive coronary artery lesions, can the exercise test be used as a prognostic tool that can encourage effective prevention of premature deaths or coronary events? Both goals take us beyond the ST segment. Reversible ST-segment depression is the characteristic finding associated with exercise-induced, demand-driven ischemia in patients with significant coronary obstruction but no flow limitation at rest. This process differs from the flow-limited acute coronary syndromes because exercise-related ischemia is generally limited to the subendocardium and is proportional to increases in myocardial oxygen demand. Ventricular waveforms of the ECG can be related to the net uncanceled transmural gradients between endocardial and epicardial myocardium, as extrapolated from the work of Holland and Brooks, among others.8–10 Accordingly, isoelectric TQ and ST segments in normal and in nonischemic patients can be related to comparable resting membrane and action potential plateau voltages in endocardial and epicardial action potentials. During exercise, progressive ischemia results in changing endocardial action potentials during both diastole and systole. Less negative endocardial cell resting membrane potential leads to current flow across the ischemic boundary during diastole, leading to elevation of the TQ …

Background: Although right bundle branch block (RBBB) delays right ventricular depolarization, its effect on cancellation of right and left ventricular forces within the QRS complex has not been quantified during stable temporal and physiological conditions. Systematic changes in QRS amplitude during transient RBBB bear directly on performance of standard ECG criteria for left ventricular hypertrophy (LVH), and these changes require quantification. Methods: We examined the instantaneous effect of RBBB on QRS amplitudes and LVH voltages in 40 patients who had intermittent complete RBBB during a single 10 sec standard 12-lead ECG recording, comprising 0.1% of approximately 400,000 consecutive ECGs in a university teaching hospital setting. Amplitudes were measured by magnifying graticule to the nearest 25 microvolts, averaged for up to 3 normal and 3 RBBB complexes, and compared by paired t test. Results: RBBB was associated with an increase in initial QRS forces (RV1, RV2, and QV6) but significant decreases in mean mid-QRS amplitudes that reflect left ventricular depolarization (RaVL [−75 microvolts], SV1 [−389 microvolts], SV3 [−617 microvolts], RV5 [−100 microvolts], and RV6 [−123 microvolts]). All late QRS forces were increased with RBBB (R'V1, SV5, SI). As a result, combined voltages used for LVH criteria were significantly reduced by RBBB: Sokolow-Lyon voltage decreased from 1520 ± 739 to 1014 ± 512 microvolts (p < 0.001), and Cornell voltage decreased from 1438 ± 683 to 746 ± 399 microvolts (p < 0.001). Conclusions: RBBB is associated with significant reduction in "left ventricular" QRS amplitudes of the standard ECG, consistent with cancellation, rather than unmasking, of left ventricular mid-QRS forces by altered septal and delayed right ventricular depolarization. Because QRS voltages that are routinely combined for the detection of LVH are reduced in RBBB, standard LVH criteria will perform with lower sensitivity in patients with RBBB.

Along with coronary artery calcium scanning, ankle-brachial index measurement, and carotid artery ultrasound, exercise electrocardiography has been proposed as a screening tool for asymptomatic subjects thought to be at intermediate risk for developing clinical coronary disease. A wealth of data indicate that exercise testing can be used to assess and refine prognosis, particularly when emphasis is placed on nonelectrocardiographic measures such as exercise capacity, chronotropic response, heart rate recovery, and ventricular ectopy. Nevertheless, randomized trial data on the clinical value of screening exercise testing are absent; that is, it is not known whether a strategy of routine screening exercise testing in selected subjects reduces the risk for premature mortality or major cardiac morbidity. The writing group believes that a large-scale randomized trial of such a strategy should be performed.

This year marks the bicentennial of the invention of the stethoscope by Rene Theophile Hyacinthe Laennec in 1816, working at the Necker Hospital in Paris. Mediate auscultation was a logical evolution within French clinical empiricism that combined elucidated physical signs with autopsy correlation to provide diagnostic insight into diseases of the lungs and heart. Over the past 2 centuries, the stethoscope has brought the doctor and patient closer together, and it has become a fundamental tool in medical practice and the symbol of the clinician.

Background —Therapeutic angiogenesis, a new experimental strategy for the treatment of vascular insufficiency, uses the administration of mediators known to induce vascular development in embryogenesis to induce neovascularization of ischemic adult tissues. This report summarizes a phase I clinical experience with a gene-therapy strategy that used an E1 − E3 − adenovirus (Ad) gene-transfer vector expressing human vascular endothelial growth factor (VEGF) 121 cDNA (Ad GV VEGF121.10) to induce therapeutic angiogenesis in the myocardium of individuals with clinically significant coronary artery disease. Methods and Results —Ad GV VEGF121.10 was administered to 21 individuals by direct myocardial injection into an area of reversible ischemia either as an adjunct to conventional coronary artery bypass grafting (group A, n=15) or as sole therapy via a minithoracotomy (group B, n=6). There was no evidence of systemic or cardiac-related adverse events related to vector administration. In both groups, coronary angiography and stress sestamibi scan assessment of wall motion 30 days after therapy suggested improvement in the area of vector administration. All patients reported improvement in angina class after therapy. In group B, in which gene transfer was the only therapy, treadmill exercise assessment suggested improvement in most individuals. Conclusions —The data are consistent with the concept that direct myocardial administration of Ad GV VEGF121.10 to individuals with clinically significant coronary artery disease appears to be well tolerated, and initiation of phase II evaluation of this therapy is warranted.

Abstract —Identification of left ventricular hypertrophy (LVH) using 12-lead ECG criteria based primarily on QRS amplitudes has been limited by poor sensitivity at acceptable levels of specificity. Because the product of QRS voltage and duration, as an approximation of the time-voltage area of the QRS complex, can improve accuracy of the 12-lead ECG for LVH, we examined the diagnostic value of true time-voltage area measurements of QRS complexes from the standard 12-lead ECG. Standard 12-lead ECGs and echocardiograms were obtained in 175 control subjects without LVH and in 74 patients with regurgitant valvular heart disease and LVH defined by echocardiographic criteria (indexed LV mass >110 g/m 2 in women and >125 g/m 2 in men). Standard voltage criteria, voltage-duration products (voltage multiplied by QRS duration), and true time-voltage areas of the QRS were calculated for Sokolow-Lyon criteria (SV 1 +RV 5/6 ) and the 12-lead sum of voltage criteria. Test sensitivities were compared using gender-specific partitions with matched specificity of 98% in the 175 subjects without LVH. Measurement of the time-voltage area significantly improved sensitivity for both criteria. The 76% sensitivity of the 12-lead sum area and 65% sensitivity of Sokolow-Lyon area were significantly greater than the 54% sensitivity of the approximation of QRS area provided by each voltage-duration product ( P P =.021) and than the 46% and 43% sensitivities of the respective simple voltage criteria (each P

Background Whether subjects identified as being at increased risk of coronary heart disease (CHD) death by heart rate adjustment of exercise-induced ST-segment depression will benefit from therapy aimed at reducing risk factors has not been examined. Methods and Results Exercise ECGs were performed in 11 880 men from the Usual Care (UC) and Special Intervention (SI) groups of the Multiple Risk Factor Intervention Trial. UC men were referred to customary sources of care in the community; SI men received counseling on smoking cessation and dietary reduction of cholesterol, and stepped-care therapy for hypertension. An abnormal ST-segment response to exercise was defined according to standard criteria as ≥100 μV of additional horizontal or downsloping ST-segment depression and by an ST-segment/heart rate (ST/HR) index >1.60 μV/bpm. After 7 years of follow-up, CHD mortality was significantly lower in SI than UC men with an abnormal ST/HR index (2.4%, 19/786 versus 5.3%, 39/729, P =.005) but was comparable in SI and UC men with a normal ST/HR index (1.6%, 84/5154 versus 1.3%, 70/5211, P =NS). Risk reduction in SI men with an abnormal ST/HR index was independent of age and other cardiac risk factors. In contrast, there was no significant difference in CHD death rate between the smaller groups of SI and UC men with an abnormal test by standard criteria (3.6%, 7/192 versus 2.7%, 5/186, P =NS). Conclusions An abnormal ST/HR index identifies men in whom therapy aimed at reducing CHD risk factors reduces the risk of CHD death by 61%. These findings support the application of heart rate adjustment of ST depression for screening of asymptomatic subjects at increased risk of CHD to identify those who will benefit most from risk factor–reduction programs.

Patients with carotid atherosclerosis have an increased risk of coronary events and an increased prevalence of echocardiographic left ventricular hypertrophy. However, little is known regarding the association between electrocardiographic abnormalities and carotid atherosclerosis. The relationship of electrocardiographic evidence of myocardial ischemia and left ventricular hypertrophy to the presence of carotid atherosclerosis was prospectively studied in 349 asymptomatic subjects who underwent echocardiography and carotid ultrasonography. Myocardial ischemia on the electrocardiogram was defined by the presence of localized T-wave inversions, and electrocardiographic hypertrophy was defined by the product of Cornell voltage and QRS duration. Carotid atherosclerosis was present in 21% (72/349) of subjects and was associated with older age, higher systolic and pulse pressures, and greater left ventricular mass. Both ischemia and hypertrophy on the electrocardiogram were strongly associated with carotid plaque. Carotid atherosclerosis was more than three times more prevalent in subjects with electrocardiographic ischemia (69% [11/16] versus 18% [61/333], P P =.0003) than in subjects without these findings. Logistic regression analysis, including standard risk factors, revealed that both ischemia and hypertrophy on the electrocardiogram remained significant independent predictors of the presence of carotid atherosclerosis, along with age and echocardiographic left ventricular mass. These findings suggest that the associations of ischemia and left ventricular hypertrophy with carotid atherosclerosis may contribute to the increased incidence of coronary events in patients with carotid atherosclerosis.

Objectives.We sought to assess the effect of heart rate adjustment of ST segment depression on risk stratification for the prediction of death from coronary artery disease. Background.Standard analysis of the ST segment response to exercise based on a fixed magnitude of horizontal or downsloping ST segment depression has demonstrated only limited diagnostic sensitivity for the detection of coronary artery disease and has variable test performance in predicting coronary artery disease mortality. Heart rate adjustment of the magnitude of ST segment depression has been proposed as an alternative approach to increase the diagnostic and prognostic accuracy of the exercise electrocardiogram (ECG). Methods.Exercise ECGs were performed in 5,940 men from the Usual Care Group of the Multiple Risk Factor Intervention Trial at entry into the study. An abnormal ST segment response to exercise was defined according to standard criteria as ≥ 100 μV of additional horizontal or downsloping ST segment depression at peak exercise. The ST segment/heart rate index was calculated by dividing the change in ST segment depression from rest to peak exercise by the exercise-induced change in heart rate. An abnormal ST segment/heart rate index was defined as >1.60 μV/beats per min. Results.After a mean follow-up of 7 years there were 109 coronary artery disease deaths. Using a Cox proportional hazards model, a positive exercise ECG by standard criteria was not predictive of coronary mortality (age-adjusted relative risk [RR] 1.5,95% condence interval [CI] 0.6 to 3.6, p = 0.39). In contrast, an abnormal ST segment/heart rate index significantly increased the risk of death from coronary artery disease (age-adjusted RR 4.1, 95% CI 2.7 to 6.0, p < 0.0001). Excess risk of death was confined to the highest quintile of ST segment/heart rate index values, and within this quintile, risk was directly related to the magnitude of test abnormality. After multivariate adjustment for age, diastolic blood pressure, serum cholesterol and cigarettes smoked per day, the ST segment/heart rate index remained a significant independent predictor of coronary death (RR 3.6, 95% CI 2.4 to 5.4, p < 0.001). Conclusions.Simple heart rate adjustment of the magnitude of ST segment depression improves the prediction of death from coronary artery disease in relatively high risk, asymptomatic men. These findings strongly support the use of heart rate-adjusted indexes of ST segment depression to improve the predictive value of the exercise ECG.

Objectives.This study sought to assess a test performance of the electrocardiogram (ECG) in relation to 1) varying definitions of left ventricular hypertrophy based on different methods of adjusting left ventricular mass for body size, and 2) the presence or absence of obesity.Background.Although left ventricular mass is most commonly indexed for body surface area or height when defining left ventricular hypertrophy, recent work suggests that normalization for height to the power of 2.7 (height2.7) may decrease variability among normal subjects and correctly identify the impact of obesity on hypertrophy.Methods.The product of Cornell voltage and QRS duration (Cornell product) and Framingham-adjusted Cornell voltage were determined from 12-lead ECGs in 212 patients. Left ventricular hypertrophy was defined on the basis of left ventricular mass indexed to body surface area, height and height2.7.Results.Using partitions with matched specificity of 95%, the sensitivity of ECG criteria varied with the definition of hypertrophy, ranging from 39% to 52% for the Cornell product and from 24% to 33% for adjusted Cornell voltage. When left ventricular mass was indexed to body surface area or to height2.7, the 52% and 39% sensitivities of the Cornell product were significantly greater than the 24% (p < 0.001) and 29% (p < 0.05) sensitivities of adjusted Cornell voltage, with a similar trend when left ventricular mass was indexed to height (43% vs. 33%, p = 0.10). Comparison of receiver operating characteristic curves confirmed the superior overall performance of the Cornell product relative to adjusted Cornell voltage for hypertrophy defined by body surface area and height2.7and demonstrated greater reproducibility of overall performance, as measured by the coefficient of variability, for the Cornell product (1.7%) than for adjusted Cornell voltage (5.8%). Sensitivity of adjusted Cornell voltage was significantly greater in obese than in nonobese subjects (50% to 59% vs. 18% to 24%, p < 0.01), but the Cornell product had only minimally higher sensitivity in nonobese than in obese subjects (40% to 54% vs. 32% to 44%, p = NS).Conclusions.The ability of ECG criteria to detect left ventricular hypertrophy differs depending on the method of indexing left ventricular mass for body size and with the presence or absence of obesity. Further, the Cornell product provides the best combination of overall accuracy and low variability of performance between definitions of hypertrophy. These findings have important implications for the clinical and epidemiologic use of 12-lead ECG criteria for the detection of left ventricular hypertrophy.

Analysis of the rate-related change in exercise-induced ST segment depression using the exercise ST segment/heart rate slope and ST segment/heart rate index can improve the accuracy of the exercise electrocardiogram (ECG) for the identification of patients with coronary artery disease, recognition of patients with anatomically or functionally severe coronary obstruction and detection of patients at increased risk for future coronary events. These methods provide a more physiologic approach to analysis of the ST segment response to exercise by adjusting the apparent severity of ischemia for the corresponding increase in myocardial oxygen demand, which in turn can be linearly related to increasing heart rate. Solid-angle theory provides a model for the linear relation of ST segment depression to heart rate during exercise and a framework for understanding the relation of the ST segment/heart rate slope to the presence and extent of coronary artery disease. False positive and false negative test results of the heart rate-adjusted methods are well known in selected populations and require further clarification. Application of these methods is also highly dependent on the type of exercise protocol, number of ECG leads examined, timing of ST segment measurement relative to the J point and accuracy and precision of ST segment measurement. These methodologic details have been an important limitation to test application when traditional protocols and measurement procedures are required. When applied with attention to required details, the heart rate-adjusted methods can improve the usefulness of the exercise ECG in a range of clinically relevant populations.

Background Fractal geometric analysis of ventricular ectopy yields a fractal dimension, which can range from zero to one and is inversely related to clustering of ventricular premature contractions (VPCs). Low values of this fractal dimension, which reflect significantly nonuniform distributions of ventricular ectopy, are found in patients with life-threatening ventricular arrhythmias and predict adverse outcomes in selected patients with congestive heart failure and with mitral regurgitation. However, the physiological mechanism and correlates of the fractal dimension are unknown. Methods and Results To explore the physiological correlates of clustered ventricular ectopy, we studied 30 patients with a history of sustained ventricular tachycardia or ventricular fibrillation who had inducible sustained monomorphic ventricular tachycardia during electrophysiological study and also underwent drug-free 24-hour ambulatory ECG. In addition to fractal dimension (determined by use of our previously described algorithm), we measured the mean RR interval (±SD) for all sinus beats preceding a sinus beat and for all sinus beats preceding a single VPC and the mean root-mean-square difference (RMSSD) of all windows of 15 successive RR intervals (excluding ectopic beats) preceding a sinus beat and preceding a single VPC. Based on the directional changes of mean RR (a measure of both sympathetic and parasympathetic tone) and of RMSSD (a measure of parasympathetic tone), each patient’s inferred relative sympathetic tone preceding ventricular ectopy was classified as increased, unchanged, or decreased. If these values changed concordantly, relative sympathetic tone was indeterminate. Fractal dimension did not correlate with the mean RR interval, SD of the RR interval, or RMSSD preceding sinus beats or preceding VPCs (all P >.10). In 20 patients, fractal dimension was significantly lower among those with increased relative sympathetic tone (n=14) than those with unchanged or decreased sympathetic tone (n=6, P =.008). Ten patients had indeterminate relative sympathetic tone. Conclusions Clustering of ventricular ectopy, as measured by the fractal dimension, is observed in patients at increased risk of sudden cardiac death. A low fractal dimension (clustered ventricular ectopy) is related to changes in heart rate and heart rate variability that are consistent with transient increases in cardiac sympathetic tone.

Objectives. This study was conducted to test the hypothesis that the time-voltage integral of the QRS complex can improve the electrocardiographic (ECG) identification of left ventricular hypertrophy.Background. Standard ECG criteria have exhibited poor sensitivity for left ventricular hypertrophy at acceptable levels of specificity. However, left ventricular mass may be more closely related to the time-voltage integral of the summed left ventricular dipole than to QRS duration or voltages used in standard ECG criteria.Methods. Standard 12-lead ECGs, orthogonal lead signal-averaged ECGs and echocardiograms were obtained in 62 male control subjects without left ventricular hypertrophy and 51 men with left ventricular hypertrophy defined by echocardiographic criteria (indexed left ventricular mass >125 g/m2). Voltage of the QRS complex was integrated over the total QRS duration in leads X, Y and Z to calculate the time-voltage integral of each orthogonal lead, of the maximal spatial vector complex and of the horizontal, frontal and sagittal plane vector complexes.Results. At matched specificity of 99%, the 73% (37 of 51) sensitivity of the time-voltage integral of the vector QMS complex in the horizontal plane was significantly greater than the 10% sensitivity of the Romhilt-Estes point score, the 16% sensitivity of QRS duration alone, the 22% sensitivity of Cornell voltage, the 33% sensitivity of the 12-lead sum of QRS voltage and the 37% sensitivity of Sokolow-Lyon voltage (each p < 0.001). Sensitivity of the horizontal plane time-voltage integral was also greater than the 10% to 51% sensitivity of the time-voltage integral calculated in the individual X, Y or Z leads (p < 0.01 to < 0.001), the 18% and 35% sensitivity of the time-voltage integrals of the frontal and sagittal plane vectors (p < 0.001) and the 49% sensitivity of the time-voltage integral of the maximal spatial vector complex calculated from all three orthogonal leads (p < 0.001). Comparison of receiver operating characteristic curves confirmed that the superior performance of the horizontal plane time-voltage integral relative to standard and other signal-averaged criteria was independent of partition value selection.Conclusions. These findings suggest that use of the time-voltage integral of the QRS complex, a method that can be readily implemented on commercially available computerized ECG systems, can improve the accuracy of ECG methods for the identification of left ventricular hypertrophy.

BACKGROUND A variety of measures of heart rate variability have been devised to measure high-frequency (0.15-0.40 Hz), low-frequency (0.04-0.15 Hz), or ultralow-frequency (< 0.0033 Hz) fluctuations in sinus cycle length. Although measures of low-frequency and ultralow-frequency heart rate variability have been shown to correlate with prognosis in several populations with ischemic heart disease, their relevance to patients with primary valvular heart disease remains to be determined. METHODS AND RESULTS Thirty-eight patients with nonischemic causes of chronic severe mitral regurgitation who were in sinus rhythm underwent 24-hour ambulatory electrocardiography as part of a prospective study of the natural history of regurgitant valvular heart disease. Patients were followed for as long as 9.2 years, and end points of mortality, progression to mitral valve surgery, and development of chronic atrial fibrillation were tabulated. Time- and frequency-domain measurements of high-frequency, low-frequency, and ultralow-frequency heart rate variability were computed and compared with resting ventricular function by radionuclide cineangiography and outcome. The standard deviation of the 5-minute mean RR intervals (SDANN), a measure of ultralow-frequency heart rate variability, was correlated with left ventricular ejection fraction (r = 0.49, p = 0.002) and right ventricular ejection fraction (r = 0.43, p = 0.007), whereas low-frequency and high-frequency heart rate variabilities were not. Heart rate, ultralow-frequency heart rate variability, and, to a lesser extent, high-frequency heart rate variability exhibited significant diurnal variation, but low-frequency heart rate variability did not. Heart rate and ultralow-frequency, low-frequency, and combined low- and high-frequency heart rate variability predicted mortality and total events. The most powerful predictor of subsequent events was SDANN: Patients with reduced SDANN were significantly more likely to develop end-point events (p < 0.001) with increased progression to mitral valve surgery (p < 0.001) as well as increased early mortality (p = 0.02). In a multivariate proportional hazards model, SDANN retained independent predictive power (p = 0.001). Likewise, SDANN was the only variable that was significantly associated with the subsequent development of atrial fibrillation (relative risk, 3.1; p = 0.03). CONCLUSIONS Ultralow-frequency heart rate variability, as measured by SDANN, correlates with right and left ventricular performance and predicts development of atrial fibrillation, mortality, and progression to valve surgery in patients with chronic severe mitral regurgitation.

Cardiac arrest due to torsade de pointes (TdP) in the acquired form of drug-induced long-QT syndrome (LQTS) is a rare but potentially catastrophic event in hospital settings. Administration of a QT-prolonging drug to a hospitalized population may be more likely to cause TdP than administration of the same drug to an outpatient population, because hospitalized patients often have other risk factors for a proarrhythmic response. For example, hospitalized patients are often elderly people with underlying heart disease who may also have renal or hepatic dysfunction, electrolyte abnormalities, or bradycardia and to whom drugs may be administered rapidly via the intravenous route. In hospital units where patients’ electrocardiograms (ECGs) are monitored continuously, the possibility of TdP may be anticipated by the detection of an increasing QT interval and other premonitory ECG signs of impending arrhythmia. If these ECG harbingers of TdP are recognized, it then becomes possible to discontinue the culprit drug and manage concomitant provocative conditions (eg, hypokalemia, bradyarrhythmias) to reduce the occurrence of cardiac arrest. The purpose of this scientific statement is to raise awareness among those who care for patients in hospital units about the risk, ECG monitoring, and management of drug-induced LQTS. Topics reviewed include the ECG characteristics of TdP and signs of impending arrhythmia, cellular mechanisms of acquired LQTS and current thinking about genetic susceptibility, drugs and drug combinations most likely to cause TdP, risk factors and exacerbating conditions, methods to monitor QT intervals in hospital settings, and immediate management of marked QT prolongation and TdP. The term torsade de pointes was coined by Dessertenne in 1966 as a polymorphic ventricular tachycardia characterized by a pattern of twisting points.1 Several ECG features are characteristic of TdP and are illustrated in Figure 1. First, a change in the amplitude and morphology (twisting) of the QRS …

Secondary prevention improves survival, yet implementation is suboptimal. We tested the impact of a systematic hospital-based educational intervention vs. usual care to improve rates of adherence to secondary prevention guidelines among women hospitalized with coronary heart disease (CHD), according to their ethnic status.Women (n = 304, 52% minorities) hospitalized with CHD were randomly assigned to a systematic secondary prevention educational intervention vs. usual care. Adherence to goals for smoking cessation, weight management, physical activity, blood pressure140/90 mm Hg, low-density lipoprotein cholesterol (LDL-C)100 mg/dL (2.59 mmol/L), and use of aspirin/anticoagulants, beta-blockers, and angiotensin-converting enzyme (ACE) inhibitors were assessed at 6 months.On admission, minority women were less likely than white women to meet the goals for blood pressure (OR = 0.46, 95% CI 0.26-0.80), LDL-C (OR = 0.57, CI 0.33-0.94), and weight management (OR = 0.40, 95% CI 0.20-0.82). There was no difference between the intervention and usual care groups in a summary score of goals met at study completion; however, minority women in the intervention group were 2.4 times more likely (95% CI 1.13-5.03) to reach the blood pressure goal at 6 months compared with minority women in usual care. White women in the intervention group were 2.86 times more likely (95% CI 1.06-7.68) to report use of beta-blockers at 6 months compared with white women in usual care. In a logistic regression model, the interaction term for ethnic status and group assignment was significant for achieving the blood pressure goal (p = 0.009).A healthcare systems approach to educate women about secondary prevention and blood pressure control may differentially benefit ethnic minority women compared with white women.

Objectives. The object of this study was to assess the hypothesis that the product of QRS voltage and duration, as an approximation of the time-voltage integral of the QRS complex, can improve the electrocardiographic (ECG) identification of left ventricular hypertrophy. Background. Electrocardiographic identification of left ventricular hypertrophy has been limited by the poor sensitivity of standard voitage criteria. However, increases in left ventricular mass can be more closely related to increases in the time-voltage integral of the summed left ventricular dipole than to changes in voltage or QRS duration alone. Methods. Antemortem ECGs were compared with left ventricular mass at autopsy in 220 patients. There were 95 patients with left ventricular hypertrophy, defined by left ventricular mass index 118 g/m2in men and 104 g/m2in women. The voltage-duration product was calculated as the product of QRS duration and Cornell voltage (Cornell product) and the 12-lead sum of QRS voltage (12-lead product). Results. At partitions with a matched specificity of 95%, each voltage-duration product significantly improved sensitivity for the detection of left ventricular hypertrophy when compared with simple voltage criteria alone (Cornell product 51 % [48 of 95] vs. Cornell voltage 36% [34 of 95], p < 0.005 and 12-lead product 45% [43 of 95] vs. 12-lead voltage 31% [30 of 95], p < 0.001). Sensitivity of both the Cornell product and 12-lead product was significantly greater than that found for QRS duration alone (28%, 27 of 95, p< 0.005) and the Romhilt-Estes point score (27%, 28 of 95, p < 0.005), and compared favorably with the sensitivity of hie complex Cornell multivariate score (44%, 42 of 95, p = NS). Comparison of receiver operating characteristic curves demonstrated that improved performance of the voltage-duration products for the detection of left ventricular hypertrophy was independent of test partition selection. In addition, test performance of the voltage-duration products was not significantly affected by the presence or absence of a bundle branch block. Conclusions. These data suggest that the simple product of either Cornell or 12-lead voltage and QRS duration can identify left ventricular hypertrophy more accurately than can voltage or QRS duration criteria alone and may approach or exceed the performance of more complex multiple regression analyses.

The detection and assessment of cardiac chamber hypertrophy has long been an important objective of clinical electrocardiography. Its importance has increased in recent years with the recognition that hypertrophy can be reversed with therapy, and that by doing so, adverse clinical outcomes can be

To assess the effect of heart rate adjustment of the magnitude of the ST integral (ST-HR integral) on exercise test performance, the exercise electrocardiogram (ECG) of 50 clinically normal subjects and 100 patients with known or suspected coronary artery disease was analyzed. At matched specificity of 96% with standard ECG criteria (≥0.1 mV of additional horizontal or downsloping ST segment depression), ar unadjusted ST integral partition of 16 μV-s identified coronary disease in the 100 patients with known or suspected disease with a sensitivity of only 41%, a value significantly lower than the 59% sensitivity of standard ECG criteria (p < 0.01) and the 65% sensitivity of an ST depression partition of 130 μV (p < 0.001).However, test performance of the ST integral was greatly improved by simple heart rate adjustment: at a matched specificity of 96%, an ST-HR integral partition of 0.154 μV-s/beat per min identified coronary disease in the 100 patients with a sensitivity of 90%, a value significantly greater than the 59% sensitivity of standard criteria and 65% sensitivity of ST depression criteria (each p < 0.001) and similar to the 91% sensitivity of the ST-HR index and 93% sensitivity of the ST-HR slope (each p = NS). Comparison of receiver-operating characteristic curves confirmed the superior overall test performance of the ST-HR integral relative to the ST integral and ST segment depression, and demonstrated improved performance that was comparable with that of the ST-HR index and the ST-HR slope.These findings support the value of heart rate adjustment of end-exercise repolarization changes during exercise electrocardiography and demonstrate that this approach significantly improves the performance of the ST integral in identifying coronary artery disease.

BACKGROUND Simple heart rate adjustment of ST segment depression during exercise (delta ST/HR index) and the pattern of ST depression as a function of heart rate during exercise and recovery (the rate-recovery loop) have been shown to improve the ability of the exercise electrocardiogram to detect the presence of coronary heart disease (CHD), but the performance of these methods for the prediction of future coronary events remains to be examined. METHODS AND RESULTS We compared the delta ST/HR index and the rate-recovery loop with standard electrocardiographic criteria for prediction of CHD events in 3,168 asymptomatic men and women in the Framingham Offspring Study who underwent treadmill exercise electrocardiography and who, at entry, were free of clinical and electrocardiographic evidence of CHD. After a mean follow-up of 4.3 years, there were 65 new CHD events: four sudden deaths, 24 new myocardial infarctions, and 37 incident cases of angina pectoris. When a Cox proportional hazards model with adjustment for age and sex was used, a positive exercise electrocardiogram by standard criteria (greater than or equal to 0.1 mV horizontal or downsloping ST segment depression) was not predictive of new CHD events (chi 2 = 0.40, p = 0.52). In contrast, stratification according to the presence or absence of a positive delta ST/HR index (greater than or equal to 1.6 microV/beat/min) and a positive (counterclockwise) rate-recovery loop was associated with CHD event risk (chi 2 = 9.45, p less than 0.01) and separated subjects into three groups with varying risks of coronary events: high risk, when both tests were positive (relative risk 3.6; 95% confidence interval, 2.4-5.4); intermediate risk, when either the delta ST/HR index or the rate-recovery loop was positive (relative risk, 1.9; 95% confidence interval, 1.3-2.8); and low risk, when both tests were negative. After multivariate adjustment for age, sex, smoking, total cholesterol level, fasting glucose level, diastolic blood pressure, and electrocardiographic evidence of left ventricular hypertrophy, the combined delta ST/HR index and rate-recovery loop criteria remained predictive of coronary events (chi 2 = 5.45, p = 0.02). CONCLUSIONS Heart rate adjustment of ST segment depression by the delta ST/HR index and the rate-recovery loop during exercise electrocardiography can improve prediction of future coronary events in asymptomatic men and women.

Compared with standard test criteria, simple heart rate (HR) adjustment of ST depression during exercise electrocardiography can improve the identification and assessment of underlying coronary artery disease. Since heart rate during exercise drives progressive ST segment depression in the presence of coronary obstruction that limits flow reserve, the ST/HR index controls for the increasing metabolic severity of ischemia that accompanies exercise. Improvement of exercise test sensitivity with the ST/HR index results from reclassification of otherwise "equivocal" and even "negative" test responses, including increased identification of one and two-vessel disease in men and in women. In addition, in population studies of low and moderate risk subjects, the ST/HR index can increase the prognostic value of the exercise electrocardiogram for prediction of cardiac risk and mortality.

Although electrocardiographic (ECG) voltage can be used to estimate left ventricular mass, day-to-day variability of voltage combinations used for this purpose must be established before ECG changes are taken as evidence of progression or regression of hypertrophy. Accordingly, serial ECGs (mean 8 days apart), derived from 10 s samples digitized at 250 Hz, were examined in 78 patients with no intercurrent change in clinical status. The coefficient of variation was calculated as 1 SD of the difference between paired voltage measurements, divided by the average mean value. Coefficient of variation for single leads was 22.3% for S v1 27.0% for R v5 or R v6 27.1% for RevL and 34.7% for S v3 . Coefficient of variation was lower for voltage combinations than for individual lead measurements: 18.5% for Sokolow-Lyon voltage (S v1 + R v5 or R v6 ), 22.3% for Gubner-Ungerleider voltage (R 1 + S3) and 24.8% for Cornell voltage (RevL + S v3 ). Serial reclassification due to variation above and below standard criteria for left ventricular hypertrophy occurred in only 3% of patients for Sokolow-Lyon voltage and 4% of patients for Cornell voltage in this group. Minute to minute reproducibility of voltage was assessed with electrodes in place in a separate group of 26 patients, and the coefficient of variation was 2.6% for Sokolow-Lyon voltage, 5.9% for Gubner-Ungerleider voltage and 2.9% for Cornell voltage. These data indicate that serial variability of computer-measured ECG voltage combinations is high, due primarily to changes in lead placement and body position, but less than the variability of computer-measured voltage in individual leads.

The assessment of functional capacity reflects the ability to perform activities of daily living that require sustained aerobic metabolism. The integrated efforts and health of the pulmonary, cardiovascular, and skeletal muscle systems dictate an individual’s functional capacity. Numerous investigations have demonstrated that the assessment of functional capacity provides important diagnostic and prognostic information in a wide variety of clinical and research settings. This scientific statement, an update of the previously published American Heart Association (AHA) document,1 highlights the major clinical and research applications of functional capacity assessment. For a comprehensive review of exercise testing, the reader is referred to the American College of Cardiology (ACC)/AHA Guidelines for Exercise Testing.2,3 Functional capacity is the ability of an individual to perform aerobic work as defined by the maximal oxygen uptake (Vo2max), that is, the product of cardiac output and arteriovenous oxygen (a−Vo2) difference at physical exhaustion, as shown in the following equation: ![Formula][1] Where HR indicates heart rate and SV indicates stroke volume. Because Vo2max typically is achieved by exercise that involves only about half of the total body musculature, it is generally believed that Vo2max is limited by maximal cardiac output rather than peripheral factors.4 Although Vo2max is measured in liters of oxygen per minute, it usually is expressed in milliliters of oxygen per kilogram of body weight per minute to facilitate intersubject comparisons. In addition, functional capacity, particularly when estimated from the work rate achieved rather than directly measured Vo, is frequently expressed in metabolic equivalents (METs), with 1 MET representing the resting energy expenditure (≈3.5 mL O2 · kg−1 · min−1). In this instance, functional capacity is commonly expressed clinically as a multiple of the resting metabolic rate. Vo2max … [1]: /embed/graphic-1.gif

This statement provides a concise list of diagnostic terms for ECG interpretation that can be shared by students, teachers, and readers of electrocardiography. This effort was motivated by the existence of multiple automated diagnostic code sets containing imprecise and overlapping terms. An intended outcome of this statement list is greater uniformity of ECG diagnosis and a resultant improvement in patient care. The lexicon includes primary diagnostic statements, secondary diagnostic statements, modifiers, and statements for the comparison of ECGs. This diagnostic lexicon should be reviewed and updated periodically.

This statement examines the relation of the resting ECG to its technology. Its purpose is to foster understanding of how the modern ECG is derived and displayed and to establish standards that will improve the accuracy and usefulness of the ECG in practice. Derivation of representative waveforms and measurements based on global intervals are described. Special emphasis is placed on digital signal acquisition and computer-based signal processing, which provide automated measurements that lead to computer-generated diagnostic statements. Lead placement, recording methods, and waveform presentation are reviewed. Throughout the statement, recommendations for ECG standards are placed in context of the clinical implications of evolving ECG technology.

In many heart diseases, exercise tolerance testing (ETT) has useful functional correlates and/or prognostic value. However, its predictive value in mitral regurgitation (MR) is undefined. To determine whether ETT descriptors predict death or indications for mitral valve surgery in patients with MR, we prospectively followed, for 7 +/- 3 end-point-free years, a cohort of 38 patients with chronic severe nonischemic MR who underwent modified Bruce ETT; all lacked surgical indications at study entry. Their baseline exercise descriptors were also compared with those from 46 patients with severe MR who, at entry, already had reached surgical indications. End points during follow-up in the cohort included sudden death (n = 1), heart failure symptoms (n = 2), atrial fibrillation (n = 4), left ventricular (LV) ejection fraction60% (n = 2), LV systolic dimensionsor =45 mm (n = 12) and40 mm (n = 11), LV ejection fraction60% plus LV systolic dimensionsor =45 mm (n = 3), and heart failure plus LV systolic dimensionsor =45 mm plus LV ejection fraction60% (n = 1). In univariate analysis, exercise duration (p = 0.004), chronotropic response (p = 0.007), percent predicted peak heart rate (p = 0.01), and heart rate recovery (p0.02) predicted events; in multivariate analysis, only exercise duration was predictive (p0.02). Average annual event risk was fivefold lower (4.62%) with an exercise durationor =15 versus15 minutes (average annual risk 23.48%, p = 0.004). Relative risks in patients with and without exercise-inducible ST-segment depression were comparable (or =1.3, p = NS) whether defined at entry and/or during follow-up. Exercise duration, but not prevalence of exercise-inducible ST-segment depression, was lower (p0.001) in patients with surgical indications at entry versus initially end-point-free patients. In conclusion, in asymptomatic patients with chronic severe nonischemic MR and no objective criteria for operation, progression to surgical indications generally is rapid. However, those with excellent exercise tolerance have a relatively benign course. Exercise-inducible ST-segment depression has no prognostic value in this population.

Important gender differences in cardiac rehabilitation utilization are well established, yet few studies have documented whether reported barriers and referrals vary by ethnicity. This is a cross-sectional study to determine whether barriers and referrals to participation in cardiac rehabilitation differed by race/ethnicity in 304 women (52% ethnic minorities) hospitalized with coronary heart disease. Nearly all subjects (92%) strongly agreed that physician referral was important to participation in rehab, but only 22% of subjects reported physician instruction to attend. Whites were more likely than minorities to report instruction to attend cardiac rehabilitation, and minorities were more likely to report financial barriers when compared with whites. These disparities need to be addressed because minority women have a worse prognosis following hospitalization for coronary heart disease, and cardiac rehabilitation has been shown to improve survival.

excluded. Results: We identified 114 patients (Mean age 59+/-15yrs; 79% male), 39 (34.2%) had isolated aortic cusp prolapse and 73 (64%) had restricted cusp motion as the primary mechanism of AR. Valve repair was performed in 26 (22.8%).Two of these patients had failed repairs requiring valve replacement. Repair was more likely in younger patients, those with leaflet prolapse, tless leaflet edge thickening and less commissural calcification. By multivariate analysis, eccentric AR jet direction and less leaflet edge thickening (