ECG diagnostics in competitive athletes. Current implications for preparticipation screening

In young competitive athletes sudden cardiac death frequently occurs as a tragic first manifestation of clinically inapparent underlying structural or electrical cardiac disorders. An increased risk may be reflected by typical electrocardiogram (ECG) alterations preceding symptoms but a correct interpretation is often challenging due to a high prevalence of training-related ECG alterations in competitive athletes mimicking such disorders. Misinterpretation may thus result in either unnecessary disqualification from competitive sports or continuation despite an increased risk or extensive diagnostic work-ups yielding additional equivocal findings. However, as observed in large athlete cohorts in recent years a variety of ECG alterations, such as isolated increased QRS voltage, early repolarization, sinus bradycardia, first degree AV block or incomplete right bundle branch block, represent common variants of ECGs of athletes reflecting physiological and training-related cardiac adaptations. These alterations do not usually require further diagnostic evaluation. In contrast, alterations such as repolarization abnormalities, complete bundle branch block, prolonged QT intervals or pathological Q waves, are strongly suggestive of underlying disorders and require further evaluation even in asymptomatic athletes. Thus, the ECG plays a pivotal role in the prevention of sudden cardiac death in competitive athletes. The present article summarizes current recommendations for the interpretation of athlete ECGs regarding the differentiation between physiological or pathological cardiac adaptation.     

Pre-participation examination of competitive athletes: role of the ECG

Sudden cardiac death in athletes is rare but has a wide social impact because it confronts the general population with the paradox that athletes perceived and admired as the fittest and healthiest suddenly drop dead during their sport. Mass media coverage is guaranteed in the case of sudden cardiac death of a top athlete, while other competitive and noncompetitive athletes of all ages, team members, sponsors, as well as huge parts of society remain puzzled and frightened. Therefore, debate is ongoing regarding how to minimize the number of fatalities, and the search continues for a cost-effective preparticipation screening for competitive athletes. Despite the fact that routine ECG screening would be widely available and rather inexpensive, debate continues regarding whether this should be part of initial screening for every athlete before starting to train at high intensity as well as during annual checkups. The role of ECGs in preparticipation examinations of competitive athletes is intensively discussed because there is a lack of strict criteria for which ECG findings should generate further workup. In this article, we analyze the main publications on sudden cardiac death, focusing on the benefit of ECG screening in preparticipation examination as it has been shown to be feasible and effective in identifying athletes at risk of sudden cardiac death.     

Electrocardiogram interpretation in the athlete

The sudden death of a young athlete is a devastating event that impacts the lay public and medical community and has attracted efforts to screen for underlying cardiovascular diseases associated with sudden death in this population. Electrocardiography (ECG) screening has been shown to increase the sensitivity of finding structural heart diseases in competitive athletes. Recent research in diverse populations of athletes has led to refinements in ECG-interpretation standards designed to improve its diagnostic accuracy. This review summarizes relevant information regarding cardiovascular screening and ECG interpretation in athletes.     

Brugada or not-Brugada: misdiagnosis of recorder-induced artifact

The Brugada-Brugada syndrome is a life threatening cardiac arrhythmia that features syncopal events or aborted sudden death in combination with electrocardiographic characteristics (ST-segment elevation of V(1)-V(3) and right bundle branch block). Typical ECG alterations were recorded in a young man who was admitted to our hospital after syncope and a Brugada-Brugada syndrome was suspected. The following days similar pathological ECG recordings of other patients were noticed. The electrocardiographic artifact was diagnosed as being caused by incorrect handling of the ECG recorder.     

Black athlete electrocardiographic repolarization pattern

There is debate over the use of the electrocardiogram (ECG) to screen athletes for disorders associated with sudden cardiac death, but if screening is completed, accurate ECG interpretation is important. Recently, there has been recognition of a normal black athlete repolarization pattern which includes J-point elevation, convex ST-segment elevation, and T-wave inversions in leads V1 to V4 occurring in 5–15% of black athletes. This pattern must be differentiated from T-wave inversions that are associated with hypertrophic cardiomyopathy or arrhythmogenic right ventricular cardiomyopathy. The combination of J-point elevation >1?mm and T-wave inversions confined to leads V1–V4 excludes cardiomyopathy. If T-wave inversions are present in the inferior or lateral leads or there is no J-point elevation, further evaluation for a cardiomyopathy is required. By recognizing this ECG pattern as a normal variant, unnecessary ancillary testing and restriction from sports can be avoided.     

Clinical significance of abnormal electrocardiographic patterns in trained athletes

BACKGROUND-The prevalence, clinical significance, and determinants of abnormal ECG patterns in trained athletes remain largely unresolved. METHODS AND RESULTS-We compared ECG patterns with cardiac morphology (as assessed by echocardiography) in 1005 consecutive athletes (aged 24+/-6 years; 75% male) who were participating in 38 sporting disciplines. ECG patterns were distinctly abnormal in 145 athletes (14%), mildly abnormal in 257 (26%), and normal or with minor alterations in 603 (60%). Structural cardiovascular abnormalities were identified in only 53 athletes (5%). Larger cardiac dimensions were associated with abnormal ECG patterns: left ventricular end-diastolic cavity dimensions were 56. 0+/-5.6, 55.4+/-5.7, and 53.7+/-5.7 mm (P<0.001) and maximum wall thicknesses were 10.1+/-1.4, 9.8+/-1.3, and 9.3+/-1.4 mm (P<0.001) in distinctly abnormal, mildly abnormal, and normal ECGs, respectively. Abnormal ECGs were also most associated with male sex, younger age (<20 years), and endurance sports (cycling, rowing/canoeing, and cross-country skiing). A subset of athletes (5% of the 1005) showed particularly abnormal or bizarre ECG patterns, but no evidence of structural cardiovascular abnormalities or an increase in cardiac dimensions. CONCLUSIONS-Most athletes (60%) in this large cohort had ECGs that were completely normal or showed only minor alterations. A variety of abnormal ECG patterns occurred in 40%; this was usually indicative of physiological cardiac remodeling. A small but important subgroup of athletes without cardiac morphological changes showed striking ECG abnormalities that suggested cardiovascular disease; however, these changes were likely an innocent consequence of long-term, intense athletic training and, therefore, another component of athlete heart syndrome. Such false-positive ECGs represent a potential limitation to routine ECG testing as part of preparticipation screening.     

Risk of competitive sport in young athletes with heart disease

The majority of sudden deaths in young athletes occur in the context of underlying inherited or genetic cardiac disorders. The evaluation of every athlete regarding underlying cardiac disease is impractical and therefore needs to be targeted at those who are at a higher risk. A practical approach would be to channel efforts towards athletes with cardiac symptoms, those with a family history of inherited cardiac disease, and those with a family history of premature sudden death. There are potential pitfalls in the evaluation of young athletes using non-invasive tests when making the distinction between physiological adaptations to exercise and cardiac pathology. Physicians evaluating young athletes need to be aware of the spectrum of physiological adaptations and to be familiar with conditions responsible for sudden death in this population.     

Prevalence of abnormal electrocardiograms in a large, unselected population undergoing pre-participation cardiovascular screening.

AIMS: The implementation of 12-lead ECG in the pre-participation screening of young athletes is still controversial and number of issues are largely debated, including the prevalence and spectrum of ECG abnormalities found in individuals undergoing pre-participation screening. METHODS AND RESULTS: We assessed a large, unselected population of 32,652 subjects [26 050 (80%) males], prospectively examined in 19 clinics associated to Italian Sports Medicine Federation. Most were young amateur athletes, aged 8-78 years (median 17), predominantly students (68%), engaged predominantly in soccer (39%), volleyball or basketball (8% each), athletics (6%), cycling (5%), swimming (4%). The ECG patterns were evaluated according to commonly used clinical criteria. The 12-lead ECG patterns were considered normal in 28 799 of the 32 652 athletes (88.2%) and abnormal in 3853 (11.8%). The most frequent abnormalities included prolonged PR interval, incomplete right bundle branch block (RBBB) and early repolarization pattern (total 2280, 7.0%). Distinct ECG abnormalities included deeply inverted T-waves in > 2 precordial and/or standard leads (751, 2.3%), increased R/S wave voltages suggestive of LV hypertrophy (247, 0.8%), conduction disorders, i.e. RBBB (351, 1.0%), left anterior fascicular block (162, 0.5%), and left bundle branch block (19, 0.1%). Rarely, cardiac pre-excitation pattern (42, 0.1%) and prolonged QTc interval (1, 0.03%) were found. CONCLUSION: In a large, unselected population of young athletes undergoing pre-participation screening, the prevalence of markedly abnormal ECG patterns, suggestive for structural cardiac disease, is low (<5% of the overall population) and should not represent obstacle for implementation of 12-lead ECG in the pre-participation screening program.     

Electrocardiogram of the failing heart

In the failing heart general specific (e.g., Q-waves after acute myocardial infarction, persistentST-elevations in post-myocardial infarction left ventricular aneurysm) and unspecific ECG changes (e.g.,left bundle branch block, right bundle branch block, ST-T-alterations due to digitalis glycosides or antiarrhythmicdrugs) may be seen in the conventional 12-lead ECG. In addition, atrial and ventricular tachy-arrhythmias maybe detected and quantified by 24-hour-Holter ECG recordings, that may be relevant for a worse prognosis of patientswith congestive heart failure. Heart rate variability as the most relevant derived ECG parameter of sympathetictone fluctuations may be of important prognostic significance in congestive heart failure patients. An abnormalsignal averaged P-wave duration may predict the incidence of atrial fibrillation, as may apply to QRS-prolongationand/or ventricular late potentials in the signal averaged ECG for the incidence of serious life-threateningventricular tachy-arrhythmias or death from pump failure. Last but not least, cardiac repolarization abnormalitiesmay be detected by QT dispersion-, QT-/QTc-fluctuation- or T-wave alternans studies, but the true prognosticsignificance of these parameters for predicting sudden cardiac death or death from pump failure in patients withcongestive heart failure remains unclear.     

Familial cardiomyopathy underlies syndrome of right bundle branch block,ST segment elevation and sudden death

Objectives. We sought to assess whether structural heart disease underlies the syndrome of right bundle branch block, persistent ST segment elevation and sudden death.Background. Ventricular fibrillation and sudden death may occur in patients with a distinctive electrocardiographic (ECG) pattern of right bundle branch block and persistent ST segment elevation in the right precordial leads.Methods. Sixteen members of a family affected by this syndrome underwent noninvasive cardiac evaluation, including electrocardiography, Holter ambulatory ECG monitoring, stress testing, echocardiography and signal-averaged electrocardiography; two patients had electrophysiologic and angiographic study. Endomyocardial biopsy was performed in one living patient, and postmortem examination, including study of the specialized conduction system, was performed in one victim of sudden death.Results. Five years before a fatal cardiac arrest, the proband had been resuscitated from sudden cardiac arrest due to recorded ventricular fibrillation. Serial ECGs showed a prolonged PR interval, right bundle branch block, left-axis deviation and persistent ST segment elevation in the right precordial leads, in the absence of clinical heart disease. Postmortem investigation disclosed right ventricular dilation and myocardial atrophy with adipose replacement of the right ventricular free wall as well as sclerotic interruption of the right bundle branch. A variable degree of right bundle branch block and upsloping right precordial ST segment was observed in seven family members; four of the seven had structural right ventricular abnormalities on echocardiography and late potentials on signal-averaged electrocardiography. A sib of the proband also had a prolonged HV interval, inducible ventricular tachycardia and fibrofatty replacement on endomyocardial biopsy.Conclusions. An autosomal dominant familial cardiomyopathy, mainly involving the right ventricle and the conduction system, accounted for the ECG changes and the electrical instability of the syndrome.     

Athlete’s heart electrocardiogram mimicking hypertrophic cardiomyopathy

Highly trained athletes show a variety of electrocardiographic (ECG) changes, including a striking increase of R or S wave voltage, either flat or deeply inverted T waves, and deep Q waves, that suggest the presence of structural cardiovascular disease, such as hypertrophic cardiomyopathy or arrhythmogenic right ventricular cardiomyopathy, which represent the most common causes of sudden death in young competitive athletes. Despite a number of previous observational surveys, the determinants and clinical significance of these abnormal ECG patterns in trained athletes are still uncertain. Therefore, ECG patterns were compared with cardiac morphology (by echocardiography) in a large population of 1005 athletes, who were engaged in a variety of 38 sporting disciplines. We found abnormal ECGs in 40% of our athletes, but structural cardiac diseases were identified in only 5%. In the absence of cardiac disease, other determinants were recognized as responsible for abnormal ECG patterns, including the extent of morphologic cardiac remodeling, participation in an endurance type of sport, and male gender. Finally, a small but important subset of athletes showed striking ECG abnormalities that strongly suggested the presence of cardiovascular disease in the absence of pathologic cardiac conditions or morphologic changes, suggesting that these ECG alterations may be the consequence of athletic conditioning itself.     

The athlete's heart: remodeling, electrocardiogram and preparticipation screening

Highly trained athletes show morphologic cardiac changes (ie, athlete's heart) that are the consequence of several determinants, including type of sport, gender, and, possibly, inherited genetic factors. The extent of physiologic cardiac remodeling may occasionally be substantial in highly trained athletes and may raise a differential diagnosis with structural cardiac disease, such as cardiomyopathies. In addition, athletes demonstrate a spectrum of alterations in the 12-lead electrocardiogram (ECG) pattern, including marked increase in precordial R-wave or S-wave voltages, ST segment or T-wave changes, and deep Q waves suggestive of left ventricular hypertrophy, that may raise the possibility of pathologic heart condition, but have also been viewed as a consequence of the cardiac morphologic remodeling induced by athletic conditioning. To evaluate the clinical significance of these abnormal ECGs, the authors compared ECG patterns to cardiac morphology and function (assessed by two-dimensional echocardiography in individual athlete) in a large population of 1005 elite athletes engaged in a variety of sporting disciplines. Forty percent of the athletes had abnormal ECGs, and a subgroup of about 15% showed distinctly abnormal and often bizarre patterns highly suggestive of cardiomyopathies, such as hypertrophic cardiomyopathy, in the absence of pathologic cardiac changes. Such alterations are likely the consequence of athletic conditioning itself and represent another potential component of athlete's heart syndrome. However, such false-positive ECGs represent a potential limitation to the efficacy of routine ECG testing in the preparticipation cardiovascular screening of large athletic populations.     

Electrocardiographic Markers of Late Sudden Death Risk in Postoperative Tetralogy of Fallot Children

Late Sudden Death Risk in Postoperative TOF. Following surgery for tetralogy of Fallot (TOP), children may develop late onset ventricular arrhythmias. Many patients have both depolarization and repolarization abnormalities, including right bundle branch block (RBBB) and QT prolongation. The goal of this study was to improve prospective risk-assessment screening for late onset sudden death. Resting ECG markers including QRS duration, QTc, JTc, and interlead QT and JT dispersion were statistically analyzed to identify those patients at risk for ventricular arrhythmias and sudden cardiac death. To determine predictive markers for future development of arrhythmia, we examined 101 resting ECGs in patients (age 12 ± 6 years) with postoperative TOF and RBBB, 14 of whom developed late ventricular tachycardia (VT) or sudden death. These ECGs were also compared with an additional control group of 1000 age- and gender-matched normal ECGs. The mean QRS (± SD) in the VT group was 0.18 ± 0.02 seconds versus 0.14 ± 0.02 seconds in the non-VT group (P < 0.01). QTc and JTc in the VT group was 0.53 ± 0.05 seconds and 0.33 ± 0.03 seconds compared with 0.50 ± 0.03 seconds and 0.32 ± 0.03 seconds in the non-VT group (P = NS). There was no increase in QT dispersion among TOF patients with VT or sudden death compared with control patients or TOF patients without VT, although JT dispersion was more common in the TOF groups. A prolonged QRS duration in postoperative TOF with RBBB is more predictive than QTc, JTc, or dispersion indexes for identifying vulnerability to ventricular arrhythmias in this population, while retaining high specificity. The combination of both QRS prolongation and increased JT dispersion had very good positive and negative predictive values. These results suggest that arrhythmogenesis in children following TOF surgery might involve depolarization in addition to repolarization abnormalities. Prospective identification of high-risk children may be accomplished using these ECG criteria.     

Athlete Screening for Cardiomyopathies: Recent Insights and Latest Guidelines

The benefits of regular moderate exercise to improve health are undisputed. However, in individuals harboring underlying cardiac disorders, there is an increased risk of adverse cardiac events during exertion, including sudden cardiac death (SCD). Subclinical cardiomyopathies are amongst the most common causes of SCD in young athletes and, importantly, SCD may be the initial presentation of a cardiomyopathy. While these tragic events are rare, the emotional effect on the athlete’s family and the community at large is profound and devastating. Therefore, pre-participation screening programs to detect silent cardiac disorders are in place in many countries. However, the optimal structure of such programs, particularly whether or not a 12-lead ECG should be included as an initial screening test, is an area of controversy. This review discusses the most recent insights and latest guidelines regarding pre-participation screening to detect cardiomyopathies in athletes.     

Sudden cardiac death and preparticipation screening: the debate continues-in support of electrocardiogram-inclusive preparticipation screening

Sudden cardiac death (SCD) is the leading cause of death in young athletes during exercise, and there is international agreement among major medical and sporting bodies that young athletes should undergo preparticipation cardiovascular screening. However, there is currently no universally accepted screening protocol, and substantial debate exists about what constitutes the ideal approach to preparticipation screening. The primary objective of preparticipation screening is the detection of intrinsic structural or electrical cardiovascular disorders that predispose an athlete to SCD. Considerable evidence exists suggesting that screening athletes with only a history and physical examination leaves most athletes with a serious underlying cardiovascular disease undetected and, thus, cannot adequately achieve the primary objective of screening. Preparticipating cardiovascular screening inclusive of an electrocardiogram (ECG) greatly enhances the ability to identify athletes at risk and is the only model shown to be cost-effective and may reduce the rate of SCD. The major obstacle to ECG screening in the United States is the lack of a physician workforce skilled in interpretation of an athlete's ECG. However, recent studies have demonstrated a capacity to distinguish physiologic ECG alterations in athletes from findings suggestive of underlying pathology that is both feasible and has a low false-positive rate. Efforts are underway to increase physician education in ECG interpretation. After 2 decades debating the proper screening strategy to identify athletes at risk, the weight of scientific evidence suggests that a screening program inclusive of ECG is the only strategy that merits promotion.     

Sudden death in young competitive athletes: clinicopathologic correlations in 22 cases

PURPOSE: To investigate the pathologic substrates of sudden death in young competitive athletes. PATIENTS AND METHODS: Twenty-two cases of sudden death in young competitive athletes occurring in the Veneto region (northern Italy) in the period January 1979 to December 1989 were studied by postmortem examination. The athletes included 19 males and three females, ranging in age from 11 to 35 years (mean, 23 years). RESULTS: In 18 cases, sudden death occurred during (16 cases) or immediately after (two cases) a competitive sport activity. In 10 subjects, sudden death was apparently the first sign of disease. Postmortem examination disclosed that this fatality was due to arrhythmic cardiac arrest in 17 cases; among these, right ventricular cardiomyopathy, also known as "right ventricular dysplasia," was the most frequently encountered cardiovascular disease (six cases), followed by atherosclerotic coronary artery disease (four cases), conduction system pathology (three cases), anomalous origin of right coronary artery from the wrong aortic sinus (two cases), and mitral valve prolapse (two cases). In two athletes, the abrupt lethal complication was "mechanical" and consisted of pulmonary embolism and rupture of the aorta; in three athletes, death was due to a cerebral cause. All athletes with right ventricular cardiomyopathy died during effort, and most had a history of palpitations and/or syncope. Whenever available, electrocardiographic (ECG) tracings showed inverted T waves in precordial leads and/or left bundle branch block ventricular arrhythmias. CONCLUSIONS: Clinicopathologic correlations indicate that in the Veneto region of Italy, right ventricular cardiomyopathy is not so rare among the cardiovascular diseases associated with the risk of arrhythmic cardiac arrest, and seems to account for the majority of cases of sudden death in young athletes; this disorder can be suspected during life on the basis of prodromal symptoms and ECG signs.     

ECG Features that suggest a potentially life-threatening arrhythmia as the cause for syncope

Syncope is a risk factor for sudden cardiac death (SCD) in many conditions associated with structural heart disease as well as inherited heart disease. The ECG in patients with syncope should be examined carefully for signs of structural heart disease, such as myocardial infarction or cardiomyopathy; signs of conduction system disease, such as bundle branch block or atrioventricular block; and signs of primary electrical disease. Important forms of cardiomyopathy accompanied by ECG changes include hypertrophic cardiomyopathy (HCM), and arrhythmogenic right ventricular dysplasia (ARVD/C). Common ECG findings in HCM include left ventricular hypertrophy by voltage, repolarization abnormalities, QRS widening, pseudoinfarction patterns, and slurred QRS upstroke mimicking delta waves. Classical ECG findings of ARVD/C include T-wave inversions and epsilon waves in the right precordial leads (V₁–V₃). Important forms of primary electrical disease which may result in syncope include Wolff–Parkinson–White syndrome, long QT syndrome, and Brugada syndrome, which is characterized by coved ST-segments in the right precordial leads, associated with a history of syncope, ventricular arrhythmia, or sudden cardiac death in probands or family member. There are three Brugada ECG patterns; however, only type I (spontaneous or induced) is considered diagnostic. Recently, studies have suggested that patients with J-point elevation or early repolarization pattern on ECG are at elevated risk of SCD. The clinical significance of finding early repolarization in a patient with syncope is unknown and should be a subject of future research.     

Resting and ambulatory ECG predictors of mode of death in dilated cardiomyopathy.

With the purpose of verifying whether the electrocardiogram (ECG) pattern alone can predict the mode of death in dilated cardiomyopathy, data from 12-lead ECGs and 48-hour arrhythmia monitoring were evaluated in 67 patients with dilated cardiomyopathy. During a mean follow-up period of 3 +/- 2 years, death from congestive heart failure occurred in 18 patients (27%), whereas 10 (15%) died suddenly (NS). Multivariate analysis showed that left bundle branch block (p < 0.001) and left atrial enlargement (p < 0.001) were independently related to death from congestive heart failure. Ventricular arrhythmias of Lown grade 4A or 4B (p < 0.001) and repolarization time, as assessed by QTc-QRS interval (p < 0.05), were independent predictors of sudden death. It is concluded that ECG features alone may be helpful for risk factor characterization of dilated cardiomyopathy patients, provided that multiple ECG criteria are utilized at time of diagnosis.     

Use of transesophageal stimulation of the left atrium in the diagnosis of ischemia and cicatricial myocardial changes in patients with complete block of the left fascicle of the bundle of His

Transesophageal stimulation of the left atrium was performed in 52 patients who had signs of complete left bundle branch block as evidenced by ECG, 48 patients having sustained block, 4, intermittent one. In 42 (80.8%) patients, the block was temporarily arrested during and/or after discontinuation of the electric stimulation, in 28 of them, the block was stopped during the stimulation without any drugs, in 1, only after obsidan, and in 13, following obsidan and atropine. When the block was being arrested, 13 patients showed ECG ischemic changes, 7 exhibited myocardial scarring alterations, 8 had nonspecific T wave alterations, 8 displayed signs of left ventricular hypertrophy with impaired repolarization. No ECG changes were found in 7 patients. The use of transesophageal electrical stimulation of the left atrium to temporarily abolish complete left bundle branch block may contribute to elucidation of the etiology of the block and choice of the most adequate therapy.     

Changes and predictive value of dispersion of repolarization parameters for appropriate therapy in patients with biventricular implantable cardioverter-defibrillators.

BACKGROUND: The impact of cardiac resynchronization therapy (CRT) on dispersion of repolarization is controversial. The benefit of CRT on sudden cardiac death has been demonstrated only after 3 years follow-up. OBJECTIVE: The purpose of this study was to explore the immediate effect of CRT on dispersion of repolarization and to define the value of dispersion of repolarization parameters as predictors of appropriate implantable cardioverter-defibrillator (ICD) therapy. METHODS: Data from 100 patients who underwent CRT-ICD placement were analyzed retrospectively. Patients had symptoms of New York Heart Association functional class III or IV heart failure, left ventricular ejection fraction < or =35%, and QRS duration >130 ms or QRS < or =130 ms with left intraventricular dyssynchrony. ECG indices of dispersion of repolarization before and immediately after CRT implantation (QT dispersion, Tpeak-Tend [Tp-e], and Tp-e dispersion) were measured. RESULTS: In patients who were upgraded to a biventricular system, Tp-e did not increase significantly after CRT. However, Tp-e increased significantly after CRT in patients with left bundle branch block or narrow QRS at baseline. After 12-month follow-up, 22 patients had received appropriate ICD therapy. ICD therapy and no ICD therapy groups had similar baseline characteristics, such as secondary prevention and ischemic cardiomyopathy. Postimplantation Tp-e was the only independent predictor of future ICD therapy (P = .02). CONCLUSION: Immediately after CRT, Tp-e did not increase in patients who received a biventricular upgrade; however, Tp-e did increase in patients with preimplantation left bundle branch block or narrow QRS. Postimplantation Tp-e was the only independent predictor of appropriate ICD therapy.