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This 40-year-old man was diagnosed with arrhythmogenic right ventricular cardiomyopathy (ARVC) 6 years prior when he presented to a different institution with ventricular tachycardia (VT), which was confirmed by an electrophysiology study. The electrophysiology study report stated that several VT origins were observed. He was advised against vigorous exercise. He visited our clinic for evaluation of recurrent episodes of palpitations despite β-blocker treatment. The baseline ECG was normal, which cast doubt on the previous diagnosis, because in a majority of patients with symptomatic ARVC ECG abnormalities are observed, the most frequent of which is the presence of negative T waves in the anterior precordial leads (V1 to V4). Cardiovascular magnetic resonance imaging was performed, which showed no abnormalities, and a new electrophysiology study was then performed. During the electrophysiology study, the ECG (Figure 1) was recorded. Figure 1. During stable wide QRS complex tachycardia, the QRS progressively narrows until it becomes a regular narrow QRS tachycardia and subsequently broadens again, showing the same morphology at the end of the tracing as at the onset. The wide QRS complex tachycardia shows the following features that suggest ventricular tachycardia: (1) QRS …

A 37-year-old woman with non-Hodgkin lymphoma undergoing chemotherapy and no other significant medical history was incidentally noted to have an irregular heart rhythm on physical examination, and a 12-lead ECG was obtained. ECG (Figure 1) showed sinus rhythm with alternating pattern of right bundle-branch block (RBBB) and left bundle-branch block (LBBB). What is the mechanism of the alternating bundle-branch block pattern noted on the ECG? Figure 1. Twelve-lead ECG showing sinus rhythm with alternating right and left bundle-branch block pattern of ventricular conduction. 1. Alternating RBBB and LBBB premature ventricular contractions 2. Alternating phase 3 block in the bundle branches 3. Alternating phase 4 block in the bundle branches 4. Interpolated premature ventricular contractions with alternating bundle-branch morphologies Please turn the page to read the diagnosis. Irregular heart rhythm in this patient is the result of frequent atrial ectopic beats occurring in a bigeminal fashion. P waves are seen within the preceding T waves during ectopy, and the atrial coupling interval is constant (440 ms), which confirms that these are premature atrial …

Background— Pathological T-wave inversion (PTWI) is rarely observed on the ECG of healthy athletes, whereas it is common in patients with certain cardiac diseases. All ECG interpretation guidelines for use within athletes state that PTWI (except in leads aVR, III and V1 and in V1–V4 when preceded by domed ST segment in asymptomatic Afro-Caribbean athletes only) cannot be considered a physiological adaptation. The aims of the present study were to prospectively determine the prevalence of cardiac pathology in athletes presenting with PTWI, and to examine the efficacy of cardiac magnetic resonance in the work-up battery of further examinations. Methods and Results— Athletes presenting with PTWI (n=155) were investigated with clinical examination, ECG, echocardiography, exercise testing, 24h Holter ECG, and cardiac magnetic resonance. Cardiac disease was established in 44.5% of athletes, with hypertrophic cardiomyopathy (81%) the most common pathology. Echocardiography was abnormal in 53.6% of positive cases, and cardiac magnetic resonance identified a further 24 athletes with disease. Five athletes (7.2%) considered normal on initial presentation subsequently expressed pathology during follow-up. Familial history of sudden cardiac death and ST-segment depression associated with PTWI were predictive of cardiac disease. Conclusions— PTWI should be considered pathological in all cases until proven otherwise, because it was associated with cardiac pathology in 45% of athletes. Despite echocardiography identifying pathology in half of these cases, cardiac magnetic resonance must be considered routine in athletes presenting with PTWI with normal echocardiography. Although exclusion from competitive sport is not warranted in the presence of normal secondary examinations, annual follow-up is essential to ascertain possible disease expression.

A 56-year-old man presented to cardiology clinic with daily episodes of chest heaviness and discomfort. He underwent an echocardiogram, which showed no evidence of structural heart disease. An exercise nuclear stress test showed average functional capacity and normal perfusion. Because of his daily symptoms, the patient wore a 24-hour Holter monitor (Figure 1A), which showed multiple episodes of T-wave inversions (Figure 1B), inconsistently associated with his symptoms of chest tightness. Because of these symptoms, he underwent coronary angiography, which showed minimal coronary artery disease. What is the mechanism of the T-wave inversions seen on Holter? Figure 1. Twenty-four hour Holter monitor obtained due to intermittent chest pain . A and B , A 24-hour Holter monitor was obtained to evaluate daily chest pain. Multiple instances of intermittent T-wave inversions were inconsistently associated with chest pain. Please turn the page to read the diagnosis. The patient had a known diagnosis of Wolf-Parkinson-White syndrome, and his baseline …

The quest to facilitate the diagnosis of the long-QT syndrome (LQTS) and even to predict genotype is neverending. The study by Sy et al1 published in the current issue of Circulation adds a new piece to the puzzle and has the potential to be very useful. Article see p 2187 Since the early days,2 diagnosis of the long-QT syndrome (LQTS) has undergone several levels of progressive upgrade. Initially, the diagnosis was made only in the presence of multiple factors, such as very bizarre T waves and marked prolongations of the QT interval in a child or teenager or abrupt loss of consciousness during emotional or physical stress, and it also required one of the few medical doctors who had heard about LQTS. The first attempt to provide diagnostic criteria for LQTS came in 19853 and, in their simplicity, they are still useful now for a first assessment (Table 1). As the disease became better known, as was bound to happen given its prevalence (1 in 2 000),4,5 a new set of more specific diagnostic criteria to discriminate between subjects likely or unlikely to be affected by LQTS was proposed and provided a quantitative score.6 View this table: Table 1. 1985 LQTS Diagnostic Criteria Those criteria, subsequently referred to as the “Schwartz criteria,” were developed before the genetic revolution, which has progressively led to the identification of 13 LQTS disease-causing genes.7 As a consequence, a lot of weight was placed on the actual duration of the QT interval. By the early 1990s, it had been recognized8 that the highest risk was for patients who had already suffered 1 cardiac event. It was thus essential not to miss the diagnosis in these patients; hence, weight was given to previous symptoms. Also, it was obvious that the disease had …

A 74-year-old woman underwent an abdominal computed tomography scan for work-up of unclear recurring abdominal discomfort because abdominal ultrasound had not been diagnostic on account of a poor acoustic window and obesity (body mass index 31). Computed tomography did not detect any abdominal pathology but revealed an unclear mass located at a left anterior position on the cranial side of the diaphragm, most likely related to the apical portions of the heart (Figure 1). Thus, the patient was referred to our hospital for further cardiological work-up. Figure 1. Abdominal computed tomography scan with oral contrast agent. The unclear mass, located at a left anterior position on the cranial side of the diaphragm and related to the apical portions of the heart, is indicated by the arrowhead. Panels I to IV appear in cranio-caudal order. Interestingly, the patient had been hospitalized twice at intervals of 4 months because of 2 episodes of severe chest pain 28 years previously, but no diagnosis could be made at that time. Routine ECG on admission revealed an abnormal electrical axis as well as high R-wave amplitudes in V2 and V3 (Figure 2). Consequently, additional right ventricular leads were obtained, demonstrating discrete ST-segment elevations (rV1 to rV4) and negative T waves (rV2 to rV6) (Figure 3), indicating possible right ventricular pathology. Because transthoracic echocardiography could …

We read with interest the recent article by Schnell et al1 regarding abnormal T waves in athletes. This was a multicenter collaboration drawing from 6372 competitive athletes who underwent cardiovascular preparticipation screening including ECG. They studied 155 athletes (2.4%) with pathological T-wave inversion (PTWI; ≥2 mm in ≥2 leads) on resting 12-lead ECG, most of whom had additional ECG abnormalities (ST depression 31%, Q waves 11%, left atrial abnormality 29%). Extensive investigations diagnosed cardiac disease in 45% (n=69) of athletes presenting with PTWI. Hypertrophic cardiomyopathy (HCM; 36%; n=56) was the most commonly identified pathology. Half of the HCM diagnoses were attributable to findings on cardiac magnetic resonance imaging, including 14 with …

Background— In large mammals and humans, the contribution of I Ks to ventricular repolarization is still incompletely understood. Methods and Results— In vivo and cellular electrophysiological experiments were conducted to study I Ks in canine ventricular repolarization. In conscious dogs, administration of the selective I Ks blocker HMR 1556 (3, 10, or 30 mg/kg PO) caused substantial dose-dependent QT prolongations with broad-based T waves. In isolated ventricular myocytes under baseline conditions, however, I Ks block (chromanols HMR 1556 and 293B) did not significantly prolong action potential duration (APD) at fast or slow steady-state pacing rates. This was because of the limited activation of I Ks in the voltage and time domains of the AP, although at seconds-long depolarizations, the current was substantial. Isoproterenol increased and accelerated I Ks activation to promote APD 95 shortening. This shortening was importantly reversed by HMR 1556 and 293B. Quantitatively similar effects were obtained in ventricular-tissue preparations. Finally, when cellular repolarization was impaired by I Kr block, I Ks block exaggerated repolarization instability with further prolongation of APD. Conclusions— Ventricular repolarization in conscious dogs is importantly dependent on I Ks . I Ks function becomes prominent during β-adrenergic receptor stimulation, when it promotes AP shortening by increased activation, and during I Kr block, when it limits repolarization instability by time-dependent activation. Unstimulated I Ks does not contribute to cellular APD at baseline. These data highlight the importance of the synergism between an intact basal I Ks and the sympathetic nervous system in vivo.

Background— The goals of this study were to compare ECG at moderate exercise in normoxia and hypoxia at the same heart rate, to provide evidence of independent predictors of hypoxia-induced ECG changes, and to evaluate ECG risk factors of severe high-altitude illness. Methods and Results— A total of 456 subjects performed a 20-minute hypoxia exercise test with continuous recording of ECG and physiological measurements before a sojourn above 4000 m. Hypoxia did not induce any conduction disorder, arrhythmias, or change in QRS axis. The amplitude of the P wave in V 1 was lower in hypoxia than in normoxia. The amplitudes of the R, S, and T waves and the Sokolow index decreased in hypoxia. Under hypoxia, the amplitude of the ST segment decreased in II and V 6 and increased in V 1 , the ST slope rose in V 5 and V 6 , and the J point was lower in II, V 5 , and V 6 . Multivariate regression of hypoxic/normoxic ratios of electrophysiological parameters and clinical characteristics showed a correlation between the decrease in Sokolow index and T-wave amplitude in V 5 with desaturation at exercise. Trained status and low body mass index were associated with a smaller decrease in T-wave amplitude in V 5 and V 6 . Comparison of ECG between subjects suffering or not suffering from severe high-altitude illness failed to show any difference. Conclusions— During a hypoxia exercise test, a dose-dependent hypoxia-induced decrease in the amplitude of the P/QRS/T waves was observed. No standard ECG characteristic predicted the risk of developing severe high-altitude illness. Further studies are required to clarify the cause of these electric changes and their potential predictive role in cardiac events.

Jiang and Qiao question whether the etiology of our patient’s chest pressure1 was elevated pulmonary venous pressures attributable to preexcitation. This is particularly salient because the patient’s symptoms resolved after catheter ablation. Changes in both hemodynamics and the …

We read with great interest the wonderful case presented by Verma and Knight1 about cardiac memory after radiofrequency ablation on a patient with Wolf-Parkinson-White syndrome with chest heaviness. However, the patient’s chest tightness with daily episodes remained unexplained, and …

Introduction: Although the vast majority of mitral valve prolapse (MVP) is benign, women with bileaflet MVP (biMVP), complex ventricular ectopy (VE), and abnormal T waves may comprise the recently described malignant biMVP syndrome. The mechanism of ventricular arrhythmia is unknown. To further characterize the arrhythmic substrate, we reviewed our center’s ablation experience in 6 biMVP patients with prior cardiac arrest and recurrent ICD shocks for drug refractory ventricular fibrillation (VF). Methods and Results: Six women with biMVP (median age 31.5 [range 24.2 - 58.7] years, EF 65 [45 - 67]%, all ≤moderate mitral regurgitation) experienced 6 (3 - 25) appropriate ICD shocks over 4.8 (2.8 - 10.7) years and underwent index ablation between 2/2007 - 10/2013. All had multiple VE morphologies (median 7 [3 - 24]) with variable coupling intervals but with a predominant VE trigger for the VF. A median 2 (1 - 4) VE foci were ablated. Sites of successful ablation of VF-triggering and other dominant VE were left ventricular papillary muscles [PM] (1 anterior, 1 posterior, 1 both), fascicles (1 anterior, 1 posterior), or both (1 both PM and posterior fascicle). Outflow tract VE was also present and targeted (1 left, 1 right)i. Two underwent repeat ablation (288 and 312 days) for recurrent complex VE without shocks, with different foci to the index ablation (1 posterior fascicle, 1 both fascicles). The VF-triggering VE in all patients was confirmed as originating from within the left fascicular system, which in 3/6 was at a papillary muscle. Acute procedural success was seen in all with no complications to date. A VF storm occurred within 24 hours of ablation in a single patient. At follow-up of a mean 662 (47 - 2099) days, 1 patient received a single shock (p=0.03 vs. preablation). Symptomatic VE was reduced in all; while 3/6 continue Class 1c antiarrhythmics and 5/6 have beta blockade. Conclusion: Malignant biMVP syndrome is characterized by fascicular and papillary muscle PVCs that trigger ventricular fibrillation, yet in all patients, the VE is multifocal. Ablation of at least one focus appears to improve symptoms and reduce shocks.

A 33-year-old man was admitted to our hospital for shortness of breath on exertion. His symptoms started suddenly a week before admission when he was driving a car and worsened daily. He was amateur football player and had no history of hypertension, dyslipidemia, diabetes mellitus, smoking, or leg injury. On admission, an arterial pulse oxygen saturation monitor showed that his arterial blood oxygen saturation was 94% with room air. His blood pressure was 114/82 mm Hg and his pulse rate was 92/min with regular rhythm. His height was 162 cm and body weight was 62 kg. No other outstanding physical abnormalities were observed. Laboratory data showed slightly an elevated C-reactive protein level of 0.87 mg/dL with a normal white blood cell count of 6100 cells/mL. Arterial blood sampling revealed a normal CO2 level of 41 mm Hg and pH of 7.42 with low oxygen tension (52 mm Hg). An ECG showed a small S wave in lead I and a small Q wave and inverted T wave in …

Background —This study examines the cellular basis for the phenotypic appearance of broad-based T waves, increased transmural dispersion of repolarization (TDR), and torsade de pointes (TdP) induced by β-adrenergic agonists under conditions mimicking the LQT1 form of the congenital long-QT syndrome. Methods and Results —A transmural ECG and transmembrane action potentials from epicardial, M, and endocardial cells were recorded simultaneously from an arterially perfused wedge of canine left ventricle. Chromanol 293B, a specific I Ks blocker, dose-dependently (1 to 100 μmol/L) prolonged the QT interval and action potential duration (APD 90 ) of the 3 cell types but did not widen the T wave, increase TDR, or induce TdP. Isoproterenol 10 to 100 nmol/L in the continued presence of chromanol 293B 30 μmol/L abbreviated the APD 90 of epicardial and endocardial cells but not that of the M cell, resulting in widening of the T wave and a dramatic accentuation of TDR. Spontaneous as well as programmed electrical stimulation (PES)-induced TdP was observed only after exposure to the I Ks blocker and isoproterenol. Therapeutic concentrations of propranolol (0.5 to 1 μmol/L) prevented the actions of isoproterenol to increase TDR and to induce TdP. Mexiletine 2 to 20 μmol/L abbreviated the APD 90 of M cells more than that of epicardial and endocardial cells, thus diminishing TDR and the effect of isoproterenol to induce TdP. Conclusions —This experimental model of LQT1 indicates that a deficiency of I Ks alone does not induce TdP but that the addition of β-adrenergic influence predisposes the myocardium to the development of TdP by increasing transmural dispersion of repolarization, most likely as a result of a large augmentation of residual I Ks in epicardial and endocardial cells but not in M cells, in which I Ks is intrinsically weak. Our data provide a mechanistic understanding of the cellular basis for the therapeutic actions of β-adrenergic blockers in LQT1 and suggest that sodium channel block with class IB antiarrhythmic agents may be effective in suppressing TdP in LQT1, as they are in LQT2 and LQT3, as well as in acquired (drug-induced) forms of the long-QT syndrome.

Background —This study probes the cellular basis for the T wave under baseline and long-QT (LQT) conditions using an arterially perfused canine left ventricular (LV) wedge preparation, which permits direct temporal correlation of cellular transmembrane and ECG events. Methods and Results —Floating microelectrodes were used to record transmembrane action potentials (APs) simultaneously from epicardial, M-region, and endocardial sites or subendocardial Purkinje fibers. A transmural ECG was recorded concurrently. Under baseline and LQT conditions, repolarization of the epicardial action potential, the earliest to repolarize, coincided with the peak of the T wave; repolarization of the M cells, the last to repolarize, coincided with the end of the T wave. Thus, the action potential duration (APD) of the longest M cells determine the QT interval and the T peak –T end interval serves as an index of transmural dispersion of repolarization. Repolarization of Purkinje fibers outlasted that of the M cell but failed to register on the ECG. The morphology of the T wave appeared to be due to currents flowing down voltage gradients on either side of the M region during phase 2 and phase 3 of the ventricular action potential. The interplay between these opposing forces determined the height of the T wave as well as the degree to which the ascending or descending limb of the T wave was interrupted, giving rise to bifurcated T waves and “apparent T-U complexes” under LQT conditions. Spontaneous and stimulation-induced polymorphic ventricular tachycardia with characteristics of torsade de pointes (TdP) developed in the presence of dl -sotalol. Conclusions —Our results provide the first direct evidence that opposing voltage gradients between epicardium and the M region and endocardium and the M region contribute prominently to the inscription of the ECG T wave under normal conditions and to the widened or bifurcated T wave and long-QT interval observed under LQT conditions. Our data suggest that the “pathophysiological U” wave observed in acquired or congenital LQTS is more likely to be a second component of an interrupted T wave, and argue for use of the term T2 in place of U to describe this event.

Background Nonuniform recovery of ventricular excitability has been demonstrated to facilitate the reentry circuits leading to the development of ventricular tachyarrhythmias. This can also occur in arrhythmogenic right ventricular dysplasia (ARVD). In fact, in patients with ARVD, abnormalities of ventricular repolarization are often observed on 12-lead ECGs, but their predictive value for the occurrence of malignant arrhythmias is yet to be established. Because body-surface potential mapping has been proved to be useful for the detection of heterogeneities in ventricular recovery even though they are not revealed by conventional 12-lead ECGs, we attempted to analyze repolarization potentials on the entire chest surface to find abnormalities that can be predictive of ventricular arrhythmias. Methods and Results Body-surface potential maps were recorded from 62 anterior and posterior thoracic leads in 22 patients affected by ARVD, 9 with episodes of sustained ventricular tachycardias (VT) and 13 without. Thirty-five healthy subjects were also studied as control subjects. The 62 chest ECGs were simultaneously recorded, digitally converted at a rate of 2000 Hz, and stored on a hard disk of a body-surface mapping computer system. In each subject, the QRST integral map was obtained by calculating at each lead point the algebraic sum of all instantaneous potentials, from the QRS onset to the T-wave end, multiplied by the sampling interval. In most ARVD patients, we observed a larger-than-normal area of negative values on the right anterior thorax. This abnormal pattern could be explained by a delayed repolarization of the right ventricle. Nevertheless, it was not related to the occurrence of VT in our patient population. To detect minor heterogeneities of ventricular repolarization, the principal component analysis was applied to the 62 ST-T waves recorded in each subject. We assumed that a low value of the first or of the first three components (components 1, 2, and 3) indicates a greater-than-normal variety of the ST-T waves, a likely expression of a more complex recovery process. The mean values of the first three components were not significantly different in ARVD patients and control subjects. Nevertheless, considering the two subsets of patients with and without VT, the values of component 1, components 1+2, and component 1+2+3 were significantly lower in the group of ARVD patients with VT. Values of component 1 < 69% (equal to 1 SD below the mean value for control subjects) were found in 6 of 9 VT patients and in 1 patient without VT (sensitivity, 67%; specificity, 92%). A low value of component 1 was the only variable significantly associated with the occurrence of VT. Conclusions Principal component analysis provides a better quantitative assessment of the complexity of repolarization than other ECG measurements. When applied to ARVD patients, principal component analysis of the ST-T waves recorded from the entire chest surface revealed abnormalities not detected by conventional ECG that can be considered indexes of arrhythmia vulnerability.

Background QT interval prolongation and dispersion have been implicated in serious arrhythmias in congestive heart failure (CHF) and the congenital and drug-induced long-QT syndromes (LQTS). In a subset of the congenital LQTS, infusion of potassium can correct QT abnormalities, consistent with in vitro increases in outward currents such as I Kr or I K1 when extracellular potassium concentration ([K + ] o ) is increased. Furthermore, increasing [K + ] o decreases the potency of I Kr -blocking drugs in vitro. The purpose of this study was to test the hypothesis that increasing [K + ] o corrects QT abnormalities in CHF and in subjects treated with quinidine. Methods and Results KCl (maximum, 40 mEq) was infused into (1) 12 healthy subjects treated with quinidine sulfate (5 doses of 300 mg/5 h) or placebo and (2) 8 CHF patients and age-matched normal control subjects. Mean [K + ] increased from 4 to 4.2 mEq/L to 4.7 to 5.2 mEq/L. Potassium infusion significantly reversed QTU c prolongation, especially in the precordial leads (quinidine, 590±79 to 479±35 [±SD] ms 1/2 , P 1/2 , P c dispersion (quinidine, 210±62 to 130±75 ms 1/2 , P 1/2 , P =.07) and was without effect in the control subjects. QT morphological abnormalities, including U waves and bifid T waves, were reversed by potassium. Conclusions Potentially arrhythmogenic QT abnormalities during quinidine treatment and in CHF can be nearly normalized by modest elevation of serum potassium.

Background In cardiac hypertrophy, ECG T-wave changes imply an abnormal sequence of ventricular repolarization. We investigated the hypothesis that this is due to changes in the normal regional differences in action potential duration. We assessed the contribution of potassium- and calcium-dependent currents to these differences. Both the altered sequence of ventricular repolarization and the underlying cellular mechanisms may contribute to the increased incidence of ventricular arrhythmias in hypertrophy. Methods and Results Rats received daily isoproterenol injections for 7 days. Myocytes were isolated from basal subendocardial (endo), basal midmyocardial (mid), and apical subepicardial (epi) regions of the left ventricular free wall. Action potentials were stimulated with patch pipettes at 37°C. The ratio of heart weight to body weight and mean cell capacitance are increased by 22% and 18%, respectively, in hypertrophy compared with controls ( P 25 ) are reduced in hypertrophy (control: endo, 11.4±0.9 ms; mid, 8.2±0.9 ms; epi, 5.1±0.4 ms; hypertrophy: endo, 11.6±0.9 ms; mid, 10.4±0.8 ms; epi, 7.8±0.6 ms). The regional differences in APD 25 are still present in 3 mmol/L 4-aminopyridine. Hypertrophy affects APD 75 differently, depending on the region of origin of myocytes (ANOVA P 75 is shortened in subendocardial myocytes but is prolonged in subepicardial myocytes (control: endo, 126±7 ms; epi, 96±10 ms; hypertrophy: endo, 91±6 ms; epi, 108±7 ms). These changes in APD 75 are altered by intracellular calcium buffering. Conclusions Normal regional differences in APD and the changes observed in hypertrophy are only partially explained by differences in I to1 . In hypertrophy, the normal endocardial/epicardial gradient in APD 75 appears to be reversed. This may explain the T-wave inversion observed and will have implications for arrhythmogenesis.

54-year-old man with childhood-onset type I diabetes mellitus who had preserved renal function but blindness secondary to his diabetes mellitus presented with a 5-day his-tory of malaise and diarrhea.On admission, he was dehydrated, hypotensive, and hypo-thermic (96.1oF/35.6oC). Initial laboratory values showed a potassium level of 9.2 (N, 3.6–5.0) mmol/L, and a sodium level of 122 (N, 137–145) mmol/L. The potassium level was confirmed on arterial samples.The initial ECG showed a regular idioventricular rhythm with bizarre, broad QRS complexes, and a frequency of 32 beats per minute (Figure A). Over a 5-hour period, on correc-tion of the hyperkalemia, he converted to sinus rhythm (Figure B and C) initially with a first-degree atrioventricular block (Figure B). Furthermore, the characteristic peaking of the T waves related to the hyperkalemia normalized (Figure C).On follow-up, an increased level of adrenocorticotropic hormone, the absence of response to synthetic adrenocorti-cotropic hormone, and strongly positive adrenal antibodies revealed that the patient had developed autoimmune adrenal insufficiency (Addison disease).Thomas Addison recognized the potential effects of adrenal insufficiency on the heart, and he described one of the marked features of the condition as “a remarkable feebleness of the hearts action” in his original monograph from 1855.

Background— T-wave inversion in right precordial leads V 1 to V 3 is a relatively common finding in a 12-lead ECG of children and adolescents and is infrequently found also in healthy adults. However, this ECG pattern can also be the first presentation of arrhythmogenic right ventricular cardiomyopathy. The prevalence and prognostic significance of T-wave inversions in the middle-aged general population are not well known. Methods and Results— We evaluated 12-lead ECGs of 10 899 Finnish middle-aged subjects (52% men, mean age 44±8.5 years) recorded between 1966 and 1972 for the presence of inverted T waves and followed the subjects for 30±11 years. Primary end points were all-cause mortality, cardiac mortality, and arrhythmic death. T-wave inversions in right precordial leads V 1 to V 3 were present in 54 (0.5%) of the subjects. In addition, 76 (0.7%) of the subjects had inverted T waves present only in leads other than V 1 to V 3 . Right precordial T-wave inversions did not predict increased mortality (not significant for all end points). However, inverted T waves in leads other than V 1 to V 3 were associated with an increased risk of cardiac and arrhythmic death ( P Conclusions— T-wave inversions in right precordial leads are relatively rare in the general population, and are not associated with adverse outcome. Increased mortality risk associated with inverted T waves in other leads may reflect the presence of an underlying structural heart disease.

To the Editor: Early repolarization (ER) was historically considered a benign ECG variant, commonly seen in the anterolateral leads of young male athletes of black ethnicity. It was defined by Wasserburger and Alt1 in 1961 as elevated take-off of the ST segment at the J junction with downward concavity of the ST segment and symmetrical T waves. In recent years it has emerged as a marker for increased risk of sudden cardiac death, particularly in the inferior ECG leads.2,3 Although ER is a common ECG finding, ER syndrome (ER with idiopathic ventricular fibrillation) is rare.2 Even in middle-aged individuals with inferior ER of ≥0.2 mV, the 3-fold …

A 29-year-old woman presented with symptoms of cough, shortness of breath, and wheezing. She was diagnosed with bronchitis, but did not improve with empirical therapy, including antibiotics, inhalers, and prednisone. She subsequently developed chest pain that was worse when lying down, and a chest X-ray demonstrated cardiomegaly. This radiographic finding prompted further investigations. Her past medical history was notable for respiratory distress at birth and small stature growing up. She was diagnosed with a heart murmur at age 15, but investigations performed at that time were unrevealing. She also suffered from hearing loss. In retrospect it was discovered that several members in her maternal family, including her mother, grandmother, and aunt, also suffered from hearing loss. In addition, her mother had type 2 diabetes and a history of stroke and seizures. On physical examination, she was a short, thin young woman with a body mass index of 17, wearing bilateral hearing aids. Her vital signs were normal. Cardiac auscultation revealed a 2/6 systolic ejection murmur. Laboratories revealed an elevated serum creatinine level of 1.36 mg/dL and a markedly elevated B-type natriuretic peptide level of 1417 pg/mL. The electrocardiogram was abnormal with evidence of right atrial enlargement, inferior Q waves, poor R wave progression, and inferolateral T wave inversions. Transthoracic echocardiography revealed severe, concentric left ventricular (LV) hypertrophy with a septal wall thickness of 17 mm (Figure 1). LV systolic function was hyperdynamic (Movie I of the online-only Data Supplement), while diastolic filling demonstrated a restrictive pattern. The right ventricle also demonstrated increased wall thickness but was of normal chamber size and function. There was a moderate-sized pericardial effusion measuring 1.8 …

We report the case of a 74-year-old woman with a history of complex congenital heart disease consisting of double-chambered right ventricle (DCRV) and situs inversus with dextrocardia. To our knowledge, this is the first reported case with the combination of these 2 congenital abnormalities. The patient was transferred to our hospital after experiencing abdominal discomfort, malaise, and cold sweats for 3 days. Initial examination revealed slightly elevated cardiac troponin T (peaked at 0.56 ng/mL). With her known history of dextrocardia, 12-lead surface electrocardiography (ECG) with both standard precordial leads (Figure 1A) and right-sided precordial leads (Figure 1B) was performed. The standard ECG was notable for inverted P waves in the lateral leads (I and aVL), suggesting rightward atrial electric forces and poor R wave progression. The right-sided precordial lead ECG showed normalized R wave progression. These summations of ECG findings are suggestive of dextrocardia. There were also pseudo-Q waves in the limb leads and T wave inversions in I and aVL, which are also consistent with dextrocardia but less specific than the other findings. In addition, her right-sided ECG showed ST depression and T wave inversion in the anterior leads, which in the …

A 36-year-old man came to the emergency department with acute onset of exertional chest pain. He had had no recent infections, and no cardiovascular risk factors were present. However, the patient had used a wheelchair since his mid-20s because of sporadic inclusion-body myositis, as established by muscle biopsy. There were no other physical findings. Inflammatory markers and troponin T were normal, and the creatine kinase was elevated 2-fold with a significant muscle brain fraction. Chest roentgenogram was normal, but ECG showed a normal sinus rhythm at 62 bpm with deep Q waves, tall R waves in the right precordial leads, interventricular conduction delay, and T wave inversion in the left lateral leads (Figure 1). Echocardiography did not reveal any abnormalities. Cardiovascular magnetic resonance (CMR) examination was next performed. Figure 1. Twelve-lead electrocardiogram demonstrating deep Q waves, tall R waves in the right precordial leads, interventricular conduction delay, and T inversion in the left lateral leads. Two-chamber (Movie I of the …

A 36-year-old Afro-Caribbean woman presented with recurrent syncope and shortness of breath after a long-haul flight. On admission, ECG revealed sinus tachycardia at 130 bpm and mildly flattened T waves in V2 through V5 (Figure 1a). D-Dimers were elevated (663 ng/mL), and blood gases showed hypoxia. Chest x-ray was unremarkable (Figure 1b). Family history revealed that the patient’s mother had suffered a previous deep venous thrombosis. Figure 1. a, ECG showing sinus tachycardia and mildly flattened T waves in V2 through V5. b, Chest x-ray with unremarkable findings. The initial clinical presentation was consistent with pulmonary embolism, confirmed by computed tomographic scan that showed a large saddle-shaped embolus in the pulmonary trunk extending into the right main pulmonary artery (Figure 2a), the right ventricle, the right atrium, and the inferior vena cava (IVC). There was also a smaller extension into the left main pulmonary artery as well as smaller, segmental, and subsegmental thrombi. Figure 2. a, Contrast-enhanced pulmonary computed tomography on admission showing a large saddle embolus in the pulmonary trunk and right main pulmonary artery. b, Contrast-enhanced pulmonary computed tomography after the first thrombolytic treatment showing resolution of the large saddle-shaped embolus in the pulmonary trunk and right main pulmonary artery. Given the extensive radiological findings along with clinical deterioration, the patient received a thrombolytic regimen with streptokinase. A repeat scan 12 hours after initiation of thrombolytic therapy showed that the saddle-shaped embolus in the pulmonary trunk had resolved (Figure 2b), but thrombotic elements in the right heart cavities and the IVC remained. An echocardiogram confirmed the presence …

BACKGROUND QRST isointegral maps (I-maps) have been useful in detecting repolarization abnormalities. We investigated the body surface distribution of abnormally low QRST areas in patients with left ventricular hypertrophy (LVH) and the relation of the abnormalities in I-map to the severity of LVH as assessed by echocardiography. METHODS AND RESULTS QRST area departure maps were constructed from electrocardiographic (ECG) data recorded in patients with LVH and precordial negative T waves resulting from aortic stenosis (AS) (10 patients), aortic regurgitation (AR) (12 patients), or hypertrophic cardiomyopathy (HCM) with asymmetric septal hypertrophy (22 patients). Fifty normal subjects served as controls. The I-map was constructed from 87 body surface electrocardiograms recorded simultaneously at a sampling interval of 1 msec. The area where the QRST area was smaller than normal limits (mean -2 SD) was designated the "-2 SD area." The echocardiographic left ventricular (LV) mass was calculated by Devereux's method. Patients with large LV masses due to AS or AR had 2 SD areas located over the left anterior chest or the midanterior chest, respectively. The 2 SD area was located over the left shoulder and left anterior chest and had a lingual shape in patients with HCM. The sum of QRST area values less than the normal range (sigma QRST) was significantly correlated with LV mass in patients with AS or AR (r = 0.83 and r = 0.69, p less than 0.01 and p less than 0.05). However, there was no significant correlation between sigma QRST and the severity of LVH in patients with HCM. sigma QRST divided by the number of electrodes in the 2 SD area was significantly greater in patients with HCM than in those with AS or AR. CONCLUSIONS These findings suggest that abnormalities in patients with HCM are manifest even in mild LVH and that there is a greater disparity of repolarization in hypertrophied left ventricles due to HCM than in LVH due to aortic valve disease. QRST isointegral departure maps may provide ECG evidence of LV mass of patients with AS or AR and of susceptibility to malignant arrhythmias in patients with HCM.

A 45-year-old man was admitted to our hospital with exertional chest pain. He had been diagnosed with membranoproliferative glomerulonephritis at the age of 20 and had undergone kidney transplantation at the age of 33. After that, he had taken some immunosuppressant drugs and steroids. Two years previously, he had presented with acute chest pain. On that occasion, cardiac enzymes were not elevated, but ECG showed the inversion of the T waves in II, III, aVF, V5, and V6 leads. We diagnosed angina pectoris and performed cardiac catheterization. Cardiac catheterization revealed a 75%-stenosed left anterior descending coronary artery (LAD) and a giant right coronary artery (RCA) aneurysm (50 mm) with intramural thrombus. Because the intravascular lumen of the RCA had been …

A white 64-year-old woman who made dresses for her livelihood was admitted to the emergency department for evaluation of acute chest pain and respiratory distress. Physical examination was unremarkable except for low arterial blood pressure (90 mm Hg systolic, 65 mm Hg diastolic), whereas ECG showed left atrial enlargement, possible previous septal myocardial infarction, negative T waves in the inferior leads, and no evidence of acute ischemia (Figure 1). Myocardial enzyme levels, including Troponin I, were within normal values after serial determination. Figure 1. ECG shows sinusal rhythm with 98 bpm, left atrial enlargement, possible previous septal myocardial infarction, and negative T waves in inferior leads. Chest x-ray was performed and showed a thin radiopaque foreign body at the 5° body of the thoracic vertebra level, near the trachea (Figure 2). When questioned specifically, the patient mentioned the possible accidental ingestion of …

To evaluate the significance of persistent negative T waves during severe ischemia, we prospectively studied 62 patients admitted for unstable angina without evidence of recent or ongoing myocardial infarction. A critical stenosis on the left anterior descending coronary artery (LAD), considered as the culprit lesion, was successfully treated by percutaneous transluminal coronary angioplasty (PTCA). The patients were divided into two groups according to the admission electrocardiogram: T NEG group (n = 32) had persistent negative T waves, and the T POS group (n = 30) had normal positive T waves on precordial leads. The two groups had similar baseline clinical, hemodynamic, and angiographic characteristics. All patients underwent a complete clinical and angiographic evaluation (coronary arteriography and left ventriculography) before undergoing PTCA and 8 +/- 3 months later. Left ventricular anterior wall motion was evaluated by the percent shortening of three areas (S1, S2, and S3) considered as LAD-related segments on left ventriculograms. Before PTCA, there was no significant difference in global ejection fraction between the two groups despite a significant depression in anterior mean percent area shortening in the T NEG compared with the T POS group (S1, 44 versus 54, p less than 0.01; S2, 39 versus 48, p less than 0.01; S3, 44 versus 50, NS). At repeated angiography, the anterior mean percent area shortening improved significantly in the T NEG group (S1, from 44 to 61, p less than 0.001; S2, from 39 to 58, p less than 0.001; S3, from 44 to 61, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

A 48-year-old man was referred to our cardiology department for the treatment of acute myocardial infarction. He had no risk factors for arteriosclerosis. Two months before this admission, he had been admitted to another hospital because of stroke with right hemiparesis; 1 month before this admission, he developed acute renal failure and hemodialysis was started. Chest radiograph demonstrated cardiomegaly and pulmonary congestion (Figure 1A). The ECG demonstrated a QS pattern in the V1 through V3 leads with ST elevation and coronary T waves in the V4 through V6 leads and left atrial overload in the V1 lead (Figure 1B). …

A 78-year-old man presented with a 1 week history of breathlessness. He had no chest pain, cough, hemoptysis or any other symptoms. Past medical history was unremarkable. Initial examination revealed normal blood pressure, resting tachycardia of 140 beats per minute and type I respiratory failure requiring oxygen (FiO2 of 0.35) to maintain normal oxygen saturation. His chest x-ray showed no evidence of pneumonia or pulmonary edema. Admission ECGs showed ST depression and T wave inversion in the precordial …

A 15-year-old male presented clinically with myocarditis. At follow-up, a 12-lead ECG (Figure 1A) and chest x-ray were performed (Figure 1B). Echocardiography was reported to show at least mildly impaired left ventricular function, and cardiovascular magnetic resonance (CMR) demonstrated a severely dilated impaired left ventricle (end-diastolic volume index, 160 mL/m2; ejection fraction, 42%), normal proximal coronary arteries, and a pattern of late gadolinium enhancement (LGE) which indicated extensive myocardial scarring as a result of myocarditis (Figure 2). The patient remained asymptomatic. Unfortunately, he died suddenly 2 years later. The post mortem distribution of scarring was concordant with the in vivo CMR LGE findings. Figure 1. A, 12 lead ECG demonstrates sinus arrhythmia with a single junctional beat and normal axis. Peaked T waves of uncertain significance are noted. B, Chest x-ray showed a cardiothoracic ratio of 0.47. Figure 2. The 12-panel figure shows echocardiographic images in the left column (from top to bottom) in parasternal long-axis, basal short-axis, mid short-axis, and apical short-axis orientations. Cine CMR images in corresponding planes are shown in the middle column with late gadolinium imaging in the right column. Of note, the cine CMR images clearly show thinning …

A 52-year-old woman presented to the emergency department complaining of atypical chest and epigastric pain. Although her neurological examination was completely normal, her ECG revealed deep, symmetric T-wave inversions in all vascular distributions, consistent with neurogenic T waves (Figure 1). Fifty minutes after the initial ECG, the patient developed left-sided hemiplegia, …

A 60-year-old white man initially presented to the outpatient clinic in 2002 complaining of atypical chest pain during the last 6 months. A resting ECG showed high R waves and giant negative T waves in the anterior leads (Figure). Cardiovascular magnetic resonance (CMR) showed the typical appearance of apical hypertrophic cardiomyopathy (Figure, A and B). Delayed enhancement imaging did not show relevant scar tissue during the baseline study (Figure, C and D). The patient was put on a β-blocker and an angiotensin-converting enzyme inhibitor and was asked to come back for a follow-up examination 2 years later. Left, …

A 43-year-old man with medical history of gastroenteritis 2 weeks previously was referred to our intensive care unit for acute chest pain. At admission, the ECG showed negative T waves in V1, V2, V3, and V4 leads, and his troponin serum level was 0.6 ng/mL. His C-reactive protein level was elevated at 70 mg/L, and the serum blood count showed hyperleukocytosis with hyperlymphocytosis and thrombocytosis. Two-dimensional transthoracic echocardiogram revealed a dilated and …

A 29-year-old man was admitted to our hospital because of recurrence of diffuse large B-cell lymphoma (DLBCL), which was initially treated with chemotherapy. Gallium scintigraphy showed abnormal accumulation in the apex of the heart, which suggested cardiac involvement of DLBCL. The thoracic CT, MRI, and transthoracic echocardiography also revealed the existence of an apical mass (Figure), and …

To the Editor: I read with great interest the contribution of Shvilkin et al.1 The issue they tackled is of utmost importance because of the high prevalence of both the postpacing T-wave inversion, cardiac memory–related changes (CM), and the ischemia-associated but similar-appearing T-wave alterations (ISC). The authors have been delving into the mechanisms of the CM ECG phenomenon from the basic science vintage for some time,2–5 and are now venturing into the clinical applications of the concept. All interested in materia electrocardiographica are now eager to put to the test of practice the authors’ contentions. I would like to offer some thoughts and direct to the authors some questions regarding their hypothesis and their methods. Considering the diverse topography of the ischemic territories, which depends on the particulars of each case, why do they feel that there will be no ischemic T-wave vectors that could be similar in …

A 26-year-old woman with congenital deafness and a lifelong “seizure disorder” presented to the emergency department with 15 episodes of syncope. She was 1 week postpartum. The ECG showed normal sinus rhythm, markedly prolonged QT …

Background— Postpacing precordial T-wave inversion (TWI), known as cardiac memory (CM), mimics ischemic precordial TWI, and there are no established ECG criteria that adequately distinguish between the two. On the basis of CM properties (postpacing sinus rhythm T vector approaching the direction of the paced QRS vector), we hypothesized that CM induced by right ventricular pacing would manifest a TWI pattern different from that of precordial ischemic TWI, thereby discriminating between the two. Methods and Results— T-wave axis, polarity, and amplitude on a 12-lead ECG during sinus rhythm were compared between CM and ischemic patients. The CM group incorporated 13 patients who were paced in DDD mode with short atrioventricular delay for 1 week after elective pacemaker implantation. The ischemic group consisted of 47 patients with precordial TWI identified among 228 consecutive patients undergoing percutaneous coronary intervention for an acute coronary syndrome. The combination of (1) positive T aVL , (2) positive or isoelectric T I , and (3) maximal precordial TWI>TWI III was 92% sensitive and 100% specific for CM, discriminating it from ischemic precordial TWI. Conclusions— CM induced by right ventricular pacing results in a distinctive T-vector pattern that allows discrimination from ischemic precordial T-wave inversions regardless of the coronary artery involved.

Early repolarization pattern (ERP) is a common ECG variant, characterized by J point elevation manifested either as terminal QRS slurring (the transition from the QRS segment to the ST segment) or notching (a positive deflection inscribed on terminal QRS complex) associated with concave upward ST-segment elevation and prominent T waves in at least two contiguous leads.1,2 The J point deflection occurring at the QRS-ST junction (also known as Osborn wave or J wave) was first described in 1938, and is seen in both extracardiac and cardiac disorders like hypothermia, hypercalcemia, brain injury, hypervagotonia, or spinal cord injury leading to loss of sympathetic tone, vasospastic angina. Besides recently described early repolarization syndrome,3–5 ERP has generally been considered a normal ECG variant with good long-term prognosis. However, this long-held concept has been challenged, and recently published population-based studies and reports of associations with ventricular fibrillation and sudden death continue to fuel more momentum.6–9 In the seminal article by Haissaguerre et al, cases of ERP associated with cardiac arrest had at least 0.1-mV J point elevation manifested as QRS slurring or notching in the 2 contiguous inferior or lateral leads.6 ERP has also emerged as a marker of increased long-term mortality (cardiac and arrhythmic) in the general population.10,11 Thus, ERP is probably not as benign as traditionally believed. Article see p 2208 The potential consequences of such an association are huge, especially as related to ECG screening and risk stratification in the general population. It is therefore extremely …

To the Editor: The editorial by Wilde and Roden1 in the December 5, 2000, issue of Circulation discussed how differences in electrocardiographic ST-T–wave patterns, together with other phenotypic differences, arise in genetically distinct forms of long-QT syndrome (LQTS).2 The authors observed how important these results can be for the investigation of the pathophysiology of ventricular repolarization. The T wave is the result of repolarization gradients across the ventricular myocardium. The LQTS ST-T–wave pattern study by Zhang et al,2 to which the editorial referred, showed that broad-based T waves are characteristic for LQT1. The editorial also referred to the work of Yan and Antzelevitch,3 …

Background — Investigators who studied ventricular defibrillation by use of optical mapping techniques failed to observe an initial defibrillation event (isoelectric window or quiescent period) shown by electrode mapping studies. This discrepancy has important implications for the mechanisms of defibrillation. The purpose of the present study was to demonstrate an optical equivalent of an isoelectric window after a near-threshold defibrillation shock. Methods and Results — We studied 10 isolated, perfused swine right ventricles. Upper limit of vulnerability was determined by shocks on T waves. A 50% probability of successful defibrillation (DFT50) was determined with an up-down algorithm. Immediately after unsuccessful defibrillation shock, new wavefronts were generated. When the shock strength was low, immediate reinitiation of reentry and ventricular fibrillation might occur without a postshock isoelectric window. However, if the shock strength was within 50 V of DFT50 (near-threshold), a synchronized activation occurred, followed by organized repolarization that ended 64±18 ms after shock. After a period of quiescence (18±24 ms), activation recurred 83±33 ms after shock and reinitiated ventricular fibrillation. Similar patterns of activation, including a quiescent period, were observed after shock was applied on the T wave of the paced beat that induced ventricular fibrillation. Upper limit of vulnerability correlated well with DFT50. Conclusions — In isolated swine right ventricles, an optical equivalent of an isoelectric window exists after near-threshold defibrillation shocks. These findings support the idea that a near-threshold defibrillation shock terminates all activation wavefronts but fails to halt ventricular fibrillation because the same shock reinitiates ventricular fibrillation after an isoelectric window.

To the Editor: Hung and colleagues1 present a very important example of a pseudo-infarction pattern presumably related to pancreatitis, one of several clinical situations in which thrombolytic therapy is either not indicated or contraindicated. I am intrigued by the pattern of the bizarre T waves in the limb leads and wonder if part or all of this phenomenon is artifact. The T waves are of unusually abrupt …

Background —Cardiac memory (CM) refers to T-wave changes induced by ventricular pacing or arrhythmia that accumulate in magnitude and duration with repeated episodes of abnormal activation. We report herein the kinetics of long-term CM and its association with the ventricular action potential. Methods and Results —Dogs were paced from the ventricles at rates of 110 to 120 bpm for ≈3 weeks. CM characterized by gradual sinus rhythm T vector rotation toward the paced QRS vector evolved in all dogs regardless of pacing site (left ventricular [LV] anterior apex or base, posterior LV, or right ventricular free wall). Cardiac hemodynamics and myocardial flow (microsphere studies) were unaltered by the pacing. Recovery time for the memory T wave to return to control increased with duration of the previous pacing. The protein synthesis inhibitor cycloheximide markedly ( P Conclusions —CM is a dynamic process for which the final T vector is predicted by the paced QRS vector and which is associated with significant changes in epicardial and endocardial but not midmyocardial cell action potential duration, such that the transmural gradient of repolarization is altered. It is unaccompanied by evidence of altered hemodynamics or flow, requires a change in pathway of activation, and appears to require new protein synthesis.

Background This study examines the contribution of transmural heterogeneity of transmembrane activity to phenotypic T-wave patterns and the effects of pacing and of sodium channel block under conditions mimicking HERG and SCN5A defects linked to the congenital long-QT syndrome (LQTS). Methods and Results A transmural ECG and transmembrane action potentials from epicardial, M, and endocardial or Purkinje cells were simultaneously recorded in an arterially perfused wedge of canine left ventricle. d -Sotalol was used to mimic LQT2, whereas ATX-II mimicked LQT3. d -Sotalol caused a preferential prolongation of the M cell action potential duration (APD 90 , 291±14 to 354±35 ms), giving rise to broad and sometimes low-amplitude bifurcated T waves and an increased transmural dispersion of repolarization (TDR, 51±15 to 72±17 ms). QT interval increased from 320±13 to 385±37 ms. ATX-II produced a preferential prolongation of the M cell APD 90 (280±25 to 609±49 ms) and caused a marked delay in the onset of the T wave and a sharp rise in TDR (40±5 to 168±40 ms). QT-, APD 90 -, and dispersion-rate relations were much steeper in the ATX-II than in the d -sotalol model. Mexiletine (2 to 20 μmol/L) dose-dependently abbreviated the QT interval and APD 90 of all cell types, more in the ATX-II than in the d -sotalol model, but decreased TDR equally in the two models. Mexiletine 2 to 5 μmol/L totally suppressed spontaneous torsade de pointes (TdP) and reduced the vulnerable window during which single extrastimuli could induce TdP in both models. Higher concentrations of mexiletine (10 to 20 μmol/L) totally suppressed stimulation-induced TdP. Conclusions Our results suggest that although pacing and sodium channel block are very effective in abbreviating the QT interval and TDR in LQT3, these therapeutic approaches may also be valuable in reducing the incidence of arrhythmogenesis in LQT2.

Background— T-wave inversion on a 12-lead ECG is usually dismissed in young people as normal persistence of the juvenile pattern of repolarization. However, T-wave inversion is a common ECG abnormality of cardiomyopathies such as hypertrophic cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy, which are leading causes of sudden cardiac death in athletes. We prospectively assessed the prevalence, age relation, and underlying cardiomyopathy of T-wave inversion in children undergoing preparticipation screening. Methods and Results— The study population included 2765 consecutive Italian children (1914 male participants; mean age, 13.9±2.2 years; range 8–18 years) undergoing preparticipation screening including an ECG. Of 229 children (8%) who underwent further evaluation because of positive findings at initial preparticipation screening, 33 (1.2%) were diagnosed with cardiovascular disease. T-wave inversion was recorded in 158 children (5.7%) and was localized in the right precordial leads in 131 (4.7%). The prevalence of right precordial T-wave inversion decreased significantly with increasing age (8.4% in children P P P P Conclusions— The prevalence of T-wave inversion decreases significantly after puberty. Echocardiographic investigation of children with postpubertal persistence of T-wave inversion at preparticipation screening is warranted because it may lead to presymptomatic diagnosis of a cardiomyopathy that could lead to sudden cardiac death during sports.

BACKGROUND The ECG recognition of diffuse pericarditis following acute myocardial infarction has been based on changes of the ST segment and, to a lesser extent, alterations of the PQ segment. No ECG criteria exist for the diagnosis of postinfarction regional pericarditis. Recently, it was observed that the T wave evolution follows an atypical pattern before fatal free wall rupture and that this pattern is due to the associated pericarditis. Therefore, this study was conducted on 200 patients with acute myocardial infarction to further elucidate the sensitivity and specificity of the atypical T wave changes in patients with regional postinfarction pericarditis without rupture and to assess the affect of lytic treatment on the rapidity and amplitude of postinfarction T wave evolution. METHODS AND RESULTS An analysis of the clinical courses and serial ECGs of 200 consecutive patients with acute myocardial infarction was performed. Among 43 patients with postinfarction pericarditis, the pattern of T wave evolution consistently differed from the customary postinfarction pattern of T wave evolution. This unusual evolutionary course was expressed as either persistently positive T waves 48 or more hours after infarction (67%) or premature, gradual reversal of inverted T waves to positive deflections (33%). The sensitivity and specificity of these T wave alterations were 100% and 77%, respectively. The only other processes identified that caused this type of postinfarction T wave evolution were cardiopulmonary resuscitation, reinfarction, and very small infarcts. Both reperfusion, as judged by the creatine kinase-MB curve, and patency, as assessed by the angiogram, were correlated with the rapidity and depth of T wave inversion. Ninety percent of patients with reperfusion attained a maximum T wave negativity of 3 mm or more within 48 hours after the onset of chest pain in the lead that initially displayed the greatest ST segment elevation. Seventy-six percent of patients without reperfusion attained a maximum negativity of 2 mm or less within 72 hours. Thus, like the ST segment, accelerated evolution and deepening of the T wave may be noninvasive markers of reperfusion. CONCLUSIONS First, premature reconcordancy of the ST segment and T wave after acute myocardial infarction is a sensitive, reasonably specific, and easily recognizable ECG manifestation of postinfarction regional pericarditis. Second, reperfusion is associated with accelerated evolution and deepening of the T waves following acute myocardial infarction.

BACKGROUND In the canine model, an upper limit of shock strength exists that can induce ventricular fibrillation during the vulnerable period of the cardiac cycle. This shock strength (the upper limit of vulnerability) closely correlates with the defibrillation threshold and supports the "upper limit of vulnerability" hypothesis of defibrillation. It is not known whether an upper limit of vulnerability exists in humans or whether this limit correlates with the defibrillation threshold. METHODS AND RESULTS In 13 patients undergoing implantable cardioverter-defibrillator implantation, the shock strengths associated with a 50% probability of reaching the upper limit of vulnerability (ULV50) and a 50% probability of reaching the defibrillation threshold (DFT50) were determined by the up-down algorithm. The ULV50 was determined only for the mid-upslope of the positive T waves and for the mid-downslope of the negative T waves. No major complications occurred during surgery. An upper limit of vulnerability was demonstrated in each patient. The ULV50 was 300 +/- 138 V or 6.8 +/- 5.8 J, which was significantly lower than the DFT50 of 347 +/- 167 V (p = 0.038) or 9.1 +/- 7.3 J (p = 0.013). The correlation between the ULV50 and the DFT50 was significant (r = 0.90, p < 0.001 for voltage; r = 0.93, p < 0.001 for energy). CONCLUSIONS An upper limit of vulnerability is present in humans. There is a significant correlation between the ULV50 and the DFT50, and the ULV50 is significantly lower than the DFT50.