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Background: Mortality in patient with acute myocardial infarction has decreased due to evolution in management system in patient with acute coronary syndrome, but mortality rate during hospitalization remains high, especially STEMI. Electrocardiography (ECG) has a role for diagnosing and predict prognosis in acute myocardial infarction. Terminal QRS distortion defined as J point elevation more than 50% of R wave in lead with qR configuration and/or loss of S wave with RS configuration. Changes of terminal QRS segment believed to be caused by electrical conduction elongation in Purkinje fiber or myocardial ischemic zone that represent severe ischemia. The purpose of this study is to assess the role of terminal QRS distortion as one of the parameter to predict major adverse cardiovascular events during hospitalization in ST elevation myocardial infarction in RSUP H. Adam Malik Methods: This is a ambispective observational study consist of STEMI patients who were hospitalized from Mei 2019 to September 2019. All subjects diagnosed with STEMI and already fulfilled the inclusion and exclusion criterias. The terminal QRS distortion on the ECGs was assessed when the patient came to emergency departement. Then during hospitalization, the patients will undergo intervention and then observed during hospitalization for MACE occurrence. Results: Of the 78 STEMI patients, 44 people had terminal QRS distortion and 34 did not have terminal QRS distortion. In group with terminal QRS distortion, 27 people experiences MACE. From the correlation analysis, there is positive correlation between terminal QRS distortion with MACE with correlation coefficient 0.317 (p value < 0.001). Multivariate analysis for most significant variable for MACE occurrence shows that terminal QRS distortion can predict MACE (OR 3.66 [1.317-10.166], 95% CI, p = 0.013) Conclusion: Terminal QRS distortion found in ECG at admission in STEMI patient correlate with major adverse cardiovascular event during hospitalization.

Background: Early repolarization pattern (ERP) is a frequent finding in asymptomatic subjects with controversial implications regarding to its prognosis. This study aims to estimate the prevalence ...

Introduction The significance of high precordial electrocardiograms in idiopathic ventricular fibrillation (IVF) is unknown. Method This study included 50 consecutive patients (48 men; age, 42 ± 18 years) who had spontaneous ventricular fibrillation not linked to structural heart disease and received implantable cardiac defibrillator therapy. IVF was diagnosed in 35 patients and Brugada syndrome was diagnosed in other 15 patients. Electrocardiograms in high intercostal space were compared between 35 patients with IVF and 105 age‐ and sex‐matched healthy controls (patient: control ratio, 1:3). Results The frequency of J point elevation ≥ 0.1 mV in the 4th intercostal spaces was similar between patients with IVF (14%) and healthy controls (7%). However, the frequency of J point elevation ≥ 0.1 mV in the 3rd intercostal space was higher in patients with IVF (40%) than controls (11%) (p

Background and objectives Takotsubo cardiomyopathy (TTC) occasionally causes life-threatening ventricular arrhythmia. J wave on surface electrocardiography (sECG) has also been associated with idiopathic ventricular fibrillation and cardiac events; therefore, we investigated whether the presence of J wave on sECG is a potential risk factor for ventricular arrhythmia in patients with TTC. Subjects and methods We performed a retrospective study in 79 patients who were diagnosed with TTC from 2010 to 2014. Among them, 20 (25.3%) were diagnosed with ventricular tachycardia (VT). The J wave on the sECG was defined as J point elevation manifested through QRS notching or slurring at least 1 mm above the baseline in at least two leads. Results A higher prevalence of ventricular tachycardia was observed in patients with J wave. The corrected QT interval (QTc) was significantly longer in the VT group than in the non-VT group. In a multivariate analysis, the presence of J wave appeared to be the only independent predictors of VT [Hazard Ratio (HR) 3.5, p = 0.019]. Conclusion Our results suggest that the presence of J wave on the sECG is significantly associated with VT, and appear to indicate that the presence of J wave is a strong and independent predictor of VT in patients with TTC.

A J wave is a common electrocardiographic finding in the general population. Individuals with prominent J waves in multiple electrocardiogram (ECG) leads have a higher risk of lethal arrhythmias than those with low-amplitude J waves. There are few reports about the relationship between thyroid function and J-wave amplitude. We report the case of a 45-year-old man who had unexpected ventricular fibrillation (VF). He had dynamic J-point elevation in multiple ECG leads. Possible early repolarization syndrome was diagnosed. He also had thyrotoxicosis caused by silent thyroiditis, and his J-wave amplitude decreased according to changes in thyroid function because of spontaneous remission of silent thyroiditis. There was a positive correlation between serum triiodothyronine levels and J-wave amplitudes. The findings in case suggested silent thyroiditis may contribute to the occurrence of VF in a patient with dynamic changes in J-point elevation in multiple ECG leads. Thyrotoxicosis is a relatively common endocrine disease; therefore, clinicians should pay attention to J-wave amplitude in the ECG of patients with thyrotoxicosis., This case suggests silent thyroiditis may contribute to the occurrence of VF associated with J-point elevation. There was a correlation between serum triiodothyronine levels and J-wave amplitudes.

Background Prevalence of early repolarisation ECG pattern (ER) has been repetitively determined in adults, but has not been reported in large unselected children populations so far. Methods ECG from 1000 successive healthy children from birth to 17years old were prospectively recorded and analyzed. ER was defined by ≥0.1mV J point elevation in at least two contiguous inferior or lateral ECG leads. Correlations with age, gender, ethnic origin, physical activity, Sokolow index and heart rate were performed. Results Prevalence of ER pattern was 23,6% (95% CI 21–26.2%) and increased after 8years of age. ER was independently correlated to a non Caucasian origin and a higher Sokolow index, but not to gender or level of physical activity. ER was independently correlated to an older age in children with heart rate Conclusion ER is present in a quarter of children of various age and is related to ethnic origin, an older age, a slower heart rate and a higher Sokolow index.

Risk Stratification in Type 1 Brugada PatternIntroduction Risk stratification of asymptomatic patients with a Brugada type 1 ECG pattern remains an unresolved clinical conundrum. In contrast to provocative pharmacological testing in Brugada syndrome, there is limited data on the role of exercise stress testing as a risk stratification modality. The objective of this study was to evaluate the utility of exercise testing in asymptomatic patients with type 1 Brugada pattern to prognosticate major arrhythmic events (MAE) during follow-up. Methods and Results Treadmill exercise testing was conducted for 75 asymptomatic patients with type 1 Brugada pattern and for 88 healthy control subjects. The clinical end point of MAE was defined as the occurrence of sudden cardiac death (SCD) or resuscitated ventricular fibrillation (VF). During a follow-up of 77.9 ± 28.9 months, eight MAE occurred (five VF and three SCD). Multivariate Cox regression analysis showed that the following were independent predictors of MAE in asymptomatic patients with a type 1 Brugada pattern: increase in S wave upslope duration ratio >30% at peak exercise (HR 1.35, 95% CI 1.08–10.97, P = 0.023), augmentation of J point elevation in lead aVR >2 mm in late recovery (HR 1.88, 95% 1.21–15.67, P = 0.011), and delayed HR recovery (HR 1.14, 95% CI 1.06–18.22, P = 0.042). A high-risk cohort was identified by the final step-wise regression model with good accuracy (specificity = 98.4%, sensitivity = 62.5%) and discriminative power (AUC = 0.93, 95% CI 0.89–0.96, P = 0.002). Kaplan–Meier analysis revealed increasing MAE in subjects with one, two, or three predictors, respectively (log rank P < 0.001). Conclusions Exercise testing in asymptomatic patients with type 1 Brugada pattern aids in identification of high-risk patients and provides a unique window of opportunity for early intervention.

The aim: to determine the prevalence of the early repolarization pattern (ERP) among patients of the 1st consultancy clinic of Kaunas clinical hospital and to evaluate age and gender influence on rate of the pattern. Objectives: 1) to determine the prevalence of the ERP among the patients of the 1st consultancy clinic of Kaunas clinical hospital. 2) to compare the occurrence of the pattern in different age and gender groups. 3) to determine the connection between the prevalence of the pattern in different leads and patients’ gender and age. Methods: 217 patients of the 1st consultancy clinic of Kaunas clinical hospital had ECGs procedure due to the different clinical reasons during the period from March 1, 2018 to May 30, 2018. 232 (n=232) patients ECGs have been selected for the research. Patients were grouped according to age and gender and ECGs were analyzed. The prevalence of the ERP and the association between age, gender and occurrence of the pattern were evaluated. Results: the ERP was observed in 27,2% of the evaluated patients EKGs. The pattern occurrence in the anterior leads was observed in 0,9%, in the lateral leads – 11,5%, in the inferior leads – 19,4% of the population. The pattern occurrence was more frequently observed in the men of age group

In 1992, R. Brugada and J. Brugada were the first to describe a syndrome characterized by right-bundle branch block (RBBB) with ST segment elevation followed by an inverted T-wave in the right precordial leads, which predisposes apparently healthy subjects to Sudden Cardiac Death (SCD).

Background Just as high-risk populations for cardiac arrest exist in patients with Brugada syndrome or long QT syndrome, high-risk and low-risk populations for cardiac arrest also exist in patients with early repolarization pattern (ERP). Hypothesis Electrocardiographic (ECG) characteristics can aid the risk stratification of patients with ERP. Methods Electrocardiographic parameters such as magnitude of J-point elevation and J/R ratio were measured. The magnitude of J-point elevation, leads with J points elevated, J/R ratio, morphology of the ST segment, and QT/QTc interval were used in comparative analysis in 2 groups: 57 patients with ERP and cardiac arrest (cardiac arrest group) and 100 patients with ERP but without cardiac arrest (control group). Results There was no statistical difference in clinical characteristics of the 2 groups. The J/R ratio in the cardiac arrest group was significantly higher than in the control group (26.8% ± 18.1% vs 16.3% ± 10.3%, respectively; P < 0.001) and the proportion of horizontal/descending ST segments (70.2%) was significantly higher than in the control group (29.0%), but the proportion of ascending/upsloping ST segments (29.8%) was significantly lower than in the control group (71.0%; P < 0.001). Multivariate logistic regression revealed that higher J/R ratio and horizontal/descending ST segment were independently associated with increased risk of cardiac arrest in patients with ERP. Conclusions In patients with ERP and cardiac arrest, J/R ratios were relatively higher and mostly with horizontal/descending ST segments, suggesting that J/R ratio and ST-segment morphology may be used as indicators for risk stratification in patients with ERP.

We report the case of a 19-year-old male who successfully recovered from sudden cardiac arrest. Careful evaluation did not reveal any electrical or structural abnormalities. He underwent implantable cardioverter defibrillator (ICD) implantation, with a diagnosis of idiopathic ventricular fibrillation (VF). Three months later, VF recurred and was successfully terminated by ICD shock. Electrocardiogram (ECG) revealed a slurred type J point elevation at the inferolateral leads with a horizontal/descending ST segment change, which was not present during the initial hospitalization. Cilostazol was prescribed to prevent further lethal ventricular arrhythmias. Subsequently, no arrhythmic events were reported, and the J wave disappeared at the follow-up ECG. However, recurrent VF episodes with an interval of 1–2 weeks occurred 1 year later, and were terminated by ICD shock. Simultaneous ECG revealed a J point elevation at the inferolateral leads. Cilostazol was replaced by quinidine. Subsequently, no arrhythmic event recurred for over 12 months. Serial follow-up ECG is needed to identify masked inherited primary arrhythmic syndromes in sudden cardiac arrest survivors diagnosed with idiopathic VF. Cilostazol and quinidine might be good therapeutic options to prevent further lethal events in cases where the J wave syndrome is present with recurrent ventricular arrhythmias.

Early repolarization (ER) pattern is a prominent J point (end-QRS notch or slur) with an elevation ≥0.1 mV in two or more contiguous leads (excluding V1-V3) in a 12-lead electrocardiogram (ECG). Furthermore, the QRS duration is required to be

Conflicting data exist regarding the associations of early repolarization (ER) with electrocardiogram (ECG) and clinical outcomes in blacks. We examined the association of ER defined by J point elevation (JPE) and all-cause mortality, and heart failure (HF) hospitalization in blacks in the Jackson Heart Study (JHS) cohort. We included JHS participants with ECGs from the baseline visit coding JPE and excluded participants with paced rhythms or QRS duration ≥120 ms. We compared the cumulative incidence of 10-year all-cause mortality and 8-year HF hospitalization by presence of JPE ≥0.1 mV in any ECG lead at baseline using Kaplan-Meier estimates and multivariable Cox models. Of the 4,978 participants, 1,410 (28%) had JPE at baseline: anterior leads 97.8%, lateral leads 8.3%, and inferior leads 2.9%. Compared with participants without JPE, those with JPE were younger, more likely to be male and current smokers, and less likely to have hypertension. Over a median follow-up of 8 years, there were no significant differences in the cumulative incidence or multivariable-adjusted hazards of all-cause mortality or HF hospitalization in participants with and without JPE in any lead (adjusted hazard ratio 0.97, 95% confidence interval 0.89 to 1.52, and adjusted hazard ratio 1.18, 95% confidence interval 0.9 to 1.54, respectively). Of the 2,523 participants who completed Exam 3 without JPE at baseline, 246 (10%) developed JPE over follow-up. In conclusion, JPE on ECG was not associated with long-term mortality or HF hospitalization in a large prospective black community cohort, suggesting that ER may represent a benign ECG finding in blacks.

Aims Anterior T-wave inversion (TWI) is a recognized variant in athletes of African/Afro Caribbean origin and some endurance athletes; however, the presence of this specific repolarization anomaly also raises the possibility of cardiomyopathy. The differentiation between physiological adaptation and cardiomyopathy may be facilitated by examining other repolarization parameters, notably the J-point and the ST-segment. Methods and results We compared the electrocardiogram pattern of anterior TWI in a series of 80 healthy athletes (median age 21 years, 75% males); 95 patients with hypertrophic cardiomyopathy (HCM) (median age 46 years, 75% males), including 26 affected athletes; and 58 patients with arrhythmogenic right ventricular cardiomyopathy (ARVC) (median age 32 years, 71% males), including 9 affected athletes. Athletes and patients were of either white/Caucasian or black/Afro Caribbean descent and showed TWI ≥1 mm in ≥2 contiguous anterior leads (V1–V4). We aimed to identify repolarization patterns for differentiating physiologic from pathologic TWI. After adjustment for age, gender, and ethnicity, J-point elevation

Background J wave, or early repolarization has recently been associated with an increased risk of lethal arrhythmia and sudden death, both in idiopathic ventricular fibrillation and in the general population. Hypercalcemia is one of the causes of J point and ST segment elevation, but the relationship has not been well studied. The aim of this study was to examine the effects of hypercalcemia on J point elevation. Methods Electrocardiographic findings were compared in 89 patients with hypercalcemia and 267 age- and sex-matched healthy controls with normocalcemia. The association of J point elevation with arrhythmia events in patients with hypercalcemia was also studied. Results The PR interval and the QRS duration were longer in patients with hypercalcemia than in normocalcemic controls. Both the QT and the corrected QT intervals were shorter in patients with hypercalcemia compared with normocalcemic controls. Conduction disorders, ST-T abnormalities, and J point elevation were more common in patients with hypercalcemia than normocalcemic controls. Following the resolution of hypercalcemia, the frequency of J point elevation decreased to a level similar to that noted in controls. During hospitalization, no arrhythmia event occurred in patients with hypercalcemia. Conclusion Hypercalcemia was associated with J point elevation.

Conflicting data exist regarding the associations of early repolarization (ER) with electrocardiogram (ECG) and clinical outcomes in blacks. We examined the association of ER defined by J point elevation (JPE) and all-cause mortality, and heart failure (HF) hospitalization in blacks in the Jackson Heart Study (JHS) cohort. We included JHS participants with ECGs from the baseline visit coding JPE and excluded participants with paced rhythms or QRS duration ≥120 ms. We compared the cumulative incidence of 10-year all-cause mortality and 8-year HF hospitalization by presence of JPE ≥0.1 mV in any ECG lead at baseline using Kaplan-Meier estimates and multivariable Cox models. Of the 4,978 participants, 1,410 (28%) had JPE at baseline: anterior leads 97.8%, lateral leads 8.3%, and inferior leads 2.9%. Compared with participants without JPE, those with JPE were younger, more likely to be male and current smokers, and less likely to have hypertension. Over a median follow-up of 8 years, there were no significant differences in the cumulative incidence or multivariable-adjusted hazards of all-cause mortality or HF hospitalization in participants with and without JPE in any lead (adjusted hazard ratio 0.97, 95% confidence interval 0.89 to 1.52, and adjusted hazard ratio 1.18, 95% confidence interval 0.9 to 1.54, respectively). Of the 2,523 participants who completed Exam 3 without JPE at baseline, 246 (10%) developed JPE over follow-up. In conclusion, JPE on ECG was not associated with long-term mortality or HF hospitalization in a large prospective black community cohort, suggesting that ER may represent a benign ECG finding in blacks.

The early repolarization pattern and J wave were recognized during the very early period after the invention of the ECG. While the J wave has been reported to become prominent in particular circumstances, i.e., hypothermia, hypercalcemia, and brain damages, early repolarization has long been considered to be a benign finding, which is attributable to the definition of early repolarization during the period that included not only end-QRS notching/slurring but also ST segment elevation continuing to the upward concave ST segment and tall T wave. The prevalence of an early repolarization pattern and its predictive value has varied widely among the studies published more recently, which presumably were due to the diversity of the definitions. In the reports, either in case control studies or population studies, showing an association between an early repolarization pattern and cardiac or arrhythmic death, the definition has been based on J point elevation with notched or slurred J wave in the inferior or lateral leads, while early repolarization based on ST segment elevation seldom has shown any increased risk. The accumulated evidence has also demonstrated that even in those with J point elevation, the arrhythmic risk does not increase with a concave ST segment morphology. The definition of an early repolarization pattern should be unified and standardized to better stratify the risk of arrhythmic death.

Whatever the terminology which will be further used, either early repolarization (ER), Haissaguerre or J wave syndrome, it should never be forgotten that the ECG pattern associating various degrees of J point elevation, slurring or notching of the terminal part of the QRS and further ST elevation has been described well before the recent growing interest of electrophysiologists for this entity and was and should be still considered – as a normal ECG variant, at least in the very largest part of the normal population. Although this introductive assumption is far from original, it is worth to be recalled, because we should never lose sight of a feature that is present in several percent of the normal population cannot be considered as abnormal. Historically, one can track the first description of this pattern as soon as 1936, followed by some other reports over the last half of the previous century. At this step, the pattern was essentially described as ST elevation with a distinct notch or slur on the downslope of the R wave and was described as a “normal variant”, “unusual RT segment deviation”, “normal RST elevation variant” related to a “persistent juvenile pattern”, reflecting the belief of lack of any harmful consequence carried by this ECG pattern at this time. The clinical relevance of the documentation of this ECG pattern in a given patient however is not negligible, since it may mimick pericarditis, acute myocardial infarction or hypothermia for example, and may be associated, although in a very limited subset of patients, to sudden death (see other chapters from this issue). If we now carefully look at the publications relying on the prevalence of “early repolarization" pattern in the normal population, we can see that very various rates have been observed (roughly 1–15% according to most of the studies compiled in Table 2). These rather large differences are believed to reflect some differences in the definition (ST elevation or J wave) or methods to diagnose the pattern (manual vs automatic analysis for example), as well as differences in the studied population. Moreover, for some authors the QRS possibly includes the J wave/slurring – so

In the past years a renewed interest has emerged in the implications of aberrant terminal R waves or J-ST segments, J point elevation and J waves on the electrocardiogram of patients without evidence of gross structural cardiac abnormalities because of the association with malignant arrhythmias and (familial) sudden death. There have been propositions to group selected clinical entities (Brugada syndrome and early repolarization syndrome) of which the principal electrocardiographic element consists of these electrographic phenomena under the broader term J wave syndromes. In this paper such a grouping is discussed

Brugada syndrome is an inherited cardiac arrhythmia condition characterized by coved-type ST elevation and J point elevation of at least 2 mm in at least 2 of the right precordial electrocardiogram (ECG) leads (V1–3). An increasing number of noncardiac agents, including psychotropic and anesthetic drugs, have been shown to induce a characteristic Brugada ECG pattern, predisposing the patient to fatal ventricular arrhythmias. However, there are scarce data regarding the clinical significance. In this case series, a typical Brugada pattern was unmasked by lithium, valproic acid, and thiocolchicoside; however, the clinical scenario was different in all 3 cases, ranging from an asymptomatic patient to sudden cardiac arrest.

Hypocalcemia is mainly the consequence of hypoalbuminemia, advanced renal impairment, cirrhosis, malnutrition, or sepsis. The most common ECG manifestation of hypocalcemia is QT prolongation as a result of ST segment lengthening. Very occasionally, hypocalcemia can manifest with ST segment elevation forcing the differential diagnosis with ST elevation MI. We described a case of severe hypocalcemia manifesting in electrocardiogram with a J point elevation, absent of ST segment and with associated short QT interval mimicking acute myocardial infarction.

THIS CASE REPORT EXPOSES A PHENOMENON WHICH, ALTHOUGH PROPOSED, HAS NOT BEEN DESCRIBED IN CLINICAL LITERATURE: transient postictal hemiplegia (Todd's paralysis) with concomitant electrocardiographic J-point deflection (Osborn waves). Although typically associated with hypothermia, a prominent J-wave on the electrocardiogram (ECG) results from a transmyocardial voltage gradient during ventricular repolarization. Rarely, the Osborn wave may be observed in a non-hypothermic setting such as hypercalcemia or cerebral hemorrhage. Transient postictal hemiplegia has been attributed to localized cerebral hypoperfusion resulting from motor cortex exhaustion following an epileptic seizure. The same central nervous system autonomic dysfunction has been theorized to produce subendocardial hypoperfusion with electrocardiographic change and cardiac troponin T elevation. This is the first described ECG evidence of a dynamically displaced J-point in the setting of postictal hemiplegia.

Gender differences in J point height exist. Previous studies suggest male sex hormones mediate effects on cardiovascular disease through myocardial repolarization. Our objective was to assess whether male and female sex hormones are associated with J point amplitude in healthy subjects. We conducted a cross-sectional study of 475 healthy, mixed racial population of men, and premenopausal women (age 33 ± 9 years, 56% male). Baseline J point amplitude (JPA) was obtained from continuous surface electrocardiograms. Plasma testosterone (T), dihydrotestosterone, estrone, 17-estradiol (E2), and sex hormone-binding globulin were measured. A free testosterone index (FTI) was calculated. Multivariate regression analysis stratified by gender and electrocardiographic lead location was used to determine independent predictors of maximum JPA. Regression analysis demonstrated FTI levels were positively associated with JPA in lateral leads (β = +0.01, p0.05) in men but not in women. Total testosterone was positively associated with anterior electrocardiographic lead JPA in women (β = +0.5, p0.02), but not in men. E2 was positively associated with inferior lead JPA (β = +1.2, p0.03) in men but not in women. Total testosterone levels were positively associated with JPA in anterior leads (β = +0.054, p0.05) in women. Male volunteers in the highest tertile of FTI demonstrated greater lateral JPA compared with the lowest tertile (p0.05). Women in the highest tertile of FTI demonstrated greater anterior lead JPA compared with the lowest tertile (p0.05). In conclusion, in a young, healthy population, the female sex hormone E2 and an FTI are independent determinants of JPA in men, whereas T is associated with JPA in women.

The early repolarization (ER) pattern on the 12-lead electrocardiogram is characterized by J point elevation in the inferior and/or lateral leads. The ER pattern is associated with an increased risk of ventricular arrhythmias and sudden cardiac death (SCD). Based on studies in animal models and genetic studies, it has been proposed that J point elevation in ER is a manifestation of augmented dispersion of repolarization which creates a substrate for ventricular arrhythmia. A competing theory regarding early repolarization syndrome (ERS) proposes that the syndrome arises as a consequence of abnormal depolarization. In recent years, multiple clinical studies have described the characteristics of ER patients with VF in more detail. The majority of these studies have provided evidence to support basic science observations. However, not all clinical observations correlate with basic science findings. This review will provide an overview of basic science and genetic research in ER and correlate basic science evidence with the clinical phenotype.

The J wave, a deflection that follows the QRS complex of the surface electrocardiogram, is usually partially buried in the R wave in humans, appearing as a J-point elevation. An early repolarization (ER) pattern characterized by J-point elevation, slurring of the terminal part of the QRS, and ST-segment elevation has long been recognized and considered to be totally benign. Recent studies have presented evidence demonstrating that an ER pattern in inferior leads or inferolateral leads is associated with increased risk for life-threatening arrhythmias, named early repolarization syndrome. Early repolarization syndrome and Brugada syndrome share similar electrocardiographic characteristics, clinical outcomes, risk factors, as well as a common arrhythmic platform related to amplification of I(to)-mediated J waves. Although Brugada syndrome and early repolarization syndrome differ with respect to the magnitude and lead location of abnormal J wave manifestation, they can be considered to represent a continuous spectrum of phenotypic expression, termed J-wave syndromes. Early repolarization syndrome has been proposed to be divided into 3 subtypes: type 1, displaying an ER pattern predominantly in the lateral precordial leads, is prevalent among healthy male athletes and rarely seen in ventricular fibrillation survivors; type 2, displaying an ER pattern predominantly in the inferior or inferolateral leads, is associated with a higher level of risk; whereas type 3, displaying an ER pattern globally in the inferior, lateral, and right precordial leads, is associated with the highest level of risk for development of malignant arrhythmias and is often associated with ventricular fibrillation storms.

Aims An association has been described between death from arrhythmia and early repolarization, an electrocardiogram pattern characterized by elevation of the QRS–ST junction (J-point). Little is known about this relationship in non-white populations. This study examines the relationship between J-point elevation (JPE) and sudden cardiac death (SCD) and whether this relationship differs by race or sex. Methods and results A total of 15 141 middle-aged subjects from the prospective, population-based Atherosclerosis Risk in Communities (ARIC) study were included in this analysis. The primary endpoint was physician-adjudicated SCD occurring from baseline (1987–1989) through December 2002, secondary endpoints were fatal and non-fatal coronary events and all-cause mortality occurring through December 2007. J-point elevation was defined as J-point amplitude ≥0.1 mV. Pre-specified subgroup analyses by sex and race were conducted. J-point elevation in any lead was present in 1866 subjects (12.3%). After adjustment for demographic, clinical, lifestyle, and laboratory variables, JPE was not significantly related to SCD in the overall sample [adjusted hazard ratio (HR), 1.23; 95% confidence interval (CI), 0.87–1.75]. However, significant interactions were present between race and JPE ( P = 0.006) and between sex and JPE ( P = 0.020). J-point elevation was significantly predictive of SCD in whites (adjusted HR, 2.03; 95% CI, 1.28–3.21) and in females (adjusted HR, 2.54; 95% CI, 1.34–4.82). Conclusion Our results suggest that JPE is associated with an increased risk of SCD in whites and in females, but not in blacks or males. Further studies are needed to clarify which subgroups of individuals with JPE are at increased risk for adverse cardiac events.

Objectives The purpose of this study was to assess the prevalence of J-point elevation among the relatives of sudden arrhythmic death syndrome (SADS) probands. Background J-point elevation is now known to be associated with idiopathic ventricular fibrillation. We hypothesized that this early repolarization phenomenon is an inherited trait responsible for a proportion of otherwise unexplained SADS cases. Methods Families of SADS probands were evaluated in an inherited arrhythmia clinic. Twelve-lead electrocardiograms were analyzed for J-point elevation defined as >0.1 mV from baseline present in 2 or more of the inferior (II, III, and aVF) or lateral (1, aVL, V4 to V6) leads. Electrocardiographic data were compared with those of 359 controls of a similar age, sex, and ethnic distribution. Results A total of 363 first-degree relatives from 144 families were evaluated. J-point elevation in the inferolateral leads was present in 23% of relatives and 11% of control subjects (odds ratio: 2.54, 95% confidence interval: 1.66 to 3.90; p Conclusions J-point elevation is more prevalent in the relatives of SADS probands than in controls. This indicates that early repolarization is an important potentially inheritable pro-arrhythmic trait or marker of pro-arrhythmia in SADS.

The electrocardiographic J wave, also referred as the Osborn wave, is a deflection with a dome or hump morphology at the junction between the QRS complex and the ST segment on the body surface ECG. Earlier studies attributed the J wave to a variety of factors including hypoxia, injury current, acidosis, delayed ventricular depolarization, and early ventricular repolarization.1 Clinical and arrhythmogenic significance of the J wave abnormalities had largely been ignored until 1996 when Yan and Antzelevitch published a study elucidating the ionic and cellular basis of the J wave, indicating that a prominent Ito-mediated action potential notch in ventricular epicardium but not endocardium may produce a transmural voltage gradient during early ventricular repolarization that could register as a J wave or J point elevation in the ECG.2 Growing evidence has since been advanced indicating that J wave abnormalities, which are often accompanied by early repolarization and ST segment elevation on the ECG, are in some cases associated with a risk of sudden cardiac death. The J wave syndromes, which represent a variable spectrum of phenotypic expression with accentuation of the J wave, can be inherited or acquired.3–6 This review attempts to summarize current knowledge about J-wave syndromes- linking bench work with the bedside.

The J wave, also referred to as an Osborn wave, is a deflection immediately following the QRS complex of the surface ECG. When partially buried in the R wave, the J wave appears as J-point elevation or ST-segment elevation. Several lines of evidence have suggested that arrhythmias associated with an early repolarization pattern in the inferior or mid to lateral precordial leads, Brugada syndrome, or arrhythmias associated with hypothermia and the acute phase of ST-segment elevation myocardial infarction are mechanistically linked to abnormalities in the manifestation of the transient outward current (I(to))-mediated J wave. Although Brugada syndrome and early repolarization syndrome differ with respect to the magnitude and lead location of abnormal J-wave manifestation, they can be considered to represent a continuous spectrum of phenotypic expression that we propose be termed J-wave syndromes. This review summarizes our current state of knowledge concerning J-wave syndromes, bridging basic and clinical aspects. We propose to divide early repolarization syndrome into three subtypes: type 1, which displays an early repolarization pattern predominantly in the lateral precordial leads, is prevalent among healthy male athletes and is rarely seen in ventricular fibrillation survivors; type 2, which displays an early repolarization pattern predominantly in the inferior or inferolateral leads, is associated with a higher level of risk; and type 3, which displays an early repolarization pattern globally in the inferior, lateral, and right precordial leads, is associated with the highest level of risk for development of malignant arrhythmias and is often associated with ventricular fibrillation storms.

Background Early repolarization, which is characterized by an elevation of the QRS–ST junction (J point) in leads other than V1 through V3 on 12-lead electrocardiography, has been associated with vulnerability to ventricular fibrillation, but little is known about the prognostic significance of this pattern in the general population. Methods We assessed the prevalence and prognostic significance of early repolarization on 12-lead electrocardiography in a community-based general population of 10,864 middle-aged subjects (mean [±SD] age, 44±8 years). The primary end point was death from cardiac causes, and secondary end points were death from any cause and death from arrhythmia during a mean follow-up of 30±11 years. Early repolarization was stratified according to the degree of J-point elevation (≥0.1 mV or >0.2 mV) in either inferior or lateral leads. Results The early-repolarization pattern of 0.1 mV or more was present in 630 subjects (5.8%): 384 (3.5%) in inferior leads and 262 (2.4%) in lateral leads,...

Objectives The purpose of this study was to determine whether J-point elevation is a marker of arrhythmic risk. Background J-point elevation has been considered an innocent finding among healthy young individuals (the “early repolarization” pattern). However, this electrocardiogram (ECG) finding is increasingly being associated with idiopathic ventricular fibrillation (VF). Methods In a case-control study, the ECG of 45 patients with idiopathic VF were compared with those of 124 age- and gender-matched control subjects and with those of 121 young athletes. We measured the height of J-point and ST-segment elevation and counted the presence of slurring in the terminal portion of the R-wave. Results J-point elevation was more common among patients with idiopathic VF than among matched control subjects (42% vs. 13%, p 0.001). This was true for J-point elevation in the inferior leads (27% vs. 8%, p 0.006) and for J-point elevation in leads I to aVL (13% vs. 1%, p 0.009). J-point elevation in V4 to V6 occurred with equal frequency among patients and matched control subjects (6.7% vs. 7.3%, p 0.86). Male subjects had J-point elevation more often than female subjects and young athletes had J-point elevation more often than healthy adults but less often than patients with idiopathic VF. The presence of ST-segment elevation or QRS slurring did not add diagnostic value to the presence of J-point elevation. Conclusions J-point elevation is found more frequently among patients with idiopathic VF than among healthy control subjects. The frequency of J-point elevation among young athletes is intermediate (higher than among healthy adults but lower than among patients with idiopathic VF). (J Am Coll Cardiol 2008;52:1231‐8) © 2008 by the American College of Cardiology Foundation

Introduction: Myocardial cooling can induce J point elevation (Osborn wave) as seen on ECG of the Brugada syndrome by activating transient outward current (Ito) and causing a spike-and-dome configuration of the monophasic action potential (MAP) in the ventricular epicardium in isolated canine ventricular wedge preparations. We determined the effect of regional epicardial cooling of the right ventricular outflow tract (RVOT) on surface ECG and ventricular vulnerability in the dog. Methods and Results: In 12 dogs, a cooling device (20-mm diameter) was attached to the RVOT epicardium, and surface ECG, epicardial MAP, and endocardial MAP were recorded. Regional cooling (29.7°C ± 2.2°C) elevated the J point from 0.05 ± 0.06 mV to 0.12 ± 0.11 mV and induced T wave inversion (from 0.02 ± 0.12 mV to −0.27 ± 0.20 mV) in lead V1 in association with “spike-and-dome” configuration of the epicardial MAP. Cooling prolonged MAP duration in the RVOT epicardium from 172 ± 27 ms to 213 ± 30 ms (P < 0.01) but not in the RV endocardium and increased transmural dispersion of MAP duration from 9 ± 8 ms to 44 ± 21 ms (P < 0.01). Cooling also prolonged the QT interval in lead V1 from 191 ± 19 ms to 212 ± 23 ms (P < 0.05), but not in lead V5, and increased spatial dispersion of QT interval from 7 ± 5 ms to 20 ± 10 ms (P < 0.01). QT interval in lead V1 correlated positively with MAP duration in the RVOT epicardium (r = 0.75). T wave amplitude in lead V1 correlated inversely with transmural dispersion of MAP duration in the RVOT (r =−0.74). Vagal nerve stimulation accentuated the cooling-induced changes. During cooling, ventricular fibrillation was induced by a single extrastimulus in 2 of 4 dogs, and additional vagal nerve stimulation during isoproterenol administration induced spontaneous ventricular fibrillation in one dog. Conclusion: Localized epicardial cooling of the RVOT could be an in vivo experimental model of Brugada syndrome. (J Cardiovasc Electrophysiol, Vol. 15, pp. 936-941, August 2004)

The early repolarization (ER) pattern is a particular EKG aspect first described in 1936 by Shipley and Hallaran as a normal variant of repolarization. Subsequently Haissaguerre et al proposed a new ER classification characterized by J point elevation associated with J wave and ST-segment elevation or a horizontal/descending ST segment. A recent meta-analysis shows that the ER pattern was associated with high risk of all-cause mortality if characterized by a notched J wave with a horizontal/descending ST elevation and T waves discordant to their respective ST-segment deviation (

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Brugada syndrome is an autosomal dominant disorder caused by loss of function mutation(s) involving the SCN5A sodium channel that is associated with sudden cardiac death. It has a characteristic pattern on ECG consisting of ST segment elevations in V1 to V3 and J point elevation of at least 2mm.

See article by Taggart et al. [50] (pages 454-462) in this issue. Studies conducted over the past dozen years or so have demonstrated that ventricular myocardium is not homogeneous, as previously thought, but is comprised of at least three electrophysiologically distinct cell types: epicardial, M and endocardial cells (see [1,2] for reviews). These three cell types have also been shown to possess different pharmacologic profiles and to respond differently to a variety of pathophysiologic states [3–8]. The three cells types differ principally with respect to repolarization characteristics. Ventricular epicardial and M cells display action potentials with a prominent transient outward current ( I to)-mediated phase 1, giving rise to a notched appearance of the action potential. The absence of a prominent notch in the endocardium is a consequence of a much smaller I to. Similar regional differences in I to are found in canine, feline, rabbit, rat and human ventricular myocytes (see [1] for references). Recent studies also indicate that I to and the action potential notch are much larger in right vs. left ventricular epicardial [9] and M [10] cells. The transmural gradient in the amplitude of the I to-mediated action potential notch underlies the normal J wave or J point elevation in the ECG [11] and its accentuation, particularly in the right ventricle, contributes to the development of life-threatening arrhythmias in patients with the Brugada syndrome and various forms of idiopathic ventricular fibrillation [12,13]. The presence of a prominent I to in right ventricular epicardium has also been shown to sensitize this tissue to the effects of ischemia [14]. Accentuation of the action potential notch and eventual loss of the dome in right ventricular epicardium but not endocardium has been shown to contribute to ischemia-induced ST segment elevation [12]. The M cells are … *Tel.: +1-315-735-2217; fax: +1-315-735-5648 ca{at}mmrl.edu

Recurrent ventricular fibrillation was observed in a 29-year-old Vietnamese man who did not exhibit structural heart disease. The patient's ECG showed prominent J (Osborn) waves and ST segment elevation in the inferior leads that were not associated with hypothermia, serum electrolyte disturbance, or myocardial ischemia. Rate-dependent change in the amplitude of J waves and ST segment elevation also were observed. An implantable cardioverter defibrillator (ICD) was implanted. Adjunctive treatment with amiodarone reduced J wave amplitude, preventing ventricular fibrillation and ICD shocks. Prominent J waves and ST segment elevation in the inferior leads may serve as an important diagnostic sign to detect high-risk individuals with a history of unexplained syncope. ICD implantation plus amiodarone is the treatment of choice.