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Background: ST-segment elevation (STE) and an increased Tpeak-Tend interval (Tp-e) have prognostic value for malignant arrhythmia events (MAEs) in patients with ST-segment elevation myocardial infarction (STEMI) and Brugada syndrome. Whether STE could predict MAEs and has an electrophysiological relationship with Tp-e in electrocardiogram (ECG) of vasospastic angina (VA) patients needs to be elucidated., Methods: Sixty-five patients with VA and 23 patients with VA complicated by MAEs were enrolled. The relationship of ECG parameters and MAEs (defined as ventricular tachycardia/ventricular fibrillation (VT/VF), syncope, and aborted sudden death) was analyzed by t-test, regression and receiver operating characteristic (ROC) curve analyses., Results: Patients with MAEs showed greater STE (P<0.001) and corrected QT dispersion (cQTd) (P=0.021), a longer corrected Tp-e interval (cTp-e) (P<0.001), and a larger Tp-e/QT ratio (P<0.001) than those in non-MAE groups. Univariate analysis revealed that cQTd (odds ratio (OR)=1.065; P=0.020), cTp-e (OR=1.159; P=0.001), Tp-e/QT (OR=1.344, P=0.002), and STE (OR=5.655, P<0.001) were significantly associated with MAEs. In the multivariate analysis, Tp-e/QT and STE remained predictors of MAEs. ROC curve analysis showed that the areas under curve (AUCs) for Tp-e/QT (AUC=0.944) and STE (AUC=0.974) were not significantly different (P>0.05), but both were significantly different than AUCs for cQTd (AUC=0.724) and cTp-e (AUC=0.841) (all P<0.05). STE was well fitted with the Tp-e/QT ratio in a multivariable linear regression model., Conclusions: STE and increased Tp-e/QT ratio had related electrophysiological properties and were independent prognostic indicators of MAEs in patients with VA., (Copyright © 2019. Published by Elsevier Inc.)

The STEMI-DTU pilot study tested the early safety and practical feasibility of left ventricular (LV) unloading with a trans-valvular pump before reperfusion. In the intent-to-treat cohort, no difference was observed for microvascular obstruction (MVO) or infarct size (IS) normalized to either the area at risk (AAR) at 3–5 days or total LV mass (TLVM) at 3–5 days We now report a per protocol analysis of the STEMI-DTU pilot study. In STEMI-DTU STUDY 50 adult patients (25 in each arm) with anterior STEMI [sum of precordial ST-segment elevation (ΣSTE) ≥4 mm] requiring primary percutaneous coronary intervention (PCI) were enrolled. Only patients who met all inclusion and exclusion criteria were included in this analysis. Cardiac magnetic resonance (CMR) imaging 3–5 days after PCI quantified IS/AAR and IS/TLVM and MVO. Group differences were assessed using Student's t -tests and linear regression (SAS Version-9.4). Of the 50 patients enrolled, 2 died before CMR imaging. Of the remaining 48 patients those without CMR at 3–5 days (n = 8), without PCI of a culprit left anterior descending artery lesion (n = 2), with OHCA (n = 1) and with ΣSTE < 4 mm (n = 5) were removed from this analysis leaving 32/50 (64 %) patients meeting all inclusion and exclusion criteria (U-IR, n = 15; U-DR, n = 17) as per protocol. Despite longer symptom-to-balloon times in the U-DR arm (228 ± 80 vs 174 ± 59 min, p < 0.01), IS/AAR was significantly lower with 30 min of delay to reperfusion in the presence of active LV unloading (47 ± 16 % vs 60 ± 15 %, p = 0.02) and remained lower irrespective of the magnitude of precordial ΣSTE. MVO was not significantly different between groups (1.5 ± 2.8 % vs 3.5 ± 4.8 %, p = 0.15). Among patients who received LV unloading within 180 min of symptom onset, IS/AAR was significantly lower in the U-DR group. In this per-protocol analysis of the STEMI-DTU pilot study we observed that LV unloading for 30 min before reperfusion significantly reduced IS/AAR compared to LV unloading and immediate reperfusion, whereas in the ITT cohort no difference was observed between groups. This observation supports the design of the STEMI-DTU pivotal trial and suggests that strict adherence to the study protocol can significantly influence the outcome. • LV unloading plus delayed reperfusion may reduce infarct size. • LV unloading plus delayed reperfusion may reduce microvascular obstruction. • This per protocol analysis supports the design of the ongoing STEMI-DTU pivotal trial. [ABSTRACT FROM AUTHOR]

Prompt diagnosis of acute ST segment elevation myocardial infarction (STEMI) by the initial ECG is important in order to perform an urgent coronary angiography as soon as possible and achieve successful revascularization, therewith improving mortality and morbidity. Several diseases and conditions can mimic an acute myocardial infarction (AMI) but may not benefit from a (percutaneous) revascularization strategy. This narrative clinical review will discuss the ECG features of some of the causes of nonischemic ST segment elevation to facilitate early recognition, prevent wrongful diagnosis and improve treatment outcomes. [ABSTRACT FROM AUTHOR]

In 1992 a new syndrome consisting of syncopal episodes and/or sudden death in patients with a structurally normal heart and a characteristic electrocardiogram (ECG) with a pattern of right bundle branch block with an ST segment elevation in leads V1 to V3 was described 1 In 1998 the poor prognosis of patients with the syndrome not receiving an implantable defibrillator was reported 2,3 In 1998 the genetic nature of the disease and its assotiation to a mutation in the cardiac sodium channel gene was described 4 . Because the diagnosis is easily made by means of the ECG, an increasing number of patients with the ECG pattern are being identified worldwide. In this article we will review our present knowledge concerning patients with the classical ECG pattern of the disease. In the Brugada syndrome, the diagnosis is based on the history of aborted sudden death with the typical electrocardiographic pattern of ST segment elevation in leads V1-V3, with or without right bundle branch block 1 ( Fig. 1). In some cases, however, the diagnosis is different because some individuals present with an abnormal electrocardiogram but are completely asymptomatic or there is a history of sudden death in the family and the electrocardiographic criteria are observed.

Brugada syndrome is characterized electrocardiographically by ST segment elevation in the right precordial leads, followed by a negative T wave unrelated to ischemia, electrolyte disturbance or drug effects and prone to rapid polymorphic ventricular tachycardia capable of degenerating into ventricular fibrillation. The ECG pattern may be dynamic and is often concealed. Sodium channel blockers, drugs, electrolyte imbalances, fever and several other clinical circumstances are recognized inducers of a Brugada type 1 ECG in susceptible patients. We describe a case of a Brugada type 1 ECG pattern induced by severe hyponatremia. Copyright © 2011 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background: Recently, we demonstrated that ajmaline caused ST segment elevation in the heart of an SCN5A mutation carrier by excitation failure in structurally discontinuous myocardium. In patients with Brugada syndrome, ST segment elevation is modulated by cardiac sodium (I Na), transient outward (I to), and L-type calcium currents (I CaL). Objective: To establish experimentally whether excitation failure by current-to-load mismatch causes ST segment elevation and is modulated by I to and I CaL. Methods: In porcine epicardial shavings, isthmuses of 0.9, 1.1, or 1.3 mm in width were created parallel to the fiber orientation. Local activation was recorded electrically or optically (di-4-ANEPPS) simultaneously with a pseudo-electrocardiogram (ECG) before and after ajmaline application. Intra- and extracellular potentials and ECGs were simulated in a computer model of the heart and thorax before and after introduction of right ventricular structural discontinuities and during varying levels of I Na, I to, and I CaL. Results: In epicardial shavings, conduction blocked after ajmaline in a frequency-dependent manner in all preparations with isthmuses ≤1.1 mm width. Total conduction block occurred in three of four preparations with isthmuses of 0.9 mm versus one of seven with isthmuses ≥1.1 mm (P<.05). Excitation failure resulted in ST segment elevation on the pseudo-ECG. In computer simulations, subepicardial structural discontinuities caused local activation delay and made the success of conduction sensitive to I Na, I to, and I CaL. Reduction of I to and increase of I CaL resulted in a higher excitatory current, overcame subepicardial excitation failure, and reduced the ST segment elevation. Conclusions: Excitation failure by current-to-load mismatch causes ST segment elevation and, like ST segment elevation in Brugada patients, is modulated by I to and I CaL. [Copyright &y& Elsevier]

Brugada Syndrome is a condition with an undetermined aetiology and a tendency for malignant arrhythmias, an electrocardiographic pattern of a right bundle branch block with persistent ST segment elevation in the right precordial leads (V1-V3) and no association with structural heart disease. We aimed to discuss the anaesthetic management of an asymptomatic 35-year-old patient with Brugada syndrome who had been diagnosed during the pre-anaesthetic assessment because of the family history of the early sudden cardiac death of his mother. As a result, we believe that detailed patient history and careful examination of laboratory tests and electrocardiography are crucial for early diagnosis of some diseases and for successful anaesthetic management. [ABSTRACT FROM AUTHOR]

Copyright of Der Kardiologe is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: Glucose-induced insulin secretion is one of the contributing factors to fluctuation of ST segment elevation in Brugada syndrome. Objectives: The purpose of this study was to explore the influence of meals on variations of ST elevation in Brugada syndrome. Methods: We assessed changes of ST segment elevation in lead V1-3 on ECG before and after taking meals, at midnight, and at 3:00 a.m. in 20 patients with Brugada syndrome. Plasma glucose, insulin, and K+ concentrations were measured. Variations of ST elevation were defined as morphological changes and/or augmentation of ST segment level by >1.0 mm. Result: Variations of ST segment morphology or elevation level after meals were observed in 15 of 20 patients (75%). ST elevation was augmented most markedly after dinner (3.3 ± 1.7 mm) and decreased both at midnight (2.6 ± 1.3 mm: P < 0.01 vs after dinner) and at 3:00 a.m. (2.4 ± 1.2 mm: P < 0.01 vs after dinner). Morphologic changes and elevation levels of ST segment were associated with changes in glucose-induced insulin levels after meals, being highest after dinner (47 ± 33 μU/mL) and decreasing significantly at midnight (7 ± 4 μU/mL) and at 3:00 a.m. (5 ± 2 μU/mL). There were no correlations between ST elevation and changes in serum K+ level or heart rate. Conclusions: The present findings suggest that variations of ST elevation are frequently associated with meals. Aggravation of ST elevation is most prominent in the evening to night after dinner rather than the period between midnight and early morning. This information may help to predict event times at high risk for life-threatening arrhythmias in Brugada syndrome. [ABSTRACT FROM AUTHOR]

ST Elevation in Brugada Syndrome. Introduction: In Brugada syndrome, ventricular fibrillation (VF) occurs mainly during sleep, and Brugada ECG signs are intensified by parasympathomimetic drugs; therefore, vagal activity could be a precipitating factor of VF. The aim of the present study was to elucidate the relation between spontaneous augmentation of ST elevation and changes in autonomic nervous activities in the daily life of patients with Brugada syndrome. Methods and Results: Twenty-three consecutive patients with Brugada syndrome were studied. Group VF(+) consisted of 7 symptomatic patients and 3 asymptomatic patients with inducible VF; group VF(–) consisted of 13 asymptomatic patients without documented or inducible VF. Two-channel unipolar lead (V1 and V2) Holter ECG was recorded. Heart rate variability was analyzed by the maximum entropy method. Spontaneous augmentation of ST elevation (≥1.5 mm/20min) occurred more frequently during 24 hours in group VF(+) than in group VF(–) (5.7 ± 2.5 times vs 2.3 ± 2.4 times, P < 0.01). ST elevation was significantly greater in group VF(+) than in group VF(–) (2.1 ± 0.2 mm vs 1.8 ± 0.2 mm, P < 0.05). Power of the high-frequency component (HF: 0.15–0.4 Hz) and RR interval increased progressively, and the ratio of low-frequency component (LF; 0.04– 0.15 Hz) to high-frequency component (LF/HF) gradually decreased toward the time of maximum ST elevation. During an entire day, daytime (0–5 P.M.), and nighttime (0–5 A.M.), both HF and LF/HF were not different between groups VF(+) and VF(–). Conclusion: In Brugada syndrome, spontaneous augmentation of ST elevation in daily life occurred along with an increase in vagal activity. ST elevation was augmented more in patients with VF than in those without VF under similar vagal tone. (J Cardiovasc Electrophysiol, Vol. 15, pp. 1-7, June 2004) [ABSTRACT FROM AUTHOR]

Copyright of Der Internist is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Increased Insulin Level and Brugada Syndrome. Introduction: ST segment elevation in patients with Brugada syndrome is known to fluctuate occasionally, influenced by multiple factors. Insulin has been shown to affect QT dispersion in healthy volunteers, as well as result in abnormality of ventricular repolarization in patients with congenital long QT syndrome. Methods and Results: To assess a possible role of insulin in ST segment elevation in patients with Brugada syndrome, an oral glucose tolerance test (OGTT) was administered to 20 patients with Brugada syndrome and 20 normal patients without ST-T changes as a control group. Plasma glucose and potassium levels, immunoreactive insulin concentration (IRI), and ST segment elevation and ST-T wave changes on 12-lead ECG during OGTT were analyzed. Augmentation (>1 mm) of ST elevation or morphologic changes in ST-T waves were observed frequently in response to increased IRI during OGTT [15/20 cases (75%)] in patients with Brugada syndrome but in none of the patients in the control group [0/20 cases (0%), P < 0.01 ]. The changes returned to baseline 180 minutes after the glucose load in 9 of 15 patients. Patients who showed coved-type ST elevation before the glucose load exhibited positive ECG changes more frequently than patients with saddleback-type elevation or transiently normalized ST segment [8/8 cases (100%) vs 7/12 (58%), P < 0.05 ]. There was no significant difference between the two groups in terms of glucose, IRI, and potassium levels during OGTT. Conclusion: The findings suggest that glucose-induced insulin secretion is one of the contributing factors to fluctuation of ST segment elevation in patients with Brugada syndrome.(J Cardiovasc Electrophysiol, Vol. 14, pp. 243-249, March 2003). [ABSTRACT FROM AUTHOR]

We report a 37-year-old man with documented aborted sudden death. After resuscitation, the patient showed no structural heart disease but the ECG showed a right bundle-branch block with a descending ST segment elevation in leads V1 and V2. After transient normalization of the ECG, the administration of ajmaline led to spontaneous development of the distinct descending ST segment elevation in the right precordial leads and therefore to the diagnosis of Brugada syndrome. The incidence of sudden cardiac death among these patients is high. The only treatment is an implantable cardioverter-defibrillator (ICD). The Brugada syndrome should therefore be borne in mind in the differential diagnosis of sudden death. [ABSTRACT FROM AUTHOR]

Transient ST segment elevation in right precordial leads with use of psychotropic drugs is reported in two cases of overdose and one case of therapeutic administration. Flecainide did not reproduce ST segment elevation. The relationship of these abnormalities to the Brugada syndrome and the electrophysiologic hypothesis are discussed. [ABSTRACT FROM AUTHOR]

We evaluated two patients without previous episodes of syncope who showed characteristic ECG changes similar to Brugada syndrome following administration of Class IC drugs, flecainide and pilsicainide, but not following Class IA drugs. Patient I had frequent episodes of paroxysmal atrial fibrillation resistant to Class IA drugs. After treatment with flecainide, the ECG showed a marked ST elevation in leads V2 and V3, and the coved-type configuration of ST segment in lead V2. A signal-averaged ECU showed late potentials that became more prominent after flecainide. Pilsicainide, a Class IC drugs induced the same ST segment elevation as tiecainide, but procainamide did not. Patient 2 also had frequent episodes of paroxysmal atrial fibrillation. Pilsicainide changed atrial fibrillation to atrial flutter with 2:1 ventricular response, and the ECG showed right bundle branch block and a marked coved-type ST elevation in leads V1 and V2. After termination of atrial flutter, ST segment elevation in leads V1 and V2 continued. In this patient, procainamide and quinidine did not induce this type of ECG change. In conclusion, strong Na channel blocking drugs induce ST segment elevation similar to Brugada syndrome even in patients without any history of syncope or ventricular fibrillation. [ABSTRACT FROM AUTHOR]

Sodium Block-Induced ST Segment Elevation. Three patients in whom Class IC sodium channel blockers induced ST segment elevation In leads V1 through V3 are described. The underlying electrophysiologic mechanism, implications for drug-induced proarrhythmia, and the relationship of the finding to the Brugada syndrome type of idiopathic ventricular fibrillation are discussed. [ABSTRACT FROM AUTHOR]

The disease known as Brugada Syndrome, the first time in 1992 in patients without structural heart disease characterized by ventricular arrhythmias and sudden cardiac death was defined as a new clinical and electrocardiographic syndrome. Components of this syndrome are as follows: right bundle branch block, precordial chest leads (V1-V3) ST segment elevation and sudden cardiac death. Our aim in this short review is to determine how should we correctly diagnose and approach to this syndrome in the light of recent information. [ABSTRACT FROM AUTHOR]