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ST‐elevation myocardial infarction (STEMI) is a life‐threatening clinical condition that requires immediate intervention, mostly caused by complete occlusion of epicardial vessels. Other diseases such as myocarditis, pericarditis, electrolyte disturbance, and early repolarization may mimic. We present a rare case of atrial lead‐related atrial perforation which mimics inferior STEMI. [ABSTRACT FROM AUTHOR]

The patient is a 73‐year‐old female with peripheral vascular disease, coronary artery disease, and systemic lupus erythematosus, who underwent mesenteric artery bypass surgery. She suffered from a pneumonia after surgery, causing acute hypoxic respiratory failure and septic shock. Due to shock, she developed acute renal failure. She was intubated, ventilated, and received continuous veno‐venous hemodialysis for renal failure. ST elevation was first observed on telemetry and subsequently confirmed on electrocardiogram. Marked ST elevation is present in the anterior leads with reciprocal ST depression in the inferior leads. A prolonged QT interval is also present. What is the most likely diagnosis? [ABSTRACT FROM AUTHOR]

Background: Early repolarization (ER) and acute ST segment elevation myocardial infarction (STEMI) are sharing the pathophysiology of J wave syndromes. It is speculated that early ventricular arrhythmias (VAs) during STEMI may be predisposed by ER. Our aim was to study the association between ER pattern and risk of VAs during acute STEMI.Methods: The study included 102 male patients with acute STEMI who were divided into two groups: cases and controls. Cases included 52 patients with sustained VAs during the first 48 hours from the onset of STEMI, while controls included 50 patients with no VAs. On 12-lead surface electrocardiogram, ER was defined as ≥ 1 mm elevation of J point in at least two inferior or lateral leads with or without ST segment elevation.Results: Mean age was 48.44 ± 10.08 years and mean left ventricular ejection fraction (LVEF) was 42.25 ± 11.1%. ER pattern was more frequent in cases than controls (29 vs 14 patients, P = 0.008). Notched J wave (P = 0.0007) and horizontal ST segment (P = 0.033) were more frequent in cases than controls. On adjusted regression model, LVEF (OR: 0.95, 95% CI: 0.91-0.99, P = 0.015) and ER (OR: 3.39, 95% CI: 1.41-8.12, P = 0.006) could predict VAs, while QTc interval (P = 0.24) and QTd (P = 0.86) did not have predictive effect. Inferior/inferolateral and global ER pattern (P = 0.044 and 0.031 respectively), notched J wave (P = 0.001), increasing J wave amplitude (P = 0.042), and ST segment elevation (P = 0.001) were associated with a higher risk of VAs.Conclusions: ER is associated with increased risk of VAs in the setting of acute STEMI. [ABSTRACT FROM AUTHOR]

Background Exact associations of gender and age with occurrence of ST segment elevation myocardial infarction are inadequately known. Design Gender and age differences in frequency and incidence of ST segment elevation myocardial infarction ( STEMI were studied using a nationwide, population-based (26 723 956 person-years) registry of hospital admissions in patients aged ≥ 30 during 2001-2008 in Finland. Data were collected from all 22 hospitals with a coronary angiolaboratory nationwide. Results The study period included 27 993 STEMI admissions. Of these patients, 65·9% were men and 34·1% women, RR 2·37 (95% CI 2·05-2·74, P < 0·0001). Women were significantly older than men (74·3 ± 11·7 vs. 64·7 ± 12·4 years, P < 0·0001). Standardized incidence rate of STEMI was 113·0/100 000 person-years overall, 170·9/100 000 in men and 66·6/100 000 in women. Men had a 3·03 (95% CI 2·86-3·21; P < 0·0001)-fold age-adjusted relative risk of STEMI compared with women with highest risk difference in population under the age of 55 years ( RR 5·94; 95% CI 5·36-6·58, P < 0·0001). Incidence increased with age up to 90 years old, with estimated gender-adjusted increase rate of 41% (95% CI 40-42%; P < 0·0001) per 5-year increase in age. Incidence rate had a slowly declining trend (−2·2%; 95% CI −3·4 to −1·0% per year, P < 0·001) during the study period. Conclusions Men have a tripled overall risk of STEMI compared with women with highest relative risk in younger adults. Incidence rate of ST segment elevation myocardial infarction increases by estimated 41% per 5-year increase in age. [ABSTRACT FROM AUTHOR]

Since the first report in 1992, Brugada pattern (BP) diagnosis is mainly based on analysis of the precordial leads. In cases with no clear BP evidence in the conventional right precordial leads (4th intercostal space), limb leads analysis resulted helpful in suspecting BP. Fluctuations within right precordial leads between the diagnostic ECG pattern and nondiagnostic ECGs are well known. For the first time, in the patient herewith reported, the transformation of BP phenotype involves both precordial and peripheral leads, confirming that the analysis of all the 12 leads has a key role in BP diagnosis. [ABSTRACT FROM AUTHOR]

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]

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]

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 present segments from a 24-hour 12-lead digital Holter recording in a 48-year-old man demonstrating transient ST elevations in the inferior leads that triggered sustained ventricular tachycardia/ventricular fibrillation (VT/VF) requiring cardioversion. The onset of VT was preceded by a gradual increase in the ST with marked QRS broadening that lacked distinction between the end of the QRS and the beginning of the ST (QRS–ST–T “triangulation”), and shortening of the QT interval not caused by an increased heart rate. This is a relatively rare documentation of the mechanisms immediately triggering sustained ventricular arrhythmias during acute myocardial ischemia obtained with 12-lead ECG. [ABSTRACT FROM AUTHOR]

We present a patient with a permanent ventricular pacemaker who was investigated for episodes of chest pain associated with syncope. Ambulatory electrocardiographic monitoring showed essentially paced rhythm. ST segment elevation of the paced beats was observed during spontaneous chest pain, but the significance of this finding was initially unclear in the context of the abnormal repolarization associated intrinsically with paced rhythm. At angiography, coronary spasm was demonstrated after ergonovine, and this was associated with ST segment elevation during paced rhythm and with chest pain. We conclude that ST segment elevation may indicate myocardial ischemia even when observed in the face of abnormal repolarization associated with paced rhythm. [ABSTRACT FROM AUTHOR]

Electrode studies have been performed with dead animal tissue and a variety of other materials immersed in saline solution and compared with studies in the canine heart (live and arrested) in an attempt to delineate both normal and anomalous signals sensed by pacemaker electrodes or obtained during diagnostic electrogram recording of cardiac activity. The data from these studies could be useful for defining the origin of artifacts and a variety of other phenomenon such us "fractured" QRS complexes, acute ST segment elevations, His bundle oscillatory signatures, and unexplained potentials synchronously associated with cardiac events. The studies verify that artifacts can he generated in an electrolyte medium by rubbing electrodes against insulators or biologic materials and by inducing motion between common pole materials of an active electrode system. The studies suggest that some of the grasping electrodes in current clinical use may be subject to self-generating artifacts associated with cardiac-induced frictional motion between the constituent materials employed in the electrode design. [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]

ST Elevation with Flecainide and Pilsicainide. Flecainide and pilsicainide, Class IC antiarrhythmic drugs with slow kinetics, were administered to a 64-year-old man experiencing ventricular tachycardia. Both drugs suppressed the arrhythmia, but caused ST segment elevation in leads II, III, and aVF. No evidence of ischemic heart disease was detected. Withdrawal of the drugs eliminated the ST change. Because these drugs frequently are used to treat tachyarrhythmias in patients who may present with chest pain, this rare ECG manifestation of Class IC drugs should be recognized to avoid misdiagnosis of acute inferior myocardial infarction. [ABSTRACT FROM AUTHOR]

In 1992, Brugada and Brugada described a syndrome characterized by right bundle branch block pattern with ST elevation in leads V, through V, and a history of sudden death due to polymorphic ventricular tachycardia or ventricular fibrillation. Since these patients bad no evidence of cardiac disease, these findings were ascribed to a distinct clinical entity. Further experience bas shown that this same pattern may be mimicked by patients with right ventricular dysplasia. acute ischemia of the right ventricle, other infiltrative cardiomyopathies, as well as tricyclic drug overdose. The pathogenesis of these changes may be due to loss of the dome configuration in the transmembrane potential of right ventricular epicardial cells, which would result in a voltage gradient producing ST elevation. Other explanations involve delayed conduction in a dysplastic right ventricle. The clinical importance of this syndrome is that it calls attention to patients at risk for sudden cardiac death. In addition, these observations have sparked the interest of basic electrophysiologists relative to the relationship of these KCG waveforms and malignant ventricular arrhythmias. Finally, the clinician must exclude other organic diseases before diagnosing this entity. [ABSTRACT FROM AUTHOR]

The article describes the case of an 85-year-old woman with longstanding atrial fibrillation and complete atrioventricular block who was referred for coil embolization for diverticular bleeding of the colon. Case highlights include patient's diagnosis with Takotsubo cardiomyopathy, characterization of bidirectional ventricular tachycardia, and apical aneurysm due to Takotsubo cardiomyopathy.

Background: It may sometimes be difficult to differentiate subtle ST-segment elevation (STE) due to anterior myocardial infarction (MI) from benign variant (BV) STE. Recently, two related formulas were proposed for this purpose. However, they have never been tested in an external population.Materials and Methods: Consecutive patients from May 2017 to January 2018, who were admitted with the diagnosis of acute anterior STEMI, were enrolled. Electrocardiograms were systematically reviewed and only subtle ones were included. First 200 consecutive patients with noncardiac chest pain were also enrolled as a control group. Relevant electrocardiographic parameters were measured.Results: A total of 379 anterior MI and 200 BV-STE cases were enrolled during study period. A total of 241 patients in STEMI group were excluded for not matching subtleness criteria, four patients in control group were also excluded because of prior left-anterior descending artery intervention. The three-variable formula, with recommended cut-point of 23.5, had a sensitivity, specificity, and diagnostic accuracy of 73.9%, 86.7%, and 81.4%, respectively. The four-variable formula, with the published cut-point of 18.2, had a sensitivity, specificity, and diagnostic accuracy of 83.3%, 87.7%, and 85.9%, respectively.Conclusion: Three- and four-variable formulas with recommended cutoffs have a reasonable sensitivity, specificity, and diagnostic accuracy in differentiating subtle STEMI with BV-STE. Although both perform well, the four-variable formula has a higher sensitivity, specificity, and diagnostic accuracy and should be preferred. [ABSTRACT FROM AUTHOR]