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The Fourth Universal Definition of Myocardial Infarction (FUDMI) focuses on the distinction between nonischemic myocardial injury and myocardial infarction (MI), along with the role of cardiovascular magnetic resonance, in order to define the etiology of myocardial injury. As a consequence, there is less emphasis on updating the parts of the definition concerning the electrocardiographic (ECG) changes related to MI. Evidence of myocardial ischemia is a prerequisite for the diagnosis of MI, and the ECG is the main available tool for (a) detecting acute ischemia, (b) triage, and (c) risk stratification upon presentation. This review focuses on multiple aspects of ECG interpretation that we firmly believe should be considered for incorporation in any future update to the Universal Definition of MI.

Background Brugada syndrome (BrS) includes a group of patients with a typical pattern of ST segment elevation in right precordial leads who are at risk for sudden cardiac death. The electrocardiogram pattern may be intermittent and unmasked by sodium channel blockers. The main objective of this study is to describe a serie of consecutive patients in whom oral administration of flecainide was used to unmask BrS type I electrocardiographic pattern. Methods We prospectively studied 14 symptomatic (palpitations/syncope) patients referred to our laboratory presenting a suggestive but not diagnostic Brugada ECG or family history of sudden death. Single oral dose of flecainide 400 mg was administered. Resting 12-lead ECG with upper and standard right precordial leads were performed after flecainide administration at 15, 30, 60 and 90 min and hourly until ECG became normal. Results Median age was 37.5 years (range = 22–50). None of them had structural heart disease. In 7 patients (50%) the typical coved-type ECG pattern of BrS was unmasked. PR interval, QRS duration and QTc median difference after-before test was 20 msec (min–max = −17–+57), 21 ms (min–max = 0 to +59) and 20 ms (min–max = −11–+77), respectively. There were no episodes of AV block, atrial or ventricular tachyarrhythmia. Conclusions In our experience we found that oral administration of flecainide in a single dose of 400 mg is useful to unmask type 1 Brugada electrocardiographic pattern.

We are in the midst of a rapidly evolving era of technology-assisted medicine. The field of telemedicine provides the opportunity for highly individualized medical management in a way that has never been possible before. Evolving medical technologies using cardiac implantable devices with capabilities for remote monitoring permit evaluation of multiple parameters of cardiovascular physiology and risk, including cardiac rhythm, device function, blood pressure values, the presence of myocardial ischaemia, and the degree of compensation of congestive heart failure. Cardiac risk, device status, and response to therapies can now be assessed with these electronic systems of detection and reporting. This document reflects the extensive experience from investigators and innovators around the world who are shaping the evolution of this rapidly expanding field, focusing in particular on implantable pacemakers, implantable cardioverter defibrillators, devices for cardiac resynchronization therapy (both with and without defibrillation properties), loop recorders, and hemodynamic monitoring devices. This document covers the basic methodologies, guidelines for their use, experience with existing applications, and the legal and reimbursement aspects associated with their use. To adequately cover this important emerging topic, the International Society for Holter and Noninvasive Electrocardiology and the European Heart Rhythm Association combined their expertise in this field. We hope that the development of this field can contribute to improve care of our cardiovascular patients.

Lead aVR is the only lead in the surface ECG that does not face the “typically” relevant walls of the left ventricle. Historically, its value has been neglected most likely due to its unusual configuration and direction, which appeared to have little correlation with other more congruous and easily diagnostic frontal leads. The isolation of the unipolar leads in the Standard surface ECG presentation may also have played an important role. Even with this “unfair” neglect, we know nowadays that it is very sensitive to locate obstructed epicardial coronary arteries. Besides helping distinguishing the culprit lesion of an infarct, lead aVR also helps recognizing other conditions that could be of clinical significance such as pericarditis, Brugada syndrome, fascicular blocks of the right branch, ectopic left atrial rhythms, etc. The purpose of this review is to revise the clinical value of lead aVR in the recognition of frequent and not so frequent clinical conditions. Ann Noninvasive Electrocardiol 2011;16(3):295–302

Several publications considering anatomical, histological, pathological, electrocardiographic, vectorcardiographic, and electrophysiologic studies have shown that the left bundle branch splits into three fascicles or in a "fan-like interconnected network" in the vast majority of human hearts. The left His system is trifascicular with a left anterior, a left posterior, and a left septal fascicle (LSF). Consequently, the classic term "hemiblock," to describe the block of one of the fascicles, established several decades ago by the Rosembaum's school, should be updated. Electrovectorcardiographic changes resulting from conduction abnormalities of the left anterior and left posterior fascicles are commonly diagnosed, mainly by their changes in the frontal plane. However, the existence of conduction defects of the LSF remains controversial. The ECG/VCG hallmark of LSF block is prominent anterior QRS forces (PAF) on the horizontal plane. This ECG/VCG phenomena should be distinguished from other conditions that also produce anterior QRS shift in the HP as: normal variants, right ventricular enlargement, misplaced precordial leads, lateral myocardial infarction, right bundle branch block, Wolff-Parkinson-White, obstructive and nonobstructive forms of hypertrophic cardiomyopahty, diastolic left ventricular enlargement, endomiocardial fibrosis, Duchenne muscular dystrophy, and dextroposition. The two highly frequent etiologies of LSFB are ischemia (coronary artery disease (CAD) with critical proximal obstruction of the left anterior descending coronary artery) and, in Latin America, Chagas' cardiomyopathy. The aims of this review are to revise the evidence of the existence of a trifascicular left Hissian system and to help in the ECG/VCG recognition of the LSFB.

Brugada Syndrome (BrS) is a low-prevalent entity (with the exception of certain endemic areas from Southeastern Asia, such as Thailand, the Philippines, and Japan) that affects the sarcolemmal channels of cardiomyocytes (channelopathy), characterized by a typical clinical-electrocardiographic pattern, occurring with great predominance in the male gender (male/female ratio—8:1 in nonAsian and 10:1 in Asian people1). The average age of the initial diagnosis is 41 ± 15 years; it is either sporadic (≈63% of the cases) or caused by a genetic mutation2 (≈37%) with dominant autosomal transmission and variable degrees of penetrance. The affected gene in ≈20% of the cases is SCN5A, located in the short arm of chromosome 3p21–23, which encodes the α subunit of the Na+ channel, a protein complex of the sarcolemma present in the contractile muscle of the atria, ventricles, and the excitoconductor system, being fundamental in the onset, conduction, excitability, excitation-contraction, and maintenance of cardiac rhythm.3 There are four genetic subtypes described as responsible for BrS1, BrS2, BrS3, and BrS4 variants4 that affect different locus, channels, and genes, and with particular clinical-electrocardiographic manifestations. BrS1: With mutation in the sodium channel: locus 3p21–23, INa+ channel, and SCN5A.Nav1.5 gene. This is the classical and predominant variety.5 BrS2:6 locus 3p24, INa+ channel, and GPD1L gene:7 more benign clinical course, with progressive conduction disease, minimal tendency to sudden cardiac death, and pharmacological test with procainamide, which does not identify the affected individuals. BrS3: With mutation in the slow calcium channel: associated to discretely short QT interval corrected by heart rate (QTc) (≤360 ms), locus 12p13.3, ICaL+2 channel, and CACNA1C.Cav1.2 gene. BrS4: locus 10p12.33, ICaL+2 channel, CACNB2b.CAvβ2b gene.8 There is a wide spectrum of mutations in the SCN5A gene with allelic phenotypes to BrS1, which led to consider the group as Na+ channel syndrome9 with overlay of clinical presentations. Mutations in the Na+ channel are responsible for variant 3 in congenital long QT syndrome, BrS, progressive conduction defect, and several mixed phenotypes.10 BrS1 necessarily occurs in the absence of any apparent demonstrable structural heart disease, even with invasive methods (except for biopsy), and not related to ischemia, electrolytic imbalances, and action of drugs. It is considered a “primary electrical heart disease.” The following factors stand out: possible positive family background for sudden cardiac death (SCD) or syncope in first-degree family members ≤40 years, a high tendency of the appearance during night sleep (rest) (>85% of the cases) of very fast malignant runs of polymorphic ventricular tachycardia (PVT) that may be aborted or degenerate into ventricular fibrillation (VF) and lead, respectively, to syncope or SCD. The annual mortality rate in Thailand has been estimated in 26 to 38 deaths per 100,000 inhabitants/year.1 Since the first consensus, three ECG patterns are acknowledged, called types 1, 2, and 3.11,12 Only type 1—much rarer—is diagnostic and characterized by presenting in the right precordial leads (V1 and V2 or V3)13 of ECG, ST-segment elevation ≥2 mm with superior convexity followed by T wave of negative polarity. Type 2 pattern displays in the right precordial leads, elevation of the J point, and the initial portion of ST segment of ≥ 2 mm and in the terminal portion ≥ 1 mm with saddleback appearance, followed by positive or biphasic T wave. In type 3, the ST segment also has saddleback configuration with elevation in J point and the onset of ST segment ≥ 2 mm and terminal portion ≤ 1 mm followed by positive T wave. Types 2 and 3 are found as normal variants, being included within the group of right end conduction delays by the fascicles of the right bundle branch of the His bundle.14 In many patients, type 1 ECG pattern is not observed, and the ECG could be transitorily normal making diagnosis difficult. The administration of certain class IA and class IC sodium channel blockers can unmask type 1 ECG pattern.15 There are different drugs and clinical circumstances that may trigger both type 1 ECG pattern and runs of PVT/VF: tricyclic antidepressants,16 vagotonic agents,17 α-agonists,18 antihistamines,19 cocaine,20 prajmalium bitartrate,21 antimalarial agents, some anesthetic agents,22 nocturnal vagotonia, and febrile states.23 In symptomatic patients, the treatment of choice is the implantable cardioverter defibrillator (ICD).24 In newborn babies and small infants, where ICD is not technically feasible, or in poor countries, where its high cost is unaffordable, oral quinidine is used with encouraging results.25 Quinidine is indicated in patients that already have an ICD implanted, to decrease the number of shocks. With very severe symptoms known as electrical storm, the therapy of choice consists of the association of isoproterenol infusion, general anesthesia, and bypass.26

Objectives: The purpose of this study was to evaluate potential interference between the Pill-cam™ video-capsule and implanted cardio-defibrillators (ICD) in both in vitro and in vivo test environments. Methods: Phase I consisted of in vitro testing utilized 6 ICD models. Each was placed in a saline gel bath in conjunction with a tool designed to emit the same wave length as the Pill-Cam™ (the Test Cap). Tests were performed at both the manufacturer's nominal and most sensitive settings with the test probe placed at 1, 5, 10, and 15 cm from three different points. There were emissions of 10-, 30-, and 60- second duration at each location. Phase II was the in vivo study utilizing patients with implanted ICDs for standard clinical reasons who were undergoing evaluation with the Test Cap. Results: In Phase I, 864 tests were performed involving the 6 ICDs. There was totally normal behavior in 5 of the devices. The Biotronik Belos (Berlin, Germany) demonstrated oversensing and delivery of inappropriate therapy. In phase II, 6 patients underwent a total number of 288 tests (48 in each patient). There were 4 men and 2 women, mean age 61 (33–77) and none demonstrated any adverse interactions. Conclusions: In patients with devices identical to those evaluated that showed no interference, the use of the Pill-Cam is safe. However, in patients with a Biotronik Belos ICD (or any other nontested ICD) the use of the Pill-Cam should be done only in-hospital, after suspended ICD therapy and in conjunction with close monitoring.

Objective: Despite the progress that has been reached in emergency medical systems and resuscitation, sudden cardiac death (SCD) continues to be the major cause of the death, and remains a significant public health problem. In this publication we are reporting our Latin American experience in the secondary prevention of SCD, by means of an ongoing registry involving seven Latin American countries and 770 patients. Methods: Every individual within the present registry to date has presented with antecedents of aborted sudden death or cardiac arrest due to ventricular tachycardia or ventricular fibrillation. Patients included have fulfilled the Class I indication for implantable cardioverter defibrillator (ICD) and they were implanted with a Biotronik ICD (all models). The study was not sponsored by Biotronik, nor did they have access to the data. A specific protocol was designed for implantation and follow-up of patients. The database was completely registered through the Internet and a personal password was assigned to each group of investigators. The primary end point was death from all causes. Secondary end points were SCD and death due to congestive heart failure (CHF). Results: The etiology of cardiac disease was found to be predominantly coronary artery disease (CAD) 39.7% (306 patients), followed by Chagas disease (ChD), 26.1% (201 patients), and idiopathic dilated cardiomyopathy (DCM), 17% (131 patients). Any remaining pathologies were included as miscellaneous 13.2% (101 patients). In 31 patients (4%) the etiology was unknown. The age did not differ within the principal pathologies, but was significantly older than the miscellaneous group (62.0 ± 11.3 years vs 48.2 ± 18.9 years, P < 0.0001). The follow-up period was 27 ± 25 months (1–113 months) for the whole group. The mortality in functional classes I–II was significantly lower than mortality for functional classes III–IV (relative risk 1.46, CI 95%, P < 0.0001). Mean left ventricular ejection fraction (LVEF) for the whole group was 37.7 ± 14.3%. Male LVEF was 36.1 ± 14.1% and female LVEF was 42.2 ± 13.8% P < 0.0001. During the follow-up period, 130 deaths were reported (global mortality 16.9 ± 9.7%), out of which 84 (64.6%) were attributed to cardiac causes (10.9 ± 5.1% of the total population). The annual adjusted cardiac mortality was 5.2 ± 1.72% (range 3.5–7.0%). Among cardiac deaths the most common cause was progressive heart failure, 48 patients (57%) including 3 patients with pulmonary embolism. The second main cause of cardiac death was SCD, 36 patients (43%), including 4 patients with electrical storm and 3 patients with electromechanical dissociation after multiple shock therapy treatments. Conclusions: Despite the differences in terms of pathologies between the ICD-LABOR (Latin American bioelectronic ongoing registry) and randomized ICD trials, a parallel evolution in all cause mortality and cardiac mortality was observed. Independent risk factors for mortality included age >70 years, male gender, NYHA III/IV, and ejection fraction

There are many diseases related to ion-channel disorders, so-called “channelopathies.” Hereditary short QT syndrome is a clinical-electrocardiographic entity with autosomal-dominant mode of transmission and it is the most recently described channelopathy. The syndrome may affect infants, children, or young adults with strong positive family background of sudden cardiac death. Short QT syndrome is characterized by short QT and heart-rate-corrected QTc intervals. It is frequently associated with tall-, peaked-, and narrow-based T waves that are reminiscent of the typical “desert tent” T waves of hyperkalemia. There is a high tendency for paroxysmal atrial fibrillation due to the heterogeneous abbreviation of action potential duration and refractoriness of atrial myocytes. The arrhythmia can also be induced by programmed electrical stimulation. The safest treatment suggested is an implantable cardioverter defibrillator, though the possibilities of inappropriate shocks have caused some concern, especially in teenagers. The ability of quinidine to prolong the QT interval has the potential to be an effective therapy for patients with short QT syndrome. This is particularly important in developing countries, where the implantable cardioverter-defibrillator therapy is not always available. Since these patients are at risk of sudden cardiac death from birth, and implantable cardioverter-defibrillator implantation has a lot of limitations in very young children, the utility of quinidine has to be evaluated further. Clinicians need to be aware of this deadly electrocardiographic (ECG) pattern as it portends a high risk of sudden cardiac death in otherwise healthy subjects with structurally normal hearts.

Andersen's Syndrome is a rare disease, hereditary with autosomal dominant transmission, of the ion channels of the sarcolemmal membranes of the cardiac and skeletal muscles (channelopathy), which affects chromosome 17 of the KCNJ2 gene, responsible for encoding the outward potassium delayed rectifier current KIR2.1, resulting in a loss or suppression of the function of this channel.

Background: The purpose of this trial was to evaluate a patient actuated transtelephonic cardiac monitoring system in order to document cardiac arrhythmias and cardiac pacemaker function. Material: Eighty-two patients were prospectively evaluated, 69 with pacemaker (group I) and 13 with symptomatic arrhythmias (group II). Two different recorders were used: a memory loop-recorder (KH) and a wrist-worn recorder (HW). Both of them were implemented using a small, portable, battery-powered transmitter, which monitors a modified V5 in KH and a lead 1 with the HW over regular nondigital pulse telephone lines. Results: In group I, 54 patients used single chamber pacemakers, 2 VDDR, and 13 used dual chamber devices. In group II, all patients included referred palpitations as their symptom. In group I, 248 registers were made using the KH and 50 with the HW. Recordings were made with KH had a 96% accuracy in the diagnosis of the ECG, while HW recordings failed to detect the QRS and the spike in 52% of the cases. Arrhythmia patients (group II) made 65 recordings with KH, all symptomatic: 28 were ventricular ectopic beats (23 isolated, 4 bigeminy, and 1 coupled ventricular ectopic beats); 9 supraventricular ectopic beats (isolated); 18 episodes of sinus tachycardia; and 10 normal sinus rhythm. Artifact was present partially in 6 other recordings, but did not affect the diagnosis. Two patients made no recordings and were excluded from the trial (group I). Conclusions: The loop-recording transtelephonic monitoring system is an excellent tool for the evaluation of patients with symptomatic arrhythmias and pacemaker. The memory KH had an excellent performance, even over regular telephone lines. The accuracy of the HW recordings was low and failed to evaluate the QRS, probably due to the direction of the AQRS vector.