Infarto agudo de miocardio inferior enmascarando el síndrome de la onda J: A propósito de cuatro observaciones
01 Jan 2008-Medicina Intensiva (Elsevier)-Vol. 32, Iss: 1, pp 48-53
TL;DR: El sindrome de the onda J puede estar oculto por un infarto agudo de miocardio inferior with depresion simultanea del segmento ST in las derivaciones precordiales derechas.
Abstract: The J wave syndrome is characterized by a prominent J wave accompanied by ST-segment elevation in the absence of structural heart disease. It includes the benign early repolarization syndrome, the highly arrhythmogenic Brugada syndrome and idiopathic ventricular fibrillation. Although acute coronary syndromes are one of the leading causes of ST-segment deviation, no clinical reports that specifically describe the modulating effects of an ischemic injury current on the ECG manifestations of the J wave syndrome have been found. This report describes four cases of patients with acute inferior ST-segment elevation myocardial infarction who had J wave (or negative deplacement of the J point) and ST-segment depression in the right precordial leads. Later, these precordial ECG alterations disappeared and were progressively replaced by prominent J (R') waves and anterior ST-segment elevations, suggesting the presence of a J wave syndrome. In conclusion, the J wave syndrome may be obscured by an acute inferior myocardial infarction with concomitant ST-segment depression in the right precordial leads. In such circumstances, early detection of the J wave (or depressed J point) may be used as ECG marker of the early repolarization syndrome or Brugada syndrome.
TL;DR: This case illustrates the possible deleterious effects of beta-blockers in patients with Brugada syndrome and the stabilizing membrane effect of high concentration of propranolol and/or inhibition of ICaL.
Abstract: This is the first report of Brugada syndrome revealed by beta-blocker intoxication. A 24-year-old healthy man ingested propranolol (2.28 g) to commit suicide. After early gastric lavage, electrolytes, cardiac enzymes, chest X-ray, and echocardiography were normal. Dosages of psychotropic drugs were negative. ECG showed a typical coved-type pattern of Brugada syndrome. Follow-up showed partial ECG normalization of the discrete saddleback-type pattern. The ajmaline- test confirmed Brugada syndrome. These ECG modifications may be explained by the stabilizing membrane effect of high concentration of propranolol and/or inhibition of ICaL. This case illustrates the possible deleterious effects of beta-blockers in patients with Brugada syndrome.
01 Jan 2011
Abstract: 136 marzo 2011 SEMG El término infarto agudo de miocardio (IAM) hace referencia a un riego sanguíneo insuficiente con daño tisular en una parte del corazón, producido por una obstrucción en una de las arterias coronarias, frecuentemente por ruptura de una placa de ateroma vulnerable. La isquemia o suministro deficiente de oxígeno resultante de la obstrucción produce la angina de pecho, que, si se recanaliza precozmente, no produce muerte del tejido cardíaco; si se mantiene esta anoxia se produce la lesión del miocardio y finalmente la necrosis, es decir, el infarto. El IAM es la principal causa de muerte, tanto en hombres como mujeres, en todo el mundo1. La facilidad de producir arritmias, sobre todo la fibrilación ventricular, es la causa más frecuente de muerte en el IAM en los primeros minutos2. Tiene una prevalencia de 0,5% de la población general y constituye el problema de salud más importante en los países desarrollados. El 5% de los IAM no son diagnosticados en el momento de la consulta y son dados de alta. Para conocer la base fisiopatológica de los síndromes coronarios agudos es fundamental manejar la anatomía coronaria básica3. El corazón esta irrigado por dos arterias principales: la coronaria izquierda y la coronaria derecha. La arteria coronaria izquierda está conformada por: • El tronco. • La descendente anterior, que da dos tipos de ramas principales: las septales y las diagonales, que irrigan los dos tercios ántero-apicales del septum interventricular y la pared ántero-lateral del ventrículo izquierdo (VI), respectivamente; también da la rama obtusa marginal que irriga la pared lateral del VI y las ramas pósterolaterales, si es dominante la descenderte posterior. • La arteria circunfleja. La coronaria derecha (CD) esta constituida por las siguientes ramas fundamentales: • Descendente posterior: irriga el tercio posterior del septum interventricular. • Aurículo-ventricular: irriga la pared posterior del VI. • Rama del nódulo sinusal: en el 60% de los casos se origina de la CD y en los restantes de la circunfleja. • Ramas ventriculares anteriores: irrigan la pared libre del ventrículo derecho (VD). • Ramas auriculares. • Rama del nodo aurículo-ventricular. Clásicamente el IAM se define por la presencia de dos de los siguientes criterios3: angor, cambios en el electrocardiograma (ECG), elevación enzimática. Según el ECG se puede clasificar en: • IAM con supradesnivel del ST (tipo Q). • IAM sin supradesnivel del ST (no Q -Tipo ST o subendocárdico). • Tipo T. • Indeterminado. • Bloqueo completo de rama izquierda (BCRI). Para realizar un buen manejo clínico y terapéutico de IAM es muy importante saber hacer un diagnóstico topográfico del mismo, es decir, conocer la localización del área del corazón infartada de acuerdo con los hallazgos en el ECG y la clínica del paciente2 (Tabla 1). Infarto agudo de miocardio póstero-inferior con “imagen en espejo” en el electrocardiograma
TL;DR: Common clinical and ECG features define a distinct syndrome in this group of patients with recurrent episodes of aborted sudden death unexplainable by currently known diseases, not explainable by electrolyte disturbances, ischemia or structural heart disease.
Abstract: Objectives. The objectives of this study were to present data on eight patients with recurrent episodes of aborted sudden death unexplainable by currently known diseases whose common clinic...
TL;DR: The present report elaborates further on the diagnostic criteria and examines risk stratification schemes and device and pharmacological approaches to therapy on the basis of the available clinical and basic science data.
Abstract: Since its introduction as a clinical entity in 1992, the Brugada syndrome has progressed from being a rare disease to one that is second only to automobile accidents as a cause of death among young adults in some countries Electrocardiographically characterized by a distinct ST-segment elevation in the right precordial leads, the syndrome is associated with a high risk for sudden cardiac death in young and otherwise healthy adults, and less frequently in infants and children Patients with a spontaneously appearing Brugada ECG have a high risk for sudden arrhythmic death secondary to ventricular tachycardia/fibrillation The ECG manifestations of Brugada syndrome are often dynamic or concealed and may be unmasked or modulated by sodium channel blockers, a febrile state, vagotonic agents, α-adrenergic agonists, β-adrenergic blockers, tricyclic or tetracyclic antidepressants, a combination of glucose and insulin, hypo- and hyperkalemia, hypercalcemia, and alcohol and cocaine toxicity In recent years, an exponential rise in the number of reported cases and a striking proliferation of articles defining the clinical, genetic, cellular, ionic, and molecular aspects of the disease have occurred The report of the first consensus conference, published in 2002, focused on diagnostic criteria The present report, which emanated from the second consensus conference held in September 2003, elaborates further on the diagnostic criteria and examines risk stratification schemes and device and pharmacological approaches to therapy on the basis of the available clinical and basic science data
TL;DR: The results provide the first direct evidence in support of the hypothesis that heterogeneous distribution of a transient outward current-mediated spike-and-dome morphology of the action potential across the ventricular wall underlies the manifestation of the electrocardiographic J wave.
Abstract: Background The J wave is a deflection that appears in the ECG as a late delta wave following the QRS or as a small secondary R wave (R′). Also referred to as an Osborn wave, the J wave has been observed in the ECG of animals and humans for more than four decades, yet the mechanism underlying its manifestation is poorly understood. The present study investigates the cellular basis for the J wave using an isolated arterially perfused preparation consisting of a wedge of canine right or left ventricle. Methods and Results A 12-lead ECG was initially recorded in vivo. After isolation and arterial perfusion of the right or left ventricular wedge, transmembrane action potentials were simultaneously recorded from epicardial, M region, and endocardial transmural sites with three floating microelectrodes. A transmural ECG was recorded concurrently. A J wave was observed at the R-ST junction of the ECG in 17 of 20 adult dogs, usually in leads II, III, aVR, and aVF and the mid to lateral precordial leads. The J wave...
TL;DR: This review deals with the clinical, basic and genetic aspects of a recently highlighted form of idiopathic ventricular fibrillation known as the Brugada syndrome and attempts to correlate the electrocardiographic manifestations with cellular and ionic heterogeneity known to exist within the heart under normal and pathophysiologic conditions so as to identify the cellular basis and thus potential diagnostic and therapeutic approaches.
Abstract: This review deals with the clinical, basic and genetic aspects of a recently highlighted form of idiopathic ventricular fibrillation known as the Brugada syndrome. Our primary objective in this review is to identify the full scope of the syndrome and attempt to correlate the electrocardiographic manifestations of the Brugada syndrome with cellular and ionic heterogeneity known to exist within the heart under normal and pathophysiologic conditions so as to identify the cellular basis and thus potential diagnostic and therapeutic approaches. The available data suggest that the Brugada syndrome is a primary electrical disease resulting in abnormal electrophysiologic activity in right ventricular epicardium. Recent genetic data linking the Brugada syndrome to an ion channel gene mutation (SCN5A) provides further support for the hypothesis. The electrocardiographic manifestations of the Brugada syndrome show transient normalization in many patients, but can be unmasked using sodium channel blockers such as flecainide, ajmaline or procainamide, thus identifying patients at risk. The available data suggest that loss of the action potential dome in right ventricular epicardium but not endocardium underlies the ST segment elevation seen in the Brugada syndrome and that electrical heterogeneity within right ventricular epicardium leads to the development of closely coupled premature ventricular contractions via a phase 2 reentrant mechanism that then precipitates ventricular tachycardia/ventricular fibrillation (VT/VF). Currently, implantable cardiac defibrillator implantation is the only proven effective therapy in preventing sudden death in patients with the Brugada syndrome and is indicated in symptomatic patients and should be considered in asymptomatic patients in whom VT/VF is inducible at time of electrophysiologic study.
TL;DR: The clinical characteristics and cellular and ionic basis for early repolarization syndrome and the characteristics of ERS need to be more fully delineated within the framework of what has been learned about the Brugada syndrome in recent years are addressed.
Abstract: Early repolarization syndrome (ERS) has traditionally been regarded as benign. In the electrocardiogram (ECG), it is characterized by a diffuse upward ST-segment concavity ending in a positive T wave in leads V2−V4 (5). Clinical interest in this ECG phenomenon has recently been rekindled because of similarities with the electrocardiographic manifestations of the highly arrhythmogenic Brugada syndrome and the potential for misdiagnosis. This article addresses the clinical characteristics and cellular and ionic basis for ERS. In experimental models, the ECG signature of ERS can be converted to that of the Brugada syndrome, raising the possibility that ERS may not be as benign as generally thought, and that under certain conditions known to predispose to ST-segment elevation, patients with ERS may be at greater risk. Further clinical and experimental data are clearly required to test these hypotheses, and the characteristics of ERS need to be more fully delineated within the framework of what has been learned about the Brugada syndrome in recent years.