1,597 research outputs found
Exercise-induced left septal fascicular block: an expression of severe myocardial ischemia
The electrocardiogram (ECG) criteria for the left septal fascicular block (LSFB) are not universally accepted and many other denominations can be seen in literature: focal septal block, septal focal block, left septal fascicular block, left anterior septal block, septal fascicular conduction disorder of the left branch, left septal Purkinje network block, left septal subdivision block of the left bundle branch, anterior conduction delay, left median hemiblock, left medial subdivision block of the left bundle branch, middle fascicle block, block of the anteromedial division of the left bundle branch of His, and anteromedial divisional block. During exercise stress test, fascicular blocks (left anterior and posterior) seem to indicate severe coronary artery narrowing of left main coronary or proximal left anterior descending artery disease1 and transient exercise-induced left septal fascicular block has been reported a few times2,3.
54-year-old male, with a history of essential arterial systemic hypertension, primary hyperlipidemia and six-month typical chest pain during exercise (Class II – Canadian Cardiovascular Society) underwent an exercise stress test. During the exercise stress test, ECG demonstrated abrupt prominent anterior forces, an increase in R wave amplitude from V1 to V4, extreme left axis deviation and minor ST segment depression in DII, DIII and aVF (Figure 1). The post-exercise period showed progressive return of the QRS axis in both frontal and horizontal planes and the ST depression worsened by 1 mm. Coronary angiogram (Figure 2A) showed a critical proximal left anterior descending artery lesion. An exercise stress test done three months after coronary artery bypass surgery grafting was normal (Figure 2B)
Prof. Dr. João Tranchesi: Chronology of a fruitful life, 8 February 1922 - 12 October 1978
Exercise Testing Score for Myocardial Ischemia Gradation
Scores aimed at contributing to the optimization of exercise testing (ET) have been developed and the experience with their application in coronary artery disease (CAD) has proven to be favorable1. Although there is debate on the use of scores in clinical practice, those that stand for it argue that they may decrease the rate of undiagnosed CAD, besides reducing the number of patients without disease that undergo highly expensive tests2. Additionally, scores may be helpful, in a more consistent and organized fashion, in prognosis evaluation and in the adoption of an appropriate plan of action for the triage of this disease in the general population
Propofol infusion syndrome and Brugada syndrome electrocardiographic phenocopy
This anesthetic drug may cause a rare condition named propofol infusion syndrome, characterized
by unexplained lactic acidosis, lipemia, rhabdomyolysis, cardiovascular collapse and
Brugada-like electrocardiographic pattern or Brugada electrocardiographic phenocopy changes
following high-dose propofol infusion over prolonged periods of time.
Several articles have contributed to our understanding of the cause of the syndrome, and the
growing number of case reports has made it possible to identify several risk factors. Uncertainty
remains as to whether a genetic susceptibility exists.
The favorable recovery profile associated with propofol offers advantages over traditional
anesthetics in clinical situations in which rapid recovery is important. Propofol is a safe
anesthetic agent, but propofol infusion syndrome is a rare lethal complication. (Cardiol J 2010;
17, 2: 130-135
The management of Brugada syndrome patients
Brugada syndrome is a congenital electrical disorder characterised by the appearance of distinctive
QRST-T patterns in the right precordial leads and an increased risk of sudden death
(SCD) in young healthy adults. Although chamber enlargement is not apparent in most cases,
autopsy and histological investigations have revealed structural abnormalities. The typical
Brugada ECG manifestation is often concealed and may be revealed by Class IC anti-arrhythmic
agents with the effect of blocking the fast component of sodium channel currents. The
syndrome may also be unmasked or precipitated by a febrile state, vagotonic agents, α-adrenergic
agonists, β-adrenergic blockers, tricyclic or tetracyclic antidepressants, a combination of
glucose and insulin and hypokalaemia, as well as by alcohol and cocaine toxicity. Since the
typical Brugada ECG pattern can be normalised by Class IA agents to block transient outward
currents (Ito) or by isoproterenol and cilostazol to boost calcium channel currents, they have
been considered pharmacological therapies aimed at rebalancing the ion channel currents
during cardiac depolarisation and repolarisation. Case studies by intra-cardiac mappingguided
ablation in the right ventricular outflow tract and Purkinje network have shown
evidence of eliminating the substrate of ventricular tachycardia/fibrillation (VT/VF) in
Brugada syndrome, which may be used as an adjunct to device therapy to abort electrical
storms. At present the most effective therapy to prevent sudden cardiac death in Brugada
syndrome is an implantable cardioverter defibrillator. (Cardiol J 2007; 14: 97–106
Basics of contemporary exercise testing
Exercise testing is a well-established procedure that has been in widespreadclinical use for many decades. Exercise testing is generally a safe procedure, but good clinicaljudgment should therefore be used in deciding which patients should undergo exercise testing.Interpretation of the exercise test should include exercise capacity and clinical, hemodynamic,and electrocardiographic response.O teste ergomĂ©trico Ă© um exame já bem estabelecido e vem sendo adotado na práticaclĂnica por várias dĂ©cadas. Ele Ă© geralmente seguro, mas deve ser considerado de formajudiciosa, indicando-se de forma apropriada qual o tipo de paciente que deve ser submetidoao exame. A interpretação do teste ergomĂ©tico inclui capacidade funcional, aspectos clĂnicos,hemodinâmicos e a resposta eletrocardiográfica
Early repolarization variant: Epidemiological aspects, mechanism, and differential diagnosis
Early repolarization variant (ERV or ERPV) is a enigmatic electrocardiographic phenomenon,
characterized by prominent J wave and ST-segment elevation in multiple leads.
Recently, there has been renewed interest in ERV because of similarities to the arrhythmogenic
Brugada syndrome (BrS). Not much is known about the epidemiology of ERV and several
studies have reported that this condition is associated with a good prognosis. Both syndromes
exhibit some similarities including the ionic underlying mechanism, the analogous responses
to changes in heart rate and autonomic tone, sympathicomimetics (isoproterenol test) as well
as in sodium channel and beta-blockers. These observations raise the hypothesis that ERV
may be not as benign as traditionally believed. Additionally, there are documents showing that
ST-segment height in the man is greatly influenced by central sympathetic nervous activity,
both at baseline and during physiologic and pharmacological stress.
Central sympathetic dysfunction regularly results in multilead ST-segment elevation or J wave
that decreases or below isoelectric baseline during low dose isoproterenol infusion.
In this review, we describe the characteristics of ERV and the main differences with acute
pericarditis, acute myocardial infraction/injury and Brugada syndrome. (Cardiol J 2008; 15: 4-16
Eletrocardiograma de Longa Duraçao: o Sistema Holter - Parte II
A eletrocardiografia ambulatorial Ă© um mĂ©todo nao-invasivo utilizado na prática clĂnica para detectar, documentar e caracterizar ocorrĂŞncias de comportamento anormal da atividade elĂ©trica cardĂaca durante as atividades diárias rotineiras. Como tais anormalidades ocorrem raramente, o eletrocardiograma deve ser registrado por longos perĂodos de tempo. Desde a introduçao, em 1961 por Norman Holter, os sistemas de eletrocardiografia ambulatorial tem sido desenvolvidos com uma ampla variedade de fidelidade de registro, peso e tamanho dos equipamentos, capacidades de análise e formatos de relatĂłrios. Existem trĂŞs tipos básicos de gravadores: gravadores contĂnuos, intermitentes (gravador de eventos) e gravadores de análise em tempo real. Gravadores contĂnuos possuem um gravador analĂłgico para capturar o eletrocardiograma continuadamente e tipicamente registram na fita dois ou trĂŞs canais do eletrocardiograma por 24 horas. Gravadores intermitentes registram somente um limitado nĂşmero de curtos segmentos de dados; sua proposta Ă© a de capturar o comportamento elĂ©trico anormal quando o paciente apresenta o sintoma para o qual o estudo foi indicado. Os registros intermitentes podem ser transmitidos por telefone no momento da ocorrĂŞncia do evento, ou os dados podem ser armazenados e transmitidos posteriormente. Os gravadores com análise em tempo real avaliam o eletrocardiograma continuamente. Os sinais eletrocardiográficos recebidos, ao invĂ©s de serem armazenados em uma fita analĂłgica, sao digitalizados e armazenados em memĂłria sĂłlida. Utilizando-se do sistema Holter, podemos tambĂ©m investigar: arritmias, efeito terapĂŞutico de drogas ou procedimentos, marcapassos e desfibriladores, doença cardĂaca isquĂŞmica e variabilidade da freqĂĽĂŞncia cardĂaca. As indicaçoes gerais para a eletrocardiografia ambulatorial seguem as recomendaçoes da Força Tarefa ACP/ACC/AHA e sao discutidas neste artigo
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