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)

Reverse atrial electrical remodeling: A systematic review

Atrial remodeling is a term introduced in 1995 to describe alterations in atrial structure or function. Atrial electrical remodeling is characterized by a reduction of refractory period and action potential duration, dispersion in refractoriness, and a reduction in conduction velocity of impulse propagation. Numerous animal and human studies have demonstrated that atrial electrical remodeling impairs normal atrial conduction and provides an environment for ectopic and re-entrant activity, thus creating a substrate for the initiation or maintenance of atrial fibrillation. Interestingly, atrial electrical remodeling has been shown to be reversible. In this systematic review, we examine the occurrence of reverse atrial electrical remodeling in various clinical settings. (Cardiol J 2011; 18, 6: 625–631

Chagas disease: State-of-the-art of diagnosis and management

Chagas’ disease or American trypanosomiasis, is a potentially lethal parasitic zoonosis prevalent and endemic only in Latin America, caused by the flagellate protozoa Trypanosoma cruzi. It has 3 differents stages, acute, indeterminate and chronic phase, with the chance of an etiological approach in the first stage and pharmacological and non-pharmacological treatment in the chronic phase. There are five main clinical forms of chronic chagasic cardiomyopathy: indeterminate, arrhythymogenic (predominantly dromotropic and extrasystolic), with ventricular dysfunction, thromboembolic and mixed forms. There are several diagnostic tests at the different stages, however, the ECG is the method of choice in longitudinal population studies in endemic areas because it is simple, with a low cost and a good sensitivity. Microscopic examination or parasitological diagnosis in the acute phase or immunodiagnostic tests are used to confirm the disease. The antiarrhythmic drug amiodarone, the most frequently prescribed agent for symptomatic ventricular arrhythmia treatment of Chagas’ disease patients, has also recently been shown to have antifungal activity. Cardiac device implantation is very common, and chronic Chagas disease patients require pacemaker implantation at a younger age in contrast with patients with other cardiac pathologies. In summary, Chagas disease is a social disease, endemic in Latin America and shows different prevalence rates in Latin American countries

Progressive conduction disturbance in myotonic dystrophy

Myotonic dystrophy (DM), the commonest dystrophy in adults, is an autosomal dominant disease characterized by a variety of multisystemic features. Two main genetically distinct forms of DM have been identified: type 1 (DM1), the classic form first described by Steinert, and type 2 (DM2), identified by Ricker. DM1 is caused by trinucleotide expansion of cytosine- -thymine-guanine (CTG) in the myotonic dystrophy protein kinase gene, whereas in DM2 the expansion of tetranucleotide repeats (CCTG) in the zinc finger protein 9 gene was identified. Both mutations are dynamic and are located in non-coding parts of the genes. Phenotype variability of DM1 and DM2 is caused by a molecular mechanism due to mutated RNA toxicity. DM1 is characterized by myotonia and multi-organ damage with major cardiac involvement. The disease is usually slowly progressive and life expectancy is reduced by the increased mortality associated with cardiopulmonary complications. Sudden death can occur as a consequence of cardiac-conduction abnormalities. We present the ECG of a 26 year-old male with DM1 and progressive conduction system disturbance characterized by syncopal episodes. (Cardiol J 2011; 18, 3: 322–325

Non-specific intraventricular conduction delay or atypical LBBB - How to predict acute coronary occlusion?

We describe two patient cases with acute coronary syndrome (ACS) and broad QRS in the acute phase electrocardiogram (ECG). The patients' ECG findings resembled left bundle branch block (LBBB), but with atypical features. Broad QRS not fulfilling the criteria for LBBB or right bundle branch block (RBBB) is diagnosed as non-specific intraventricular conduction delay (NSIVCD). The case report deals with the challenges of predicting acute coronary occlusion in patients with NSIVCD in their acute phase ECG. In one of the cases, the ECG changed from typical LBBB to NSIVCD or atypical LBBB with the development of systolic dysfunction and clinical heart failure.publishedVersionPeer reviewe