PubMed · 7357729
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A Mayorga-Cortes, A Castellanos, R J Myerburg. 1980. LAHB obscuring RBBB.. https://pubmed.ncbi.nlm.nih.gov/7357729/
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BACKGROUND: Patients with heart failure were candidates for cardiac resynchronization therapy (CRT) regardless of underlying aetiology. This study observed the effect of CRT in patients with ischaemic or nonischaemic cardiomyopathy. METHODS: One hundred and forty-two patients with refractory chronic heart failure and left bundle branch block received cardiac resynchronization therapy, 91 men and 51 women, average age 60 years. Left ventricular ejection fraction (LVEF) was severely depressed (mean 29%), left ventricular end diastolic diameter (LVEDD) enlarged (mean 72 mm) and QRS width was lengthened (mean 147 ms). Ninety-eight had nonischaemic cardiomyopathy and 44 had ischaemic cardiomyopathy. RESULTS: After cardiac resynchronization therapy, the heart function was significantly improved. The mean LVEF increased from 29% to 36% after pacing. In patients with nonischaemic cardiomyopathy, the LVEF was improved from 28% to 37%, and in patients with ischaemic cardiomyopathy, the LVEF was improved from 30% to 36%. No significant difference of the improvement was found between the two groups (P > 0.05). CONCLUSIONS: Cardiac resynchronization therapy could significantly improve cardiac function in patients with chronic heart failure regardless of the underlying heart disease.
Brugada syndrome is characterized by the presence of an electrocardiographic pattern of ST-segment elevation in leads V1 to V3 and a history of sudden cardiac death in the absence of structural heart disease [Brugada P, Brugada J. Right bundle branch block, persistent ST segment elevation and sudden cardiac death: a distinct clinical and electrocardiographic syndrome. A multicenter report. J Am Coll Cardiol 1992;20(6):1391]. The disease usually affects individuals in their 40s, at the prime of their life, and the appearance of cardiac arrest in these otherwise healthy individuals brings an important burden to families and to health care. Brugada syndrome is in several instances a familial disease, caused by mutations in SCN5A in up to 25% of the individuals [Chen Q, Kirsch GE, Zhang D, Brugada R, Brugada J, Brugada P, et al. Genetic basis and molecular mechanism for idiopathic ventricular fibrillation. Nature 1998;392(6673):293]. The identification of the electrocardiographic pattern in an individual will therefore trigger an important cascade of events in the families. Several family members, including children, will be under the scrutiny of a cardiologist to decide on preventive measures, especially if there is a history of sudden death in the family. The presence of abnormal repolarization patterns, which in otherwise sporadic individuals might be classified under normal variations, have become a diagnostic challenge for clinicians facing a family with the disease [Hong K, Brugada J, Oliva A, Berruezo-Sanchez A, Potenza D, Pollevick GD, et al. Value of electrocardiographic parameters and ajmaline test in the diagnosis of Brugada syndrome caused by SCN5A mutations. Circulation 2004;110(19):3023].
The prevalence of conduction disturbances, particularly left bundle branch block (LBBB), is strongly correlated with age and with the presence of cardiovascular disease. LBBB has been reported to affect approximately 25% of the heart failure (HF) population and it is likely that the deleterious role of such conduction disorders in the progression to HF has been underestimated. The purpose of this article is to review the data from the literature indicating that LBBB may have a causative role, mediated through the resulting intra-ventricular asynchrony, in the deterioration of cardiac function and the development of cardiac remodelling and HF. It also aims to address the potential for future clinical therapies for this conduction disorder.