PubMed · 4441012
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P Nicolai, M Delaage, J L Medvedowsky, C Barnay. [Left posterior hemiblocks. Current data].. https://pubmed.ncbi.nlm.nih.gov/4441012/
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BACKGROUND: Analysis of the surface ECG can predict the locations of pacing foci but is of limited value for locating arrhythmogenic substrates causing ventricular tachycardia because of the effects of myocardial infarction, ischaemia, and bundle branch block on ventricular activation. AIM: To determine whether analysis of the initial 60 ms segment of the surface QRS improves the accuracy of the ECG for predicting ventricular tachycardia origin we correlated the locations of 37 arrhythmogenic areas present in 20 patients with the 3D vectors of the ventricular tachycardias generated by each respective area. METHODS: The 3D vector of each ventricular tachycardia morphology was calculated from the integrals of the initial 60 ms of the surface vectorcardiogram and from the entire QRS recorded in each lead of the Frank orthogonal lead vectorcardiogram. Sixty eight-morphologies of ventricular tachycardia were mapped using simultaneous recordings from 60 catheter electrodes. RESULTS: Ventricular tachycardias with 3D vectors directed inferiorly and posteriorly or superiorly and anteriorly were more likely to originate from the septum, P = 0.04, whereas tachycardias directed superiorly and to the right were more likely to originate from the inferior wall and the cardiac apex, P = 0.001. However, the same arrhythmogenic area could generate multiple ventricular tachycardias with different 3D vectors. In addition, ventricular tachycardias with similar 3D vectors were generated by arrhythmogenic areas in the septal, apical and inferior walls. The variances of the mean 3D vectors of ventricular tachycardias originating from each of 12 different cardiac regions were no different when based on the initial 60 ms of the surface QRS than on the entire surface QRS. CONCLUSION: Analysis of the surface ECG provides only an approximate guide to the locations of arrhythmogenic areas generating ventricular tachycardia even when analysis is restricted to the initial forces in the surface QRS. Therefore, detailed mapping is needed to accurately determine the number and location of arrhythmogenic areas.
BACKGROUND: Progressive familial heart block type I (PF-HBI) is a dominantly inherited cardiac bundle-branch conduction disorder that has been traced through nine generations of a large South African kindred. Similar conduction disorders have been reported elsewhere; however, the cause of these diseases is unknown. The aim of the present study was to determine by linkage analysis the approximate chromosomal position of the gene causing PFHBI, thereby allowing family-based diagnosis and the development of positional cloning strategies to identify the causative gene. METHODS AND RESULTS: Eighty-six members of three pedigrees, 39 members of which were affected with PFHBI, were genotyped at four linked polymorphic marker loci mapped to chromosome 19, bands q13.2-q13.3 (chromosome 19q13.2-13.3). Maximum two-point logarithm of the odds scores (which represent the logarithm of the odds ratio of detecting linkage versus nonlinkage) generated were 6.49 (theta = 0) for the kallikrein locus, 5.72 (theta = 0.01) for the myotonic dystrophy locus, 3.44 (theta = 0) for the creatine kinase muscle-type locus and 4.51 (theta = 0.10) for the apolipoprotein C2 locus. The maximum multipoint logarithm of the odds score was 11.6, with the 90% support interval positioning the PFHBI locus within a 10 cM distance centering on the kallikrein 1 locus. CONCLUSIONS: The gene for PFHBI maps to an area of approximately 10 cM on chromosome 19q13.2-13.3. There are several candidate genes in this interval; although a recombination event ruled out the myotonic dystrophy locus from direct involvement with PFHBI, the proximity of these two loci may be relevant to the observed cardiac abnormalities of myotonic dystrophy. The results provide a means of DNA-based diagnosis in the families studied and a foundation for cloning studies to identify the causative gene.
The indications, method, results and complications of various thrombolytic medical treatment options in acute myocardial infarction is discussed. The thrombolytic treatment decreases the in-hospital and late mortality of patients and prevents the deterioration of left ventricular function. The earlier the treatment is initiated, the better result may be expected. The indication of thrombolysis may be expanded for patient with left bundle branch block, higher age groups, and also for late admissions after the onset of chest pain.