P. Torner

Electrophysiological mechanisms of the SI SII SIII electrocardiographic morphology

We studied three groups of individuals by means of spatial-velocity electrocardiograms and thallium-201 myocardial imaging to figure out the electrophysiological explanation of the SI SII SIII electrocardiographic morphology. We studied twelve healthy individuals without SI SII SIII, seven healthy individuals with SI SII SIII and fifteen patients with chronic obstructive pulmonary disease with SI SII SIII. The average values of the QRS-E and QRS-F intervals were higher in the second (P less than 0.05 and P less than 0.005) and third groups (P less than 0.01 and P less than 0.001) than in the first. One patient of the second group and thirteen of the third showed right ventricular enlargement. The slowing down of the right ventricular conduction explained the SI SII SIII morphology in normal individuals in more than half the cases. In patients with chronic obstructive pulmonary disease with SI SII SIII the conduction delay plays an important part in the electrogenesis of the right ventricular enlargement electrocardiographic morphology. We think that these observations can give further data about the electrophysiologic mechanism of the SI SII SIII morphology.

Study of the Evolution of Masked Bifascicular Block

Masked bifascicular block (MBB) (absent or minimal S in I and VL. high R in V; and ÂQRS approximately ‐60°) is a rare condition. We have found 16 such cases in the last 12 years, thirteen male and three female, mean age 70 ± 9 years. The conventional electrocardiogram was tabulated and the clinical features and evolution of the patients were followed over 39.1 ± 32 months. Ten patients required pacemakers, nine because of complete atrioventricular (AV) block or increase in the previous AV block. Seven patients died (follow‐up 27.3 ± 32 months), five from heart failure. This study shows: (1) MBB is a subgroup of patients with a high risk of advanced atrioventricular block; (2) a pacemaker implant does not significantly reduce the high mortality in this group because of the severity of the underlying disease; (3) these results should be evaluated in a larger series of patients in order to confirm our provisional results.

Heart Rate Variability Early After Successful Radiofrequency Catheter Ablation of Left- and Right-Sided Accessory Pathways and After Selective Ablation of the Slow Pathway

Inappropriate sinus tachycardia (1ST) and alterations in heart rate variability (HRV) may survene after radiofrequency catheter ablation (RFCA). The objective of this study was to analyze and to compare HRV after RFCA of supraventricular tachycardia.

Sudden cardiac death 1990: An update

In most cases, over 80% in our experience (Figure 1) [1–4], ambulatory sudden death (ASD) is due to the onset of malignant ventricular arrhythmia. In 50% of these, ventricular fibrillation (VF) preceded by classic ventricular tachycardia (VT) is responsible for ASD. In the remaining cases of malignant ventricular arrhythmia, VF is of abrupt onset or is preceded by “torsades de pointes”. In the 20% not due to malignant ventricular arrhythmia, the cause of ASD is bradyarrhythmia.

Imagen de seudocaptura por microdesplazamiento del electrodo en un marcapasos VDD

Los nuevos marcapasos secuenciales auriculoventriculares(AV) han mejorado la individualizacionen el modo de estimulacion para cada paciente. Lacomplejidad de los sistemas hace en ocasiones dificildetectar algunas malfunciones. En el caso clinicoque presentamos se expone como un fallo decaptura por microdesplazamiento del electrodopuede pasar desapercibido en un control sencillode marcapasos, al unirse varios factores como presentarconduccion AV normal en ese momento, laconcordancia entre la espicula y el QRS conducidoy la similar morfologia entre el complejo QRS conducidoy el estimulado.

Acute drug test

Initially introduced by Lown et al.. [1–4], these authors demonstrated the efficacy of this test in the treatment of patients with malignant ventricular arrhythmias. The test consists of the administration of acute oral doses of antiarrhythmic drug so as to determine whether the drug can suppress the premature ventricular contractions. If this is the case, it is probable that chronic administration of the antiarrhythmic will be useful. The acute drug test also allows us to know if the drug has an arrhythmogenic effect. The aims of the acute drug test, therefore, are: a) to identify therapy for arrhythmias more scientifically and less empirically; b) to objectively prove whether the therapeutic efficacy of the drugs administered acutely is maintained with chronic administration; c) to avoid iatrogenic risks (specially arrhythmogenesis) of antiarrhythmic drugs.