PubMed · 1157254
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T G Steffans. 1975. Letter: Automaticity and conduction.. https://pubmed.ncbi.nlm.nih.gov/1157254/
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The presence of left ventricular hypertrophy (LVH) in either hypertensives -H- or in normotensives -N-, suggests that not only blood pressure is determining this anatomic change, but various factors, as neural or endocrine ones, could be involved in its genesis. In order to evaluate the role of sympathetic dys-reactivity on LVH, we studied three groups of subjects: a) 12 -H- (SBP 159+/-9; DBP 99.6+/-7; FC 80+/-7) with LVH, diagnosed by echocardiogram. b) 12 -N- (SBP 138.2+/-8; DBP 83+/-2; FC 75.6+/-4) with LVH. c) 12 -N- (SBP 136.6+/-11; DBP 81.8+/-5; FC 76.3+/-5) without LVH. Using computer interfaced equipment, we measured beat to beat, hemodynamic and extra-cardiovascular autonomic functions, during a session of stressors (Mental Arithmetic, Color Word Stroop, Cold Pressure and Handgrip Tests), preceded and followed by 10' of observation. Among the various considered indexes, we evaluated the Percentual Total Activity Index (PTAI), as percentual total activity change + percentual total recovery change. Our findings point out that the PTAI of N with LVH is significantly higher for SCL, PHT, HR, SV, CO, TPR than either in H with LVH or N without LVH. These data seem to demonstrate a prolonged reactivity in N without LVH and are according to the hypothesis that LVH could also be supported by a hyper-adrenergic state with sympathetic dys-reactivity, independently from high blood pressure values.
A three-dimensional finite-elements model of the left and right ventricles has been developed to study the process of myocardial electrical activation. The experimentally measured velocity is known to depend on membrane processes, the cellular shape, fiber orientation, and the interaction with neighboring cells. The simulated process is, therefore, governed by the geometry and by the directional conduction velocity at each point in the myocardial volume. The geometry of the ventricles is described by ellipsoidal shape, and divided to layers and sections, each filled with "cells" of preassigned properties. It allows for taking into account the local orientation of the myocardial fibers and their distributed velocities and refractory periods. The values are Gaussly distributed around the mean, and the mean and variance differ at each section. A conduction network of Purkinje "cells" is included on the endocardial surface. The anisotropic properties are demonstrated during simulation of an abnormal cardiac cycle, when propagating is initiated at an ectopic ventricular site. Ischemia is simulated by low conduction velocities in the ischemic zone and wide dispersion of values in nearby locations; automaticity is described by restimulating "cells" in the injured area; the dangerous effects of a premature beat leading to reentry are simulated by reduction of propagation velocity in "cells" that are reactivated while they repolarize. The different activation patterns are calculated throughout the myocardium and on its surface. The generated surface activation maps are not sensitive to minute changes in location of the foci of activation within the normal conduction system. The maps show sensitivity to pathological velocities, ischemic areas, and the existence of ectopic foci.(ABSTRACT TRUNCATED AT 250 WORDS)
Sotalol has a virtually unique antiarrhythmic profile in that it combines the properties of the Class II beta-blocking agents with the Class III properties that prolong repolarization. The Class II action exerts a marked effect on atrioventricular nodal conduction and makes sotalol a suitable drug for the treatment of adrenergic-induced supraventricular tachycardias. Sotalol helps to prevent or slow supraventricular arrhythmias involving the atrioventricular node as part of a reentrant pathway and also helps to control the ventricular rate during supraventricular arrhythmias conducted to the ventricles over the normal atrioventricular pathway. The capacity of conduction of accessory pathways is diminished by sotalol, thereby decreasing the ventricular rate during atrial fibrillation in the Wolff-Parkinson-White syndrome. The effects of sotalol on conduction of the cardiac impulse (Class I effects) have been probably overlooked and those on true refractoriness (Class III effects) overestimated.