In this report, we dealt with ventricular activation abnormalities in 30 patients with previous non-Q myocardial infarction (Mi) by means of the CARD1AG 128.1 device, which enables analysis of ECGs, VCGs and body surface potential maps. The diagnosis was verified by left ventriculography, echocardiography and perfusion scintigraphy. Twenty-nine healthy subjects served as the control group. Morphological findings confirmed the presence of a significant subgroup with serious left ventricular asynergy. Seven electrocardiological variables, which significantly differed from control values, disclosed that non-Q Ml is responsible for localized activation time prolongation, and that inferoposterior scars tend to delay the entire activation of ventricles, and to cause disturbances of the terminal depolarization phase together with a decrease in voltage production during QRS. Lesions of the anterior wall and the apicomesial part of the inferoposterior wall affect the distribution of the Q wave more often than the posterior basal ones. The probability of such abnormalities increases with the degree of asynergy. Some VCG criteria increase the sensitivity of electrocardiological analysis. These parameters will be used for evaluating the diagnostic value of electrocardiological analysis in the chronic non-Q Ml. Non-Q myocardial infarctions represent a heterogeneous group of infarctions from both electrophysiological and morphological aspects.
The aim of this contribution was to review the possibilities of presentation of orthogonal ECG signals and to evaluate the progress in computerized electrocardiography achieved in Czechoslovakia. The information about the cardiac electric field in orthogonal electrocardiography is defined and consequently displayed as a fixed single dipole (vector). The spatial trajectory of vector end-point (spatial vectorcardiographic loop) can be presented in different ways — as orthogonal electrocardiogram, polarcardiogram, planar vectorcardiogram and decartogram, respectively. The advantages of particular methods of presentation, as well as their limitations are discussed. Computer-assisted electrocardiography was introduced in Czechoslovakia in 1974. The original AVA program has been further developed in the Research Institute of Medical Informatics (formerly Research Institute of Medical Bionics). The currently developed system CardioSys allows the utilization of all the possibilities of orthogonal ECG and vectorcardiographic presentation for clinical and epidemiological cardiology as well as for the research.
In 77 young healthy volunteers of both sexes the dependence of the QT interval of ECG on the heart rate was investigated during normal ventilation (control) and after 1, 2, 3, 4 min of voluntary hyperventilation, after 6 min of hypoxic-hypercapnic ventilation (through an enlarged dead space) and during the Valsalva manoeuvre. The absolute coefficients (a) of the regression lines QT = a + b . HR were significantly different in all groups. The slopes of regression lines (b) were significantly different in all groups with the exception of 4 min hyperventilation. Our results indicate that short-term alterations of pulmonary ventilation may change not only the duration of the QT interval but also its dependence on the heart rate. Voluntary hyperventilation lasting 1-2 min and the Valsalva manoeuvre decrease the rate dependence of the QT interval and this change may cause its prolongation at higher heart rates.
The Frank orthogonal corrected ECG and its first derivation were recorded in 27 healthy volunteers (women aged 19-22 years) during normal ventilation at rest (control group), after voluntary hyperventilation lasting 75 seconds, and during hypoxic-hypercapnic ventilation (through the enlarged dead space) lasting 5 min. The projections of the magnitude and direction of the positive and negative QRS derivation maxima into the horizontal, frontal, left sagittal planes and their spatial distribution were constructed. The magnitude of the positive and negative QRS derivation maxima was significantly decreased during hypoxic-hypercapnic ventilation. A significant alteration in the direction only arose at the positive maximum during hypoxic-hypercapnic ventilation in the frontal plane. The intrinsicoid deflection was not significantly altered. The normal values of the maxima of the first QRS derivation in young healthy women are given. It is supposed that the decrease in amplitude of the maxima of the first QRS derivation is caused by slowed propagation of the depolarization wave under hypoxic- hypercapnic conditions and alteration of the direction of the positive maximum is caused by a greater participation of the right ventricle at the origin of the resulting QRS vector.
A brief description of the methodology of analysis of the electric heart field using electrocardiograms, vectorcardiograms, diagrams of potential maxima/minima and body surface potential maps is presented. The text is focused on the description of different kinds of isopotential and isointegral maps and their diagnostic possibilities. A detailed description of the diagram of potential maxima/minima and its place in diagnostic of different disturbances of the heart muscle and conduction defects is given.
The influence of some pulmonary ventilation alterations (the normal ventilation at rest = control), the hyperventilation (HV) lasting 75 s, the hypoxic-hypercapnic ventilation (HXV) lasting 3 and 6 min) on the instantaneous QRS vectors was investigated in 42 young healthy women (19-24 years old). The magnitude and the direction of instantaneous QRS vectors in the 10th to the 70th ms and in QRS max were constructed from the Frank lead ECG. The significant alterations of the direction (angle) were found in the 30th ms and QRS max at HXV and in the 60th ms at HV. A significant decrease in the magnitude of instantaneous vectors was found in the 10th to 50th ms after 6 min of HXV, in the 30th to 50th ms at 3 min of HXV, in the 40th to 50th ms at HV. These alterations were the most marked in the horizontal plane. We suggest that the alterations of the instantaneous QRS vectors were caused by the influence of the autonomic nervous system or humoral agents, but not by heart position, Brody’s effect or lung hyperinflation.