[Risks and precautions in stress testing].
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Biomedical subjects
Publications and source records attributed to M L Simoons.
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Multiple dipole models of activation of the heart, in combination with a model of the thorax as an electrical conductor relate the action of individual cells to features of the electrocardiogram. The models can be used to develop diagnostic electrocardiographic criteria for ventricular hypertrophy, myocardial infarction or conduction disorders. Criteria derived with the use of Holt, Barnard and Lynn's model proved to be superior to well-established empirical rules. Their approach restricts position, direction and polarity of the current dipole vectors in the model. In the Selvester model, and later in the Ritsema van Eck model, in addition to these restrictions time-constraints are imposed on the dipole activity. In a validation study of the Ritsema van Eck model activation of a beating dog heart is compared in detail with simulated activation in a computer replica of the same heart. Myocardial spread of activation is found to be stimulated correctly. Simulated spread of activation along the Purkinje fiber network however, differs considerably from reality. In apical regions excitation spreads in reality much faster than in the model, in basal regions much slower. The model can be improved by slowing endocardial excitation from apex to base with the time-course of activation. Further improvement is obtained by the use of a more detailed pattern of endocardial excitation, based on studies of endocardial excitation in opened ventricles. The model can predict the time-course of activation with an accuracy of 5% of total ventricular activation time.
In 34 patients with chest pain the spatial orientation of the ST-vectors in the exercise electrocardiogramm 30 and 80 msec after the end of QRS were compared with the location of exercise induced local defects of myocardial uptake of 201Tl. The following results were obtained: 1. The sensitivity and specifity of myocardial perfusion imaging after exercise were the same as those of exercise electrocardiograms; 2. No relation could be observed between the location of reduced 201Tl uptake during exercise and the spatial orientation of the ST-vectors.
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The ECG changes during exercise are described in 71 patients with a previous anteroseptal or anterolateral infarction (ANT-MI) and in 73 patients with an old posterior or inferior wall infarction (INF-MI). Left ventricular angiograms in 95 patients yielded a good correlation between areas of dyssynergy and the QRS pattern at rest. The ST changes in patients with coronary artery disease and a normal ECG at rest, and in normal subjects, were oriented toward the right, posteriorly and superiorly. In patients with INF-MI and inferior wall dyssynergy, the ST changes were more inferiorly oriented. Anteriorly-oriented ST changes were associated with anterior wall or apical dyssynergy and with ANT-MI. Thus the spatial direction of the ST changes during exercise is related to three independent factors: those factors which cause the ST changes in normal subjects, the degree of myocardial ischemia in that particular case, and the extent of dyssynergic areas in the wall of the left ventricle.
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