Abstract:
In this study we evaluated the validity of well-known human electrocardiographic markers of myocardial pathology in Dorper sheep. These markers are all properties of PVC`s, namely the duration of the QRS complex of PVC`s, the presence of notching of the QRS complex of PVC`s and change in the ST segment of PVC`s. It was shown that these three electrocardiographic phenomena correlate with myocardial pathology in the hearts of Dorper sheep. We also described a new electrocardiographic indicator of myocardial pathology in the hearts of Dorper sheep, namely an increase in the frequency of cardiac memory T waves, induced by PVC`s, as a new electrocardiographic surrogate for myocardial pathology. This study was possible, because we knew from a pilot study that our specific method of inducing right ventricular PVC`s is known to induce structural alterations in the myocardium of Dorper sheep. The guidewire was situated in the right ventricle and we examined the histological appearance of only the left ventricle, in order to exclude any possible changes caused by the wire itself. Although this study was not designed to answer the question of whether PVC`s can be a cause of, rather than a consequence of, structural myocardial disease, it is an important method, because in this way every wether serves as it`s own histological control for electrocardiographic changes. We started with normal Dorper wethers, induced right ventricular PVC`s and these PVC`s had certain characteristics, as described in chapter 3. We know what the normal histological appearance of Dorper wethers are and the electrocardiographic appearance of PVC`s in the normal heart. At the end of the study certain changes appeared in the PVC`s, namely the QRS duration increased, notching appeared and the ST segment disappeared. Furthermore, at this stage the histological appearance of the left ventricle resembled that of myocarditis. At the end of the study (abnormal myocardial histology) we also noted an increase of 42 % in the incidence of cardiac memory T waves following PVC`s, when compared to the beginning of the study (normal myocardial histology). What might the reason be for the abnormal left ventricular histology ? As this study was not designed to answer that question this is open to debate. It might be the anaesthetic, the wire itself or the PVC`s. As already discussed we induced right ventricular PVC`s and afterwards we examined the left ventricles, therefore these histological alterations cannot be a direct consequence of the guidewire itself. It is suggested that it will be worthwhile to explore the possibility that PVC`s may be a cause of myocardial disease and that it is not always a consequence of established myocardial disease.
