W. Gordon
1918 The Lancet  
458 however, that some factor other than the aortic lesion was concerned in the production of this delay ; this is shown by the fact that when the anginal attack had subsided no delay in the nervous transmission occurred. (See Plate 2.) Severe aortic disease is known to be associated with high intraventricular pressure. One of the theories of the causation of angina is that the attack is due to vaso-motor spasm, and the resulting increase of peripheral resistance raises the general blood
more » ... e, and consequently the intraventricular pressure. The above curve would appear to confirm this in a measure, for the patient was not thoroughly "at home " in the cardiograph room, and fear of the unknown was probably sufficient to produce the rise of blood pressure which precipitated the attack. Clearly, as the second plate shows, the aortic lesion alone was not responsible for the delay in the bundle, ior here, when the seizure had passed, the nervous disturbance also vanished. But there is another feature of the records which is interesting and difficult of explanation. The T wave is always erect in lead 2 of a cardiogram from a healthy individual. Here, during an attack of angina pectoris which might have proved fatal, wave T was erect. Compare lead 2 of Plate 2. The dangerous attack had now subsided, yet the T wave has become inv6rted. Whatever caused the attack was, therefore, also affecting the musculature at the base of the aorta or the path by which the stimulating wave was propagated. , It appears that the rise of intraventricular pressure was i sufficient during the attack to produce distress and consequent delay in the right branch of the auriculo-ventricular bundle. All three leads in Plate 1 demonstrate this delay excellently. Again, the disturbance was sufficient to cause a profound effect on the musculature at the aortic base, to the extent of producing inversion of the wave T due to its contraction.
doi:10.1016/s0140-6736(00)76030-2 fatcat:wvn36xz6qrax7oimhajyoj4hym