89 



we know, from abundant pathological evidence in man, 

 the association of coronary and myocardial impairment 

 with fatal angina. Further, the clinical features of many 

 recorded anginal cases, where sudden death took place 

 either in an attack of pain or apart from such, are very 

 noteworthy in their similarity to those attendant on death 

 by ventricular fibrillation. The significance of these facts 

 taken together need not be enlarged upon. 



If we accept the view, which has commended itself to 

 many observers, that an important factor in the production 

 of pain in angina is to be found in the heart muscle working 

 with a defective blood supply, it becomes plain how increased 

 demands on the oi'gan by muscular ejffoi't or emotional stress 

 may excite an attack by leading to a relative anaemia, the 

 blood supply, which was sufficient during rest to ensure the 

 absence of pain, now becoming inadequate for the muscle. 

 Such a conception might be brought into relation with the 

 results obtained in an ischaemic limb where, on working a 

 muscle, acute pain is caused long before the fatigue point 

 (as indicated by inability to raise the weight in ergograph 

 experiments) is reached — a mechanism of pain production 

 apparently different from that present in a muscle 

 working to fatigue while its normal circulation is going on 

 (MacWilliam and Webster'^). 



It may be conceived that in the close and striking asso- 

 ciation of angina and sudden death we see the working of 

 distinct but related mechanisms, based in part at least 

 on a common underlying process, essentially similar in 

 character but differing in intensity and in the fatal or 

 non-fatal issues, these issues being no doubt also influenced 

 by other conditions which affect the results of the funda- 

 mental process. A conception of this kind would include 

 two categories of dangerous anginal conditions — one with 

 more or less transient attacks of pain of varying grades of 

 severity, the other with the process, common to the two 

 categories, going further in some directions, attaining 

 greater intensity, and culminating in ventricular fibrilla- 

 tion. But the pros and cons of the vexed question of pain 

 production in angina are beyond the scope of this paper. 



In connexion with the well known fact that pronounced 

 coronary sclerosis very frequently exists without angina, it 

 has to be borne in mind that an essential point is, not the 

 structural change in the arterial wall, but the amount of 

 actual defect of blood supply through the sclerosed vessels 

 from greater or less narrowing of their channels, the 

 presence or absence of contraction in their muscular coats, 

 the state of the capillary field, etc. Much depends no doubt 

 on the more or less gradual development of obstructive 

 change, the establishment of more or less efficient collateral 

 circulation, etc. It is known that life may go on after the 

 gradual development of complete occlusion of one coronary 

 while the other may be found to be very greatly reduced in 

 calibre; also after complete blocking of a large branch. 



