88 



which may last after the general blood pressure has again 

 risen to its former level. The spasm hypothesis has been 

 subjected to searching criticism by Sir Clifford AUbutt, who 

 among many other considerations states that amyl nitrite 

 gives no relief in transitory hemiplegias and aphasias. 

 There is also the occurrence of dyspnoea in coronary 

 obstruction from sudden thrombosis or embolism (as estab- 

 lished post mortem) and its absence as a necessary feature 

 of typical angina; but a possible explanation of this 

 difference can be suggested. 



Evidence of the occasional presence of strong contraction 

 of large arteries (brachial, etc.) in diseased conditions in 

 man was obtained by the present writer, in conjunction with 

 Professor G. Spencer Melvin^* and Dr. J. E. Kesson,^^ in 

 an investigation of blood pressure a number of years ago, 

 and surviving sclerosed arteries from the legs of old horses 

 were found to show extraordinarily intense contraction, 

 causing complete obliteration of their lumen and an 

 enormous resistance to attempts to force blood through 

 them. 



In relation to the question of arterial spasm, doubt as to 

 the existence, at least in effective degree, of vasomotor 

 innervation of the coronary arteries is not a consideration 

 of decisive moment. For there is no proof that the forms 

 of excessive contraction now under discussion — for example, 

 in the brachial artery or the horse's leg, etc. — are vaso- 

 motor phenomena ; it is more probable that they are directly 

 dependent on morbid conditions present in the arterial 

 muscle at the time. 



It may be argued that the foregoing considerations point 

 to the feasibility of the hypothesis of coronary spasm, in 

 view of there being no sufficient reason to assume that the 

 coronary vessels — specially prone as they are to sclerotic 

 changes — should in diseased states be immune from such 

 functional disturbances as seem to occur in other arteries. 

 But the question is far from being closed. 



Fatal and Non-Fatal Angina. 



It is necessary to discriminate clearly between the separate 

 questions of (1) the mechanism of pain production in anginal 

 attacks, and (2) the mechanism of death occurring during 

 or between attacks, sometimes without warning. 



The striking tendency of the graver forms of angina to 

 terminate in sudden death need not be emphasized. There 

 is every reason to believe that, in many cases at least, the 

 end comes by ventricular fibrillation, and that the different 

 issue in fatal and non-fatal cases hangs on the supervention 

 of fibrillation in the former and its absence in the latter. 

 The development of fibrillation as a frequent and charac- 

 teristic result of defective coronary blood supply, as demon- 

 strated experimentally, has already been described; and 



