Abnormal Left Coronary Artery of Ox Heart 69 



1*5 cm. as it lies in direct relationship with the wall of the dilated portion; it 

 then becomes thicker, approximating to its original size. 



(7) Branch of abnormal coronary artery. 

 Healthy arterial wall. 



(8) Branch of right coronary artery. 

 Nothing abnormal to be noted. 



(9) and (10) Coronary arteries from normal ox heart. 



Left: the larger vessel; wall of left varies in thickness considerably. 

 Conclusions in regard to: 



I. Course taken by blood during life in the abnormal vessel. 



(1) During systole. Probably regurgitation occiu'red from the left ventricle 

 throughout the greater part of systole through the abnormal communication 

 at the apex. This would give rise to a pulse wave apart from the question of 

 the quantity of blood regurgitated. Another pulse wave would be sent along 

 the abnormal vessel from the aorta. In this way the abnormal vessel would 

 be subjected to strain, and the cyst-like part would be subjected probably to 

 the greatest strain. The movement of blood in the abnormal vessel would 

 perhaps be from the apex of the left ventricle towards the aorta. 



(2) During diastole. The blood-flow in the abnormal vessel would in all 

 likelihood be from the aorta to the left ventricle. The diastolic pressure in 

 the left ventricle and in the abnormal coronary would be high, viz. aortic 

 pressure. Hence conditions would be favourable for increased strain on the 

 abnormal vessel and dilated part during diastole and on the dilated part more 

 particularly during diastole. On the whole, there would be a relative stagnation 

 of blood in the abnormal vessel. 



II. Respective proportions of the abnormality, congenital and acquired. 

 It would appear clear that the communication between the left ventricle 



and the coronary was developmental wholly. The pseudo-valvular structure 

 must have been present before birth as a congenital peculiarity. 



That the abnormal coronary and dilated portion were subjected to abnormal 

 pressures and in consequence became expanded is concluded from the 

 following : 



( 1 ) Varying thickness of the wall of the abnormal coronary and dilated part. 



(2) The wall does not show the typical structure of a normal artery. 



(3) Irregular arrangement of bundles of unstriped muscle etc. in wall. 



(4) Evidence of impaired nutrition of portions of the wall of the abnormal 

 vessel. 



(5) High diastolic pressure. 



In all probability, had the animal not been killed, it would have died at 

 some period of rupture into the pericardial sac through one of the thinned 

 portions of the wall of the dilated portion at the apex. 



I am indebted to Professor J. A. MacWilliam for his help and permission 

 to publish the above, and to Mr George C. Kelly for the sketches. 



