360 DISEASES OF THE HEART. 



The anatomical changes which cause insuflicience are usually 

 shrinking and shortening of the valves, so that, even if spread out by 

 the blood, they would not meet. But thickening, and rigidity too, may 

 prevent closure, the pressure of the blood becoming insufficient to make 

 the leaves flap together. Much more rarely we find adhesion of the 

 valve to the arterial wall, or laceration or detachment of one of the 

 leaves from its insertion, as a palpable cause of insufficience. 



Besides these changes at the root of the aorta, we constantly find 

 in the cadaver a degree of excentrie hypertrophy of the left ventricle 

 greater than is observed under almost any other circumstances. The 

 wall of the ventricle may be an inch in thickness, its cavity is often 

 capable of containing a fist. We have already seen that dilatation of 

 the left ventricle is the necessary result of severe pressure sustained by 

 it from within while in a state of relaxation, and that hypertrophy fol- 

 lows in consequence of the augmented effort which it must make in 

 order to propel the increased volume of blood which it holds. A large 

 number of the signs of aortic insufficience are due to this enormous hy- 

 pertrophy of the left ventricle. In a former chapter we have fully de- 

 tailed all the alteration which the shape of the heart undergoes from 

 this enlargement. We have seen that the rest of the organ participates 

 hi a less degree in the affection, and that bulging of the septum into the 

 right ventricle materially encroaches upon the capacity of that chamber. 



The mouth of the aorta may contract to such a degree as barely to 

 admit the insertion of the end of the little finger into the narrowed open- 

 ing. The anatomical changes which occasion such strictures are gen- 

 erally the thickening and shrinking of the flaps described above. These 

 flaps may form unyielding prominences at the root of the aorta ; so 

 that it becomes equally impossible for the stream of blood to lay them 

 back against the aortic wall during systole, and for the weight of the 

 blood during diastole to force them together again. Cohesion of the 

 semilunar flaps is the next cause of stenosis, and is the more marked 

 the more the point of adhesion approaches the centre of the valve. Old 

 vegetations on the valves, of cartilaginous hardness, and which are often 

 the seat of calcareous deposit, assist in blocking up the constricted pas- 

 sage, although they rarely constitute the sole cause. 



In simple stricture of the aortic valve, the left ventricle has no in 

 crease of pressure to support during diastole, and hence does not be- 

 come dilated ; it has, however, to propel its blood through a contracted 

 orifice, and becomes hypertrophied on account of the greater amount 

 of effort thus required from it. In contradistinction, then, to what we 

 meet with in insufficience of the semilunar valves, we find a simple hy- 

 pertrophy, instead of excentrie hypertrophy of the left ventricle, when 

 the aortic outlet is contracted. 



