DISEASES OF THE HEAHT. — VALVULAr. DEFECTS. 287 



apex of the left ventricle in sucli an overvvlielming majority of 

 cases that I may fairly confine my remarks to these two localities, 



E. Valvular defects. 



§ 255. Those coarser distortions of the orifices of the heart 

 which are caused by chronic endocarditis are embraced under 

 the general head of valvular defects. These are always made up 

 of three distinct anatomical factors, which have to be considered 

 separately in every case : 1. Thickening — the immediate result of 

 overgrowth of the connective tissue. Slight degrees of thickening 

 are extremely common at the base of the aortic valves and along 

 the " line of contact " of the mitral ; they do not Fig. 



affect the functional activity of the valves. Higher 

 deo^rees of the same alteration mve rise to rouo^h 

 elevations, hardened by earthy deposit; along the 

 '' line of contact" of the mitral valve these are 

 usually confined to one surface only; in the \'^^^^ — ^^v^ 

 aortic valves thev usually affect both. They '"'^1^^^.'^ 



cover the entire surface of the semilunar valves Ins^^fficiency and 



stenosis of the 

 w^ith a layer several lines thick, so that instead aortic orifice, 

 of three delicate, sigmoid flaps, we ultimately Thickening and 

 find three rigid, tuberculated bodies festooned ^-^^ valve-flaps. 

 round the wall of the aorta (fig. 89). Natural size. 



2. Retraction. This results from shrinking of the hyperplastic 

 connective tissue. Together with the thickening, it gives us the 

 impression that the entire mass of the valve is crumpled into a 

 small, elongated roller — that the curtain is rolled up. Curiously 

 enough, the narrow borders of the aortic valve beyond the "line 

 of contact" often remain unaltered, and hang from the free 

 edges of the shrunken valves like flexible bands. At the mitral 

 orifice, where the process extends to the chords tendineae, the 

 shortening causes the valve to be dragged down into the ventri- 

 cular cavity, thus fixing it in the attitude which it ought only to 

 occupy after the close of each systole (fig. 90). 



3. Adhesion. The tissue of the inflamed valve, notwith- 

 standing its rigidit}^, is capable of a certain degree of internal 

 movement ; it is in a state of inflammatory fluxion, wdiich allows 

 it to adhere to its fellows, wherever they happen to touch. So long 

 as the valvular apparatus retains its normal mobility, any two 



