Manual of pathology : including bacteriology, the technic of postmortems, and methods of pathologic research . ssue that has been lost. As itis not improbable that in cardiachypertrophy new fibers are formed, with the associated enlargement ofexisting fibers, the possibility of a similar change following the subsidenceof the disorder at present under consideration must be admitted. 2. The second form of fatty degeneration is sometimes spoken of aspartial or local. It is due to a local ischemia, such as results from ath-eroma, calcification, embolic plugging, or thrombosis of some branch ofthe
Manual of pathology : including bacteriology, the technic of postmortems, and methods of pathologic research . ssue that has been lost. As itis not improbable that in cardiachypertrophy new fibers are formed, with the associated enlargement ofexisting fibers, the possibility of a similar change following the subsidenceof the disorder at present under consideration must be admitted. 2. The second form of fatty degeneration is sometimes spoken of aspartial or local. It is due to a local ischemia, such as results from ath-eroma, calcification, embolic plugging, or thrombosis of some branch ofthe coronary arteries, which are, to a certain extent, terminal. Thelesion is manifested by the presence of a softened spot in the ventricularwall, pale yellowish-brown in color, frequently greasy to the touch, andoccasionally containing oil globules, visible macroscopically. Some-times the degenerated area is surrounded by a zone of hyperemia. Therapidity with which the process develops varies in different cases, de-pending upon the promptness with which the cause acts. When there^Med. Record, Feb. 16, ;..»o: Fig. 247.—Fatty Degexeratiox of the Heart.(Specimen fi-xed in osmic acid, rendering the fatglobules black.) Near the center of the drawing are a number of red blood-cells. {From a case oj pernicious anemia in the Jej-jerson Medical College Hospital, seriice oj ProfessorJ. C. Wilson.) VASCULAR SYSTIiM. 495 has been a sudden occlusion of tlie l)lood-sui»i)ly. the process will com-monly be rapid. On the other hand, when the local change is broughtabout by gradual encroachment ui)on the lumen of the coronary arteryor a-branch, the lesion is delayed, and opportunities are afforded for anassociated overgrowth of fibrous tissue. As a rule, the degenerativechange is limited to a single focus, which is located on the anterior aspectof the left ventricle near the apex. Less commonly, a correspondingpoint on the wall of the right ventricle is involved. The degeneratedarea is
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