threads of fibrin; later, more as an interwoven network forming a thick layer in which are inclosed varying numbers of leukocytes. The deposition of fibrin, which is the result of the exudation of plasmatic fluid from the dilated vessels followed by coagulation, may attain a considerable degree, forming a thick, reticular membrane or long, hairy-like projections upon the surface (cor villosum). (Plate 7, Figs. I and II. Compare also Plate 60, Fig. I.) In the underlying connective-tissue layer of the pericardium various cellular processes also run their course. The connective-tissue cells produce, through mitosis, short spindle-shaped or polygonal cell-elements with large vesicular nuclei (epithelioid cells, fibroblasts), while the endothelial cells of the lymph and blood-vessels also undergo proliferation. Between these appear a great number of lymphocytes and leukocytes.

Later, the blood-vessels give off sprouts, which, at first solid, become hollow and pass into the loosened and cellular layer of connective tissue and out toward the fibrin, which is gradually infiltrated with new cells and eventually completely substituted by granulation tissue. And now the new vessels gradually disappear, the cells diminish, and the granulation tissue changes into connective tissue which is at first rich in spindle-shaped cells, but later becomes more and more fibrillated at the expense of the cells.

In this way the fibrinous deposit is gradually changed into cicatricial tissue, which produces either flat, glistening, opaque thickenings in the epicardium (so-called tendinous spots, "soldier-spots"), or more or less extensive adhesions of the pericardial layers up to a complete fibrous obliteration of the pericardial cavity.

In tuberculous pericarditis the processes described-of exudation, proliferation, and organization-run their course in the same manner; but, in addition, there appear in the granulation tissue, under the fibrinous layer, typical tubercles, generally composed of radially arranged epi

PLATE 7.

FIG. I. Acute Fibrinous Pericarditis (Cor Villosum). Fibrin stain. 64. 1, Myocardium; 2, subepicardial fat-tissue; 3, thickened and richly cellular epicardium; 4, fibrin deposit, in the meshes of which leukocytes are seen; 5, blood-vessels growing toward the fibrin and filled with leukocytes.

FIG. II.-Fibrinous Pericarditis, Organizing. ×127. 1, Pericardial connective tissue; 2, young, connective-tissue layer with numerous, thin-walled blood-vessels, epithelioid (fibroblasts) and round cells; 3, fibrin layer (stained red with eosin); 4, the fibrin penetrated by new blood-vessels and fibroblasts.

thelioid cells, giant cells, and round cells, the center early becoming the seat of caseous necrosis.

The confluence of nodules and caseous areas leads to the formation of extensive necrotic layers, which are surrounded by granulation tissue or fibrous tissue. New tubercles spring up in the young connective tissue externally, undergo the same degeneration, and become covered by a new layer of fibrin and of granulation tissue; in this way thick masses are formed, which consist of, at times, numerous alternating layers of granulation tissue and caseous and necrotic material. Usually, this process goes on in the same way in both the pericardial layers, which become firmly adherent and thus obliterate the pericardial cavity.

PLATE 8.

FIG. I.-Subacute Tuberculous Pericarditis. 50. 1, Heartmuscle; 2, subepicardial fat-tissue greatly infiltrated with small round cells; 3, thickened pericardium; 4, tubercle with cheesy center and epithelioid cells arranged in a radiating manner; 5, giant cells; 6, fibrin deposit.

FIG. II. Sclerotic or Milk Spots of the Epicardium. 65. 1, Transverse section of the heart-muscle; 2, normal epicardial connective tissue; 3, layer of greatly thickened sclerotic connective-tissue fibers.