Notwithstanding the diminished proportion of fibrin in typhoid fever, and the impossibility of explaining, in many cases, any increase of the plasticity by local inflammatory disorders, cardiac concretions have been observed by Huss, Virchow, and Hardy.26 Bucquoy also relates, after Huxham, an epidemic which reigned at Plymouth in 1742 amongst sailors who came from a long cruise, characterized by dyspnoea, cardiac palpitations, and intermittences of the pulse. Many of those attacked died, and at the autopsies made polypoid concretions of considerable elasticity and adherent to the walls of the heart were found. Another similar occurrence took place amongst the soldiers of the garrison of Rocroy in 1746. Quite a number succumbed after having shown symptoms similar to those of the sailors of Huxham. Cadaveric sections discovered in the left ventricle several hard, consistent cardiac thrombi.
26 Quoted by Bucquoy, Des Concrétions sanguines, Paris, 1863, p. 36.
III. Endocarditis.—Whatever may be the opinion of different authors in regard to the frequency of endocarditis when intra-cardiac thrombi are present, it is certain that if it does exist the explanation of the presence of these deposits is clear and ample. In endocarditis we have both a local and mechanical cause and also a vital condition of fibrinous deposits in the heart. As a mechanical cause we know that often it is the cause of the stenoses of orifice which are present, and that further, by its effect in producing roughening or fissuring of surface, it offers a strongly predisposing cause of the deposit of fibrin. Ulcerative endocarditis acts still more efficiently in this direction, owing to the fact that it produces its effects as much on the surface of the valve, aortic and mitral, near the adherent portion and in the neighborhood of the cardiac orifice, as between its layers. The result is, that the surface is rough, unequal, presenting often cauliflower excrescences, and showing sometimes, in the midst of a mass of fibrin that has become deposited by degrees, portions of a softened, partially-detached valve which was the nucleus of the outer layers of fibrin. Further, endocarditis of both forms acts as a vital and efficient cause of cardiac thrombosis, in that it belongs to the class of inflammatory diseases which occasions an absolute increase in the proportion of fibrin of the blood (from 25/1000, concrete fibrin 3, and metalbumen 22, to 56/1000, concrete fibrin 17, metalbumen 36); and also, more especially in ulcerous endocarditis, by the transport of infectious materials into the blood, which still further tend to cause coagulation.27
27 At times there is complete deprivation of epithelium over a limited area, and in rare cases slight ulcerations of membrane. These two conditions are efficient factors of the exudation of plastic lymph.
SYMPTOMATOLOGY.—According to Laennec,28 it is equally erroneous to attribute to cardiac thrombosis many symptoms which properly belong to an organic lesion of the heart (notably hypertrophy) as it is to believe that intra-cardiac thrombi never begin to form until the terminal period of life. According to him, Haller, Vinckler, Staneari, and Bonaroli29 have observed obliterations of the internal jugular vein and carotid artery by very firm concrete fibrin, and he himself has seen a similar production in the inferior vena cava for the space of four fingers' breadth. Although these concretions were evidently formed during life, they occasioned no symptoms indicative of their presence, nor were there any obstructions in the course of the circulation which could explain their origin. Reasoning from these facts and from the phenomena which occur in aneurismal tumors, it seems highly probable that the blood should coagulate in the heart also during life. Later writers frankly admitted that coagulations in the veins caused partial dropsies, a usual instance of which is the white swelled leg, or phlegmasia alba dolens, from obliteration of the femoral vein.30 This is not invariable, for I have seen, in patients who have succumbed to diphtheria, both venæ cavæ obstructed by coagula, without having observed during life either local or general oedema.31
28 A Treatise on Diseases of the Chest, p. 183, Philada., 1823.
29 Quoted by Morgagni, Epist. 64.
30 Vide Bouillaud, Archiv. gén. de, Méd., t. ii. et v., quoted by Hope.
31 Thrombose cardiaque dans la Diphthérie, Paris, 1872, p. 43.
Scarcely any contemporary author doubts that cardiac thrombosis gives rise to more or less well-defined symptoms. What these are we shall now consider. Of course we are far less liable to-day, when the diagnosis of organic cardiac disease is so accurate, to attribute to intra-cardiac thrombi the signs, physical or rational, which properly belong to them, and which ancient observers could not differentiate. Nevertheless, there are complex cases in which one is at fault even in regard to this problem.