I. Amongst the mechanical causes we should mention all organic lesions of the heart, all obstacles in the pulmonary circulation, and possibly, by analogy, certain badly-defined lesions of the pneumogastric nerves. All the stenoses and dilatations of orifices, all irregularities of the valves or heart-walls, all depressions or roughened parts of the walls,13 may determine the beginning of a concretion. In the same way, a small mass of fibrin deposited on a calcareous valve after transport from one of the veins of the limbs may originate a voluminous heart-clot. Dilatation of the heart, pericarditis, every cardiac change which weakens the contractile power, is a predisposing cause of cardiac thrombosis. Every organic lesion of the heart tending toward that final stage of asystolism so often encountered, and which weakens so greatly cardiac contractility; pouching of different portions of the cardiac wall, or aneurism; pressure upon the right heart by a mediastinal tumor or a sacculated aneurism of the arch of the aorta,14—all these have great power in producing intra-cardiac thrombi. The mechanism of these different lesions was familiar to Kreyssig, Laennec, and Hope. At the same time it must be admitted that these changes in the heart are not of themselves always sufficient to give rise to fibrinous deposits. We encounter stenoses and regurgitations at orifices very frequently, and concretions, on the other hand, are relatively rare. Moreover, we find heart-clot at times when there is no cardiac alteration. We believe, therefore, that the heart lesion is an aiding factor—that in the last moments of life, when the force of the heart's contraction is weakened and the conditions of the blood favor coagulation, they will act with special power.
13 Pathol. Society's Trans., vol. xiv. p. 71, cases by J. W. Ogle.
14 Walshe, Dis. of the Heart, Lond., 1873.
Among the mechanical causes which are removed or distant should be mentioned all those which interfere with the pulmonary circulation. Such are the effects left behind by pneumonia, pleuro-pneumonia, or the compression of the blood-vessels by old congestion of the lungs. In these cases, when the vis a tergo is impaired somewhat, and an obstacle is placed in the pulmonary capillary circulation, even if cardiac thrombosis does not directly result at first, we may have thrombi form in the pulmonary veins. In the same way, the nervous affections which are accompanied with slowing of the circulation tend to produce coagulation of the blood. All lesions, as we have said, of the pneumogastrics act in the same direction. In proof of this we should cite the experiments of Meyer of Bonn, of Longet, and of Blondet, who produced fibrinous concretions in the hearts of animals by tying or cutting the pneumogastric nerves. At the same time, the heart-beats became more rapid, wavering, unequal, and less energetic than in ordinary physiological conditions. After all, however, all these mechanical causes are but predisposing causes, for they do not always produce cardiac concretions. Frequently, as we have said already, the obstruction to the circulation may be present, and yet at the autopsy no fibrinous deposit be found in the heart. In order that the mechanical causes act efficiently to produce coagula, it is essential that they be aided by the conditions of the blood which favor it.
All concretions do not form with the same rapidity nor are they of the same size. At times their production is sudden, and but a few hours elapse before the fatal termination is reached. Again, it is affirmed that weeks, and even months, may pass before the concretion has reached a volume sufficient to cause entire stoppage of the heart's contractions. In the former category are found, of course, the softer, least consistent coagula—usually, however, very voluminous; in the latter are the smaller, more elastic, and resistant concretions, at times even presenting a stratified structure15 and surrounded habitually by a clot formed during the latter moments of life, and having a large proportion of cruor in its composition. The heart affected with fatty degeneration should, if we consider its weakened power and deficient contractility, be a predisposing cause of stagnation first, and finally of the formation of intra-cardiac thrombi. As a matter of observation in the dead-house, however, such hearts are not frequently accompanied with fibrinous deposits in their cavities.
15 According to Legroux, roughening of the walls or valves gives rise to stratified coagula of moderate size, or else to those small clots which deposit on the surface or margin of the valves (Dict. Encycl. des Sci. méd., article "Concrétions sanguines," Paris, 1876).
All diseases which by their nature and duration produce great exhaustion of the vital powers tend strongly to produce fibrinous coagula in the heart. This is eminently true of those which at the same time do not occasion a diminished plasticity of the blood. It is often assumed that mere stasis in the blood-current through the heart is essential to the formation of clots in its cavities, and to lend support to this belief reference is made to the phenomena which take place in bleeding. It is not true, however, that stasis is necessary to coagulation, and the proof is afforded when we take a bundle of twigs and by beating the blood forcibly produce the separation of the fibrin. Besides a slowness of the circulation, there must be, once again, an obstacle in the heart itself, and even then polypoid concretions are not always formed.16
16 Gaz. hébdomadaire, Paris, 1856.
II. The Vital or Pathological Causes.—In this class of conditions leading to cardiac thrombosis are included all diseases in which certain special changes have taken place in the blood itself. Among these we should mention, first, certain sthenic inflammatory affections in which the proportion of the plasmin (fibrin and metalbumen) is notably elevated, and in which, on this account, there is a strong tendency to the separation of fibrin from the blood and to the formation of cardiac concretions. In fibrinous pneumonia and acute rheumatism this is particularly true, and amongst the numerous accidents we have to dread in the course of these diseases none strike us with more dread than the possible production of intra-cardiac thrombi. In fibrinous pneumonia this complication is so frequent that Bouillaud has enunciated the following pathological law: "Fibrinous concretions exist constantly in patients who succumb to a frank, acute pleuro-pneumonia, well characterized, which has reached the second stage."17 According to Raynaud, this is without question a great exaggeration, and results from the confusion this learned author evidently made between terminal clots and those formed some time previous to death. Nevertheless, there is here a proof of the great frequency of coagula occasioned by this disease, and of the strong tendency to their formation which the condition of the blood must afford. What we have said of fibrinous pneumonia and acute articular rheumatism is not true, singular to say, of lobular or broncho-pneumonia. The lesions of this form of pneumonia are those of a catarrhal inflammation of the lung, and the blood does not offer during its course the remarkable tendency to coagulation that is shown in fibrinous pneumonia. Usually, the heart-cavities and the vessels are filled after death with a liquid of a black or violet-brown color, very often sticky.18 The fibrin in the heart-cavities in pneumonia is fibrillar, and does not present those changes which indicate that it has been deposited for a long while. Moreover, these coagula do not present physical characters which show any considerable degree of age. They are usually terminal coagula, or at least formed within a few days of the fatal termination. Do globular vegetations occur in pneumonia? At times they do, but they are at least very rare as compared with the fibrinous conditions just referred to.
17 Gazette méd., 1843, vol. xi. p. 270, quoted by Armand, Thèse de Paris, 1857, p. 41.