The clanger to the heart is all the greater if previous pathologic changes of this organ exist, such as weak heart, fatty heart, valvular defects, or arteriosclerosis. We repeatedly saw, as also did Drasche, cases with stationary, fully compensated valvular lesions occasionally suffer, as a result of influenza, from a transitory or sometimes a permanent injury to the heart, which some weeks or months later caused death, due to cardiac incompetence, with or without recurrence of the endocarditis. Kahler repeatedly saw death follow in patients with heart disease "within a short space of time, always with the signs of acute purulent bronchitis." On the other hand, as Krehl, Warfvinge, and we have remarked, many individuals with cardiac disease passed through an uncomplicated attack of influenza with the same ease as healthy individuals.
Pignoll and Teissier described cases of "acute dilatation of the heart," particularly of the left ventricle, following directly on influenza.
Some processes, as well as the previously mentioned severe attacks of cardiac weakness and acute cardiac failure, point undoubtedly to changes in the heart muscle. Yet Peter, Pawinski, Stiller, Teissier, and particularly Huchard consider the influence of the influenza toxin on the nervous mechanism of the heart to be the chief factor; they, therefore, speak of a "fatal disturbance of the cardiac innervation, " of a " nervous cardiac death," or of " death due to vagus paralysis." Although these hypotheses go perhaps too far, there can be no doubt of the nervous origin of the numerous and often severe affections of the heart in influenza.
In support of this view the following considerations may be added: The transitory character of many of the cardiac disturbances and their acute occurrence-e. g., the stenocardia, the arhythmia in young individuals with previously quite healthy hearts, and in subfebrile or mild attacks of the influenza; also the fact that these cardiac manifestations, even when chronic, occur without any sign of disturbed circulation, without congestion of the liver or the kidneys, and without anasarca, which could hardly be absent with degenerative processes of the heart muscle. In favor of the neuropathic nature of these severe cardiac manifestations after influenza is the fact that the frequent post influenzal neurasthenia often seems to have a cardiac basis in that it is accompanied by marked subjective and objective cardiac manifestations (palpitation of the heart, heart anxiety, tachycardia, bradycardia, and arhythmocardia).
There are but few reports from competent pathologists on the pathologic changes in the heart; the most exhaustive are by Kuskow. Since influenza is generally fatal through inflammatory complications, especially from pneumonia, the cardiac changes found are probably due to these rather than to influenza. The changes which occur are those usually found in acute infectious diseases,-that is, myocarditis,- especially parenchymatous and fatty degeneration, often combined with consecutive dilatation of the ventricle (Wallis, Marchand, Bollinger, Stewart, Kuskow). Lenhartz found in one case of influenza pneumonia combined with pleurisy and pericarditis, and several small metastatic abscesses containing streptococci in the heart substance.
Several cases of "primary" endocarditis verrucosa sive ulcerosa have been described by various authors as a sequel of influenza (Em minghaus, Fiessinger, Engesser, Gerhardt, Surmont, Pawinski, Teissier, Huchard, Hefforn, official reports from Switzerland and from Germany).
But the endocarditis is more frequently due to inflammatory processes in the lung and the pleura, and is the result of mixed infection, especially with streptococci, which were shown to be present in the vegetations by Oulmont and Barbier. Influenza bacilli have, up to the present time, not been found in them. Endocarditis following acute articular rheumatism complicating influenza ("synovitis grippalis") is repeatedly mentioned (Miiller in Zurich, Swiss report), and especially often endocarditis pneumonica.
Cases of influenzal pericarditis with fibrinous or purulent exudate are reported from Bassi, Tyson, and in many official reports and collective investigations. But much more often pericarditis is a sequela of pneumonia, pleurisy, and the complicating acute articular rheumatism.
By analogy with the modern doctrine of "uremic pericarditis" it has also been assumed that the influenza toxin is capable of directly causing pericarditis, but it is not likely that the toxins do more than damage the tissues, and thereby facilitate the invasion by the specific inflammatory micro organisms.
Hemorrhagic, serofibrinous, and purulent mediastinitis sometimes follow pneumonia, pleurisy, pericarditis, and gangrene of the lung, and have been observed in several cases by Krannhals.
An important and relatively more frequent sequela of influenza is phlebitis with venous thrombosis; of this there are numerous records in literature. It is unnecessary to give a list of the names of all the authors. In the official and private collective investigations of all countries this complication is noted, and accompanied by examples; the German collective investigation mentions 25.
The favorite seat of the post influenzal thrombosis is, like in other infectious diseases and conditions of cardiac weakness, the veins of the lower extremities, particularly the femoral veins and the veins of the leg. Frequently the affection is bilateral and symmetric.
Although as a whole rare, yet relatively much more frequent than in other acute infectious diseases, is influenza thrombophlebitis affecting also the large veins of the upper extremities (brachial vein and even the axillary vein).
Another peculiarity of influenzal venous thrombosis is its not infrequent association with a mild and short attack of influenza. Naturally it occurs most often in severe cases, especially in those characterized by cardiac weakness and tachycardia, the "forme cardiaque " of influenza.
Another characteristic which we noticed in two cases of thrombosis of the veins of the upper arm is its very acute onset and progress. In a physician of Cologne, strong and in the prime of life, we saw, after a severe cardiac influenza, thrombosis of the veins of the upper arm, which, within twenty four hours, caused a marked swelling and blue discoloration of the whole extremity. Possibly the acute character of the influenzal venous thrombosis explains the remarkable fact, repeatedly mentioned in the literature, that venous thrombosis had caused gangrene of the affected extremity. This, as is well known, hardly ever occurs in venous thrombosis, and one would be tempted to suppose that these cases resulting in gangrene were due to arterial obstruction, were it not that in some cases the affected extremity first became very swollen and edematous-a characteristic of venous obstruction.