Retrocession of gout from the extremities to the heart is a rare in cident, but there are well-attested cases of this accident. As a con of refrigeration of the inflamed joint, or of violent agitation of mind and body, swelling and pain have abandoned the affected member, and their disappearance has been speedily followed by car diac collapse. It is probable that in such instances the overwhelm ing disturbance of the heart is clue to perturbation of the nervous centres, and to over-stimulation succeeded by paralysis of the cardiac excito-motor nerves. The debilitated condition of the organ and the inordinate irritation of its nervous tissue, consequent upon chronic arthritism, must not be forgotten in estimating the causes of collapse under such conditions.
The influence of gout in the production of atheroma in the arteries is beyond question. Yet, like the course of arthritic degeneration in other structures and organs of the body, it is often the case that atheroma is the result of the causes that have also produced gout, rather than the direct consequence of gouty disorder.
So many factors may contribute to the production of arterial de generation, such as old age, intemperance, errors of diet, etc., that it is sometimes difficult to assign to each its exact share in the work of destruction. The remote consequences of an atheromatous condi tion of the blood-vessels are very numerous, and when that condition is due to gout or to the arthritic diathesis, they may be reckoned among the secondary or remote results of arthritism. Thus, for ex ample, thrombosis and hemorrhage in the brain may follow disease of the cerebral arteries. In the heart, an atheroma of the coronary arteries leads to starvation, degeneration, and rupture of the cardiac muscle. Gangrene of the extremities has also been attributed to a corresponding state of the vascular walls in the limbs, but the coin paratively frequent occurrence of diabetes as the antecedent of such mortification should lead to careful inquiry as to the possibility of that as the cause. The connection between diabetes and the arthritic diathesis is, however, so intimate that in many instances gangrene, glycosuria, and gout can all be referred to the same predisposing cause or causes.
Angina pectoris is an incident of not infrequent occurrence among gouty patients. It is usually experienced by the victims of chronic arterial degeneration in whom the aorta has become atheromatous. The onset of an attack is often the first indication of the existence of the disease that has insidiously undermined the vitality of the vascu lar tissue. It may be an unusual muscular effort or a fit of indiges
tion that excites the first paroxysm of pain; but the real anatomical cause consists in the altered structure of the atheromatons vessel.
True angina pectoris thus originated is a far more serious inci dent than its counterfeit, that form of cardialgia that occurs among youthful subjects who have not yet acquired an atheromatous degen eration of their arteries. Such patients, as a consequence of indiges tion, or of the excessive use of tobacco, tea, or coffee, may suffer severely with attacks of intensely painful neuralgia in the precordial region. The paroxysm is characterized by violent pain and a feeling of constriction about the inferior portion of the thorax. Painful ir radiations penetrate the interscapular space, and sometimes reach the neck and shoulders, or extend into the arms, and follow the track of the nerves as far as the tips of the fingers. Breathing seems difficult; perspiration covers the surface of the body; the face is pallid and expressive of the utmost anxiety and distress. The pulse is small, rapid, and feeble, so that the tips of the fingers grow cool. Every thing testifies to the existence of arterial spasm, rather than the loss of contractility that follows degeneration of the arterial coats. After a variable period of suffering the paroxysm subsides, unless cut short by therapeutic measures, and all goes on as before. Such ex periences are frequently connected with ordinary dyspepsia, but they are also common among the gouty. During the early stages of the disease, such attacks often precede and usher in the articular crisis; and they are not uncommon among neurotic members of the arthritic family long before the occurrence of articular manifestations. These early neuralgic pseudo-anginas are rarely attended with. danger, but the genuine form of angina pectoris is usually fatal—if not at the time of the first attack it may destroy life in any subsequent par oxysm. Post-mortem section reveals chronic inflammation of the aortic walls with atlieroma and constriction of the lumen of the nutrient arteries of the heart. In such cases death is the result of an arrest of circulation in the cardiac wall, and it is only indirectly con nected with gout. Thus produced, death is the direct consequence of arterial disease, and should not be ascribed to retrocession of the articular disease.