The immediate, precipitating condi tions of a paroxysm are not known, but they are supposed to be connected with disturbances of the vagus, or; perhaps, the sympathetic nerves. Nothnagel re ported a series of cases under the title "Angina Pectoris Vasomotoria" which seemed to be due to a pure neurosis. They followed exposure to cold, and were ushered in by spasm of the peripheral arterioles, which presumably produced the cardiac disturbance because of the in creased exertion demanded of the heart in order to propel the blood through nar-1 rowed channels. Cases of this sort must be rare. Authors quote Nothnagel with out mentioning similar personal observa tions.
From a neuralgia or a neurosis true angina pectoris differs in being usually fatal, in attacking men ten times as often as women, and in being associated with organic changes in the neighboring structures, viz.: the heart and aorta.
Lesions of the cardiac plexus and the branches of the vagus have been found in repeated instances of angina pectoris, but that such lesions are invariably pres ent and essential to the disorder has not vet been proved. "The cardiac nerves may be seriously implicated in aneurism, in mediastinal tumors, in adherent peri cardium, and in the exudate of acute pericarditis, without causing the slight est pain." (Osier.) The late Sir Benjamin W. Richardson regarded angina pectoris as an actual disease analogous (as Trousseau held) to epilepsy, and due to a disturbance in the sympathetic nervous system.
Debove says that in tabetic angina pectoris there is no organic lesion of the heart or large vessels and that the at tack must be regarded as a visceral crisis. Dana refers cardiac crises in tabes to a degenerative irritation of the vagus.
[It should, however, be remembered that aortic disease is rather frequent in tabetic patients. H. F. VICKERY.] In regard to the causation of attacks of angina pectoris in the graver cases which are associated with serious struct ural disease of the heart and vessels, J. Burney Yeo states that in by far the greater number of deaths from organic disease of the heart all the various lesions may be present which have been found in fatal cases of angina and yet no true attacks have ever been com ,, plained of. In his opinion there is some additional circumstance needed to ac count for the angina. The most serious forms of angina seem to have a complex causation. First, there must be a ncu nasal element; the nerves of the cardiac plexus suffer irritation, and an intense cardiac nerve-pain is excited; this acts as a shock to the motor nerves of the heart, and thus reacts on the heart-mus cle, which, in fatal cases, is already on the verge of failure from organic causes; and, if there should be excited at the same time some reflex arterial spasm, the heart will have to encounter an increased peripheral resistance as well. In such
cases the rapidity of the fatal issue is no argument against the neuralgic nature of the angina. In certain conditions, espe cially in habitual high arterial tension, strain is apt to fall (when the aortic valves are competent) rather on the first part of the aorta than on the ventricular surface, and anginal attacks are more prone to occur in these cases, as this part of the aorta is in such close relation with the nerves of the cardiac plexus, rather than in those cases in which the strain is felt on the interior of the cardiac cavi ties. The causation of the less grave and more remediable forms of angina is also, in many instances, complex. A cardio vascular system, feeble and poorly nour ished, on account of anremia. may be submitted to undue strain: or there may be some intoxication—such as that of tea, tobacco, alcohol, gout, or some intes tinal toxin—irritating the cardiac and vasomotor nerves, increasing peripheral resistance, and so exciting anginal at tacks, which may altogether pass away and be completely recovered from. Va somotor spasm, as a unique cause of at tacks of angina, must be set aside as inconsistent with extended clinical ex perience. Cases of angina pectoris. both of the milder and graver forms, occur without any evidence of vasomotor spasm or of heightened arterial tension; and the conditions of heightened arterial ten sion. together with a feeble cardiac mus cle, very commonly co-exist, without any tendency whatever to the development of anginal attacks. The argument in favor of a vasomotor causation has been inferred from therapeutic experiment and the relief to the paroxysm which has attended the use of agents which cause arterial relaxation. But most, if not all, of these vasodilators are also ansthetics, and, as Balfour has pointed out, it is probably to their anodyne action on the sensory cardiac nerves that they owe their chief efficacy; Grainger Stewart has also pointed out that nitrite of amyl has a direct effect on nervous structures, and that it relieves other forms of neuralgia.