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ossification of the coronary arteries and fatty degeneration of the heart-walls. Again, there are many cases which commence gradually, and with great mildness, and with little appearance of danger to life in the first attacks; but the subsequent attacks are progressively more severe and dangerous up to a fatal result, after weeks, months, or years. On the other hand, I have known three instances in which the first attacks of spasmodic heart-pain very nearly proved fatal, but the subsequent fits were milder (in one there was no second attack): all those patients are living, six, eight, and three years respectively, after their first attacks.
It can hardly be doubted that neuralgic spasm is the true cause of sudden death in some cases of stenosis of the aortic orifice, which, but for some accidental circumstances, would not have died suddenly at all, but would have gone through a long and gradual course of deterioration. I particularly remember an instance in which extreme and calcareous constriction of the aortic orifice, in a boy not yet come to puberty, was entirely unsuspected, until one day, in running fast, he screamed out and fell down, and was almost instantaneously dead. I remember another case very similar, in which extreme mitral constriction produced almost as sudden death, apparently from painful spasm, under the same kind of exertion. On the other hand, sudden death, when produced by the form of heart-disease which (as Dr. Walshe points out) is most likely to cause such a catastrophe, viz., aortic regurgitation pure, without hypertrophy, does not seem to be due to painful spasm, but to simple and complete failure of the muscular power, and is perhaps partly of the nature of paralysis from a syncopal condition of the brain, the unhypertrophied heart having become for the moment unable to supply blood enough to the brain to carry on nervous function at all.
