Muscular cramp, in relation with the phenomena of angina pectoris and 'intermittent claudication of the extremities' / by F. Parkes Weber.

  • Weber, Frederick Parkes, 1863-1962.
Date:
1894
Catalogue details

Licence: Public Domain Mark

Credit: Muscular cramp, in relation with the phenomena of angina pectoris and 'intermittent claudication of the extremities' / by F. Parkes Weber. Source: Wellcome Collection.

Provider: This material has been provided by The Royal College of Surgeons of England. The original may be consulted at The Royal College of Surgeons of England.

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    nary theory; but in these cases spasm of the coronaries may explain the attacks, as was maintained in the fatal case attributed by Huchard to the poison of tobacco (see Huchard, op. cit., pp. 626 and 712). These are the chief objections to the coronary artery theory, and they are not unanswerable; whilst, on the other side, the well-known action of nitrite of amyl and trinitrin affords support to this theory. The bene- ficial action of nitrite of amyl in some cases of angina pectoris was first discovered by Dr. Lauder Brunton,1 and has since been abundantly confirmed. He considered that it acted by lowering the peripheral resistance to the arterial stream and thereby diminishing the amount of the heart's work. It is obvious, then, how this therapeutic explanation of Dr. Brunton may be adduced in support to some extent of the theory that in patients with angina pectoris the coronary arteries are stenosed, and that, owing to this, the blood-supply to the cardiac muscle is limited, allowing it to do only a limited amount of work. More detailed evidence from post-mortem statistics as to the presence of coronary disease in fatal cases of angina pectoris is given, amongst recent authors, by Huchard,2 and it would be out of place to repeat it here ; this paper deals with the part played by cramp in angina pectoris, and the coronary theory has been practically assumed. It now rests with me to recapitulate the chief points in my paper: True angina pectoris has long been 'separated from the nervous cases, or pseudo-anginas; it has been regarded as due to stenosis of the coronary arteries and as analogous to certain premonitory signs of dry gangrene, due to stenosis of arteries in the extremities. In the present paper I do not pretend to have discussed these questions in their en- tirety, but have confined myself to the rdle played by muscular cramps in relation to the other phenomena. In this paper it is main- tained that muscular cramp does not take any necessary part in angina pectoris or in the phenomena preceding senile gangrene in an extremity, but that cramp is likely to occur in any muscle where an accumulation of waste products takes place, whether this accumulation be caused in healthy muscles by rapid catabolism due to excessive exercise, or by insufficient removal of the waste products/ in cases of disease due to stenosis of the main arteries and consequent diminution of the blood-stream through the affected part. It is further held that these cramps, when they do occur in angina pectoris, are expressed by the syncope, which may accompany the attack and lead to a fatal ter- mination. not examined. In a later case, examined by Hunter (narrated by Dr. J. Fothergill, in Medical Observations and Inquiries, 1776, vol. v. p. 225), ossification of the coronary arteries was found, and on Hunter's own death, in 1793, from angina pectoris, Sir Everard Home, fore- warned by Jenner, discovered that the coronary arteries were diseased. i See Dr. Lauder Brunton : Nitrite of Amyl in Angina Pectoris, Clin. Soc Reports, Feb- ruary, 1870, vol. iii. a Huchard, op. cit., pp. 798-847. 10 Grosvenor Street, London, Eng.