Sindrome coronario lateral

Sindrome coronario lateral


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ESTUDO PATOL~GICO ~.4 A#o DO TABAC~ DESNICOTINIZADO SBBRE OS VASOS SANGUINEOS DO RATO BRANCO: By J. Lopes de Faria, Universidade de Minas Gerais. Grafica Queizoz Breiner Ltda., Belo Horizonte, Brazil, 1943, 107 pages, 56 illust,rations. Forty-one rats were injected with a denicotinized extract of tobacco which was prepared according to Harkavy’s technique. Thirteen rats served as controls, and were injected with saline solution. In the latter parts of the experiments, which lasted 114 days, doses of 4 times as much and then 18 times as much of the extract as Harkavy used were injected. Chronic endocardit,is, myocarditis, and pericarditis were noted on microscopic examination of both test animals and control animals. The author concludes that nicotine-free extracts of tobacco, specifically that grown in Minas Gerais, do not produce pathologic changes in the bloo,d vessels of the hearts and extremities of white rats. He was thus unable to c.onfirm the studies of Harkavy. This, he believes, may be due to the fact that the tobacco which he used had a lower “antigen power” than that employed by Harkavy. EDGAR SINDRO~~E ologia Aires.


CORONARIO LATERAL : By Guillermo A. BOSCO, Professor Titular de Semiy Clinica. Propedeutica de la Facultad de Ciencias Medicas de Buenos Imprenta Ferrari Hnos., Buenos Aires, 1943, 168 pages, 83 illustrations.

As is made clear in the introduction, this monographic t,he “lateral coronary syndrome ’ ’ as an anatomicoclinical together with the “ anterior ’ ’ and ‘ Lposterior ’ ’ coronary

study strives to establish entity to be considered syndromes.

The syndrome is caused by occlusion of the left circumflex artery in its terminttl portion. This artery is distributed over the lateral portion of the left ventricle in about 80 per cent of all persons, and over the posterior part of the septum and the right ventricle in the others. The author states that this possibly L‘anomalous ’’ distribution need not be taken into account, for only the left ventricle might show the effects of acute ischemia; it is the reviewer’s opinion that this is not valid. The first is illustrated

part of the book by exceptionally

is devoted to an anatomic and pathologic study, and clear photographs. A physiopathologic study follows.

The clinical signs of the “lateral syndrome” are discussed in detail. In spite of the author’s efforts, they do not seem to be essentially different from those caused by occlusion of other coronary arteries. The cardiac manifestations are sinus tachycardia, gallop rhythm, friction rub, functional mitral systolic murmur, and ventricular alternation. It is emphasized that attacks of either left ventricular premature beats or left ventricular tachycardia may occur. The early electrocardiographic abnormalities are depression of the S-T segment in Leads I and IVF and elevation of the S-T segment in Lead III. Differentiation from posterior infarction may be difficult at times. The author agrees with Wood




au11 his co-workers, but nclt with Katz, who Ilescribes changes in the S.T segment in Leads I and III similar tf, those associatetl with posterior infarction, and changes in the precondial lea~ls like those which occur with anterior infawtiou, i.e.. a special electroc~arcliographi~~ pattern. Ko mention is made of the original description of the syndrome t)y Wood. fVolferth, and Bellet (Ax. HEAFLT .J., 16: SXij 193X), nor is there any historical approach or quotation from the literature. In spite of the efforts of the author, a differentiation between this and other c~oronarp syntlromes does not always sfwn possible. Wood and his co-workers emphasized the frequency of auricular fibrillation, but Bosco, on the other hamI, stresses ventricular premature beats and ventricular tachg. caxlia. This differenw of opinion undoubtedly le.aves a field for future investigation. Am0