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Familial Cardiomegaly Br Heart J: first published as 10.1136/hrt.11.1.68 on 1 January 1949. Downloaded from FAMILIAL CARDIOMEGALY BY WILLIAM EVANS From the Cardiac Department of the London Hospital Received November 8, 1948 When valvular, hypertensive, and congenital heart While under observation for two mqnths, the disease have been excluded as causes of cardiac extrasystoles became more frequent and when attacks enlargement, some rarer condition should be sought, of paroxysmal tachycardia increased in number and but only after excluding bradycardia, pericardial severity, the patient was handicapped in his work at disease, sternal depression, or an elevated diaphragm, times by giddiness. At last, when tachycardia which by themselves without real enlargement pro- (Fig. 2) persisted for two days, pulmonary aedema duce an exaggerated cardiac silhouette on cardio- (Fig. 4) developed and he died on the third day. scopy. Such being eliminated, there remains a Summary of Necropsy (P.M. 121/1947). By group where the cause of cardiac enlargement is Professor Dorothy Russell of the Bernhard Baron obscure, and it is the purpose of this paper to Institute of Pathology. describe cases with common subjective and objective Acute pulmonary a?dema. Heart failure. Familial symptoms, and to propose a syndrome that serves Cardiomegaly. Clear yellow pericardial effusion to explain a hitherto ambiguous form of cardiac (4 oz.). Slight whitish opacity of most of visceral enlargement and facilitates clinical diagnosis of the pericardium over both ventricles. Milk-spot (2X5 condition. by 1X2 cm.) on anterior surface of right ventricle. Foramen ovale patent (about 1 cm. diameter), the NoTEs OF THREE CASES IN ONE FAMILY orifice being valvular. Great thickening (up to http://heart.bmj.com/ Case 1. Male, aged 18 years. He was referred 4 cm.) of myocardium of left ventricle, without by a service medical board which sought an explana- appreciable dilatation, composed of pale brown tion for the displacement of his apex beat. He moderately firm tissue blotched with numerous ill- admitted to no symptoms at the time and he appeared defined pale areas of fibrosis (Fig. 5). Similar pro- to be a well-developed healthy youth. The pulse portionate thickening of other chambers of heart was irregular from extrasystoles with brief periods (Fig. 6), but least marked of left auricle (5 cm. of paroxysmal tachycardia. The blood pressure diameter; 04 cm. thick). All valves normal apart was 120/80. The apex beat was forcible and was from congenital fenestration oftwo pulmonary cusps. on September 30, 2021 by guest. Protected copyright. displaced as far as the left anterior axillary line. Coronary arteries normal and enlarged in propor- The heart sounds were clear and there were no mur- tion to ventricles; no atheroma. Aorta of normal murs. A triple rhythm was present from the addi- circumference (6 cm. at ring, and 0-2 to 0-25 cm. tion ofthe third heart sound. There was no enlarge- thick). Very slight atheroma. Early mucinous ment of the liver or spleen, and further examination degeneration of media of aorta found micro- found no abnormal signs elsewhere including the scopically. central nervous system. The Wassermann reaction Clear yellow pleural effusions (right, 12 oz.; left, was negative. The blood sugar and cholesterol 5 oz.). Almost solid cedema of right lung, showing were both normal, and so was the sugar tolerance microscopically variable numbers of red corpuscles test; there was no ketosis. The cardiogram (Fig. 1) and phagocytes in alveolar spaces; purulent showed extrasystoles and exceptionally wide QRS bronchitis and early broncho-pneumonia present in complexes with inverted T waves. On cardioscopy a few places. Left lung similar but showing, (Fig. 3) there was great enlargement of the heart, microscopically, a layer of fibrin coating respiratory and particularly of the left ventricle; the border of bronchioles and some alveoli. Enlargement of which was remarkably quiet compared with the gland at tracheal bifurcation, and another above mobile right auricle. right bronchus, by miliary and larger caseous 68 Br Heart J: first published as 10.1136/hrt.11.1.68 on 1 January 1949. Downloaded from FAMILIAL CARDIOMEX/ALY669- 1' 111---W----==X= --... ................P -L 0 I--Tn~~~~~~~~~~~~~~~5 ec T -r l-N-- U:FEXtt+TSsll~~~~tr 7 ~ ~~~~~~~~~~~~~~~~ --u;"'''"'-'L~~~~~~~~~~~V_L l'!E-t III - = i X~~~~~r r T t'1_T -=-- '''''1' X 4 UT> 1/ sec I f#- ...sAZ tt5X~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~.¢..... v h i0~~~~~~~~~~~~~~~~1 http://heart.bmj.com/ FIG. 1 -Electrocardiogram from Case 1. Sinus rhyl FIG. 2.-Electrocardiogram from Case 1. on September 30, 2021 by guest. Protected copyright. with extrasystoles; exceptionally wide QRS comple Paroxysmal tachycardia with a high with four R waves showing in IVR, and deep invers auricular rate and A-V dissociation. of the T waves in many leads. tubercles, with considerable focal fibrosis. No cutaneous cedema. A well developed and well tuberculosis found in lungs. Central congestion of nourished young man. liver. Chronic congestion and cedema of spleen, Weights. Body, 62-5 kg. (height, 1-7 m.); heart, showing microscopically two miliary tubercles in 1134 g.; liver, 1921 g.; kidneys, 333 g.; spleen, pulp. One old infarct in spleen and one in right 333 g.; brain, 1495 g.; suprarenals, 13 g.; thyroid, kidney. Congestion and severe post-mortem 56 g.; thymus, 20 g.; testes, 21 g. ; pituitary, degeneration of kidneys. Persistent glandular 0-6 g. thymus. No abnormality, macroscopic or micro- Microscopic examination. Portions of the left scopic, in endocrine glands. (Only one para- ventricle and right auricle were fixed in Bouin's thyroid identified.) Post-mortem digestion of fixative. The rest of the heart was fixed in formalde- stomach. No macroscopic or microscopic ab- hyde, blocks being taken on the following day from normality found in brain or spinal cord. Middle both ventricles, interventricular septum, and sino- ears normal. Cyanosis of extremities. No sub- auricular node. In addition to haematoxylin and Br Heart J: first published as 10.1136/hrt.11.1.68 on 1 January 1949. Downloaded from 70 WILLIAM EVANS FIG. 3.-Teleradiogram from Case 1. Great enlarge- FIG. 4.-Teleradiogram from Case 1. Pulmonary ment of the heart and especially of the left cedema (1) is added to the great cardiac enlarge- ventricle (1); much pulmonary congestion (2). ment seen in Fig. 3. eosin, iron hematoxylin and van Gieson and spindle cells and occasional small lymphocytes phosphotungstic-acid hematoxylin, sections from which are mostly perivascular. Occasional larger all blocks were stained by Best's carmine for glyco- clumps of small round cells appear to be due to gen. Frozen sections of a piece of left ventricle submiliary granulomatous tubercles, one being were stained with Sudan III for fat. identified with certainty in the interventricular Heart. In all parts examined there is dense patchy septum, and one in the pericardium of the left fibrosis of the myocardium, especially beneath the ventricle. The pericardium elsewhere is little http://heart.bmj.com/ endocardium and pericardium, and gross hyper- affected; there are a few small lymphocytes about trophy of the muscle fibres (Fig. 7). The hyper- the vessels, which are engorged. No changes were trophy often appears greatest where there is most found in the special muscle fibres of the conducting fibrosis. In ordinary stains the fibres are occasion- system. ally greatly vacuolated, but vacuolation in general Liver. In a block fixed in Bouin's fluid there is is rather inconspicuous, except in phosphotungstic- great congestion and atrophy of the centres of the acid haematoxylin preparations, where high magni- lobules; in places adjacent atrophied areas are fications frequently reveal clusters of small vacuoles confluent. There is no fibrosis. A good deal of on September 30, 2021 by guest. Protected copyright. in the centres of fibres, or groups of reddish-brown glycogen is present as fine cytoplasmic granules in granules in a similar situation. In such fibres the the better preserved cells of the periportal longitudinal fibrils are restricted to the periphery of parenchyma. the muscle cell and cross-striation is lost. Cross- Muscle. Portions of the tongue and vastus striation is preserved in many fibres devoid of externus muscle were fixed in Bouin's fluid. In the vacuoles and granules. There is no fatty degenera- tongue glycogen is restricted to the squamous tion. The Bouin-fixed sections show conspicuous epithelium and some cells of the mucous glands. deposits of glycogen in many scattered fibres in both In the vastus externus large quantities of glycogen left ventricle and right auricle. There are no are present, some being in the muscle fibres but most circumscribed areas in which all or most fibres are has escaped into the interstitial tissue. Patchy so affected; the change is diffuse. A good deal of vacuolation of the fibres is demonstrated by other finely granular material stained by Best's carmine is stains, but the degree of vacuolation appears trivial present in the intermuscular connective tissue and in in comparison with the amount of glycogen. A the walls of capillaries. In the formalin-fixed tissue, special search for glycogen was made in Bouin-fixed however, there is little evidence of glycogen. The material from the kidney, spleen, and central nervous fibrous tissue in the myocardium contains few system with negative results. Br Heart J: first published as 10.1136/hrt.11.1.68 on 1 January 1949. Downloaded from FAMILIAL CARDIOMEGALY 71 http://heart.bmj.com/ on September 30, 2021 by guest. Protected copyright. FIG. 5.-Photogram of the heart in Case 1. There is very great general hypertrophy and especially of the left ventricle (1) which shows grey patches of fibrosis (2). Case 2. Male, aged 20 years. His appearance pressure was 125/80. The apex beat was near the was healthy and he complained of no symptoms left anterior axillary line and was forcible.
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