Peripheral gangrene caused by the extreme vaso-constriction that accompanies severe circulatory failure in such a disease as cholera is well recognized. Its occurrence, however, as a complication of myocardial infarction is such an uncommon event, to judge from the literature, that the reporting of two cases seems to be justified. On admission he was severely dyspnoeic at rest. There was no cedema. He was pale and it was noted that the end of his nose was blue and cold. The pulse was impalpable at the wrist and the blood pressure was 80/60. The apex rate was 100 a minute and the rhythm was regular. The heart showed no clinical enlargement and the heart sounds were normal. There was no pericardial friction. There were loud moist sounds all over both lungs, especially towards the bases. The liver was not enlarged.He remained seriously ill with a heart rate of around 110 a minute until December 30th, when he seemed to be a little better, but it was found that the right foot had become cold and blue up to the level of the ankle, and was anmsthetic over the same area. No pulse could be felt at the ankle, though the femoral pulses were present on both sides. On this day also it was noted that the whole of the nose was blue, livid, cold and anesthetic, and that there was a clear line of demarcation with the normal skin at the base of the nose. The tips of the ears and the tongue were unaffected, but there were some blotchy blue areas on the hands. The fingers were unaffected. Anti-coagulant treatment was started on this day.On December 31st, the left foot became affected in exactly the same way, and the right foot remained blue, cold and anesthetic. The prothrombin time was 36 seconds and a normal control was 25 seconds.He remained gravely ill, and on January 3, 1949, a blood pressure reading of 60 mm. systolic with no diastolic end point was made: he died on this day. Electrocardiograms on the fourth and tenth day of the illness showed evidence of extensive myocardial infarction (Fig. 1).Necropsy. There was gangrene of the nose with a well-defined line of demarcation, and small bulli over the healthy skin at the junction. Both feet showed gangrene, with the skin black, swollen, and wrinkled (Fig. 2). The fingers and ears did not show gangrene.
The general features of acute non-specific (benign) pericarditis are now well known from the large number of cases reported from the United States (Barnes and Burchell, 1942;Carmichael et al., 1951; Scherl, 1956;Chapman and Overholt, 1957) and Scandinavia (Krook, 1954). Accounts from this country are limited to smaller numbers of patients (Davies, 1952;Bower et al., 1953;Will and Fleming, 1958). A clear pattern emerges from these reports and it is not proposed to describe the syndrome in elaborate detail but rather to emphasize certain unusual features and difficulties that have occurred in the present series of fourteen patients.The clinical picture of the ordinary uncomplicated case of acute non-specific pericarditis (ANSP) is usually that of a young man who complains of severe retrosternal pain which is made worse by movement and breathing. The temperature is raised and pericardial friction is present. The electrocardiogram shows uniform elevation of the S-T period in most leads, without abnormal Q waves, followed in a few days by lowering of the T waves as the S-T period returns to the isoelectric level. T wave inversion follows and the tracing then returns to normal ( Fig. 1 and 2). Radiological enlargement of the heart shadow due to pericardial effusion is commonly seen and there may be pleural effusion (Fig. 3). Increase of jugular venous pressure may occur. After a period of days or weeks all the abnormalities disappear and full recovery takes place. An upper respiratory infection often precedes or accompanies the onset of the illness.In the present series five cases followed this course and call for no special comment, but others showed unusual and sometimes puzzling features which will be mentioned in more, detail. All the patients were men and their ages ranged from 19 to 75 years. One patient died (see Table).Pericardial friction is not invariably heard. It was absent in three patients-and in another it was heard on one day only (Case 2). The occurrence of ANSP without friction has been previously noted; there were 13 (26%y) in Carmichael's (1951) 50 patients and 11 (37°4) in Scherl's (1956) 30 patients. No friction was heard in the fatal case of Pomerance et al. (1952).The number of patients who had repeated attacks, sometimes over long periods, is a striking feature of this series. In Case 1 there was a history of 17 attacks of retrosternal pain during 16 years: in two of these a friction rub was heard by doctors and in most of the others by the patient and his wife. In Case 5 there were 8 attacks of pain, 6 of which were observed, during 5 years: friction was heard in only one of the attacks. Another patient, Case 11, had 5 attacks of pain during 8 months but no rub was ever heard. Three attacks occurred in two patients, Cases 3 and 12, and 2 in one, Case 4. Recurrences have been frequently observed and were noted by Carmichael et al. (1951)inprobably 9 (18%) of their patients. Krook (1954)
The purpose of this paper is to give a brief account of present-day knowledge of the effects of haemochromatosis upon the heart after which we shall describe two cases of the disease in which cardiac involvement was a prominent feature stimulating our interest in this subject. The involvement of the heart in hkmochromatosis is well known. Infiltration of hemosiderin varies from wedge-shaped deposits at the nuclear poles of the muscle fibres to the extreme degree in which the fibres may be replaced by a mass of pigment granules contained within the muscle sheath. HLmosiderin may also be found in the connective tissue, lying free in the lymph spaces, or within fibroblasts and mononuclear cells. An increase of fibrous tissue has been considered to be rare. Hmmofuscin is also found in the muscle fibres arranged in the same way as hlmosiderin (Sheldon, 1935). In his review of 311 cases of haemochromatosis Sheldon states that myocardial failure is uncommon and he places it as the cause of death in a miscellaneous group (15 per cent of 119 cases in which the cause of death was evident) which includes various intercurrent conditions. Within the past seventeen years a number of reports have appeared of cases of himochromatosis in which cardiac symptoms followed by death in congestive heart failure have occurred. We have selected ten reports comprising fourteen cases which are arranged in Table I. It is a pity that the pathological data are often very meagre. Significant coronary sclerosis or valvular lesions were not described except in the case of Blumer and Nesbit (1938) in which there was a moderate degree of coronary atheroma. Cardiac enlargement was noted in eleven cases, in four on clinical grounds only and in the remainder on radiography or necropsy or both. Electrocardiographic findings are given for twelve cases. Four were normal, one after having shown T wave changes. Three showed low voltage; seven showed T wave changes other than in lead III; there were three examples of auricular fibrillation and one of auricular flutter; there was one paroxysm of supraventricular tachycardia. There were two cases of complete heart block and one of prolonged P-R interval. Substernal pain is mentioned in five cases. In two it was severe and in one it was often related to exertion. In one case, pain over a period of three weeks occurred three years before his death in heart failure. Necropsy in two instances showed myocardial fibrosis but there was coronary disease in only one (Blumer and Nesbit, 1938) and it was not severe. No myocardial infarction was found in any case. Congestive heart failure closed the illness in all the fatal cases. On the subject of the heart in hlmochromatosis, there have been a number of reports by French authors who have striven to invoke an endocrine origin for the observed heart failure without satisfying the reader or, apparently, themselves. The clinical reports describe cases that are comparable with the present series and doubtless represent the same disease process (de Gennes et al., 1936; Ouma...
The downward displacement into the right ventricle of a deformed tricuspid valve is the characteristic feature of Ebstein's anomaly. There is a large proximal cavity composed of the right atrium and part of the right ventricle and a distal cavity formed by the rest of the right ventricle. There is usually a large defect of the atrial septum. The association of the lesion with cardiac arrhythmia and bundle branch block has been stressed by Taussig (1947) and Brown (1950). Engle et al. (1950) reviewed the reported cases and, with three of their own, brought the total number to 26 at that time. None had been diagnosed before death. Baker et al. (1950) reported two cases with necropsy control in one of which crural embolism followed cardiac catheterization. Reynolds (1950) published the first report of a case diagnosed during life; angiocardiography and cardiac catheterization showed evidence of a very large right atrium and a defect of the atrial septum. Soloff et al. (1951) also made the diagnosis in life mainly on angiocardiographic evidence. van Lingen et al. (1952) described two further cases in which the diagnosis was suggested by catheter findings.Case Report A man, aged 26, was found to have an abnormal heart at the age of four and on medical advice he led a restricted life, avoiding strenuous exertion, but was able to work as a mining engineer. Two days before admission he felt rapid palpitation after cycling and his breathing became distressed. On admission he was noted to be a well-built man. He was dyspnceic and cyanosed at rest, but there was no clubbing of the fingers. The apex rate was 110 a minute and the rhythm was auricular fibrillation. The blood pressure was 110/75; the jugular veins were distended to a height of 4 cm. above the sternal angle in the erect posture. There was no other clinical evidence of heart failure. The apex beat was in the sixth interspace outside the mid-clavicular line. There was no thrill. The first heart sound was split at the apex, and the second sound at the left border of the sternum was split but not exceptionally loud. A very soft early diastolic murmur was later heard to the left of the sternum. A blood count showed 7,410,000 red cells per c.mm. and haemoglobin 17-8 g. per 100 ml.Radioscopy on admission showed a very large heart with apparent marked enlargement of the right atrium and right ventricle and slight enlargement of the left atrium but no dilatation of the pulmonary artery; there was pulmonary congestion but no hilar dance. The heart rate slowed in response to digitalis. Next day the apex rate was 80 a minute and the lungs were free from radiological signs of congestion (Fig. 1).The electrocardiogram showed auricular fibrillation and right bundle branch block. Regular rhythm returned two days after cardiac catheterization and has since been maintained; the bundle branch block persists (Fig. 3).Atrial septal defect was first suspected but the absence of enlargement of the pulmonary artery and of a hilar dance with such a large heart were against this d...
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