"Idiopathic" Hypertrophy of the Heart in a Young Man.

Whittle, Christina

doi:10.1016/s0140-6736(00)85431-8

Cited by 33 publications

(7 citation statements)

References 2 publications

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“…Whenever a single example of unexplained enlargement of the heart is seen the need to find the precise cause has not appeared so important, but,'when two WILLIAM EVANS or more such cases appear, a search for a common aetiology becomes more vital. When the pathological findings have not been available or are equivocal in these odd instances ofcardiac enlargement they have been described under such titles as 'idiopathic enlargement,' or 'unexplained enlargement of the heart in young subjects' (Whittle, 1929;Kugal and Stoloff, 1933;Levy and Rousselot, 1933;Mahon, 1939;Levy and von Glahn, 1937;Case Records of Massachusetts General Hospital, 1942;Norris and Pote, 1946;and Vulliamy, 1947). When inflammatory changes or fibrosis of the myocardium has been an obvious finding at necropsy, they have appeared as acute non-specific myocarditis (Helwig and Wilhelmy, 1939;Candel and Wheelock, 1945), myocardial fibrosis in young men (Sellars and Phillips, 1946), and chronic fibroblastic myocarditis (Ware and Chapman, 1947).…”

Section: Discussionmentioning

confidence: 99%

Familial Cardiomegaly

Evans¹

1949

Heart

181

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Section: Discussionmentioning

confidence: 99%

Familial Cardiomegaly

Evans¹

1949

Heart

181

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“…However, as Apelt pointed out, there was no constant feature in any case by which one could say hypertrophy would be present or not. More recently, Whittle (1929) reported the case of a young man, aged 20, who collapsed and died in the street; other than a recent attack of influenza, there was no record of any previous illness. The autopsy revealed a heart weighing 793 g., with a general enlargement chiefly affecting the left ventricle; the descending aorta was hypoplastic, but it was not specifically stated whether the thoracic aorta was of normal calibre; the remaining organs were normal though the heart was not tested for glycogen.…”

Section: Discussionmentioning

confidence: 99%

Extreme cardiac hypertrophy: Report of two cases with aortic hypoplasia and endocrine disorders

1944

American Heart Journal

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Cardiac hypertrophy exceeding 1000 grams in weight is rare. Golden and Brams (1937) could only find 37 cases recorded, excluding the 9 that they themselves reported. They did not include in their survey the cases occurring in acromegaly, to which Courville and Mason (1938) drew attention. In the two cases here reported the hearts weighed 1350 and 900 grams respectively and were associated with aortic hypoplasia and disorders of the endocrine system, one having diabetes mellitus, the other an interauricular septal defect and acromegaly. NOTES OF FIRST CASEThis man had suffered with chronic nasal infection for many years and in 1935 he underwent drainage of the left frontal sinus. In 1936, when 28 years old, he began to lose weight and to be extremely thirsty; diabetes mellitus was diagnosed. He was treated with 60 units of soluble insulin and a diet containing 90 g. of carbohydrate daily.He first attended the diabetic clinic of the Birmingham United Hospital in November, 1937.The same dietary and insulin regime was continued. Physical examination at that time showed a wellbuilt man, 5 ft. 10 in. tall and 141 lb. in weight. The heart was enlarged and there was a systolic murmur and thrill of moderate intensity, just internal to the apex beat. The rhythm was regular at a rate of 80-85 beats a minute and the blood pressure varied between 100/70 and 120/80. At the diabetic clinic his blood sugar rose to between 300 and 400 mg. per 100 c.c. after lunch, but in spite of this he felt well and was able to do heavy work as a foundry worker. Six months later, however, on the same dosage of insulin and diet he began to have frequent hypoglycxmic attacks and for the next six months he was stabilized with 30 units daily, but then the blood sugar levels again climbed to between 300-400 mg. per 100 c.c. with no obvious change in the patient's well being. In 1938 he was admitted to hospital on account of hypoglycaemic coma, and careful examination at that time suggested a diagnosis of interventricular septal defect. The electrocardiogram showed a normal P-R interval, marked left axis deviation, and inverted T waves in leads I and II. Radioscopy showed the transverse measurement of the heart was 16 5 cm., with a chest diameter of 29 5 cm. (Fig. 1). Physical examination did not show any change and the blood pressure still remained at the same level.In July, 1940, he was again admitted for investigation. He was then complaining of marked weakness and inability to work over the previous five weeks. He had noted, also, profuse sweating even when at rest and some breathlessness and palpitations on exertion. Again, physical examination was essentially as before, his Wasserman was negative, while his basal metabolic rate was +28 per cent with a basal pulse rate of 88.At this time he was taking 150 g. of carbohydrate and 25 units of soluble insulin twice a day. He was treated with rest in bed and improved rapidly. After this he gave up his job as a foundry worker and took on that of a bread salesman. In January, 1941, he was admitted w...

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“…The next key clinical-pathologic observation in the unfolding story of HCM was the association of ventricular hypertrophy of unknown etiology with sudden death in 1929 [ 6 ]. In 1944, Levy and von Glahn published an infl uential paper describing ten patients entitled "Cardiac Hypertrophy of Unknown Cause" [ 7 ].…”

Section: Sudden Deathmentioning

confidence: 99%

“…In 1929, Whittle described an asymptomatic 20 year old man who collapsed while riding a bicycle and died before reaching the hospital [ 6 ]. At post mortem examination he had marked left ventricular hypertrophy of unknown etiology.…”

Section: Prevention Of Sudden Deathmentioning

confidence: 99%

Hypertrophic Cardiomyopathy: The Past, the Present, and the Future

Braunwald

2014

Hypertrophic Cardiomyopathy

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Patients with left ventricular hypertrophic cardiomyopathy (HCM) were described in the middle of the nineteenth century. Clinico-pathologic correlations carried out in the fi rst half of the twentieth century revealed that HCM is characterized by familial occurrence, hypertrophy of the interventricular septum, dynamic obstruction to left ventricular outfl ow, impaired left ventricular fi lling, and rarely, sudden death or heart failure.The clinical diagnosis can usually be confi rmed by echocardiography. Treatment includes beta blockade and invasive therapy to reduce obstruction (septal myectomy or catheter induced alcohol septal ablation). In patients at high risk for sudden death, an implanted defi brillator is indicated. HCM is a disease of sarcomeric proteins; more than 1,500 mutations on ten genes have been described.Future challenges include learning more about patients with characteristic mutations but normal phenotypes and the development of drugs that are specifi cally directed at the molecular abnormalities. KeywordsFamilial heart disease • Ventricular hypertrophy • Sudden death • Septal myectomy • Beta-blockade • Echocardiography • Implanted defi brillator

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"Idiopathic" Hypertrophy of the Heart in a Young Man.

Cited by 33 publications

References 2 publications

Familial Cardiomegaly

Familial Cardiomegaly

Extreme cardiac hypertrophy: Report of two cases with aortic hypoplasia and endocrine disorders

Hypertrophic Cardiomyopathy: The Past, the Present, and the Future

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