The prognosis for 115 rheumatic fever patients subsequently receiving regular intramuscular penicillin prophylaxis for at least 5 years was studied. Average follow-up was 9.3 years, and 57 patients were followed for 10 years or longer. Of the 79 patients with acute mitral regurgitation, 70% lost their murmur from 4 days to 8.5 years after it was first heard. This is in contrast to those with acute aortic regurgitation which persisted in 73%. No patient developed mitral or aortic stenosis: this suggests that regular prophylaxis may prevent the development of stenosis. Congestive failure, cardiomegaly, and arrhythmia correlated closely with persistence of murmurs, but increased P-R interval, acute QRS or T-voltage variation or both, and ST-T abnormalities did not.
The Mustard operation corrects the effects of congenital transposition of the great arteries by creating an intraarterial baffle to direct pulmonary venous blood to the tricuspid orifice and systemic venous blood to the mitral orifice. To identify the long-term effects of this procedure, we followed 372 patients with complete transposition of the great arteries who survived the Mustard operation for at least three months. The mean follow-up period was 4.5 years (range, 0.4 to 15.9); the mean age at operation was 2.0 years. Mean resting heart rates were consistently lower than those for age-matched normal children. Seventy-six per cent of the patients had sinus rhythm during the year of operation--a figure that decreased to 57 per cent by the end of the eighth postoperative year. Twenty-five patients died during the follow-up period, nine suddenly. Life-table analysis revealed a cumulative survival rate of 91 per cent for 11 years and 71 per cent for 15 years after the operation. No strong risk factor for sudden unexpected death identified. This study demonstrates that extended survival among patients with transposition can be expected after the Mustard operation. However, over time there is a decreasing prevalence of normal sinus rhythm in survivors, as well as a small risk of sudden death.
The natural history of transposition of the great arteries between 1957 and 1964 is presented based on a total of 742 cases. The area of study was the State of California and included 290 cases from 14 selected hospital centers. It is clear that in this era of more successful surgery, no such study will ever again be possible.Of major importance has been a compilation of a life table so that present day cardiologists and surgeons, when evaluating whether surgery should be undertaken in a particular patient, can weigh the risk of the operative procedure against the expected number of years of life remaining if surgery is not done.For the whole group the age of death was as follows: by 1 week, 28.7%; by 1 month, 51.6%; and by 1 year, 89.3%.The average life expectancy at birth was 0.65 years; at 1 week of age, 0.87 years; at 1 month, 1.12 years; and at 1 year, 3.92 years.Associated lesions had a marked effect on prognosis. The life tables presented tell a more complete story, and the pertinent data are presented in detail. (See longer summary at end of paper for further information.)
SUMMARY The effects of variations in the volume conductor properties of the torso on the electrocardiogram were studied by means of a theoretical eccentric spheres model. The model includes a blood cavity, cardiac muscle layer, pericardium, lung region, skeletal muscle layer, and subcutaneous fat. The source of the field is a double-layer spherical cap located within the myocardium. The following effects regarding the electrocardiogram (ECG) potentials were determined: (1) blood augments the potential, but less than predicted by simpler published models; (2) in anemia, high potentials are expected, whereas in polycythemia, voltages are reduced; (3) abnormally low lung conductivity (emphysema) causes low surface potentials whose magnitude is controlled by the low conductivity skeletal muscle layer; (4) low voltages result both from low and high pericardial conductivities; (5) the surface potential increases with increasing myocardial conductivity; (6) low skeletal muscle conductivity (Pompe's disease) causes high surface potentials; (7) obesity lowers the potential only slightly; (8) a thick myocardium, protruding into the lung region, slightly augments the potential; (9) an increase in the thickness of the myocardium at the expense of the blood cavity causes a decrease in potential; (10) the potential increases with increasing heart size; and (11) the location of the heart within the torso has a very significant effect on the surface potential distribution. Ore Res 104-111, 1979
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