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Biomedical subjects

B O Eriksson

Publications and source records attributed to B O Eriksson.

77 records · Page 5Linked to original sources

Endomyocardial biopsy in heart-transplanted children: comparison of sheaths to guide biopsy forceps.

The risk of perforation during 65 endomyocardial biopsies (380 specimens) was investigated using two different sheaths to guide the biopsy forceps in five heart-transplanted children aged 1.6-12.9 years. One of the sheaths guided the biopsy forceps simply into the right ventricle (prefabricated 110 degrees curved tip); the other (specially curved sheath) had two curves, the distal one of which guided the forceps posteriorly toward the interventricular septum. The position of the sheath was evaluated by biplane fluoroscopy and, in children </=4 years of age, also by transesophageal echocardiography (TEE). Perforation was defined as clinical perforation (chest pain and pericardial effusion as judged by transthoracic echocardiography or TEE) and "near perforation" (epicardial fat in specimens). The prefabricated sheath was associated with 10 incidents of perforation (one clinical and nine near perforations) after 16 biopsies and 96 specimens (10.4%) compared with 2 near perforations after 49 biopsies and 284 specimens (0.7%) after using the specially curved sheath (p < 0.001). We conclude that the risk of perforation during endomyocardial biopsy can be reduced by using a specially curved sheath to guide the biopsy forceps toward the interventricular septum.

Adolescent↗

Mitochondrial myopathy and cardiomyopathy in siblings.

Two siblings with infantile lactic acidosis and mitochondrial myopathy are described. The first child, a girl, died at 5 months of age from severe lactic acidosis after about 3 weeks of progressive muscular hypotonia. The younger brother had congenital lactic acidosis but no other symptoms until 6 months of age when progressive muscle weakness appeared. Treatment with dichloroacetate lowered the serum lactic acid level but did not affect his clinical condition. At 13 months of age, cardiomyopathy was diagnosed and he died at the age of 29 months of circulatory failure. Both children had mitochondrial myopathy. Postmortem examination of the boy revealed marked morphologic changes of the mitochondria in both skeletal muscle and the myocardium; biochemical investigation of skeletal muscle mitochondria demonstrated deficiencies in both complex I (NADH ferricyanide reductase) and complex IV (cytochrome c oxidase). The disease in these siblings differs in several respects from previously reported patients with mitochondrial myopathy and cytochrome c oxidase deficiency.

Acidosis, Lactic↗