Myocardial connexin43 expression in left ventricular hypertrophy resultingfrom aortic regurgitation

Intercellular conduction in the working myocardium of the mammalian heart i s mediated by gap junctions composed of connexin43 or 45. Recently, it has been shown that myocardial connexin expression is malleable and may be alte red with disease. To better understand myocardial conduction in left ventri cular hypertrophy resulting from volume overload, we used indirect immunofl uorescence microscopy to examine cardiac connexin43 expression in 10 New Ze aland white rabbits with surgically induced aortic regurgitation (AR) and i n 10 age-matched sham-operated controls. Animals were sacrificed at approxi mately 1 month or greater than or equal to 2.5 years after operation. All A R animals developed eccentric hypertrophy; none evidenced heart failure. Th e heart-to-body weight ratios for the I month AR and control groups were 2. 9 +/- 0.8 vs 1.8 +/- 0.2 g/kg (p less than or equal to 0.01) while ratios f or the greater than or equal to 2.5 year AR and control groups were 2.4 -/ 0.3 vs 1.9 +/- 0.3 (p less than or equal to 0.05). No significant differen ces in posterior wall thickness were found among any of the groups. Althoug h the overall pattern of connexin43-like immunoreactivity was similar for a ll four groups, staining in the 1 month AR animals tended to be less than t hat of age-matched controls; staining was increased in the greater than or equal to 2.5 year AR animals and was greater than control (p < 0.05), in wh ich staining did not change with animal age. This disease duration-related increase differs from the long-term decrease in connexin43 expression assoc iated with other forms of heart disease and suggests that alterations in co nnexin expression may play a role in the rhythm abnormalities commonly seen in AR. (C) 1998 by Elsevier Science Inc.