Abstract
Aortic regurgitation differs from mitral regurgitation in that it is a result of combined volume and pressure overload, while the latter represents an almost pure volume overload. In this study, we tested the possibility that these two forms of left ventricular volume overload exert different effects on beta-adrenoceptor density. Lymphocyte (n = 33) and myocardial (n = 22) beta-adrenoceptor densities were evaluated by [125I]-iodocyanopindolol binding in volume-overload patients with left heart valvular disease, compared with 31 healthy donor blood and 15 donor heart controls, made available as a result of failing to get matching recipient. The total lymphocyte (LC) beta-adrenoceptor density decreased from 43.4 +/- 5.5 fmol mg-1 protein in controls to 9.2 +/- 2.7 fmol (P < 0.001) in heart valvular patients. In the myocardial controls, the left ventricular (LV)-receptor density was 126.7 +/- 19.5 fmol; right ventricular (RV), 123.1 +/- 14.6 fmol; left atrial (LA), 81.6 +/- 10.5 fmol; and right atrial (RA), 108.1 +/- 14.5 fmol mg-1 protein. Compared to this group, the total LV-receptor density of the patients decreased by 63%, RV by 54%, LA by 31% and RA by 34%. The decrease in receptor density exhibited a positive correlation with increasing ejection fractions in both the left (r = 0.38) and right (r = 0.44) ventricles, indicating that the former was dependent on the extent of the disease. These changes were accompanied by a 44% increase in plasma epinephrine, 13% in norepinephrine and a 27% decrease in dopamine levels. Based on the predominant left ventricular volume overload classified as aortic regurgitation (AVR), mitral regurgitation (MVR), and mixed aortic and mitral regurgitation (MOL), the attenuation in myocardial-receptor densities showed the following trend: MOL > AVR > AVR. The results show a global reduction in myocardial and LC beta-adrenoceptor density, which depends on the origin and the gravity of the LV volume overload.
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