RELATIONSHIP BETWEEN ALTERATIONS IN LYMPHOCYTE AND MYOCARDIAL β‐ADRENOCEPTOR DENSITY IN PATIENTS WITH LEFT HEART VALVULAR DISEASE

We have evaluated the possibility that alterations in lymphocyte beta-adrenoceptor density may be related to changes in the myocardial population in left heart valvular diseases. Receptor density and their binding affinities were estimated using [125I]-iodocyanopindolol. 2. The lymphocyte (LC) beta-adrenoceptor density was 43.4 +/- 5.6 fmol/mg protein in the controls (n = 35) and 81% lower in heart valvular patients (n = 86). In myocardial controls (n = 18), the left ventricular (LV) receptor density was 167.2 +/- 29.8 fmol/mg protein, right ventricular (RV) density was 123.1 +/- 14.6 fmol/mg, left atrial (LA) density was 81.6 +/- 10.5 fmol/mg and right atrial (RA) 108.1 +/- 14.5 fmol/mg. Compared with this group, the receptor density of the study patients (n = 47) decreased by 67, 43, 24 and 32% in the LV, RV, LA and RA, respectively. The decrease in LC was twice that of the average total myocardial receptor density. 3. When patients were classified according to their left ventricular load conditions as having either left ventricular pressure overload (LVP), left ventricular volume overload, mixed lesions (MOL) and no left ventricular overload (mitral stenosis; NOL), the attenuation in LC receptor density reached statistical significance for all four groups, without showing significant difference between the individual groups. In contrast, the decrease in all chambers was predominantly due to volume overload. MOL and NOL exerted intermediate effects that were significant in the LV, while LVP did not contribute to the changes in the LA. 4. Accordingly, the reduction in peripheral beta-adrenoceptor density may reflect the extent to which particularly the volume overload exerts its influence on myocardial beta-adrenoceptors in left heart valvular patients.