[The effect of carvedilol on cardiac function and autoantibodies against the cardiac receptors].
OBJECTIVE
To evaluate the effect of carvedilol on the cardiac function and autoantibodies against the cardiac beta(1), beta(2) and alpha(1)-adrenergic receptors in patients with chronic heart failure (CHF).


METHODS
54 patients with CHF were divided randomly into two groups, one was regular treatment group treated with ACE inhibitor, digoxin and diuretic, another was carvedilol treatment group treated with carvedilol on the basis of above regular treatment. All the patients were followed up for six months and measured the changes of cardiac function and three autoantibodies by echocardiography and enzyme-linked immunosorbent assay (ELISA) respectively.


RESULTS
(1) After carvedilol treatment, LVEDD and LVESD (57.50 +/- 7.29) mm and (43.17 +/- 8.27) mm were smaller than that in regular treatment group [(64.09 +/- 7.40) mm and (52.93 +/- 8.35) mm], and LVEF [(50.41 +/- 10.91)%] was higher than that [(41.70 +/- 7.45)%] in regular treatment group (P < 0.01). (2) After carvedilol treatment, the positive ratios and average titers of autoantibodies against the cardiac beta(1), beta(2) and alpha(1)-adrenergic receptors all decreased significantly compared with that of pre-treatment (P < 0.05). The positive ratios of autoantibodies against the three receptors in carvedilol treatment group were lower than those in regular treatment group (P < 0.05). The average titers of autoantibodies against the cardiac beta(1), beta(2) and alpha(1)-adrenergic receptors in carvedilol treatment group (1:72.44, 1:61.66 and 1:67.30) were lower than those in regular treatment group (1:113.24, 1:110.66 and 1:113.24), P < 0.05.


CONCLUSIONS
Carvedilol decreased positive ratio and average titer of autoantibodies against the beta(1), beta(2) and alpha(1) receptors accompanied with the obvious improvement of cardiac function though the blockade of beta(1), beta(2) and alpha(1) receptors. It suggests that the autoantibodies might be involved in the process of pathophysiology and development of CHF. Carvedilol can inhibit this process.
Chen
Jin
J
Heart Centre, Beijing Chaoyang Hospital, Capital University of Medical Sciences, Beijing 100020, China.
Hu
Da-yi
DY
Zhang
Lin
L
Liu
Xiu-lan
XL
Wu
Ya-feng
YF
Li
Jing
J
D000328:Adult; D000368:Aged; D001323:Autoantibodies / Q000097:blood*; D002227:Carbazoles / Q000627:therapeutic use*; D000077261:Carvedilol; D005260:Female; D005500:Follow-Up Studies; D006333:Heart Failure / Q000188:drug therapy / Q000276:immunology* / Q000503:physiopathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D011412:Propanolamines / Q000627:therapeutic use*; D018340:Receptors, Adrenergic, alpha-1 / Q000276:immunology; D018342:Receptors, Adrenergic, beta-1 / Q000276:immunology; D018343:Receptors, Adrenergic, beta-2 / Q000276:immunology; D055815:Young Adult
D001323:Autoantibodies; D002227:Carbazoles; D011412:Propanolamines; D018340:Receptors, Adrenergic, alpha-1; D018342:Receptors, Adrenergic, beta-1; D018343:Receptors, Adrenergic, beta-2; D000077261:Carvedilol