Haemodynamic changes induced by the correction of anaemia by erythropoietin: role of antiplatelet therapy.
BACKGROUND
In a retrospective study, antiplatelet therapy has been shown to be associated with a decreased incidence of erythropoietin-induced hypertension. In order to ascertain the role of antiplatelet drugs in the haemodynamic response to the correction of anaemia by rHuEpo, 18 patients on chronic haemodialysis who started rHuEpo therapy were prospectively studied.


METHODS
The subjects were randomly assigned to receive or not, one of the following antiplatelet drugs: ditazole (3 patients), ticlopidine (3 patients) or aspirin plus dipyridamole (3 patients). Cardiac index (CI) by echo-Doppler, total peripheral resistance (TPR) and mean arterial pressure (MAP) were determined at baseline 10 and 20 weeks following the initiation of rHuEpo therapy. rHuEpo therapy was administered subcutaneously at the same dose (40 U/kg thrice weekly) during the first 10 weeks. Ten uraemic patients on haemodialysis who had never received rHuEpo therapy served as the control group.


RESULTS
One patient in the group without antiplatelet drugs discontinued the study due to the development of severe hypertension after 12 weeks on rHuEpo therapy. There were no significant differences in the haemodynamic parameters at baseline. At 10 weeks, MAP was higher in patients without than with antiplatelet drugs or controls untreated with rHuEpo (128.5 +/- 28 versus 100.6 +/- 13.5 versus 98.7 +/- 14 mmHg respectively, P = 0.0047), TPR was also higher in patients without antiplatelet drugs than in the 2 other groups (1919 +/- 433 versus 1576 +/- 359 versus 1418 +/- 324 din.seg.cm-5m2 respectively, P = 0.0231), but CI did not differ among the three groups. At 20 weeks, MAP was still higher in patients without antiplatelet drugs than in patients with antiplatelet drugs or controls not on rHuEpo therapy respectively (112.9 +/- 24.6 versus 91.0 +/- 9.0 versus 101.7 +/- 14.1 mmHg respectively, P = 0.075), but at this stage TPR and Cl did not differ among the three groups.


CONCLUSIONS
These data reinforce the previous observation that antiplatelet therapy may prevent the development of rHuEpo-induced hypertension.
Caravaca
F
F
Servicio Nefrología, Hospital Infanta Cristina, Extremadura University, Badajoz, Spain.
López-Minguez
J R
JR
Arrobas
M
M
Cubero
J
J
Pizarro
J L
JL
Cid
M C
MC
Sanchez-Casado
E
E
Miranda
M P
MP
D000328:Adult; D000368:Aged; D000740:Anemia / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology*; D001241:Aspirin / Q000627:therapeutic use; D004176:Dipyridamole / Q000627:therapeutic use; D004921:Erythropoietin / Q000627:therapeutic use*; D005260:Female; D006439:Hemodynamics / Q000187:drug effects* / Q000502:physiology; D006801:Humans; D008297:Male; D008875:Middle Aged; D010080:Oxazoles / Q000627:therapeutic use; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D011446:Prospective Studies; D011994:Recombinant Proteins / Q000627:therapeutic use; D006435:Renal Dialysis / Q000009:adverse effects; D013988:Ticlopidine / Q000627:therapeutic use; D013997:Time Factors; D014511:Uremia / Q000150:complications / Q000503:physiopathology / Q000628:therapy
D010080:Oxazoles; D010975:Platelet Aggregation Inhibitors; D011994:Recombinant Proteins; D004921:Erythropoietin; D004176:Dipyridamole; C084774:ditazol; D013988:Ticlopidine; D001241:Aspirin