Effects of atenolol and propanolol on platelet aggregation in moderate essential hypertension.

To the Editor: We read the paper “Effects of atenolol and propranolol on platelet aggregation in moderate essential hypertension: randomized crossover trial” by Punda et al with great interest (1). However, we would like to point out some issues which we found conflicting. Firstly, the presence of hypertension in patients, used for comparing the effects of two distinct -blockers on platelet functions, is an independent factor which could directly influence the results. The mechanisms of platelet activation in hypertension include high shear force, activation of renin-angiotensin system, endothelial changes, and presence of comorbid conditions. The treatment of high blood pressure brings about a reversal of the changes seen in the cell. This could in part be due to the direct effect of the drug on the megakaryocyte and/or the platelets themselves, or it might simply be due to the reduction in blood pressure (2). The possibility that the regulation of hypertension could solely correct the platelet functions makes the comparison of the effects of the two drugs questionable. Secondly, the authors imply that there is no clear evidence that atenolol has an effect on platelet aggregation. In 1997, Knight et al reported that atenolol treatment did not alter platelet aggregation in unstimulated samples, lead an increment in fibrinogen binding as a response to thrombin activation, and did not block the effect of epinephrine on platelet fibrinogen binding (3). According to the results of this study, atenolol did not alter platelet activation significantly. At this point, it does not seem logical to create a model comparing the effects of propranolol and atenolol when there are reports addressing the ineffectiveness of atenolol on hypertension. Additionally, a metaanalysis by Carlberg et al, cited by Punda et al, found that antihypertensive effect of atenolol was not superior to placebo and was inferior to other antihypertensives in cardiovascular morbidity and mortality (4). According to this metaanalysis (4), it does not seem appropriate to administer atenolol to one arm of the hypertensive patients, as Punda et al did. Thirdly, the authors noted that the effects of propranolol on platelet aggregation were reported to be different in previous studies. They argue that these differences could originate from different doses of propranolol and a difference in the methods for measuring platelet aggregation. They claim that they studied spontaneous aggregation, despite the fact that others studied induced aggregation. In this case, is the method the authors chose for measuring the effects of propranolol on platelet aggregation appropriate for the exact determination of the effects of propranolol on platelet aggregation? It is unclear why this method could not be performed in vivo by using flow cytometry (5). Moreover, the serotonergic effects of platelets should not be overlooked as it is influenced by propranolol (6).