Sir, The correspondence (1986;55:112-3) arising out of the paper by Dr Walker and colleagues' prompts us to make the following comments. We agree with Dr Walker that the conclusions of the study should be confined to the specific clinical setting and should not be extended to encompass the view that it is never harmful to stop atenolol abruptly in patients with coronary artery disease.Walker et al saw no serious coronary events in 20 patients with stable angina in the six days after atenolol was stopped. This is not surprising because few would regard the risk of serious consequences from abrupt / blocker withdrawal as being high under these circumstances. They also noted no rebound in heart rate or blood pressure measured daily-this is also not surprising because these variables were recorded under unstressed conditions (which is why the earlier formal investigations into the phenomenon produced negative results). Furthermore, they saw no rebound in the consequences of treadmill exercise testing five days after atenolol was stopped-again this is not unexpected since these tests were probably on the late side and treadmill exercise is not the only form, and not necessarily the most potent form, of sympathetic stimulation to which patients may be exposed. These negative findings certainly do not demonstrate that the phenomenon of ,B adrenergic hypersensitivity is absent after treatment with atenolol has been stopped, nor that it wouid be safe to ignore the possibility of this consequence in clinical practice.The manifestation of increased (B adrenergic sensitivity as it gradually declines after the end of ,B blocker treatment will depend upon the net level of ( adrenoceptor stimulation, and this in turn will depend upon the competition between sympathetic drive and the declining concentration of the (B blocking drug. Our data showed that the phenomenon is indeed present after atenolol is stopped; under the particular circumstances of our study (in which heart rate was measured when the patient was standing after sublingual glyceryl trinitrate) the rebound was significantly greater for the group as a whole only at four days and not at five days. It occurred 2-3 days after propranolol, oxprenolol, "slow release" oxprenolol, and acebutolol.2 3 Exercise, moreover, is only one way of increasing sympathetic drive, and the increased sympathetic drive with exercise is only one component cause of the increase in heart rate and myocardial energy requirements. Emotional stress, the reflex response to vasodilator drugs, or operation, can all cause very high ,B adrenergic activity and it would not be wise to regard this as always being innocent. . Abrupt withdrawal of atenolol in patients with severe angina: comparison with effects of treatment. Br HeartJ 1985;53:276-82. 2 Ross PJ, Lewis MJ, Sheridan DJ, Henderson AH. Adrenergic hypersensitivity after beta-blocker withdrawal. Br Heart J 1981;45:637-42. 3 Singh H, Rimmer A, Lewis MJ, Henderson AH. Beta-adrenergic hypersensitivity after stopping oxprenolol: discrepant findings n...
