Blood pressure and bone cement.

SIR,-I read with interest "Angina Pectoris-I" (27 February, p. 501) and "Angina Pectoris-II" (6 March, p. 545) and I thoroughly enjoyed the discussion. May I be allowed to make a comment regarding "Mechanism" of angina pectoris? The causes of angina, brilliantly listed in the diagram, embrace everything but aortic valvular disease, which may be listed under provoking factors (B) and sub-heading-reduced coronary blood flow (5). Aortic stenosis may result in angina pectoris because of interference with coronary blood flow in the small vessels during systole due to high intraventricular pressure, and in aortic regurgitation coronary perfusion may be impaired by low diastolic pressure. In both forms of aortic valvular disease increased size and work of the heart may contribute to coronary insufficiency by augmenting the need for blood. May I also have the opinion of the readers regarding the treatment of angina pectoris with (3-blockers. At present three 8-blockers are available: propranolol, practolol, and oxprenolol. Dr. J. C. Petrie has rightly mentioned that practolol is less likely to cause bronchoconstriction, but practolol is less potent than the other two and it has been used more for arrhythmias than for angina. Oxprenolol, as the manufacturers claim, has got intrinsic sympathomimetic activity and is less likely to cause cardiac failure. In our Unit during the last three months we have used oxprenolol in ten patients with angina pectoris. The results of treatment are extremely satisfactory, but three patients developed intractible cardiac failure even on very low doses of oxprenolol. How common is this unwanted side effect in others' experience?-I am, etc., M. AHMED