Distal Coronary-Artery Constriction in Angina Pectoris

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Abstract
Pupita et al. (Aug. 23 issue)1 have sought to explain myocardial ischemia during exercise in patients with stable angina and single coronary-artery occlusion on the basis of a change in the caliber of collateral or distal coronary arteries. They argue against any change in left ventricular load and myocardial oxygen demand on the basis of determinations of the rate—pressure product, using measurements of pressure in the brachial artery. The problem with this approach is that it fails to consider the effects of exercise and vasoactive drugs (nitroglycerin and ergonovine) on other systemic arteries, on wave reflection, and on the amplification of systolic pressure between the central and the peripheral arteries.2 , 3 The effects of nitroglycerin may be explained on the basis of this drug's effect on ascending aortic impedance4 , 5 — an effect that is underestimated in the measurement of systolic pressure in a peripheral artery.6 The authors may be correct in their major conclusions, but they are wrong in assuming that systolic pressure is the same in the brachial artery and the ascending aorta under different conditions, and that myocardial oxygen requirements can be determined accurately from recordings of peripheral blood pressure.