No abstract

It has been shown in different groups of patients with variant angina that coronary spasm can be reproduced by physiologic maneuvers Received Feb. 4, 1986; revision accepted Aug. 14, 1986. Presented in part at the 58th Scientific Sessions of the American Heart Association, November 11-14, 1985, Washington, D.C.Vol. 74, No. 6, December 1986 In patients with variant angina focal coronary spasm can be reproduced by ergonovine"922 and, less frequently, also by hyperventilation.2"25 Isolated reports suggest that coronary spasm can also be provoked by a number of physiologic maneuvers2"29 and pharmacologic agents such as histamine,9 epinephrine,3 metacholine,5 and dopamine.30 It has therefore become apparent in patients with variant angina that particular segments of their epicardial coronary arteries exhibit an abnormal reactivity to stimuli that produce only minor degrees of coronary constriction, if any, in normal individuals or in patients with other forms of angina.3'The aim of our study was to investigate whether the abnormal coronary reactivity exhibited by patients with vasospastic angina results from specific abnormal agonist-receptor interactions or from a local, nonspecific supersensitivity to different stimuli. To this end, we studied the responses of patients with vasospastic angina to a series of provocative tests known to induce coronary spasm through different mechanisms.

CT-based AC of SPECT images consistently improved overall diagnostic performance of readers with different interpretive attitudes and experience. CT-based AC is well suited for routine use in clinical practice.

PET with C15O2 inhalation provides an accurate noninvasive quantitative method for measuring regional myocardial blood flow in patients.

Regional myocardial perfusion and exogenous glucose uptake were assessed with rubidium-82 (82Rb) and 18F-2-fluoro-2-deoxyglucose (FDG) in 10 normal volunteers and 12 patients with coronary artery disease and stable angina pectoris by means of positron emission tomography. In patients at rest, the myocardial uptake of 82Rb and FDG did not differ significantly from that measured in normal subjects. The exercise test performed within the positron camera in eight patients produced typical chest pain and ischemic electrocardiographic changes in all. In each of the eight patients a region of reduced cation uptake was demonstrated in the 82Rb scan recorded at peak exercise, after which uptake of 82Rb returned to the control value 5 to 14 min after the end of the exercise. In these patients, FDG was injected in the recovery phase when all the variables that were altered during exercise, including regional myocardial 82Rb uptake, had returned to control values. In all but one patient, FDG accumulation in the regions of reduced 82Rb uptake during exercise was significantly higher than that in the nonischemic regions, i.e., the ones with a normal increment of 82Rb uptake on exercise. In the nonischemic areas, FDG uptake was not significantly different from that found in normal subjects after exercise. In conclusion, myocardial glucose transport and phosphorylation seem to be enhanced in the postischemic myocardium of patients with exercise-induced ischemia. Circulation 74, No. 1, 81-88, 1986. IT HAS LONG been known that myocardial glucose utilization is enhanced as a consequence of faster anaerobic glycolysis during conditions of reduced oxygen availability, as proved by the greater lactate production.' The importance of coronary flow and washout of the interstitial space in maintaining an accelerated glycolytic rate has been emphasized by studies in isolated working rat hearts submitted to anoxia and ischemia.24 Both anoxia and ischemia produce an initial acceleration of the glycolytic rate caused by rapid activation of glycogen breakdown, which lasts less than 10 min. Thereafter, as tissue glycogen is depleted, the glycolytic rate remains accelerated in the anoxic heart because of a greater utilization of exogenous glucose. In contrast, in the ischemic heart, the From the M.