Myocardial perfusion imaging findings and the role of adenosine in the warm-up angina phenomenon

OBJECTIVES This study examined the roles of myocardial perfusion and adenos ine in warm-up angina. BACKGROUND In warm-up angina, neither the role of an adenosine-mediated mec hanism, as is found in experimental ischemic preconditioning, nor of increa sed myocardial perfusion is well defined. METHODS In substudy A, a single-photon emission computed tomography (SPECT) -thallium-201 exercise test was performed by 12 subjects with ischemic hear t disease on three occasions one week apart. The third test was preceded by a warm-up test. The extent of the thallium deficit and its intensity on th e third test were compared with the baseline tests controlling for the hear t rate-systolic blood pressure product (RPP) at thallium injection. In subs tudy B, 12 similar subjects did two successive exercise tests at two separa te sessions and received the adenosine antagonist, aminophylline (intraveno us 5 mg/kg bolus and 0.9 mg/kg/h infusion) at one session, and equivalent s aline at the other session. Change in ischemic threshold (RPP at 1 mm ST se gment depression) and in maximum ST depression adjusted for RPP were analyz ed. RESULTS In substudy A, despite a significant attenuation of electrocardiogr am indexes of myocardial ischemia between the baseline and third (warmed-up ) tests, the thallium extent deficits (20.8 +/- 15.1% and 16.8 +/- 12.4%) a nd intensity deficits (41.2 +/- 12.6% and 39.3 +/- 12.6%) did not differ si gnificantly. In substudy B, the increase in ischemic threshold on re-exerci se was unaffected by aminophylline. Adjusted maximum ST depression even dec reased to a greater extent on re-exercise with aminophylline (by 51 +/- 21% ) than with saline (by 32 +/- 19%) (p = 0.012). CONCLUSIONS While warm-up angina is associated with a significant attenuati on of exercise electrocardiogram indexes of ischemia, it is unaccompanied b y significant changes in SPECT perfusion and does not appear to be mediated by an adenosine-dependent mechanism since it is not blocked by aminophylli ne. Thus, its mechanism, which appears distinct from experimental ischemic preconditioning, remains unidentified. (C) 2001 by the American College of Cardiology.