CLINICAL STUDY: MYOCARDIAL ISCHEMIA
Myocardial perfusion imaging findings and the role of adenosine in the warm-up angina phenomenon
Peter Bogaty, MDa,
John G. Kingma, PhD, FACCa,
Jean Guimond, MDa,
Paul Poirier, MDa,
Luce Boyer, RNa,
Lyne Charbonneau, RNa and
Gilles R. Dagenais, MD, FACCa
a Quebec Heart Institute/Laval Hospital, Laval University, Sainte-Foy, Quebec, Canada
Manuscript received March 15, 2000;
revised manuscript received September 18, 2000,
accepted October 26, 2000.
Reprint requests and correspondence: Dr. Peter Bogaty, Quebec Heart Institute/Laval Hospital, 2725 Chemin Sainte-Foy, Sainte-Foy, Quebec, Canada G1V 4G5
peter.Bogaty{at}med.ulaval.ca
OBJECTIVES
This study examined the roles of myocardial perfusion and adenosine in warm-up angina.
BACKGROUND
In warm-up angina, neither the role of an adenosine-mediated mechanism, as is found in experimental ischemic preconditioning, nor of increased 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 heart 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 the third test were compared with the baseline tests controlling for the heart rate-systolic blood pressure product (RPP) at thallium injection. In substudy B, 12 similar subjects did two successive exercise tests at two separate sessions and received the adenosine antagonist, aminophylline (intravenous 5 mg/kg bolus and 0.9 mg/kg/h infusion) at one session, and equivalent saline at the other session. Change in ischemic threshold (RPP at 1 mm ST segment depression) and in maximum ST depression adjusted for RPP were analyzed.
RESULTS
In substudy A, despite a significant attenuation of electrocardiogram 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%) and intensity deficits (41.2 ± 12.6% and 39.3 ± 12.6%) did not differ significantly. In substudy B, the increase in ischemic threshold on re-exercise was unaffected by aminophylline. Adjusted maximum ST depression even decreased 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 attenuation of exercise electrocardiogram indexes of ischemia, it is unaccompanied by significant changes in SPECT perfusion and does not appear to be mediated by an adenosine-dependent mechanism since it is not blocked by aminophylline. Thus, its mechanism, which appears distinct from experimental ischemic preconditioning, remains unidentified.
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Abbreviations and Acronyms
| | CAD | = coronary artery disease | | ECG | = electrocardiographic, electrocardiogram | | K+-ATP | = adenosine triphosphate-sensitive potassium channel(s) | | RPP | = heart rate-systolic blood pressure product | | SPECT | = single-photon emission computed tomography (or tomographic) | | STD | = ST segment depression | | Tl-201 | = thallium-201 |
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