Myocardial perfusion imaging findings and the role of adenosine in the warm-up angina phenomenon.
OBJECTIVE
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.
Bogaty
P
P
Quebec Heart Institute/Laval Hospital, Laval University, Sainte-Foy, Canada. peter.Bogaty@med.ulaval.ca
Kingma
J G
JG
Guimond
J
J
Poirier
P
P
Boyer
L
L
Charbonneau
L
L
Dagenais
G R
GR
D000241:Adenosine / Q000502:physiology*; D000328:Adult; D000368:Aged; D000628:Aminophylline / Q000008:administration & dosage; D000787:Angina Pectoris / Q000000981:diagnostic imaging* / Q000503:physiopathology; D001794:Blood Pressure / Q000502:physiology; D003327:Coronary Disease / Q000000981:diagnostic imaging* / Q000503:physiopathology; D004562:Electrocardiography / Q000187:drug effects; D005080:Exercise Test; D005260:Female; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D019157:Ischemic Preconditioning, Myocardial; D008297:Male; D008875:Middle Aged; D011237:Predictive Value of Tests; D013599:Systole / Q000502:physiology; D015899:Tomography, Emission-Computed, Single-Photon
D000628:Aminophylline; D000241:Adenosine