High-dose adenosine overcomes the attenuation of myocardial perfusion reserve caused by caffeine.
OBJECTIVE
We studied whether an increase in adenosine dose overcomes caffeine antagonism on adenosine-mediated coronary vasodilation.


BACKGROUND
Caffeine is a competitive antagonist at the adenosine receptors, but it is unclear whether caffeine in coffee alters the actions of exogenous adenosine, and whether the antagonism can be surmounted by increasing the adenosine dose.


METHODS
Myocardial perfusion scintigraphy (MPS) was used to assess adenosine-induced hyperemia in 30 patients before (baseline) and after coffee ingestion (caffeine). At baseline, patients received 140 microg/kg/min of adenosine combined with low-level exercise. For the caffeine study, 12 patients received 140 microg/kg/min of adenosine (standard) and 18 patients received 210 microg/kg/min (high dose) after caffeine intake (200 mg). Myocardial perfusion was assessed semiquantitatively and quantitatively, and perfusion defect was characterized according to the presence of reversibility.


RESULTS
Caffeine reduced the magnitude of perfusion abnormality induced by standard adenosine as measured by the summed difference score (SDS) (12.0 +/- 4.4 at baseline vs. 4.1 +/- 2.1 after caffeine, p < 0.001) as well as defect size (18% [3% to 38%] vs. 8% [0% to 22%], p < 0.01), whereas it had no effect on the abnormalities caused by high-dose adenosine (SDS, 7.7 +/- 4.0 at baseline vs. 7.8 +/- 4.2 after caffeine, p = 0.7). There was good agreement between baseline and caffeine studies for segmental defect category (kappa = 0.72, 95% confidence interval: 0.65 to 0.79) in the high-dose group. An increase in adenosine after caffeine intake was well tolerated.


CONCLUSIONS
Caffeine in coffee attenuates adenosine-induced coronary hyperemia and, consequently, the detection of perfusion abnormality by adenosine MPS. This can be overcome by increasing the adenosine dose without compromising test tolerability.
Reyes
Eliana
E
National Heart and Lung Institute, Imperial College London, United Kingdom. e.reyes@rbht.nhs.uk
Loong
Chee Y
CY
Harbinson
Mark
M
Donovan
Jackie
J
Anagnostopoulos
Constantinos
C
Underwood
S Richard
SR
D000241:Adenosine / Q000008:administration & dosage / Q000627:therapeutic use*; D000368:Aged; D002110:Caffeine / Q000097:blood / Q000494:pharmacology*; D000697:Central Nervous System Stimulants / Q000097:blood / Q000494:pharmacology*; D003069:Coffee; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging / Q000188:drug therapy*; D003331:Coronary Vessels / Q000187:drug effects*; D004347:Drug Interactions; D005260:Female; D006801:Humans; D006940:Hyperemia / Q000139:chemically induced / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000188:drug therapy; D055414:Myocardial Perfusion Imaging; D011446:Prospective Studies; D058915:Purinergic P1 Receptor Antagonists; D018047:Receptors, Purinergic P1 / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects; D014665:Vasodilator Agents / Q000008:administration & dosage / Q000627:therapeutic use*
D000697:Central Nervous System Stimulants; D003069:Coffee; D058915:Purinergic P1 Receptor Antagonists; D018047:Receptors, Purinergic P1; D014665:Vasodilator Agents; D002110:Caffeine; D000241:Adenosine