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Caffeine is a non-selective antagonist at the adenosine receptors, which is expected to reverse both the intended (coronary vasodilation) and unintended (hypotension, flushing) effects of exogenously administered adenosine and adenosine-related compounds. In the past, several studies were conducted to characterize the effect of caffeine on vasodilator myocardial perfusion imaging (MPI) with conflicting results. However, new evidence supports earlier observations and shows that recent caffeine intake attenuates vasodilator-induced myocardial hyperaemia and may therefore reduce the sensitivity of radionuclide MPI for the detection of inducible perfusion abnormality in patients with coronary artery disease. Although the magnitude of this effect and hence its clinical significance are dose dependent, the acute response to equivalent doses of caffeine varies largely among individuals, and this might be explained by differences in caffeine exposure and genetically determined variations in caffeine metabolism. Abstinence from caffeinated foods and beverages for a minimum of 12 hours before vasodilator stress is therefore recommended although longer abstention might be required in order to prevent the potentially blocking effect of residual caffeine on vasodilator-mediated actions.

Objectives: 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.