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CLINICAL RESEARCH: CARDIAC IMAGING

High-Dose Adenosine Overcomes the Attenuation of Myocardial Perfusion Reserve Caused by Caffeine

Eliana Reyes, MD^_*,,_*, Chee Y. Loong, MRCP^_*,, Mark Harbinson, MD, MRCP, Jackie Donovan, MSc, DipRCPath, Constantinos Anagnostopoulos, MD, PhD, FRCP, FRCR, FESC and S. Richard Underwood, MD, FRCP, FRCR, FESC, FACC^_*,

^_* National Heart and Lung Institute, Imperial College London, United Kingdom
Nuclear Medicine Department, Royal Brompton Hospital, London, United Kingdom
Clinical Biochemistry Department, Royal Brompton Hospital, London, United Kingdom

Manuscript received April 15, 2008; revised manuscript received July 21, 2008, accepted August 19, 2008.

^_* Reprint requests and correspondence: Dr. Eliana Reyes, Nuclear Medicine Department, Royal Brompton Hospital, Sydney Street, London SW3 6NP, United Kingdom (Email: e.reyes{at}rbht.nhs.uk).

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 µg/kg/min of adenosine combined with low-level exercise. For the caffeine study, 12 patients received 140 µg/kg/min of adenosine (standard) and 18 patients received 210 µg/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.

Key Words: caffeine • adenosine • myocardial perfusion scintigraphy • coronary artery disease

Abbreviations and Acronyms   CAD = coronary artery disease   MI = myocardial infarction   MPS = myocardial perfusion scintigraphy   SDS = summed difference score   SSS = summed stress score   TID = transient ischemic dilation

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