Although coffee is a widely used, pharmacologically active beverage, its impact on
the cardiovascular system is controversial. To explore the effect of acute caffeine
ingestion on brachial artery flow-mediated dilation (FMD) in subjects without coronary
artery disease (CAD; controls) and patients with CAD, we prospectively assessed brachial
artery FMD in 40 controls and 40 age- and gender-matched patients with documented
stable CAD on 2 separate mornings 1 week to 2 weeks apart. After overnight fasting,
discontinuation of all medications for ≥12 hours, and absence of caffeine for >48
hours, participants received capsules with caffeine 200 mg or placebo. One hour after
drug ingestion, participants underwent brachial artery FMD and nitroglycerin-mediated
dilation (NTG) using high-resolution ultrasound. As expected, patients with CAD were
more oftein diabetic, hypertensive, obese, dyslipidemic, and smoked more than controls
(p <0.01 for all comparisons). Aspirin, Clopidogrel, angiotensin-converting enzyme
inhibitors, β blockers, and statins were significantly more common in patients with
CAD than in controls (p <0.01 for all comparisons). At baseline, FMD, but not NTG,
was significantly lower in patients with CAD compared to controls. Acute caffeine
ingestion significantly increased FMD (patients with CAD 5.6 ± 5.0% vs 14.6 ± 5.0%,
controls 8.4 ± 2.9% vs 18.6 ± 6.8%, p <0.001 for all comparisons) but not NTG (patients
with CAD 13.0 ± 5.2% vs 13.8 ± 6.1%, controls 12.9 ± 3.9% vs 13.9 ± 5.8%, p = NS for
all comparisons) and significantly decreased high-sensitivity C-reactive protein (patients
with CAD 2.6 ± 1.4 vs 1.4 ± 1.2 mg/L, controls 3.4 ± 3.0 vs 1.2 ± 1.0 mg/L, p <0.001
for all comparisons) in the 2 groups compared to placebo. In conclusion, acute caffeine
ingestion significantly improved endothelial function assessed by brachial artery
FMD in subjects with and without CAD and was associated with lower plasma markers
of inflammation.
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Article info
Publication history
Published online: February 25, 2011
Accepted:
December 21,
2010
Received in revised form:
December 21,
2010
Received:
October 30,
2010
Identification
Copyright
© 2011 Elsevier Inc. Published by Elsevier Inc. All rights reserved.
