Impact of Acute Caffeine Ingestion on Endothelial Function in Subjects With and Without Coronary Artery Disease

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 wi...

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Published in:The American journal of cardiology 2011-05, Vol.107 (9), p.1255-1261
Main Authors: Shechter, Michael, MD, MA, Shalmon, Guy, RD, Scheinowitz, Mickey, PhD, Koren-Morag, Nira, PhD, Feinberg, Micha S., MD, Harats, Dror, MD, Sela, Ben Ami, PhD, Sharabi, Yehonatan, MD, Chouraqui, Pierre, MD
Format: Article
Language:English
Subjects:
ACE inhibitors
Biological and medical sciences
Biomarkers
Brachial Artery - drug effects
Brachial Artery - physiology
Caffeine
Caffeine - pharmacology
Cardiology. Vascular system
Cardiovascular
Cardiovascular disease
Case-Control Studies
Coffee
Comparative analysis
Coronary Artery Disease
Coronary heart disease
Double-Blind Method
Effects
Endothelium, Vascular - drug effects
Endothelium, Vascular - physiology
Female
Heart
Humans
Male
Medical sciences
Middle Aged
Phosphodiesterase Inhibitors - pharmacology
Plasma
Regional Blood Flow
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Sela, Ben Ami, PhD
Sharabi, Yehonatan, MD
Chouraqui, Pierre, MD
description 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
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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 &gt;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 &lt;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 &lt;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 &lt;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 &lt;0.001 for all comparisons) in the 2 groups compared to placebo. 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Vascular system ; Cardiovascular ; Cardiovascular disease ; Case-Control Studies ; Coffee ; Comparative analysis ; Coronary Artery Disease ; Coronary heart disease ; Double-Blind Method ; Effects ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - physiology ; Female ; Heart ; Humans ; Male ; Medical sciences ; Middle Aged ; Phosphodiesterase Inhibitors - pharmacology ; Plasma ; Regional Blood Flow</subject><ispartof>The American journal of cardiology, 2011-05, Vol.107 (9), p.1255-1261</ispartof><rights>Elsevier Inc.</rights><rights>2011 Elsevier Inc.</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2011 Elsevier Inc. All rights reserved.</rights><rights>Copyright Elsevier Sequoia S.A. 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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 &gt;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 &lt;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 &lt;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 &lt;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 &lt;0.001 for all comparisons) in the 2 groups compared to placebo. 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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 &gt;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 &lt;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 &lt;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 &lt;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 &lt;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.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>21349479</pmid><doi>10.1016/j.amjcard.2010.12.035</doi><tpages>7</tpages></addata></record>
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subjects ACE inhibitors
Biological and medical sciences
Biomarkers
Brachial Artery - drug effects
Brachial Artery - physiology
Caffeine
Caffeine - pharmacology
Cardiology. Vascular system
Cardiovascular
Cardiovascular disease
Case-Control Studies
Coffee
Comparative analysis
Coronary Artery Disease
Coronary heart disease
Double-Blind Method
Effects
Endothelium, Vascular - drug effects
Endothelium, Vascular - physiology
Female
Heart
Humans
Male
Medical sciences
Middle Aged
Phosphodiesterase Inhibitors - pharmacology
Plasma
Regional Blood Flow
title Impact of Acute Caffeine Ingestion on Endothelial Function in Subjects With and Without Coronary Artery Disease
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