cardiovascular health


Effect of alcohol consumption on biological markers associated with risk of coronary heart disease: systematic review and meta-analysis of interventional studies. PDF Print E-mail

BMJ. 2011 Feb 22;342:d636. doi: 10.1136/bmj.d636.
Effect of alcohol consumption on biological markers associated with risk of coronary heart disease: systematic review and meta-analysis of interventional studies.
Brien SE, Ronksley PE, Turner BJ, Mukamal KJ, Ghali WA.
Department of Community Health Sciences, Faculty of Medicine, Calgary Institute for Population and Public Health, University of Calgary, Alberta, Canada T2N 4Z6.
Abstract
OBJECTIVE: To systematically review interventional studies of the effects of alcohol consumption on 21 biological markers associated with risk of coronary heart disease in adults without known cardiovascular disease.
DESIGN: Systematic review and meta-analysis.
DATA SOURCES: Medline (1950 to October 2009) and Embase (1980 to October 2009) without limits.
STUDY SELECTION: Two reviewers independently selected studies that examined adults without known cardiovascular disease and that compared fasting levels of specific biological markers associated with coronary heart disease after alcohol use with those after a period of no alcohol use (controls). 4690 articles were screened for eligibility, the full texts of 124 studies reviewed, and 63 relevant articles selected.
RESULTS: Of 63 eligible studies, 44 on 13 biomarkers were meta-analysed in fixed or random effects models. Quality was assessed by sensitivity analysis of studies grouped by design. Analyses were stratified by type of beverage (wine, beer, spirits). Alcohol significantly increased levels of high density lipoprotein cholesterol (pooled mean difference 0.094 mmol/L, 95% confidence interval 0.064 to 0.123), apolipoprotein A1 (0.101 g/L, 0.073 to 0.129), and adiponectin (0.56 mg/L, 0.39 to 0.72). Alcohol showed a dose-response relation with high density lipoprotein cholesterol (test for trend P = 0.013). Alcohol decreased fibrinogen levels (-0.20 g/L, -0.29 to -0.11) but did not affect triglyceride levels. Results were similar for crossover and before and after studies, and across beverage types.
CONCLUSIONS: Favourable changes in several cardiovascular biomarkers (higher levels of high density lipoprotein cholesterol and adiponectin and lower levels of fibrinogen) provide indirect pathophysiological support for a protective effect of moderate alcohol use on coronary heart disease.
PMID: 21343206 [PubMed - indexed for MEDLINE]

 
Is red wine a SAFE sip away from cardioprotection? Mechanisms involved in resveratrol- and melatonin-induced cardioprotection. PDF Print E-mail


J Pineal Res. 2011 Feb 23. doi: 10.1111/j.1600-079X.2010.00853.x. [Epub ahead of print]
Is red wine a SAFE sip away from cardioprotection? Mechanisms involved in resveratrol- and melatonin-induced cardioprotection.
Lamont KT, Somers S, Lacerda L, Opie LH, Lecour S.
Hatter Institute for Cardiovascular Research, Department of Medicine, Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa.
Abstract
Epidemiological studies suggest that regular moderate consumption of red wine confers cardioprotection but the mechanisms involved in this effect remain unclear. Recent studies demonstrate the presence of melatonin in wine. We propose that melatonin, at a concentration found in red wine, confers cardioprotection against ischemia-reperfusion injury. Furthermore, we investigated whether both melatonin and resveratrol protect via the activation of the newly discovered survivor activating factor enhancement (SAFE) prosurvival signaling pathway that involves the activation of tumor necrosis factor alpha (TNFα) and the signal transducer and activator of transcription 3 (STAT3). Isolated perfused male mouse (wild type, TNFα receptor 2 knockout mice, and cardiomyocyte-specific STAT3-deficient mice) or rat hearts (Wistars) were subjected to ischemia-reperfusion. Resveratrol (2.3 mg/L) or melatonin (75 ng/L) was perfused for 15 min with a 10-min washout period prior to an ischemia-reperfusion insult. Infarct size was measured at the end of the protocol, and Western blot analysis was performed to evaluate STAT3 activation prior to the ischemic insult. Both resveratrol and melatonin, at concentrations found in red wine, significantly reduced infarct size compared with control hearts in wild-type mouse hearts (25 ± 3% and 25 ± 3% respectively versus control 69 ± 3%, P < 0.001) but failed to protect in TNF receptor 2 knockout or STAT3-deficient mice. Furthermore, perfusion with either melatonin or resveratrol increased STAT3 phosphorylation prior to ischemia by 79% and 50%, respectively (P < 0.001 versus control). Our data demonstrate that both melatonin and resveratrol, as found in red wine, protect the heart in an experimental model of myocardial infarction via the SAFE pathway.
© 2011 John Wiley & Sons A/S.
PMID: 21342247 [PubMed - as supplied by publisher]

 
Resveratrol and endothelial cell function PDF Print E-mail

Biofactors. 2010 Aug 20. [Epub ahead of print]
Effect of resveratrol on endothelial cell function: Molecular mechanisms.
Schmitt CA, Heiss EH, Dirsch VM.
Wolfson Institute for Biomedical Research, University College London, London, United Kingdom.
Abstract
The polyphenolic natural product resveratrol (RV), best known for its occurrence in grape skin and red wine, is considered a candidate drug for prevention and treatment of cardiovascular diseases. This review aims to summarize the molecular effects of RV on endothelial cells, which line the inner walls of blood vessels and play a key role in the development of those diseases. We describe how RV enhances endothelial nitric oxide production, improves endothelial redox balance and inhibits endothelial activation in response to pro-inflammatory and metabolic insults. Furthermore, we summarize effects of RV on endothelial senescence, apoptosis, endothelin-1 release, and endothelial progenitor cell function. As many of RV's actions seem to be mediated by SIRT1, different mechanistic possibilities how RV may lead to SIRT1 activation are discussed.

 
Nitric oxide and vasodilation PDF Print E-mail

Vascular Actions of Nitric Oxide as Affected by Exposure to Alcohol.
Toda N, Ayajiki K.
Toyama Institute for Cardiovascular Pharmacology Research, 7-13, 1-Chome, Azuchi-machi, Chuo-ku, Osaka 541-0052, Japan.
Abstract
Vasodilator substances liberated from endothelial cells, mainly nitric oxide (NO), play important roles in physiologically regulating blood flow and blood pressure and preventing pathological vascular damage. Impairment of these actions promotes the genesis of cardiovascular diseases such as hypertension, cerebral and cardiac hypoperfusion, impaired vasodilatation and atherosclerosis. Low concentrations of alcohol induce increased release of NO from the endothelium due to activation and expression of NO synthase (NOS). In contrast, administration of high concentrations of alcohol or its chronic ingestion impairs endothelial functions in association with reduced NO bioavailability. The endogenous NOS inhibitor asymmetric dimethylarginine may participate in decreased synthesis of NO. Chronic alcohol intake also impairs penile erectile function possibly by interfering with endothelial, but not nitrergic nerve, function. This review article summarizes the vascular actions of NO derived from endothelial and neuronal NOS as affected by alcohol, other than wine, and acetaldehyde in healthy individuals, human materials and various experimental animals.
PMID: 20522422 [PubMed - as supplied by publisher]

 
Resveratrol, estradiol, and heart muscle PDF Print E-mail


J Clin Endocrinol Metab. 2010 Jun 9. [Epub ahead of print]
Resveratrol, a Red Wine Constituent, Blocks the Antimitogenic Effects of Estradiol on Human Female Coronary Artery Smooth Muscle Cells.
Dubey RK, Jackson EK, Gillespie DG, Zacharia LC, Imthurn B, Rosselli M.
Department of Obstetrics and Gynecology (R.K.D., B.I., M.R.), Clinic for Reproductive Endocrinology, University Hospital Zurich, Zurich CH-8091, Switzerland; Zurich Center for Integrative Human Physiology (R.K.D.), University of Zurich, Zurich CH-8057, Switzerland; and Center for Clinical Pharmacology (R.K.D., E.K.J., D.G.G., L.C.Z.) and Departments of Medicine (R.K.D., E.K.J., D.G.G., L.C.Z.) and of Pharmacology and Chemical Biology (E.K.J., L.C.Z.), University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15260.
Abstract
Context: Antimitogenic effects of estradiol on vascular smooth muscle cells (VSMCs) may be cardioprotective, and these effects are mediated by estrogen receptor-alpha-dependent and -independent mechanisms, with the latter involving the conversion of estradiol to 2-hydroxyestradiol/2-methoxyestradiol by CYP450. Because resveratrol inhibits CYP450 and is an estrogen-receptor-alpha antagonist, resveratrol may abrogate the antimitogenic effects of estradiol. Objective: The objective of the study was to examine the interaction of pharmacologically relevant concentrations of resveratrol with estradiol, 2-hydroxyestradiol, and 2-methoxyestradiol in human female coronary artery VSMCs. Methods and Results: In human female coronary VSMCs, resveratrol (0.1-10 muM) alone did not influence serum-induced DNA or collagen synthesis or cell proliferation or migration; however, resveratrol abrogated the inhibitory effects of estradiol, but not 2-hydroxyestradiol or 2-methoxyestradiol, on these responses. Resveratrol also abrogated the inhibitory effects of estradiol on positive growth regulators (cyclin A, cyclin D, MAPK phosphorylation) and the stimulatory effects of estradiol on negative growth regulators (p21, p27). In microsomes and cells, dietarily relevant levels of resveratrol (0.001-1 muM) inhibited the metabolism of estradiol to 2-hydroxestradiol/2-methoxyestradiol. Propylpyrazoletriol (estrogen receptor-alpha agonist, 100 nmol/liter), but not diarylpropionitrile (estrogen receptor-beta agonist, 10 nmol/liter), inhibited VSMC mitogenesis, and this effect was blocked by resveratrol (5 mumol/liter). Higher concentrations (>25-50 muM) of resveratrol, never attainable in vivo, inhibited VSMC growth, an effect blocked by GW9662 (peroxisomal proliferator-activated receptor-gamma antagonist). Conclusion: In conclusion, dietarily relevant levels of resveratrol abrogate the antimitogenic effects of estradiol by inhibiting CYP450-mediated estradiol metabolism and blocking estrogen receptor-alpha.
PMID: 20534756 [PubMed - as supplied by publisher]

 
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