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Biomedical subjects

Michel de Lorgeril

Publications and source records attributed to Michel de Lorgeril.

18 recordsLinked to original sources
PubMed2006

Cholesterol lowering and mortality: time for a new paradigm?

Sudden cardiac death is the main cause of cardiac mortality. Is blood cholesterol a determinant of sudden cardiac death? Does cholesterol lowering result in fewer sudden cardiac deaths? Answering these two questions may shed new light on the epidemiology of coronary heart disease and on prevention options. In fact, careful analysis of the available data, including randomised trials, indicates that, contrary to a widespread opinion, cholesterol lowering does not appear to be a very effective way of reducing cardiac and overall mortality in the general population.

Anticholesteremic Agents↗
PubMed2006

Selenium and antioxidant defenses as major mediators in the development of chronic heart failure.

Increased oxidative stress is involved in the pathogenesis of chronic heart failure (CHF), the common end result of most cardiac diseases. Selenium is an "essential" trace element, which means that it must be supplied by our daily diet and that its blood and tissue concentrations are extremely low. Selenium has a variety of functions. It is a key component of several functional selenoproteins required for normal health. The best known of these are the antioxidant glutathione peroxidase (GPx) enzymes, which remove hydrogen peroxide and the harmful lipid hydroperoxides generated in vivo by oxygen-derived species. GPx deficiency exacerbates endothelial dysfunction, a major contributing factor in the severity of CHF symptoms, in various conditions such as hyperhomocysteinemia. This suggests that homocysteine may be involved in the CHF associated endothelial dysfunction through a peroxide-dependent oxidative mechanism. Selenium also plays a role in the control of thyroid hormone metabolism and in protection against organic and inorganic mercury. One possible additional mechanism by which low selenium may compromise cardiovascular condition may be through the effect of selenium on the synthesis and activity of deiodinases, enzymes converting thyroxin into the biologically active triiodothyronine. Selenium and iodine actually interact in cardiovascular physiology, and further studies are needed to examine their role, in isolation and in association, in the development of CHF. Thus, selenium (through its role in selenoenzymes, thyroid hormones, and interactions with homocysteine and endothelial function) appears to be a major mediator in several pathways potentially contributing to CHF development.

Antioxidants↗
PubMed2006

The Mediterranean-style diet for the prevention of cardiovascular diseases.

OBJECTIVES: To discuss present knowledge about Mediterranean diet and cardiovascular diseases. DESIGN: Review of existing literature. SETTING AND RESULTS: Epidemiological studies as well as randomised dietary trials suggest that Mediterranean diet may be important in relation to the pathogenesis (and prevention) of CHD. For instance, a striking protective effect of an ALA-rich Mediterranean diet was reported in the Lyon Diet Heart Study with a 50 to 70% reduction of the risk of recurrence after 4 years of follow-up in CHD patients. According to our current knowledge, dietary ALA should represent about 0.6 to 1% of total daily energy or about 2 g per day in patients following a Mediterranean diet, whereas the average intake in linoleic acid should not exceed 7 g per day. Supplementation with very-long-chain omega-3 fatty acids (about 1 g per day) in patients following a Mediterranean type of diet was shown to decrease the risk of cardiac death by 30% and of sudden cardiac death by 45% in the GISSI trial. CONCLUSIONS: In the context of a diet rich in oleic acid, poor in saturated fats and low in omega-6 fatty acids (a dietary pattern characterising the traditional Mediterranean diet), even small doses of omega-3 fatty acids (about 1 g EPA+DHA the form of fish oil capsules or 2 g alpha-linolenic acid in canola oil and margarine) might be very protective. These data underline the importance of the accompanying diet in any dietary strategy using fatty acid complements.

Cardiovascular Diseases↗
PubMed2006

A mediterranean diet is cost-effective in patients with previous myocardial infarction.

This evaluation aimed to assess the economic performance of the Mediterranean diet for patients after a first acute myocardial infarction (AMI). A cost utility analysis using a Markov model was used to compare the Mediterranean diet to a prudent Western diet over a time frame of 10 years. After a systematic review of the literature, program effectiveness was based on the Lyon Diet Heart Study (605 patients, mean age 54 y, randomized to the Mediterranean diet delivered by a dietician and cardiologist, or a prudent Western diet). Costs were estimated in AU$ [and converted to US$ and Euros (euro)] based on the resource use to which published unit costs were applied. Cost and benefits were discounted at 5% per annum. The main outcome measure was cost per quality-adjusted life year (QALY) gained. Extensive 1-way sensitivity analyses were performed. The Mediterranean diet compared with a prudent Western diet was estimated to cost AU$1013 (US$703, euro579) per QALY gained per person. There was a mean gain in life years of 0.31/person and a gain in quality-adjusted life years of 0.40/person. Based on the published results from the Lyon Diet Heart Study and conservative assumptions, the Mediterranean diet is highly cost-effective for persons after a first AMI and represents an exceptional return on investment. Policy makers should strongly consider the generalizability of results to their own setting.

Cost-Benefit Analysis↗
PubMed2006

The Mediterranean diet in secondary prevention of coronary heart disease.

Epidemiological studies as well as randomised dietary trials suggest that Mediterranean diet may be important in relation to the pathogenesis and prevention of coronary heart disease (CHD). A striking protective effect of a Mediterranean diet rich in alpha-linolenic acid (ALA) was reported in the Lyon Diet Heart Study with a 50 to 70% reduction of the risk of recurrence after four years of follow-up in CHD patients. According to current knowledge, dietary ALA should represent about 0.6 to 1% of total daily energy or about 2 g per day in patients who follow a traditional Mediterranean diet. Supplementation with very long chain omega-3 fatty acids (c.1g per day) in patients following a Mediterranean type of diet was shown to decrease the risk of cardiac death by 30% and of sudden cardiac death by 45% in the GISSI trial. Thus, in the context of a diet rich in oleic acid, poor in saturated fats and not high in omega-6 fatty acids (a dietary pattern characterizing the traditional Mediterranean diet), even a small dose of very long chain omega-3 fatty acids (one gram under the form of capsules) might be very protective. These data underline the importance of the accompanying diet in any dietary strategy using fatty acid complements.

Coronary Disease↗
PubMed2005

Lipid-lowering drugs and essential omega-6 and omega-3 fatty acids in patients with coronary heart disease.

BACKGROUND AND AIM: There are only little data about the effects of lipid-lowering drugs (LLDs) on the metabolism of essential n-6 and n-3 fatty acids in patients with established coronary heart disease (CHD). METHODS AND RESULTS: Male patients with CHD and high cholesterol levels (>6.2 mmol/L) were randomized (double-blind protocol) to receive either simvastatin 20mg (S) or fenofibrate 200mg daily (F) for 3 months. Dietary habits and plasma fatty acids were not different in the two groups at baseline. After treatment, there were significant changes in both the groups for the main n-6 fatty acids, with an increase in arachidonate (from 6.5+/-1.7% of total fatty acids to 7.5+/-2.1, p<0.001 in S and from 6.2+/-1.4 to 6.8+/-1.4, p<0.005 in F) and a decrease in linoleate (from 26.9+/-3.9 to 24.2+/-3.6, p<0.001, and from 27.8+/-3.4 to 26.1+/-4.2, p<0.05, in S and F, respectively). In addition, there was a decrease in two major n-3 fatty acids (alpha-linolenate and docosahexanoate, both p<0.05), but only in F. CONCLUSIONS: For the first time in a double-blind randomized study in CHD patients, we report that LLDs significantly alter the metabolism of essential fatty acids that are critically important for the pathogenesis and prevention of CHD. Further studies are urgently needed to examine the effects of higher dosages of statins (as currently proposed to reduce more cholesterol) on these essential fatty acids in the clinical setting and the crucial questions of whether specific dietary intervention (combining low intake of n-6 fatty acids and high intake of n-3 fatty acids) may improve the effectiveness of these drugs.

Analysis of Variance↗
PubMed2004

Cardioprotective effect of chronic low dose ethanol drinking: insights into the concept of ethanol preconditioning.

The reason why low-to-moderate alcohol drinking is associated with reduced cardiovascular mortality is not elucidated. While data suggested that ethanol drinking may have a protective effect on global cardiac ischemia, the effect of chronic low dose ethanol drinking (CLEthD) on myocardial infarct size has not been evaluated in a model of regional ischemia. Using an isolated rat heart model to exclude the effect of various in vivo confounders, we have studied the effect of CLEthD on infarct size (IS) and left ventricular function after 30 min of regional ischemia and 120 min of reperfusion. The effect of CLEthD was compared with ischemic preconditioning (IPC) and protein kinase C (PKC) isoforms were analysed in the myocardium before the 30-min ischemia. Ethanol-fed rats received 9% (v/v) ethanol in their drinking water for 7 weeks. Four groups of rats were studied: (1) control, (2) ethanol, (3) control + IPC, (4) ethanol + IPC. Compared with controls (59 +/- 10), IS (as percent of risk zone) was smaller in the ethanol (39 +/- 6) and IPC (31 +/- 8) groups (both p < 0.05). Combination of ethanol and IPC in the same rats further decreased IS (-46% vs. ethanol, p < 0.05). PKC analyses did not show sustained isoform translocation in that model. These data indicate that chronic low dose ethanol drinking actually induces in the rat heart a chronic protective state that is independent from an effect on the traditional (lipid and coagulation) risk factors. Further studies are required to elucidate the mechanisms of that protection.

Alcohol Drinking↗
PubMed2004

Preischemic selenium status as a major determinant of myocardial infarct size in vivo in rats.

Prospective epidemiological studies have shown that the incidence of numerous cardiovascular pathologies is correlated with body selenium status. However, it remains unclear whether selenium status also influences the outcome of myocardial infarction. The aim of the present study was to test whether dietary selenium intake affects myocardial necrosis induced by transient regional ischemia in vivo in rats. For this purpose, male Wistar rats received either a high-selenium (High-Se: 1.5 mg of Se/kg) or a low-selenium (Low-Se: 0.05 mg of Se/kg) diet for 10 weeks. Animals were subjected to 30 min of myocardial ischemia induced by coronary artery ligation followed by 60 min of reperfusion. Pre- and postischemic blood samples were collected for glutathione (GSH and GSSG) determination and for glutathione peroxidase (GSH-Px) assessment. Our results show that high-selenium intake reduces myocardial infarct size (High-Se: 25.16 +/- 1.19% versus Low-Se: 36.51 +/- 4.14%, p < 0.05), preserves postischemic GSH/GSSG ratio (High-Se: 1.37 +/- 0.37 versus Low-Se: 0.47 +/- 0.10, p < 0.05), increases plasma GSH-Px activity, and improves postischemic mean arterial pressure. In conclusion, preischemic body selenium status is a major determinant of the outcome of myocardial ischemia in vivo in rats probably because it influences the cellular redox status.

Animals↗
PubMed2004

Ethanol, wine, and experimental cardioprotection in ischemia/reperfusion: role of the prooxidant/antioxidant balance.

It is now well established that oxidative stress resulting from reactive oxygen species (ROS) that are generated in cardiac myocytes subjected to ischemia/reperfusion plays a causative role in the development of heart failure and may contribute to promote cell death. During the last decade, several groups have reported that, in animal models of myocardial ischemia/reperfusion, certain nutrients, including ethanol and nonethanolic components of wine, may have a specific protective effect on the myocardium, independent of the classical risk factors implicated in vascular atherosclerosis and thrombosis. Mechanisms through which the consumption of alcoholic beverages protects against ischemia-induced cardiac injury are still unknown. One major open question is whether ethanol and nonethanolic components of wine are cardioprotective, at least in part, by interfering with the myocardial prooxidant/antioxidant balance. Important concepts, such as cardiac preconditioning, are now entering the field of nutrition, and recent experimental evidence suggests that ethanol and/or nonethanolic components of wine might exert preconditioning effects in animal models of myocardial ischemia/reperfusion. There is no doubt that such an observation, if confirmed in human subjects, might open new perspectives in the prevention and treatment of ischemic coronary heart disease.

Animals↗
PubMed2002

Wine drinking and risks of cardiovascular complications after recent acute myocardial infarction.

BACKGROUND: Scientific data on the clinical impact of moderate alcohol consumption after a recent acute myocardial infarction (AMI) are limited, and the specific effect of wine ethanol has not been studied. METHODS AND RESULTS: In survivors of a recent AMI, we analyzed the association between ethanol intake and the risk of recurrence. The patients were classified according to the amount of ethanol that they consumed regularly during follow-up. Major prognostic factors, including the severity of the prior AMI and drug treatment, were recorded and included in the analyses. Only patients with at least 2 reliable assessments of drinking (and dietary) habits were included (n=437). The average ethanol intake was 7.6% of the total energy intake, wherein wine ethanol represented 92% of the total. Among these patients, 104 cardiovascular complications occurred during a mean follow-up period of 4 years. In comparison with abstainers, the adjusted risk of complications was reduced by 59% (95% confidence interval: 17 to 80) in patients whose average ethanol intake was 7.7% of the total energy intake (about 2 drinks/day), and by 52% (95% confidence interval: 4 to 76) in those whose average ethanol intake was of 16% of energy (about 4 drinks/day). CONCLUSION: Whereas moderate wine drinking was associated with a significant reduction in the risk of complications in this homogenous population of coronary heart disease patients, further studies are required to confirm the data, define the clinical and biological profile of the patients who would most benefit from wine drinking after recent AMI, and examine whether the relations found are due to ethanol or other wine ingredients.

Cardiovascular Diseases↗