Hyperlipidemias: Poirier P

Poirier P. · Faculté de pharmacie de l'Université Laval, Institut universitaire de cardiologie et de pneumologie, Hôpital Laval, 2725, chemin Sainte-Foy, Sainte-Foy, Québec, G1V 4G5 Canada. · Med Sci (Paris). · Pubmed #19116122 No free full text.

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Lemieux I, Poirier P, Bergeron J, Alméras N, Lamarche B, Cantin B, Dagenais GR, Després JP. · Hôpital Laval Research Centre, Quebec. · Can J Cardiol. · Pubmed #17932584 No free full text.

Abstract: The worldwide increase in the prevalence and incidence of type 2 diabetes represents a tremendous challenge for the Canadian health care system, especially if we consider that this phenomenon may largely be explained by the epidemic of obesity. However, despite the well-recognized increased morbidity and mortality associated with an elevated body weight, there is now more and more evidence highlighting the importance of intra-abdominal adipose tissue (visceral adipose tissue) as the fat depot conveying the greatest risk of metabolic complications. In this regard, body fat distribution, especially visceral adipose tissue accumulation, has been found to be a key correlate of a cluster of diabetogenic, atherogenic, prothrombotic and inflammatory metabolic abnormalities now often referred to as the metabolic syndrome. This dysmetabolic profile is predictive of a substantially increased risk of coronary artery disease (CAD) even in the absence of hyperglycemia, elevated low-density lipoprotein cholesterol or hypertension. For instance, some features of the metabolic syndrome (hyperinsulinemia, elevated apolipoprotein B and small low-density lipoprotein particles--the so-called atherogenic metabolic triad) have been associated with a more than 20-fold increase in the risk of ischemic heart disease in middle-aged men enrolled in the Quebec Cardiovascular Study. This cluster of metabolic complications has also been found to be predictive of a substantially increased risk of CAD beyond the presence of traditional risk factors. These results emphasize the importance of taking into account in daily clinical practice the presence of metabolic complications associated with abdominal obesity together with traditional risk factors to properly evaluate the cardiovascular risk profile of patients. From a risk assessment standpoint, on the basis of additional work conducted by several groups, there is now evidence that the simultaneous presence of an elevated waist circumference and fasting triglyceride levels (a condition that has been described as hypertriglyceridemic waist) may represent a relevant first-step approach to identify a subgroup of individuals at higher risk of being carriers of the features of the metabolic syndrome. Moreover, a moderate weight loss in initially abdominally obese patients is associated with a selective mobilization of visceral adipose tissue, leading to improvements in the metabolic risk profile predictive of a reduced risk of CAD and type 2 diabetes. In conclusion, hypertriglyceridemic waist as a marker of visceral obesity and related metabolic abnormalities is a useful and practical clinical phenotype to screen persons at risk for CAD and type 2 diabetes.

St-Pierre J, Vohl MC, Després JP, Gaudet D, Poirier P. · Dyslipidemia, Diabetes and Atherosclerosis Research Group, Chicoutimi Hospital, Chicoutimi, Quebec. · Can J Cardiol. · Pubmed #15729423 links to  free full text

Abstract: Diabetes mellitus is a source of great concern in contemporary cardiology. It is a heterogeneous disease and patients are often characterized by features of the insulin resistance syndrome, also referred to as the metabolic syndrome. The objectives of the present review were to discuss some genes that potentially modulate the risk of coronary artery disease in diabetes mellitus; to address how the genes' respective contributions could possibly influence the global risk assessment of coronary artery disease among diabetic patients; and to present simple clinical markers, such as plasma glycerol concentration and the 'hypertriglyceridemic waist' phenotype, that could help to identify high-risk individuals.

Poirier P, Després JP. · Institut universitaire de cardiologie et de pneumologie, Centre de recherche de l'Hôpital Laval, 2725, chemin Sainte-Foy, Sainte-Foy, Québec, G1V 4G5, Canada. · Med Sci (Paris). · Pubmed #14613004 links to  free full text

Abstract: Available evidence clearly indicates a rapid progression in the prevalence of obesity worldwide. As a consequence, there has also been a marked increase in the prevalence of type 2 diabetes all over the world and this chronic metabolic disease is now considered as a coronary heart disease risk equivalent. However, even in the absence of the hyperglycaemic state which characterizes type 2 diabetic patients, non diabetic individuals with a specific form of obesity, named abdominal obesity, often show clustering metabolic abnormalities which include high triglyceride levels, increased apolipoprotein B, small dense low density lipoproteins and decreased high density lipoproteins-cholesterol levels, a hyperinsulinemic-insulin resistant state, alterations in coagulation factors as well as an inflammatory profile. This agglomeration of abnormalities has been referred to as the metabolic syndrome which can be identified by the presence of three of the five following variables: abdominal obesity, elevated triglyceride concentrations, low HDL-cholesterol levels, increased blood pressure and elevated fasting glucose. Post-mortem analyses of coronary arteries have indicated that obesity (associated with a high accumulation of abdominal fat measured at autopsy) was predictive of earlier and greater extent of large vessels atherosclerosis as well as increase of coronary fatty streaks. Metabolic syndrome linked to abdominal obesity is also predictive of recurrent coronary events both in post-myocardial infarction patients and among coronary artery disease men who underwent a revascularization procedures. It is suggested that until the epidemic progression of obesity is stopped and obesity prevented or at least properly managed, cardiologists will be confronted to an evolving contribution of risk factors where smoking, hypercholesterolemia and hypertension may be relatively less prevalent but at the expense of a much greater contribution of abdominal obesity and related features of the metabolic syndrome.

Bogaty P, Dagenais GR, Poirier P, Boyer L, Auclair L, Pépin G, Jobin J, Arsenault M. · Quebec Heart Institute, Laval Hospital, Ste-Foy, Quebec, Canada. · Am J Cardiol. · Pubmed #14609594 No free full text.

Abstract: To investigate whether marked and sustained lipid-lowering in subjects with stable angina pectoris and dyslipidemia reduces exercise-induced myocardial ischemia, 17 subjects were treated with dose-adjusted atorvastatin over 1 year and underwent serial evaluation of exercise electrocardiographic ischemic parameters, serum biomarkers, and brachial artery endothelial function. Endothelial function improved progressively and C-reactive protein, P-selectin, and tissue plasminogen activator inhibitor levels decreased, but there was no decrease in exercise electrocardiographic ischemia.

Capell WH, DeSouza CA, Poirier P, Bell ML, Stauffer BL, Weil KM, Hernandez TL, Eckel RH. · Department of Medicine, University of Colorado Health Sciences Center, Denver 80262, USA. · Arterioscler Thromb Vasc Biol. · Pubmed #12588776 links to  free full text

Abstract: OBJECTIVE: The objective of this study was to investigate the effects of lowering plasma triglycerides (TGs) on endothelial function and gain insight into the role played by free fatty acids (FFAs) in hypertriglyceridemia-associated vascular dysfunction. METHODS AND RESULTS: Eleven hypertriglyceridemic subjects without coronary artery disease, diabetes, elevated low-density lipoprotein cholesterol, tobacco use, or hypertension were studied using a randomized, double-blinded, crossover design (fenofibrate and placebo, 14 days). After each regimen, forearm blood flow was assessed by plethysmography in response to arterial acetylcholine, nitroprusside, and verapamil infusion. Hourly plasma TGs, FFA, glucose, and insulin were measured during a 24-hour feeding cycle to characterize the metabolic environment. Changes in plasma FFA after intravenous heparin were used to estimate typical FFA accumulation in the luminal endothelial microenvironment. Fenofibrate lowered plasma TG (P<0.001), total cholesterol (P<0.01), and apolipoprotein B (P<0.01) without altering high-density lipoprotein or low-density lipoprotein cholesterol concentrations. Forearm blood flow in response to acetylcholine (P<0.0001), nitroprusside (P<0.001), and verapamil (P<0.0001) improved after fenofibrate. Fenofibrate lowered 24-hour (P<0.0001) and post-heparin (P<0.001) TG and tended to lower 24-hour (P=0.054) and post-heparin (P=0.028) FFA. CONCLUSIONS: Vascular smooth muscle function significantly improves after lowering plasma TG without changes in confounding lipoproteins or insulin resistance. The data raise additional questions regarding the role of FFA in hypertriglyceridemia-associated vascular dysfunction.

Plenge JK, Hernandez TL, Weil KM, Poirier P, Grunwald GK, Marcovina SM, Eckel RH. · Division of Endocrinology, Metabolism, and Diabetes, University of Colorado Health Sciences Center, Denver, Colo 80262, USA. · Circulation. · Pubmed #12234946 links to  free full text

Abstract: BACKGROUND: The early response of C-reactive protein to initiation of a hydroxymethylglutaryl coenzyme A reductase inhibitor (statin) is not known. The purpose of this study was to determine the rate at which highly sensitive C-reactive protein (hsCRP) levels change after initiation of simvastatin and whether this occurs independently of the change in LDL cholesterol. METHODS AND RESULTS: The study was a crossover, double-blind design including 40 subjects with elevated LDL cholesterol. Subjects were randomly assigned to 1 of 2 groups: simvastatin 40 mg for 14 days, then placebo for 14 days, or placebo first, then simvastatin. Simvastatin decreased LDL cholesterol by 56+/-4 mg/dL (P<0.0001) at day 7 and by an additional 8+/-3 mg/dL (P=0.02) at day 14. Baseline log(hsCRP) levels were similar in the 2 groups. By day 14, log(hsCRP) was significantly lower in patients on simvastatin when compared with placebo (P=0.011). Although there was no significant difference in fibrinogen levels, simvastatin produced a modest increase in log[lipoprotein(a)] (P=0.03) at days 7 and 14. There were no relationships between the decrease in LDL cholesterol and the decrease in hsCRP. CONCLUSIONS: Simvastatin lowers hsCRP by 14 days, independent of its effect on LDL cholesterol. This rapid impact of a statin on hsCRP has potential implications in the management of acute coronary syndromes.

Poirier B, Baillot R, Bauset R, Dagenais F, Mathieu P, Simard S, Dionne B, Caouette M, Hould FS, Doyle D, Poirier P. · Département de chirurgie cardiaque, Institut universitaire de cardiologie et de pneumologie, Hôpital Laval, Ste-Foy, Québec. · Can J Surg. · Pubmed #12812238 links to  free full text

Abstract: INTRODUCTION: To evaluate the prevalence, risk factors and morbidity associated with gastrointestinal (GI) complications after cardiac surgery, with and without cardiopulmonary bypass, we carried out a retrospective cohort study at a university teaching hospital. METHODS: We divided the 11,405 eligible adult patients into 2 groups: group A (operated on between January 1992 and June 1996) (4657 patients) and group B (operated on between July 1996 and December 2000) (6748 patients). RESULTS: We found 147 GI complications in 134 (1.2%) patients. The incidence of GI morbidity was similar for the 2 groups of patients (group A, n = 59/4657 [1.2%]; group B, n = 75/6748 [1.1%]. Patients from group B were older, obese, diabetic and presented with more peripheral and cerebrovascular disease. Bleeding, gastritis and ulcer with perforation, the most common of these GI events, were associated with the esophagus and stomach (67/147 [45.5%]). Other events that we documented included cholecystitis 10 (6.8%), pancreatitis 13 (8.8%), episodes of small and large bowel ischemia 17 (11.6%), pseudomembranous colitis 12 (8.3%) and diverticulitis 5 (3.4%). Mesenteric ischemia was responsible for 11 (37.9%) of the 29 deaths. Two hundred and ninety-three patients were revascularized without extracorporeal circulation during this study. In this group, we were able to pinpoint 5 (1.7%) GI complications with 3 cases of mesenteric ischemia. Multivariate analysis identified renal insufficiency, prolonged intubation and sepsis as significant, predictive variables of GI complications for the 2 groups of patients whereas the Parsonnet score and stroke were predictive for the second group. CONCLUSIONS: Although cardiac surgery is now being performed on older patients with significant comorbidity, we could not demonstrate a significant increase of GI complications after cardiac surgery. Off-pump coronary artery bypass does not seem to protect patients from these complications.