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(B1)
Circulation. 2002;105:354.)
(c) 2002 American Heart Association, Inc.
Basic Science Reports
Social Environment Influences the Progression of Atherosclerosis in the Watanabe Heritable Hyperlipidemic Rabbit
Philip M. McCabe, PhD; Julie A. Gonzales, PhD; Julia Zaias, DVM; Angela Szeto, BA; Mahendra Kumar, PhD; Alan J. Herron, DVM; Neil Schneiderman, PhD
From the Department of Psychology (P.M.M., J.A.G., A.S., N.S.), University of Miami, Coral Gables, Fla; Division of Comparative Pathology (J.Z.) and Department of Psychiatry (M.K.), University of Miami Medical School, Miami, Fla; and Section of Pathology (A.H.), Institute of Comparative Medicine, Columbia University, New York, NY.
Correspondence to Philip M. McCabe, PhD, Department of Psychology, University of Miami, P.O. Box 248185, Coral Gables, FL 33124. E-mail pmccabe@miami.edu
Background- Although there is evidence that emotionally stressful behavior can accelerate the progression of atherosclerosis, there is less data to support the notion that affiliative social behavior can slow disease progression. The present study examines the influence of social environment on the progression of atherosclerosis in the Watanabe Heritable Hyperlipidemic (WHHL) rabbit, a model that spontaneously develops lesions because of a genetic defect in lipoprotein clearance.
Methods and Results- WHHL rabbits were assigned to 1 of 3 social or behavioral groups: an unstable group, in which unfamiliar rabbits were paired daily, with the pairing switched each week; a stable group, in which littermates were paired daily for the entire study; and an individually caged group. The stable group exhibited more affiliative social behavior and less agonistic behavior than the unstable group and significantly less aortic atherosclerosis than each of the other 2 groups. Although the unstable and individually caged groups had comparable aortic lesion areas, the severity of the disease progressed faster in the unstable group, as indexed by a larger area of calcification and increased fibrous cap thickness in complex lesions. The unstable group showed increased agonistic behavior and signs of chronic adrenocortical and gonadal activation, whereas the individually caged group was relatively sedentary, had low glucocorticoid levels, and was hyperinsulinemic compared with the other groups.
Conclusions- The present study demonstrates that social environment can slow, as well as accelerate, the progression of atherosclerosis. It also emphasizes the importance of behavioral factors in atherogenesis, even in a model of disease with strong genetic determinants.
Key Words: behavior • social environment • atherosclerosis • rabbits *
(B2)
Hypertension. 2001;38:155.) (c) 2001 American Heart Association, Inc.
Scientific Contributions
DASH (Dietary Approaches to Stop Hypertension) Diet Is Effective Treatment for Stage 1 Isolated Systolic Hypertension
Thomas J. Moore; Paul R. Conlin; Jamy Ard; Laura P. Svetkey; for the DASH Collaborative Research Group
From the Department of Medicine, Boston University Medical Center (T.J.M.), Boston, Mass; Department of Medicine, Brigham and Women's Hospital (R.R.C.), Boston, Mass; Duke University Medical Center, Duke Hypertension Center (L.P.S., J.A.), Durham, NC; and Sarah W. Stedman Center for Nutritional Studies (L.P.S.), Durham, NC.
Correspondence to Thomas J. Moore, MD, Office of Clinical Research, Boston University Medical Center, Room A206, 715 Albany St, Boston, MA 02118. E-mail tmoore@bu.edu
Abstract-- Use of the DASH (Dietary Approaches to Stop Hypertension) diet, which is rich in fruits, vegetables, and low-fat dairy foods, significantly lowers blood pressure. Among the 459 participants in the DASH Trial, 72 had stage 1 isolated systolic hypertension (ISH) (systolic blood pressure, 140 to 159 mm Hg; diastolic blood pressure, <90 mm Hg). We examined the blood pressure response in these 72 participants to determine whether the DASH diet is an effective treatment for stage 1 ISH. After a 3-week run-in period on a typical American (control) diet, participants were randomly assigned for 8 weeks to 1 of 3 diets: a continuation of the control diet (n=25), a diet rich in fruits and vegetables (n=24), or the DASH diet (n=23). Sodium content was the same in the 3 diets, and caloric intake was adjusted during the trial to prevent weight change. Blood pressure was measured at baseline and at the end of the 8-week intervention period with standard sphygmomanometry. Use of the DASH diet significantly lowered systolic blood pressure compared with the control diet (-11.2 mm Hg; 95% confidence interval, -6.1 to -16.2 mm Hg; P<0.001) and the fruits/vegetables diet (-8.0 mm Hg; 95% confidence interval, -2.5 to -13.4 mm Hg; P<0.01). Overall, blood pressure in the DASH group fell from 146/85 to 134/82 mm Hg. Similar results were observed with 24-hour ambulatory blood pressure measurements. In the DASH diet group, 18 of 23 participants (78%) reduced their systolic blood pressure to <140 mm Hg, compared with 24% and 50% in the control and fruits/vegetables groups, respectively. Our results indicate that the DASH diet, which is rich in fruits, vegetables, and low-fat dairy foods, is effective as first-line therapy in stage 1 ISH.
Key Words: diet • clinical trials • hypertension, systolic, isolated • blood pressure • aging *
(B3)
J Am Coll Cardiol. 2001 Jun 1;37(7):1929-1935.
Post-prandial remnant lipids impair arterial compliance.
Nestel PJ, Shige H, Pomeroy S, Cehun M, Chin-Dusting J.
Baker Medical Research Institute, Melbourne, Australia. paul.nestel@baker.edu.au
OBJECTIVES: We sought to examine the effects of plasma lipids, especially in remnants after a fat meal, on systemic arterial compliance (SAC), a newly recognized cardiovascular risk factor. BACKGROUND: Post-prandial remnants correlate with coronary heart disease events through mechanisms that may include vascular dysfunction, although the effect on SAC has not been studied. METHODS: Systemic arterial compliance was measured non-invasively over 6 h after a fat meal in 16 subjects with varying plasma triglyceride levels. Changes were related to rises in plasma lipids and remnant lipids. Systemic arterial compliance was measured in 20 subjects after a control low-fat meal. RESULTS: The fat meal induced increments in plasma triglyceride and remnant cholesterol and triglyceride (respectively +54%, 50% and 290% at 3 h, analysis of variance <0.001). Systemic arterial compliance fell at 3 h and 6 h by 25% and 27% (analysis of variance <0.001). Baseline SAC correlated significantly with all lipid concentrations at 0, 3 h and 6 h, but only with triglyceride on stepwise regression analysis. The SAC response to the low-fat meal was very small and not significant. CONCLUSIONS: This is the first demonstration of SAC becoming impaired after a fat meal. Remnant lipids and plasma total triglyceride appeared to contribute to the fall in SAC.
COMMENT
High-Fat Meals Significantly Reduce Systemic Arterial Compliance
WESTPORT, CT (Reuters Health) Jun 01 - Meals high in fat appear to significantly reduce systemic arterial compliance, apparently because of increased remnant lipids and triglyceride, Australian researchers report in the June 1st issue of the Journal of the American College of Cardiology.
Dr. Paul J. Nestel, from the Baker Medical Research Institute in Melbourne, and colleagues measured systemic arterial compliance in 16 subjects with varying triglyceride levels over 6 hours following a high-fat meal, and in 20 subjects who were given a low-fat meal.
Three hours after the high-fat meal, plasma triglyceride had increased by 54%, remnant cholesterol had increased by 50% and triglyceride had increased by 290%, the researchers report. Systemic arterial compliance was reduced 25% by 3 hours after the high-fat meal and 27% at 6 hours. The low-fat meal had only a small and nonsignificant effect on systemic arterial compliance.
At baseline, and at 3 and 6 hours, systemic arterial compliance correlated significantly with all lipid concentrations, Dr. Nestel's team found. Stepwise regression analysis showed that the strongest correlation was with plasma triglyceride.
"Our findings suggest that people should generally avoid meals rich in total fat," Dr. Nestel said in a journal statement. "That is especially relevant to people who have coronary heart disease and to those who have high lipid levels," he added, noting that reduced arterial compliance has been linked to an increased risk of myocardial infarction.*
(B4)
JAMA. 2004;291:1071-1080.
Effect of Intensive Compared With Moderate Lipid-Lowering Therapy on Progression of Coronary Atherosclerosis
A Randomized Controlled Trial
Steven E. Nissen, MD; E. Murat Tuzcu, MD; Paul Schoenhagen, MD; B. Greg Brown, MD; Peter Ganz, MD; Robert A. Vogel, MD; Tim Crowe, BS; Gail Howard, MS; Christopher J. Cooper, MD; Bruce Brodie, MD; Cindy L. Grines, MD; Anthony N. DeMaria, MD; for the REVERSAL Investigators
Context Statin drugs reduce both atherogenic lipoproteins and cardiovascular morbidity and mortality. However, the optimal strategy and target level for lipid reduction remain uncertain.
Objective To compare the effect of regimens designed to produce intensive lipid lowering or moderate lipid lowering on coronary artery atheroma burden and progression.
Design, Setting, and Patients Double-blind, randomized active control multicenter trial (Reversal of Atherosclerosis with Aggressive Lipid Lowering [REVERSAL]) performed at 34 community and tertiary care centers in the United States comparing the effects of 2 different statins administered for 18 months. Intravascular ultrasound was used to measure progression of atherosclerosis. Between June 1999 and September 2001, 654 patients were randomized and received study drug; 502 had evaluable intravascular ultrasound examinations at baseline and after 18 months of treatment.
Interventions Patients were randomly assigned to receive a moderate lipid-lowering regimen consisting of 40 mg of pravastatin or an intensive lipid-lowering regimen consisting of 80 mg of atorvastatin.
Main Outcome Measures The primary efficacy parameter was the percentage change in atheroma volume (follow-up minus baseline).
Results Baseline low-density lipoprotein cholesterol level (mean, 150.2 mg/dL [3.89 mmol/L] in both treatment groups) was reduced to 110 mg/dL (2.85 mmol/L) in the pravastatin group and to 79 mg/dL (2.05 mmol/L) in the atorvastatin group (P<.001). C-reactive protein decreased 5.2% with pravastatin and 36.4% with atorvastatin (P<.001). The primary end point (percentage change in atheroma volume) showed a significantly lower progression rate in the atorvastatin (intensive) group (P = .02). Similar differences between groups were observed for secondary efficacy parameters, including change in total atheroma volume (P = .02), change in percentage atheroma volume (P<.001), and change in atheroma volume in the most severely diseased 10-mm vessel subsegment (P<.01). For the primary end point, progression of coronary atherosclerosis occurred in the pravastatin group (2.7%; 95% confidence interval [CI], 0.2% to 4.7%; P = .001) compared with baseline. Progression did not occur in the atorvastatin group (-0.4%; CI -2.4% to 1.5%; P = .98) compared with baseline.
Conclusions For patients with coronary heart disease, intensive lipid-lowering treatment with atorvastatin reduced progression of coronary atherosclerosis compared with pravastatin. Compared with baseline values, patients treated with atorvastatin had no change in atheroma burden, whereas patients treated with pravastatin showed progression of coronary atherosclerosis. These differences may be related to the greater reduction in atherogenic lipoproteins and C- reactive protein in patients treated with atorvastatin.
Author Affiliations: Departments of Cardiovascular Medicine (Drs Nissen, Tuzcu, Schoenhagen, and Mr Crowe) and Diagnostic Radiology (Dr Schoenhagen), Cleveland Clinic Lerner School of Medicine, Cleveland, Ohio; Department of Medicine, University of Washington, Seattle (Dr Brown); Department of Medicine, Brigham and Women's Hospital, Boston, Mass (Dr Ganz); Department of Medicine, University of Maryland, Baltimore (Dr Vogel); Pfizer Inc, New York, NY (Ms Howard); Department of Medicine, Medical College of Ohio, Toledo (Dr Cooper); LeBauer Cardiovascular Research Foundation, Greensboro, NC (Dr Brodie); Cardiac Catheterization Laboratory, Division of Cardiac Diseases, William Beaumont Hospital, Royal Oak, Mich (Dr Grines); and Department of Medicine, University of California, San Diego (Dr DeMaria). *
(B5)
JAMA. 1998;280:2001-2007. (Vol. 280 No. 23, December 16, 1998)
Intensive Lifestyle Changes for Reversal of Coronary Heart Disease
Dean Ornish, MD; Larry W. Scherwitz, PhD; James H. Billings, PhD, MPH; K. Lance Gould, MD; Terri A. Merritt, MS; Stephen Sparler, MA; William T. Armstrong, MD; Thomas A. Ports, MD; Richard L. Kirkeeide, PhD; Charissa Hogeboom, PhD; Richard J. Brand, PhD
Context.- The Lifestyle Heart Trial demonstrated that intensive lifestyle changes may lead to regression of coronary atherosclerosis after 1 year.
Objectives.- To determine the feasibility of patients to sustain intensive lifestyle changes for a total of 5 years and the effects of these lifestyle changes (without lipid-lowering drugs) on coronary heart disease.
Design.- Randomized controlled trial conducted from 1986 to 1992 using a randomized invitational design.
Patients.- Forty-eight patients with moderate to severe coronary heart disease were randomized to an intensive lifestyle change group or to a usual-care control group, and 35 completed the 5-year follow-up quantitative coronary arteriography.
Setting.-Two tertiary care university medical centers.
Intervention.- Intensive lifestyle changes (10% fat whole foods vegetarian diet, aerobic exercise, stress management training, smoking cessation, group psychosocial support) for 5 years.
Main Outcome Measures.- Adherence to intensive lifestyle changes, changes in coronary artery percent diameter stenosis, and cardiac events.
Results.- Experimental group patients (20 [71%] of 28 patients completed 5-year follow-up) made and maintained comprehensive lifestyle changes for 5 years, whereas control group patients (15 [75%] of 20 patients completed 5-year follow-up) made more moderate changes. In the experimental group, the average percent diameter stenosis at baseline decreased 1.75 absolute percentage points after 1 year (a 4.5% relative improvement) and by 3.1 absolute percentage points after 5 years (a 7.9% relative improvement). In contrast, the average percent diameter stenosis in the control group increased by 2.3 percentage points after 1 year (a 5.4% relative worsening) and by 11.8 percentage points after 5 years (a 27.7% relative worsening) (P=.001 between groups. Twenty-five cardiac events occurred in 28 experimental group patients vs 45 events in 20 control group patients during the 5-year follow-up (risk ratio for any event for the control group, 2.47 [95% confidence interval, 1.48-4.20]).
Conclusions.- More regression of coronary atherosclerosis occurred after 5 years than after 1 year in the experimental group. In contrast, in the control group, coronary atherosclerosis continued to progress and more than twice as many cardiac events occurred.
From the Department of Medicine (Dr Ornish), and the Division of Cardiology (Dr Armstrong), California Pacific Medical Center, San Francisco; the Department of Medicine (Dr Ornish), the Division of Cardiology, Cardiac Catheterization Laboratory, Cardiovascular Research Institute (Dr Ports), and the Division of Biostatistics (Drs Brand and Hogeboom), School of Medicine, University of California, San Francisco; the Division of Cardiology, University of Texas Medical School, Houston (Drs Gould and Kirkeeide); and the Preventive Medicine Research Institue, Sausalito, Calif (Drs Ornish Scherwitz, and Billings, Mr Sparler, and Ms Merritt). *
(B6)
Arch Intern Med. 2004;164:370-376.
Dietary Fiber and Risk of Coronary Heart Disease A Pooled Analysis of Cohort Studies
Mark A. Pereira, PhD; Eilis O'Reilly, MSc; Katarina Augustsson, PhD; Gary E. Fraser, MBChB, PhD; Uri Goldbourt, PhD; Berit L. Heitmann, PhD; Goran Hallmans, MD, PhD; Paul Knekt, PhD; Simin Liu, MD, ScD; Pirjo Pietinen, DSc; Donna Spiegelman, ScD; June Stevens, MS, PhD; Jarmo Virtamo, MD; Walter C. Willett, MD; Alberto Ascherio, MD
Background Few epidemiologic studies of dietary fiber intake and risk of coronary heart disease have compared fiber types (cereal, fruit, and vegetable) or included sex-specific results. The purpose of this study was to conduct a pooled analysis of dietary fiber and its subtypes and risk of coronary heart disease.
Methods We analyzed the original data from 10 prospective cohort studies from the United States and Europe to estimate the association between dietary fiber intake and the risk of coronary heart disease.
Results Over 6 to 10 years of follow-up, 5249 incident total coronary cases and 2011 coronary deaths occurred among 91 058 men and 245 186 women. After adjustment for demographics, body mass index, and lifestyle factors, each 10-g/d increment of energy-adjusted and measurement error-corrected total dietary fiber was associated with a 14% (relative risk [RR], 0.86; 95% confidence interval [CI], 0.78-0.96) decrease in risk of all coronary events and a 27% (RR, 0.73; 95% CI, 0.61-0.87) decrease in risk of coronary death. For cereal, fruit, and vegetable fiber intake (not error corrected), RRs corresponding to 10-g/d increments were 0.90 (95% CI, 0.77-1.07), 0.84 (95% CI, 0.70-0.99), and 1.00 (95% CI, 0.88-1.13), respectively, for all coronary events and 0.75 (95% CI, 0.63-0.91), 0.70 (95% CI, 0.55-0.89), and 1.00 (95% CI, 0.82-1.23), respectively, for deaths. Results were similar for men and women.
Conclusion Consumption of dietary fiber from cereals and fruits is inversely associated with risk of coronary heart disease.
From the Division of Epidemiology, School of Public Health, University of Minnesota, Minneapolis (Dr Pereira); Departments of Nutrition (Ms O'Reilly and Drs Willett and Ascherio), Epidemiology (Drs Spiegelman, Willett, and Ascherio), and Biostatistics (Dr Spiegelman), Harvard School of Public Health, Harvard Center for Cancer Prevention (Dr Willett), Channing Laboratory, Department of Medicine (Dr Willett), and Division of Preventive Medicine (Dr Liu), Brigham and Women's Hospital and Harvard Medical School, Boston, Mass; Department of Medical Epidemiology, Karolinska Institute, Stockholm, Sweden (Dr Augustsson); Center for Health Research, Loma Linda University School of Medicine, Loma Linda, Calif (Dr Fraser); Section of Epidemiology and Biostatistics, Henry N. Neufeld Cardiac Research Institute, Sheba Medical Center, Tel Hashomer, Israel (Dr Goldbourt); Institute of Preventive Medicine, Copenhagan University Hospital, Copenhagan, Denmark (Dr Heitmann); Department of Public Health and Clinical Medicine, Umea University, Umea, Sweden (Dr Hallmans); National Public Health Institute, Helsinki, Finland (Drs Knekt, Pietinen, and Virtamo); and Departments of Nutrition and Epidemiology, School of Public Health, University of North Carolina, Chapel Hill (Dr Stevens). The authors have no relevant financial interest in this article. *
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(B7)
Hypertension. 2000;36:423.)
(c) 2000 American Heart Association, Inc.
Scientific Contributions
Enhanced NO Inactivation and Hypertension Induced by a High-Fat, Refined-Carbohydrate Diet
Christian K. Roberts; Nosratola D. Vaziri; Xiu Q. Wang; R. James Barnard
From the Department of Physiological Science (C.K.R., R.J.B.), University of California, Los Angeles, and the Division of Nephrology and Hypertension (N.D.V., X.Q.W.), Department of Medicine, University of California, Irvine.
Correspondence to R. James Barnard, PhD, Department of Physiological Science, UCLA, PO Box 951527, Los Angeles, CA 90095-1527. E-mail jbarnard@ucla.edu
Abstract-We have recently demonstrated that long-term consumption of a high-fat, refined-carbohydrate (HFS) diet induces hypertension (HTN) in normal rats compared with a low-fat, complex-carbohydrate (LFCC) diet. Limited evidence suggests that high-fat or high-sugar diets cause enhanced generation of reactive oxygen species (ROS). We therefore hypothesized that by inducing oxidative stress, the HFS diet may promote nitric oxide (NO) inactivation and HTN. To test this hypothesis, female Fischer rats were placed on either the HFS or the LFCC diet starting at 2 months of age. Blood pressure, urinary NO metabolites (NOx), and total renal NO synthase activity were monitored, and the tissue abundance of nitrotyrosine (NT), which is the stable "footprint" of NO oxidation by ROS, was determined. The HFS diet group exhibited a gradual rise in arterial blood pressure and were hypertensive by 18 months. This trend was accompanied by a marked accumulation of NT in all tested tissues, an initial rise and a subsequent fall in NO synthase activity, and a fall in urinary NOx excretion. The HFS diet-fed animals had a blunted blood pressure response to the NO synthase inhibitor N-nitro-L-arginine methyl ester (L-NAME) compared with the LFCC diet group, which showed a marked hypertensive response to L-NAME. L-NAME-induced HTN was reversible with L-arginine in the LFCC diet group; however, HTN was not corrected by L-arginine supplementation in the HFS diet group. These findings point to enhanced ROS-mediated inactivation and sequestration of NO, which may contribute to the reduction of bioactive NO and HTN in the HFS diet-fed animals.
Key Words: arginine • endothelial • free radicals • insulin resistance • L-NAME • nitric oxide *
(B8)
Circulation. 2002;106:2530.)
(c) 2002 American Heart Association, Inc.
Brief Rapid Communications
Effect of Diet and Exercise Intervention on Blood Pressure, Insulin, Oxidative Stress, and Nitric Oxide Availability
Christian K. Roberts, PhD; Nosratola D. Vaziri, MD; R. James Barnard, PhD
From the Department of Physiological Science, University of California, Los Angeles (C.K.R., R.J.B.), and the Division of Nephrology and Hypertension, Department of Medicine, University of California, Irvine (C.K.R., N.D.V.).
Correspondence to R. James Barnard, Department of Physiological Science, UCLA, P.O. 951527, Los Angeles, CA 90095-1527. E-mail jbarnard@physci.ucla.edu
Background- Diet and exercise can affect blood pressure and atherosclerotic risk.
Methods and Results- The present study was designed to examine the effects of a short-term, rigorous diet and exercise intervention on blood pressure, hyperinsulinemia, and nitric oxide (NO) availability. Men (n=11) were placed on a low-fat, high-fiber diet combined with daily exercise for 45 to 60 minutes for 3 weeks. Pre- and post fasting blood was drawn for serum lipid, insulin, 8-isoprostaglandin F2 (8-iso-PGF2), and glucose measurements. Anthropometric parameters, blood pressure (BP), and 24-hour urinary NO metabolite excretion (NOX), a marker of NO bioavailability, were measured. Systolic (P<0.01) and diastolic BP (P<0.01) and 8-iso-PGF2 decreased (P<0.05), whereas urinary NOX increased (P<0.05). There was a significant reduction in fasting insulin (P<0.01) and a significant correlation between the decrease in serum insulin and the increase in urinary NOX (r2=0.68, P<0.05). All fasting lipids decreased significantly, and the total cholesterol to high-density lipoprotein cholesterol ratio improved. Although body weight and body mass index (P<0.01) decreased, obesity was still present and there were no correlations between the change in body mass index and the change in insulin, BP, or urinary NOX.
Conclusions- This intervention resulted in dramatic improvements in BP, oxidative stress, NO availability, and the metabolic profile within 3 weeks, mitigating the risk for atherosclerosis progression and its clinical sequelae.
Key Words: hypertension • free radicals • oxygen • insulin *
(B9)
Nature 362, 801 - 809 (1993); doi:10.1038/362801a0
review article
The pathogenesis of atherosclerosis: a perspective for the 1990s
Russell Ross
Atherosclerosis, the principal cause of heart attack, stroke and gangrene of the extremities, is responsible for 50% of all mortality in the USA, Europe and Japan. The lesions result from an excessive, inflammatory-fibroproliferative response to various forms of insult to the endothelium and smooth muscle of the artery wall. A large number of growth factors, cytokines and vasoregulatory molecules participate in this process. Our ability to control the expression of genes encoding these molecules and to target specific cell types provides opportunities to develop new diagnostic and therapeutic agents to induce the regression of the lesions and, possibly, to prevent their formation. *
(B10)
Circulation. 1999;99:2192-2217.)
(c) 1999 American Heart Association, Inc.
Clinical Cardiology: New Frontiers
Impact of Psychological Factors on the Pathogenesis of Cardiovascular Disease and Implications for Therapy
Alan Rozanski, MD; James A. Blumenthal, PhD; Jay Kaplan, PhD
From the Division of Cardiology, Department of Medicine, St Luke's/Roosevelt Hospital Center, and the Department of Medicine, Columbia University College of Physicians and Surgeons, New York, NY (A.R.); the Department of Psychiatry and Behavioral Sciences, Duke University Medical Center, Durham, NC (J.A.B.); and the Department of Pathology (Comparative Medicine) and Anthropology, Wake Forest University School of Medicine and Wake Forest University, Winston-Salem, NC (J.K.).
Correspondence to Alan Rozanski, MD, Division of Cardiology, St Luke's/Roosevelt Hospital Center, 114th Street and Amsterdam Avenue, New York, NY 10025. E-mail ar77@columbia.edu
Abstract
Recent studies provide clear and convincing evidence that psychosocial factors contribute significantly to the pathogenesis and expression of coronary artery disease (CAD). This evidence is composed largely of data relating CAD risk to 5 specific psychosocial domains: (1) depression, (2) anxiety, (3) personality factors and character traits, (4) social isolation, and (5) chronic life stress. Pathophysiological mechanisms underlying the relationship between these entities and CAD can be divided into behavioral mechanisms, whereby psychosocial conditions contribute to a higher frequency of adverse health behaviors, such as poor diet and smoking, and direct pathophysiological mechanisms, such as neuroendocrine and platelet activation. An extensive body of evidence from animal models (especially the cynomolgus monkey, Macaca fascicularis) reveals that chronic psychosocial stress can lead, probably via a mechanism involving excessive sympathetic nervous system activation, to exacerbation of coronary artery atherosclerosis as well as to transient endothelial dysfunction and even necrosis. Evidence from monkeys also indicates that psychosocial stress reliably induces ovarian dysfunction, hypercortisolemia, and excessive adrenergic activation in premenopausal females, leading to accelerated atherosclerosis. Also reviewed are data relating CAD to acute stress and individual differences in sympathetic nervous system responsivity. New technologies and research from animal models demonstrate that acute stress triggers myocardial ischemia, promotes arrhythmogenesis, stimulates platelet function, and increases blood viscosity through hemoconcentration. In the presence of underlying atherosclerosis (eg, in CAD patients), acute stress also causes coronary vasoconstriction. Recent data indicate that the foregoing effects result, at least in part, from the endothelial dysfunction and injury induced by acute stress. Hyperresponsivity of the sympathetic nervous system, manifested by exaggerated heart rate and blood pressure responses to psychological stimuli, is an intrinsic characteristic among some individuals. Current data link sympathetic nervous system hyperresponsivity to accelerated development of carotid atherosclerosis in human subjects and to exacerbated coronary and carotid atherosclerosis in monkeys. Thus far, intervention trials designed to reduce psychosocial stress have been limited in size and number. Specific suggestions to improve the assessment of behavioral interventions include more complete delineation of the physiological mechanisms by which such interventions might work; increased use of new, more convenient "alternative" end points for behavioral intervention trials; development of specifically targeted behavioral interventions (based on profiling of patient factors); and evaluation of previously developed models of predicting behavioral change. The importance of maximizing the efficacy of behavioral interventions is underscored by the recognition that psychosocial stresses tend to cluster together. When they do so, the resultant risk for cardiac events is often substantially elevated, equaling that associated with previously established risk factors for CAD, such as hypertension and hypercholesterolemia.
Key Words: coronary disease • stress • psychology *
(B11)
Circulation. 2004;109:78-83.)
(c) 2004 American Heart Association, Inc.
Clinical Investigation and Reports
Differences Between Mainstream and Sidestream Cigarette Smoke Extracts and Nicotine in the Activation of Platelets Under Static and Flow Conditions
David Rubenstein; Jolyon Jesty, PhD; Danny Bluestein, PhD
From the Department of Biomedical Engineering (D.R., D.B.) and the Division of Hematology, School of Medicine (J.J.), Stony Brook University, Stony Brook, New York.
Correspondence to Danny Bluestein, PhD, Department of Biomedical Engineering, Health Sciences Center, Stony Brook University, Stony Brook, NY 11794-8181. E-mail danny.bluestein@sunysb.edu
Received March 24, 2003; de novo received July 17, 2003; revision received September 19, 2003; accepted September 22, 2003.
Background- Cigarette smoke is a primary risk factor for cardiovascular diseases. Enhanced function of the hemostatic system, in which platelets play a major role, is a significant underlying mechanism in cardiovascular disease and its progression. Epidemiological studies, complemented by physiological and biochemical data, show that cigarette smoke adversely affects platelet function, both in smokers and in nonsmokers exposed to sidestream smoke.
Methods and Results- The thrombogenic potential of platelets subjected to mainstream smoke extracts, sidestream extracts, and nicotine was measured in vitro under static and dynamic flow conditions. Platelet activation state was measured with a modified prothrombinase-based method. Mainstream and sidestream smoke extracts caused increased platelet activation. Although low-tar mainstream extracts activated platelets less than high-tar extracts, the sidestream extracts were almost equally potent. Modification of the filters of low-tar cigarettes, by blocking the air-bypass holes, raised activation rates by mainstream extracts to the level of high-tar extracts. Nicotine (50 nmol/L and 5 µmol/L) inhibited platelet activation under both flow and static conditions.
Conclusions- Cigarette smoke extracts directly cause platelet activation but also markedly increase the susceptibility of platelets to activation by shear stress. In contrast, nicotine, although also a constituent of cigarette smoke, significantly reduces platelet susceptibility to shear stress.
Key Words: platelets • smoking • thrombosis • cardiovascular diseases *
(B12)
Journal of the American College of Nutrition, Vol. 20, No. 5, 494-501 (2001) http://www.jacn.org/cgi/content/abstract/20/5/494
Effects of Long versus Short Bout Exercise on Fitness and Weight Loss in Overweight Females
W. Daniel Schmidt, PhD, Craig J. Biwer, MS and Linda K. Kalscheuer, BS
Department of Physical Education and Health Promotion, University of Wisconsin-Oshkosh Oshkosh, Wisconsin (W.D.S.)
Northern Michigan University, Marquette, Michigan (C.J.B.)
Arizona State University, Tempe, Arizona (L.K.K.)
Address reprint requests to: Dr. W. Daniel Schmidt, Department of Physical Education and Health Promotion, Albee Hall, The University of Wisconsin-Oshkosh, Oshkosh, WI 54901. E-mail: schmidtw@uwosh.edu.
Objective: The specific aim of this study was to determine if three 10 minute bouts of exercise per day (3 x 10) and two 15 minute bouts per day (2 x 15) were as effective as one 30 minute bout per day (1 x 30) for improving VO2 max and weight loss.
Methods: Overweight, female college students (body mass index =" src="/math/ge.gif" border=028 kg/m2) were recruited and assessed at baseline and post-treatment for aerobic fitness (Astrand maximal cycle test), weight, skinfold thickness (7-site), and circumference measures (4-site). Following measurement of resting energy expenditure (REE), subjects were asked to follow a self-monitored calorie restricted diet (80% of REE) for the twelve week duration of the study and were assigned (non-random) to one of four treatment groups: 1) a nonexercising control group (control, n = 8), 2) a 30 minutes continuous exercise group (1 x 30, n = 12), 3) a 30 minutes accumulated exercise group (2 x 15, n = 10) and 4) a second 30 minutes accumulated exercise group (3 x 10, n = 8). The exercising subjects participated in aerobic exercise training at 75% of heart rate reserve three to five days per week with all exercise monitored.
Results: VO2 max increased significantly while weight, body mass index, sum of skinfolds, and sum of circumferences decreased significantly from baseline to post-treatment in the 1 x 30, 2 x 15 and the 3 x 10 groups, but not in the control group. A tertiary finding was that exercise participation did not differ among the exercising groups with regard to the average number of days per week.
Conclusions: These results support the hypothesis that exercise accumulated in several short bouts has similar effects as one continuous bout with regard to aerobic fitness and weight loss during caloric restriction in overweight, young women.
Key words: aerobic fitness, heart rate reserve, body mass index *
(B13)
Circulation. 2004;109:843-848.)
(c) 2004 American Heart Association, Inc.
Clinical Investigation and Reports
Urinary 8-iso-Prostaglandin F2 as a Risk Marker in Patients With Coronary Heart Disease A Matched Case-Control Study
Edzard Schwedhelm, PhD; Asja Bartling, MD; Henrike Lenzen, MD; Dimitrios Tsikas, PhD; Renke Maas, MD; Jens Brümmer, MD; Frank-Mathias Gutzki, Ing Chem; Jürgen Berger, PhD; Jürgen C. Frölich, MD, FRSM; Rainer H. Böger, MD
From the Clinical Pharmacology Unit, Institute of Experimental and Clinical Pharmacology (E.S., R.M., R.H.B.), Institute of Clinical Chemistry (J. Brümmer), and Institute of Mathematics and Data Processing in Medicine (J. Berger), University Hospital Hamburg-Eppendorf, and the Institute of Clinical Pharmacology (A.B., H.L., D.T., F.-M.G., J.C.F.), Hannover Medical School, Germany.
Correspondence to Dr rer nat Edzard Schwedhelm, Institut für Experimentelle und Klinische Pharmakologie, Universitätsklinikum Hamburg-Eppendorf, Martinistraße 52, D-20246 Hamburg, Germany. E-mail schwedhelm@uke.uni-hamburg.de
Received September 24, 2003; revision received November 7, 2003; accepted November 18, 2003.
Background- Oxidative stress is involved in the pathophysiology of atherosclerosis, diabetes mellitus, hypertension, obesity, and cigarette smoking, all of these being risk factors for coronary heart disease (CHD). We tested the hypothesis that risk factors of CHD are associated with abundant systemic oxidative stress.
Methods and Results- We conducted a case-control study with 93 CHD patients and 93 control subjects frequency-matched by age and sex. Urinary excretion of the F2-isoprostane 8-iso-prostaglandin (PG) F2 and its major urinary metabolite, 2,3-dinor-5,6-dihydro-8-iso-PGF2, were measured by gas chromatography-tandem mass spectrometry. Body mass index, systolic blood pressure, and C-reactive protein were elevated in CHD patients (P<0.01). Urinary 8-iso-PGF2 and 2,3-dinor-5,6-dihydro-8-iso-PGF2 also differed, from 77 (interquartile range, 61-101) to 139 (93-231) pmol/mmol creatinine and from 120 (91-151) to 193 (140-275) pmol/mmol in control subjects and case subjects, respectively (P<0.001). 8-iso-PGF2 and its metabolite were highly correlated (Spearman's =0.664, P<0.001). HDL cholesterol was diminished in CHD patients (P<0.001). All of these characteristics predicted CHD in univariate analysis. In a multivariate model, the odds ratios were increased only for 8-iso-PGF2 (=" src="/math/ge.gif" border=0131 pmol/mmol, P<0.001) and C-reactive protein (>3 mg/L, P<0.01), ie, by 30.8 (95% CI, 7.7-124) and 7.2 (1.9-27.6), respectively. 8-iso-PGF2 was found to be a novel marker in addition to known risk factors of CHD, ie, diabetes mellitus, hypercholesterolemia, hypertension, and smoking. Urinary excretion of 8-iso-PGF2 correlated with the number of risk factors for all subjects (P<0.001 for trend).
Conclusions- 8-iso-PGF2 is a sensitive and independent risk marker of CHD.
Key Words: prostaglandins • coronary disease *
(B14)
2004 Statin IVUS plaque reduction
Circulation. 2004;110:1061-1068.)
(c) 2004 American Heart Association, Inc.
Original Articles
Early Statin Treatment in Patients With Acute Coronary Syndrome
Demonstration of the Beneficial Effect on Atherosclerotic Lesions by Serial Volumetric Intravascular Ultrasound Analysis During Half a Year After Coronary Event: The ESTABLISH Study
Okazaki Shinya, MD; Takayuki Yokoyama, MD; Katsumi Miyauchi, MD; Kazunori Shimada, MD; Takeshi Kurata, MD; Hitoshi Sato, MD; Hiroyuki Daida, MD
From the Department of Cardiology, Juntendo University School of Medicine, Tokyo, Japan.
Correspondence to Shinya Okazaki, MD, Department of Cardiology, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku Tokyo 113-8421 Japan. E-mail shinya@med.juntendo.ac.jp
Received February 10, 2004; revision received May 6, 2004; accepted May 18, 2004.
Background- Recent clinical trials have demonstrated that aggressive lipid lowering by statins could prevent recurrent events after acute coronary syndrome (ACS). We hypothesized that this efficacy was caused by a significant reduction in plaque volume by aggressive LDL cholesterol (LCL-C) lowering. The present study investigated the effect of early statin treatment on plaque volume of a nonculprit lesion by serial volumetric intravascular ultrasound in patients with ACS.
Methods and Results- Seventy patients with ACS were enrolled. All patients underwent emergency coronary angiography and percutaneous coronary intervention (PCI). They were randomized to intensive lipid-lowering therapy (n=35; atorvastatin 20 mg/d) or control (n=35) groups after PCI. Volumetric intravascular ultrasound analyses were performed at baseline and 6-month follow-up for a non-PCI site in 48 patients (atorvastatin, n=24; control, n=24). LDL-C level was significantly decreased by 41.7% in the atorvastatin group compared with the control group, in which LDL-C was increased by 0.7% (P<0.0001). Plaque volume was significantly reduced in the atorvastatin group (13.1±12.8% decrease) compared with the control group (8.7±14.9% increase; P<0.0001). Percent change in plaque volume showed a significant positive correlation with follow-up LDL-C level (R=0.456, P=0.0011) and percent LDL-C reduction (R=0.612, P<0.0001), even in patients with baseline LDL-C <125 mg/dL.
Conclusions- Early aggressive lipid-lowering therapy by atorvastatin for 6 months significantly reduced the plaque volume in patients with ACS. Percent change in plaque volume showed a significant positive correlation with percent LDL-C reduction, even in patients with low baseline LDL-C.
Key Words: atherosclerosis • lipids • plaque • statins • coronary disease *
(B15)
Circulation. 2002;105:e9105.)
(c) 2002 American Heart Association, Inc.
Cardiovascular News
Ruth SoRelle, MPH
Circulation Newswriter
Leisure-Time Exercise Better Than Walking or Biking to Work
Perhaps in part explaining the mystery of the French conundrum, a group of French and Northern Irish researchers have found that leisure-time exercise (a form more common to the French) seems to have a greater positive cardiovascular effect than walking or cycling to work (the exercise more common to those who live in Northern Ireland).
The study, published in this week's issue of Circulation (Circulation. 2002;105:2247-2252) and led by Aline Wagner, MD, of the Laboratoire d'Epidemiologie et de Sante Publique in Strasbourg, France, and Chantal Simon, MD, PhD, of the Groupe d'Etudes et de Recherche en Nutrition at Strasbourg, examined information from the Prospective Epidemiological Study of Myocardial Infarction (the PRIME Study) to determine the effects of activity levels and patterns on both major coronary events and angina. (The PRIME Study Group included research groups from France and the Queen's University Belfast, Northern Ireland. The PRIME Study consisted of 9758 men aged 50 to 59 years who were recruited between 1991 and 1993 and who had no signs of coronary heart disease. They were monitored for 5 years.)
During the follow-up period, 321 coronary events were recorded, of which 167 (106 in France, 61 in Northern Ireland) were either fatal or nonfatal myocardial infarctions or coronary deaths. There were 154 instances of angina pectoris (94 in France, 60 in Northern Ireland). The researchers found that the individuals who exercised hardest as a leisure-time activity had the lowest risk of fatal or nonfatal myocardial infarction or coronary deaths. However, walking or bicycling to work did not appear to have a positive effect on such coronary disasters. "Those who walked or cycled to work tended to have a higher incidence of angina," the researchers wrote.
"In our study, surprisingly, a significant increase in the incidence of angina was observed for the most active subjects," they wrote. "The mechanism behind such pain is still unclear," they wrote, "and it hasn't yet been proven if what is seen is a true increase or an under-diagnosis of angina in more sedentary individuals."
"In conclusion, these prospective data from a European cohort of middle-aged men show a beneficial effect of leisure-time physical activity (EE) on the incidence of fatal or nonfatal myocardial infarction and coronary deaths. These results could partly explain the unfavorable rate of coronary heart disease in Northern Ireland compared to France." *
(B16)
Circulation. 2002;105:2817.)
(c) 2002 American Heart Association, Inc.
Brief Rapid Communications
Mental Stress Induces Prolonged Endothelial Dysfunction via Endothelin-A Receptors
Lukas E. Spieker, MD; David Hürlimann, MD; Frank Ruschitzka, MD; Roberto Corti, MD; Frank Enseleit, MD; Sidney Shaw, PhD; Daniel Hayoz, MD; John E. Deanfield, MD; Thomas F. Lüscher, MD; Georg Noll, MD
From Cardiology (L.E.S., D.H., F.R., R.C., F.E., T.L., G.N.), University Hospital, Zürich; the Department of Clinical Research (S.S.), Inselspital, Bern; Division of Hypertension and Vascular Medicine (D.H.), Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland; and Cardiology (J.E.D.), Great Ormond Street Hospital for Children, London, UK.
Correspondence to Georg Noll, MD, FESC, Cardiology, University Hospital, CH-8091 Zürich, Switzerland. E-mail karnog@usz.unizh.ch
Background- Mental stress is a risk factor for atherosclerosis and may precipitate myocardial ischemia and infarction. Because endothelial dysfunction is an early manifestation of atherosclerosis, we investigated the impact of mental stress on endothelial function.
Methods and Results- The effects of a 3-minute mental stress task on endothelium-dependent vasodilation were studied in healthy subjects without cardiovascular risk factors. Flow-mediated (FMD) and nitroglycerin (0.4 mg sublingual)-induced vasodilation were studied before and after mental stress by high-resolution ultrasound of the radial artery. Additionally, FMD was assessed before and 10 to 45 minutes after mental stress during intraarterial infusion of a selective endothelin A receptor antagonist (BQ-123, 1 nmol/min) or saline, respectively. Endothelium-dependent vasodilation was reduced by half for about 45 minutes (8.0±1.1% versus 4.1±1.0%; P<0.002), whereas endothelium-independent vasodilation to nitroglycerin remained unaffected (15.6±1.6 versus 14.3±1.3%; NS). Intraarterial infusion of BQ-123, a selective endothelin-A receptor antagonist, but not saline prevented the impairment of endothelium-dependent vasodilation (8.6±1.2 versus 9.4±1.3%; NS). In contrast, intraarterial infusion of norepinephrine of similar duration as mental stress did not inhibit FMD.
Conclusions- Mental stress induces prolonged endothelial dysfunction, which is prevented by selective endothelin-A receptor antagonism. This represents a novel and important link between mental stress and atherosclerotic vascular disease.
Key Words: atherosclerosis • endothelin • nitric oxide • reactive hyperemia *
(B17)
J Am Coll Cardiol 2000 Dec;36(7):2185-2191
Oral glucose loading acutely attenuates endothelium-dependent vasodilation in healthy adults without diabetes: an effect prevented by vitamins C and E.
Title LM, Cummings PM, Giddens K, Nassar BA. Division of Cardiology, Laboratory Medicine at the Queen Elizabeth II Health Sciences Center, Halifax, Nova Scotia, Canada. ltitle@is.dal.ca
OBJECTIVES: The goal of this study was to determine whether postprandial hyperglycemia, induced by oral glucose loading, attenuates endothelial function in healthy subjects without diabetes and whether coadministration of vitamins C and E could prevent these postprandial changes. BACKGROUND: Epidemiologic evidence suggests that postprandial hyperglycemia, below diabetic levels, is a risk factor for cardiovascular disease. Postprandial hyperglycemia may promote atherosclerosis through endothelial dysfunction and oxidative stress. METHODS: We evaluated the acute effects of oral glucose loading (75 g), alone and with vitamins C (2 g) and E (800 IU), on endothelium-dependent flow-mediated dilation (FMD) of the brachial artery, in a randomized, double-blind, placebo-controlled, crossover study of 10 healthy volunteers. Changes in the levels of markers of oxidative stress (plasma malondialdehyde and erythrocyte glutathione, glutathione peroxidase and superoxide dismutase) were also assessed. RESULTS: Increases in plasma glucose and insulin after glucose loading were unaffected by vitamin coadministration. With glucose loading alone, FMD fell from 6.5+/-2.2 at baseline to 5.4+/-1.7, 3.7+/-2.1*, 4.1+/-3.5* and 5.7+/-1.9% at 1, 2, 3 and 4 h (*p < 0.05 vs. 0 h). In contrast, FMD did not change significantly after glucose plus vitamins (6.4+/-1.3, 7.6+/-1.8, 7.9+/-2.7, 6.9+/-2.3, 6.9+/-1.9% at 0, 1, 2, 3 and 4 h). By two-way repeated measures analysis of variance we found a significant interaction between vitamin treatment and time (p = 0.0003), indicating that vitamins prevented the glucose-induced attenuation of FMD. Oxidative stress markers did not significantly change with glucose loading alone or with vitamins. CONCLUSIONS: Oral glucose loading causes an acute, transient decrease of FMD in healthy subjects without diabetes, which is prevented by vitamins C and E. *
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(B18)
Circulation. 2002 Nov 12;106(20):
Smoking a Single Cigarette Rapidly Reduces Combined Concentrations of Nitrate and Nitrite and Concentrations of Antioxidants in Plasma
Masahiko Tsuchiya, MD; Akira Asada, MD; Emiko Kasahara; Eisuke F. Sato, MD; Mitsuo Shindo, MD; Masayasu Inoue, MD
From the Department of Biochemistry and Molecular Pathology (M.T., E.K., E.F.S., M.I.) and the Department of Anesthesiology and Intensive Care Medicine (M.T., A.A., M.S.), Osaka City University Medical School, Abenoku, Osaka, Japan.
Correspondence to Dr Masahiko Tsuchiya, c/o Prof Masayasu Inoue, Department of Biochemistry and Molecular Pathology, Osaka City University Medical School, 1-4-3 Asahimachi, Abenoku, Osaka 545-8585, Japan. E-mail oxymasa@ea.mbn.or.jp
Background- Cigarette smoking is a well-known risk factor for the development of cardiovascular disease, yet the mechanism of action involved is not completely understood. Because cigarette smoke contains superoxide and other reactive oxygen species, it has been hypothesized that some of the adverse effects of smoking may result from oxidative damage to endothelial cells, which results in nitric oxide (NO) shortage. However, little information is available regarding the acute effects of smoking on plasma concentrations of NO and antioxidants. We measured the changes in the combined plasma concentrations of nitrate and nitrite as an index of NO concentration, as well as changes in concentrations of major serum antioxidants (ascorbic acid, cysteine, methionine, and uric acid) in smokers after smoking a single cigarette.
Methods and Results- A randomized crossover study of the effects of smoking a single cigarette was performed in 20 smokers. Smoking a sham cigarette induced no significant changes in all assayed parameters. However, smoking a single cigarette significantly decreased nitrate and nitrite plasma concentrations by 3.5±1.2 and 3.4±1.1 µmol/L, compared with plasma concentrations at presmoking and sham smoking, respectively. The concentrations of ascorbic acid and other antioxidants were also significantly lower after smoking a single cigarette. These parameters returned to preexperimental levels 60 minutes after smoking cessation.
Conclusion- The present findings indicate that smoking a single cigarette temporarily decreases nitrate, nitrite, and serum antioxidant concentrations in the plasma. These transient changes may partially contribute to coronary vasoconstriction, which is routinely observed after smoking.
Key Words: smoking • nitric oxide • free radicals • antioxidant • endothelium *
(B19)
Circulation. 2002;105:2247.
http://circ.ahajournals.org/cgi/content/abstract/105/19/2247
(c) 2002 American Heart Association, Inc.
Clinical Investigation and Reports
Physical Activity and Coronary Event Incidence in Northern Ireland and France The Prospective Epidemiological Study of Myocardial Infarction (PRIME)
Aline Wagner, MD; Chantal Simon, MD, PhD; Alun Evans, MD; Jean Ferrières, MD; Michèle Montaye, MD; Pierre Ducimetière, PhD; Dominique Arveiler, MD, on behalf of the PRIME Study Group
From Laboratoire d'Epidémiologie et de Santé Publique, Strasbourg, France (A.W., D.A.); Groupe d'Etudes et de Recherche en Nutrition, Strasbourg, France (C.S.); the Department of Epidemiology and Public Health, The Queen's University Belfast, United Kingdom (A.E.); INSERM U558, Département d'Epidémiologie, Toulouse, France (J.F.); INSERM U508, Institut Pasteur, 59019 Lille, France (M.M.); and INSERM U258, Villejuif Cedex, France (P.D.).
Correspondence to Dr Chantal Simon, Service de Médecine Interne et de Nutrition, Hôpital de Hautepierre, 67098 Strasbourg Cedex, France. E-mail chantal.simon@medecine.u-strasbg.fr
Background- The influence of physical activity on the incidence of angina pectoris and hard coronary events (myocardial infarction and coronary deaths) was examined in Northern Ireland and France at contrasting risk for coronary heart disease (CHD) and with different physical activity patterns.
Methods and Results- Participants of the Prospective Epidemiological Study of Myocardial Infarction (PRIME) (n=9758; age, 50 to 59 years), free of CHD at baseline, were followed up for 5 years: 167 hard CHD and 154 angina events were recorded. Net energy expenditure (EE) as the result of physical activity was assessed by means of the MONICA Optional Study of Physical Activity Questionnaire (MOSPA-Q). Leisure-time physical activity EE was calculated; subjects were also categorized as to whether they performed high-intensity leisure-time activities or walked or cycled to work. After multivariate adjustment, leisure-time physical activity EE was associated with a lower risk of hard CHD events (P<0.04), whereas walking or cycling to work was not independently related to hard CHD events. No interaction by country was found. The beneficial effect of leisure-time physical activity was also present among subjects who did not report high-intensity activities (P<0.04), with similar results in France and Northern Ireland. In contrast, an increasing level of leisure-time physical activity was associated with a higher risk of angina in both countries.
Conclusions- These data indicate a beneficial effect of leisure-time physical activity EE on hard CHD incidence in middle-aged men, which could partly explain the unfavorable rate of CHD in Northern Ireland. The higher level of leisure-time activities in France could, in part, explain its lower rate of CHD.
Key Words: angina • coronary disease • follow-up studies • men • exercise *
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