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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.
Obesity and Cardiovascular Disease
Paul Poirier, MD, PhD, FRCPC, and Robert H. Eckel, MD
Address
Institut Universitaire de Cardiologie et de Pneumologie, Hôspital Laval,
2725 Chemin Sainte-Foy, Sainte-Foy, Québec G1V 4G5, Canada.
Current Atherosclerosis Reports 2002, 4:448–453
Current Science Inc. ISSN 1523–3804
Copyright © 2002 by Current Science Inc.
Introduction
Calorie imbalance, in part due to excess calorie con-
sumption, is related to a rising prevalence of obesity. Popu-
lations of industrialized countries are becoming more
overweight as a result of changes in lifestyle, and obesity
may well become the most common health problem of the
21st century [1,2,3•]. Obesity is a major contributor to
the prevalence of cardiovascular disease (CVD) in the
developed world, and yet has only recently been afforded
the same level of attention as other risk factors of coronary
artery disease (CAD).
It was recently stated by the Public Health Approaches
to the Prevention of Obesity (PHAPO) working group
of the International Obesity Task Force (IOTF) that "In
every country in the world today, depending on its stage of
epidemiologic transition, chronic non-communicable
diseases such as CVD, cancer, diabetes, and osteoporosis
are either newly appearing, rapidly rising, or already estab-
lished at high levels" [3•]. Thus, obesity is a major con-
tributor to the global burden of disease and disability
because it is a risk factor for numerous medical conditions
such as heart disease, diabetes, hypertension, stroke, pul-
monary emboli, certain cancers, osteoarthritis, gallbladder
disease, and respiratory abnormalities [1]. Indeed, deaths
from noncommunicable diseases are expected to rise from
28.1 million to 49.7 million a year, an increase in absolute
numbers of 77% [3•], and ischemic heart disease is pre-
dicted to become the leading worldwide cause of disease
burden in 2020 (Table 1).
The Metabolic Syndrome
A high body mass index (BMI) is significantly associated
with myocardial infarction, coronary insufficiency, and
sudden death; the association seems strongest with sudden
death [4]. Although, obesity per se is considered a major
modifiable risk factor for ischemic heart disease [2], it is of
importance to remember that a remarkable heterogeneity
exists among obese subjects, and the presence of visceral obe-
sity generally worsens the metabolic portrait that is assoc-
iated with a cluster of traditional and nontraditional risk
factors, which are all potentially synergistic and deleterious
(Table 2). Because not all obese individuals are at increased
risk of CVD, the challenge for the clinician is to screen the
obese patients who are at risk (ie, the obese state associated
with the metabolic syndrome). Using the criteria established
by the National Cholesterol Education Panel (NCEP) [5••],
the metabolic syndrome is defined as three or more of the
following: 1) waist circumference for men greater than
102 cm and for women greater than 88 cm; 2) fasting tri-
glycerides of 150 mg/dL or greater (1.7 mmol/L); 3) high-
density lipoprotein (HDL) cholesterol less than 40 mg/dL
(<1.0 mmol/L) for men and less than 50 mg/dL (<1.3
mmol/L) for women; 4) blood pressure greater than 130/85
mm Hg; and 5) fasting plasma glucose of 110 mg/dL or more
(6.1 mmol/L). Presently, the "metabolic syndrome" is a
working definition only, and it remains unclear as to whether
the five components provide equal risk to the development
of cardiovascular disease events.
Obesity is a major contributor to the prevalence of
cardiovascular disease in the developed world, and yet has
only recently been afforded the same level of
attention as other risk factors of coronary artery disease.
Obesity is a chronic metabolic disorder associated with
cardiovascular disease and increased morbidity and mortal-
ity. It is apparent that a variety of adaptations/alterations in
cardiac structure and function occur as excessive adipose
tissue accumulates, even in the absence of comorbidities.
Shifts toward a less physically demanding lifestyle are
observed today throughout different populations, and this
scourge associated with obesity implicates a corresponding
increase in the number of individuals afflicted with the met-
abolic syndrome, which defines the obese patient as being
"at risk." Adipose tissue is not simply a passive storehouse
for fat, but an endocrine organ that is capable of
synthesizing and releasing into the bloodstream a variety
of molecules that may impact unfavorably the risk
factor profile of a patient. Indeed, obesity may affect
atherosclerosis through unrecognized variables and risk
factors for coronary artery disease such as dyslipidemia,
hypertension, glucose intolerance, inflammatory markers,
and the prothrombotic state. By favorably modifying
lipids, decreasing blood pressure, and decreasing levels
of glycemia, proinflammatory cytokines, and adhesion
molecules, weight loss may prevent the progression of
atherosclerosis or the occurrence of acute coronary
syndrome events in the obese high-risk population.
Obesity and Cardiovascular Disease • Poirier and Eckel 449
There is ample evidence suggesting that the presence of
excess fat in the abdomen in proportion to total body fat is
an independent predictor of CVD [6–8], and the features of
the metabolic syndrome are most often the consequence of
an excessive accumulation of abdominal fat (especially when
accompanied by a high accumulation of visceral adipose
tissue) [9–13]. For instance, among equally overweight and
obese individuals, patients with a high accumulation of
visceral adipose tissue are characterized by disturbances in
plasma glucose/insulin homeostasis; elevated triglycerides
(TG) and apolipoprotein B concentrations; low HDL choles-
terol levels; an increased proportion of small dense low-
density lipoprotein (LDL) and small dense HDL particles;
and by postprandial hyperlipidemia, reflecting a more
saturated system for the clearance of TG-rich lipoproteins
either of exogenous or endogenous origin [9-13]. This profile
is also accompanied by a prothrombotic, inflammatory state
[14–18]. Abdominal distribution of body fat is associated
with increased plasma levels of fibrinogen, factor VII and
factor VIIIc coagulant activities, and tissue plasminogen acti-
vator (tPA) antigen and plasminogen activator inhibitor I
(PAI-I) antigen and activity [19–22]. This hypercoagulable
state, which accompanies excessive central fat deposition,
may also be associated with impaired endothelial function
[23,24]. Therefore, the abdominally obese patient with the
features of the metabolic syndrome is characterized by an
atherogenic, prothrombotic, and inflammatory profile,
which probably substantially increases the risk of an acute
coronary syndrome [25].
From a pathophysiologic viewpoint, it is important to
keep in mind that adipose tissue is not simply a passive
storehouse for fat, but an endocrine organ that is capable
of synthesizing and releasing into the bloodstream a vari-
ety of molecules [1]. Of clinical consideration, circulating
concentrations of PAI-1, angiotensin II, C-reactive protein
(CRP), fibrinogen, and tumor necrosis factor α (TNF-α)
are all related to BMI [15,20]. It has been estimated that
in vivo, approximately 30% of the total circulating con-
centrations of interleukin 6 (IL-6) originate from adipose
tissue [15,26]. This is of importance because IL-6 modu-
lates CRP production in the liver, and CRP may be a
marker of a chronic inflammatory state that predisposes to
acute coronary syndromes [27–30].
Thus, when obesity is associated with the metabolic
syndrome, attention from the clinician is needed; this is
not an uncommon relationship [31]. The metabolic syn-
drome was encountered in approximately 10% of subjects
with normal glucose tolerance, approximately 50% of the
subjects with impaired fasting glucose/impaired glucose
tolerance, and approximately 80% of those with type 2
diabetes [32]. From an epidemiologic perspective, a recent
report indicated that 20% to 25% of the adult US
population has the metabolic syndrome [33••]. This is
of concern because the magnitude of risk associated with
insulin resistance (ie, the metabolic syndrome) may be of
the same magnitude as that of hypercholesterolemia [34].
From a clinical point of view, abdominal obesity-associ-
ated metabolic syndrome can be assessed easily, at least in
men. It was reported in men with a waist circumference
greater than 90 cm and with triglycerides greater than
2.0 mmol/L that this may identify as many as 80% of the
subjects with the insulin resistance syndrome; this is assoc-
iated with a cluster of risk factors for CVD [9,35]. However,
the waist circumference cutoff may lose predictive power in
patients with a BMI of 35 kg/m
2
or more [36].
Atherosclerosis
An important early event in the development of athero-
sclerosis is endothelial cell dysfunction and inflammation of
the vessel wall [37]. Atherosclerosis begins in childhood with
deposits of cholesterol in macrophages and smooth muscle
cells located in the intima of large muscular arteries to form
fatty streaks [38,39]. As individuals age, fibrous plaques
develop and progress to complicated lesions wherein hemor-
rhage or rupture may lead to acute coronary events [29,30].
In adults, obesity is often associated with advanced
atherosclerosis. Indeed, examination of arteries post-
mortem from young individuals (15 to 34 years of age)
who died from accidental injury, homicide, or suicide
demonstrates that the extent of fatty streaks and raised
lesions (fibrous plaques and plaques with calcification or
ulceration) in the right coronary artery (RCA) and in
the abdominal aorta were associated with obesity and
abdominal panniculus [40–43]. The prevalence of obesity,
defined as the thickness of panniculus adiposus and BMI
Table 1. The five leading causes of disease burden worldwide as measured in disability-adjusted
life years in the 1990s and the 2020s
1990s 2020s (predicted)
1. Lower respiratory infections 1. Ischemic heart disease
2. Diarrheal diseases 2. Unipolar major depression
3. Perinatal conditions 3. Road traffic accidents
4. Unipolar major depression 4. Cerebrovascular disease
5. Ischemic heart disease 5. Chronic obstructive disease
Adapted from Kumanyika et al. [
3•
].
450 Nutrition
of 30 kg/m
2
or more, in the Pathobiological Determinants
of Atherosclerosis in Youth (PDAY) study was 14.3% [44•].
Obesity in young men, as defined by BMI, was associated
with both fatty streaks and raised lesions in the RCA and
with microscopic atherosclerosis and stenosis in the
left anterior descending artery. Black subjects had more
extensive fatty streaks than white subjects in all arterial
segments, and men had more extensive raised lesions in
the RCA than women [44•]. The prevalence of total athero-
sclerosis (fatty streaks and raised lesions) in the RCA
increased from approximately 60% in the youngest age
group (15 to 19 years) to greater than 80% in men and
approximately 70% in women in the oldest age group
(30 to 34 years) [44•]. There was a 5% increase in arterial
surface involved with lesions for each 5-year age increase
[44•]. Importantly, when BMI and panniculus thickness
were used together in males, a BMI of 30 kg/m
2
or more
was associated with RCA raised lesions only within the
higher (17 mm) classification of panniculus thickness,
reinforcing that central fat distribution is more important
than total fat as a risk for CVD [44•]. Lesion prevalence was
greatest in the first 2 to 3 cm of the RCA, and in men the
effects of adiposity on raised lesions in this region were
evident even before the age of 25 years [45••]. Moreover
the association between adiposity and RCA lesions after
adjusting for other risk factors, namely non-HDL and HDL
cholesterol concentration, hypertension, smoking, and
glycohemoglobin, was still statistically significant; these
risk factors accounted for only 15% of the effects on
atherosclerosis [45••]. On the other hand, there was little
association of adiposity with coronary atherosclerosis in
young women, with a nonsignificant trend for an assoc-
iation between BMI and fatty streaks in women who
presented a thick panniculus adiposus [45••]. Of note,
however, raised lesions in coronary arteries in young
women lag behind those in young men by about 10 years,
independently of risk factor status [45••]. The same
parallel probably applies to postmenopausal women, who
often present with clinically significant atherosclerosis 10
years later than men. In the proximal left anterior descend-
ing (LAD) artery, obesity and hypertension were associated
with grade 4 and 5 lesions, which were defined as raised
or advanced lesions with necrotic lipid cores that may be
clinically significant [44•,46]. These data provide evidence
that obesity in adolescents and young adults accelerates
the progression of atherosclerosis decades before clinical
manifestations appear. Thus, the control of childhood
obesity is justified for the prevention of CVD as well as
other chronic disease associated with it.
Although the relationship between obesity and athero-
sclerosis is often dependent on obesity-related comorbidities
(eg, hypertension, glucose intolerance, and dyslipidemia),
after a follow-up of 26 years, the Framingham Heart Study
[47] and the Manitoba Study [4] have both documented
that obesity is an independent predictor of CVD, particularly
among women. This association was more pronounced in
individuals younger than 50 years of age, reinforcing the idea
that obesity leads to premature atherosclerosis. There is
evidence, however, that dyslipidemia, smoking, obesity,
and hyperglycemia are related to fatty streaks in the second
decade of life, and the same risks factors, along with hyper-
tension, are associated with plaques in the third decade
of life [40]. Hence the American Heart Association has
stated that obesity is a major modifiable risk factor, rather
than independent risk factor, for atherosclerotic cardio-
vascular disease [2,48].
Childhood Obesity and the Development
of Cardiovascular Disease
Childhood obesity has reached epidemic proportions.
During the past three decades, the number of overweight
children in the United States has more than doubled.
In 1983, 18.6% of preschool children in the United States
were defined as overweight and 8.5% were defined as
obese, whereas in 2000, 22% of preschool children were
overweight and 10% were obese [49]. Similar increases in
the prevalence of obesity have been observed worldwide
[50]. Obesity has a substantial influence on the cardio-
vascular system [1], and it is of importance to recognize
that childhood obesity is directly linked to abnormalities
in risk profile of both CAD and diabetes [51]. Indeed, over
40 years ago it was suggested that atherosclerosis was at
least in part a pediatric nutrition problem [52]. Because
modification of risk factors should occur before the ages
when the effects of atherosclerosis are observed, simple
risk factor modification (including diet, physical activity,
and weight control) should begin early in life, at least by
the late teens [53]. This has been recently demonstrated by
the observations that the secular trend toward obesity in
children is accompanied by detrimental risk factors for the
eventual development of CVD [54••,55].
Coronary Artery Disease and
Revascularization Therapy
The metabolic syndrome should probably be treated
aggressively following revascularization therapy. Indeed,
abnormal glucose tolerance may be an important determi-
nant for long-term prognosis after coronary angioplasty
[56]. Moreover, following coronary artery bypass graft
(CABG), the components of the metabolic syndrome are
associated with angiographic progression of athero-
sclerosis in nongrafted coronary arteries [57].
The cardiac catheterization laboratory at Duke Univer-
sity has observed an increase in obesity from 20% to 33%
in over 9000 patients studied between 1986 and 1997 [58].
Although obesity was associated with younger age, comor-
bidities, and only single-vessel disease at baseline [58,59],
obesity was associated with more clinical events during
the post–30-day period after cardiac catheterization [58].
In another study [59], obesity was associated with higher
Obesity and Cardiovascular Disease • Poirier and Eckel 451
cumulative in-patient medical costs and significant differ-
ences in unadjusted survival at 10 years [58]. This was not
true in the study of Gruberg et al. [59].
Coronary Artery Bypass Graft
Rightfully, surgeons often quote obesity as a risk factor for
perioperative morbidity and mortality. The presence of
comorbidities like hypertension, CAD, dyslipidemia, and
type 2 diabetes mellitus, as well as the technical difficulties
inherent to the surgical and postsurgical care of obese
patients, likely contribute to this perception. Obese patients
have been shown to have a higher incidence of postoperative
thromboembolic disease in noncardiac surgery, and the
high risk of thromboembolic disease in obese patients may
necessitate an aggressive approach to deep venous thrombo-
sis prophylaxis [60]. In contrast to frequent beliefs, obesity
is not associated with increased mortality or postoperative
cerebrovascular accidents following CABG. There is, however,
an increased risk of sternal and superficial wound infection,
saphenous vein harvest site infection, and atrial dysrhyth-
mias in obese patients undergoing bypass surgery [61,62].
Clinical Trials and Cardiovascular Disease
Outcome in Patients with Obesity
There is some evidence that patients with obesity and/or
the metabolic syndrome with coronary heart disease (or
with coronary heart disease risk) may respond better to
lipid-modifying interventions in clinical trials. In the
Helsinki Heart Study [63], men with hypercholesterolemia
with a BMI greater than 26 kg/m
2
and either hypertri-
glyceridemia plus low levels of HDL cholesterol and/or three
to four additional risk factors for coronary heart
disease appeared to respond better to the gemfibrozil inter-
vention than patients without obesity. Moreover, in patients
with coronary heart disease and baseline levels of HDL
cholesterol less than 40 mg/dL, the metabolic syndrome
predicted a superior reduction in coronary heart disease
events with gemfibrozil [64]. Whether this relative benefit of
obese patients with or without the metabolic syndrome
extends to other cardiovascular disease risk factors remains
unexamined, but it is clearly worthy of additional attention.
Conclusions
Obesity is a chronic metabolic disorder associated with CVD
and increased morbidity and mortality. It is apparent that a
variety of adaptations/alterations in cardiac structure and
function occur as excessive adipose tissue accumulates, even
in the absence of comorbidities. Large shifts towards a less
physically demanding lifestyle are observed today through-
out different populations, and this scourge associated with
obesity implicates a corresponding increase in the number
of individuals afflicted with the metabolic syndrome. This
deleterious trend endangers the advances made in reducing
morbidity and mortality from CVD over the past two
decades [65]. It also poses a challenge to physicians to mod-
ify their practice to place more emphasis on lifestyle changes
[53]. More prevalent cardiac risk factors in obese and very
obese CAD patients at baseline seemed to counteract poten-
tial survival benefits derived from the younger age and less
extensive CAD of these individuals. Consequently, the long-
term clinical burden of illness is greater [58]. Of note, the
impact of excess body fat on mortality is delayed and may
not be seen in short-term studies [58] compared with other
ones [25,28,45••,47]. Indeed, cardiovascular mortality
assessed in 3606 subjects with a median follow-up of 6.9
years was increased substantially in subjects with the fea-
tures of the metabolic syndrome (12.0% vs 2.2%) [32], and
it was shown recently that abdominal obesity is associated
with increased risk of acute coronary events in men [28].
Obesity may affect atherosclerosis through risk factors
like dyslipidemia, hypertension, glucose intolerance,
inflammatory markers, and the prothrombotic state. Many
of these are components of insulin resistance. Although
there are no prospective studies to date demonstrating that
weight loss increases survival, there is strong evidence that
weight loss in "at risk" overweight and obese individuals
reduces the incidence of diabetes [66,67], and because
diabetes is a CAD equivalent, probably CVD as well. By
favorably modifying lipids and by decreasing blood pres-
sure, levels of glycemia, proinflammatory cytokines (ie,
TNF-α, IL-6, CRP) [68–70], and adhesion molecules (ie, P-
selectin, circulating inter-cellular adhesion molecule-1,
vascular adhesion molecule-1) [68], weight loss may pre-
vent the progression of atherosclerosis or the occurrence of
acute coronary syndrome events. Moreover, weight loss
translates into improvement in endothelial function [68].
If the current worldwide epidemic of childhood obesity
cannot be averted, its full public health impact will be felt
in the contemporary cardiology world as affected children
become adults and the long-term complications of obesity
develop. The best way to treat a disease is to prevent it. For
obesity, this is where the emphasis needs to be placed.
References and Recommended Reading
Papers of particular interest, published recently, have been
highlighted as:
Of importance
•• Of major importance
1. Poirier P, Eckel RH:
The heart and obesity.
In
Hurst's The
Heart.
Edited by Fuster V, Alexander RW, King S,
et al.
:
New York: McGraw-Hill; 2000:2289–2303.
2. Eckel RH, Krauss RM:
American Heart Association call to
action: obesity as a major risk factor for coronary heart
disease. AHA Nutrition Committee. Circulation
1998,
97:
2099–2100.
3.• Kumanyika S, Jeffery RW, Morabia A, Ritenbaugh C, Antipatis
VJ:
Obesity prevention: the case for action. Int J Obes Relat
Metab Disord
2002,
26:
425–436.
Statement from an international task force group on obesity.
452 Nutrition
4. Rabkin SW, Mathewson FA, Hsu PH:
Relation of body weight
to development of ischemic heart disease in a cohort of
young North American men after a 26 year observation
period: the Manitoba Study. Am J Cardiol
1977,
39:
452–458.
5.••
Executive Summary of The Third Report of The National
Cholesterol Education Program (NCEP) Expert Panel
on Detection, Evaluation, And Treatment of High Blood
Cholesterol In Adults (Adult Treatment Panel III).
JAMA
2001,
285:
2486–2497.
Guidelines for the management of dyslipidemia and definition of the
metabolic syndrome that defines the obese patient as being "at risk."
6. Larsson B, Svardsudd K, Welin L,
et al.
:
Abdominal adipose
tissue distribution, obesity, and risk of cardiovascular
disease and death: 13 year follow up of participants in the
study of men born in 1913. BMJ
1984,
288:
1401–1404.
7. Folsom AR, Kaye SA, Sellers TA,
et al.
:
Body fat distribution
and 5-year risk of death in older women. JAMA
1993,
269:
483–487.
8. Rexrode KM, Carey VJ, Hennekens CH,
et al.
:
Abdominal
adiposity and coronary heart disease in women. JAMA
1998,
280:
1843–1848.
9. Lemieux I, Pascot A, Couillard C,
et al.
:
Hypertriglyceridemic
waist: a marker of the atherogenic metabolic triad
(hyperinsulinemia; hyperapolipoprotein B; small, dense
LDL) in men? Circulation
2000,
102:
179–184.
10. Tchernof A, Lamarche B, Prud'homme D,
et al.
:
The dense LDL
phenotype. Association with plasma lipoprotein levels,
visceral obesity, and hyperinsulinemia in men. Diabetes Care
1996,
19:
629–637.
11. Couillard C, Bergeron N, Prud'homme D,
et al.
:
Postprandial
triglyceride response in visceral obesity in men. Diabetes
1998,
47:
953–960.
12. Pascot A, Lemieux I, Prud'homme D,
et al.
:
Reduced HDL
particle size as an additional feature of the atherogenic
dyslipidemia of abdominal obesity. J Lipid Res
2001,
42:
2007–2014.
13. Lemieux S, Després JP:
Metabolic complications of visceral
obesity: contribution to the etiology of type 2 diabetes
and implications for prevention and treatment. Diabetes
Metab
1994,
20:
375–393.
14. Juhan-Vague I, Alessi MC:
PAI-1, obesity, insulin resistance
and risk of cardiovascular events. Thromb Haemost
1997,
78:
656–660.
15. Yudkin JS, Stehouwer CD, Emeis JJ, Coppack SW:
C-reactive
protein in healthy subjects: associations with obesity,
insulin resistance, and endothelial dysfunction: a potential
role for cytokines originating from adipose tissue?
Arterioscler Thromb Vasc Biol
1999,
19:
972–978.
16. Hak AE, Stehouwer CD, Bots ML,
et al.
:
Associations
of C-reactive protein with measures of obesity, insulin
resistance, and subclinical atherosclerosis in healthy,
middle-aged women. Arterioscler Thromb Vasc Biol
1999,
19:
1986–1991.
17. Pascot A, Poirier P, Lemieux I, Després JP:
Caractère
distinct de la plaque athéromateuse du patient insulino-
résistant diabétique. Ann Endocrinol (Paris)
2001,
62:
267–273.
18. Yudkin JS, Kumari M, Humphries SE, Mohamed-Ali V:
Inflammation, obesity, stress and coronary heart disease:
is interleukin-6 the link? Atherosclerosis
2000,
148:
209–214.
19. Folsom AR, Qamhieh HT, Wing RR,
et al.
:
Impact of weight
loss on plasminogen activator inhibitor (PAI-1), factor VII,
and other hemostatic factors in moderately overweight
adults. Arterioscler Thromb
1993,
13:
162–169.
20. Cigolini M, Targher G, Bergamo AI,
et al.
:
Visceral fat
accumulation and its relation to plasma hemostatic factors
in healthy men. Arterioscler Thromb Vasc Biol
1996,
16:
368–374.
21. Svendsen OL, Hassager C, Christiansen C, Nielsen JD,
Winther K:
Plasminogen activator inhibitor-1, tissue-type
plasminogen activator, and fibrinogen: effect of dieting
with or without exercise in overweight postmenopausal
women. Arterioscler Thromb Vasc Biol
1996,
16:
381–385.
22. Licata G, Scaglione R, Avellone G,
et al.
:
Hemostatic function
in young subjects with central obesity: relationship with
left ventricular function. Metabolism
1995,
44:
1417–1421.
23. Steinberg HO, Chaker H, Leaming R,
et al.
:
Obesity/insulin
resistance is associated with endothelial dysfunction.
Implications for the syndrome of insulin resistance.
J Clin Invest
1996,
97:
2601–2610.
24. Hashimoto M, Akishita M, Eto M,
et al.
:
The impairment of
flow-mediated vasodilatation in obese men with visceral fat
accumulation. Int J Obes Relat Metab Disord
1998,
22:
477–484.
25. Grundy SM:
Obesity, metabolic syndrome, and coronary
atherosclerosis. Circulation
2002,
105:
2696–2698.
26. Mohamed-Ali V, Goodrick S, Rawesh A,
et al.
:
Subcutaneous
adipose tissue releases interleukin-6, but not tumor
necrosis factor-alpha, in vivo. J Clin Endocrinol Metab
1997,
82:
4196–4200.
27. Ridker PM:
Novel risk factors and markers for coronary
disease. Adv Intern Med
2000,
45:
391–418.
28. Lakka HM, Lakka TA, Tuomilehto J, Salonen JT:
Abdominal
obesity is associated with increased risk of acute coronary
events in men. Eur Heart J
2002,
23:
706–713.
29. Bogaty P, Poirier P, Simard S,
et al.
:
Biological profiles in
subjects with recurrent acute coronary events compared with
subjects with long-standing stable angina. Circulation
2001,
103:
3062–3068.
30. Bogaty P, Robitaille NM, Solymoss S,
et al.
:
Atherogenic,
hemostatic, and other potential risk markers in subjects
with previous isolated myocardial infarction compared with
long- standing uncomplicated stable angina. Am Heart J
1998,
136:
884–893.
31. Alberti KG, Zimmet PZ:
Definition, diagnosis and classifi-
cation of diabetes mellitus and its complications. Part 1:
diagnosis and classification of diabetes mellitus provisional
report of a WHO consultation. Diabetes Med
1998,
15:
539–553.
32. Isomaa B, Almgren P, Tuomi T,
et al.
:
Cardiovascular morbidity
and mortality associated with the metabolic syndrome.
Diabetes Care
2001,
24:
683–689.
33.•• Ford ES, Giles WH, Dietz WH:
Prevalence of the metabolic
syndrome among US adults: findings from the third National
Health and Nutrition Examination Survey.
JAMA
2002,
287:
356–359.
Analysis of data on 8814 men and women aged 20 years or older from
the Third National Health and Nutrition Examination Survey (1988
to 1994) to determine the prevalence of the metabolic syndrome.
34. Pyorala M, Miettinen H, Laakso M, Pyorala K:
Hyperin-
sulinemia predicts coronary heart disease risk in healthy
middle- aged men: the 22-year follow-up results of the
Helsinki Policemen Study. Circulation
1998,
98:
398–404.
35. Després JP, Lamarche B, Mauriege P,
et al.
:
Hyperinsulinemia
as an independent risk factor for ischemic heart disease.
N Engl J Med
1996,
334:
952–957.
36. Clinical Guidelines on the Identification, Evaluation, and
Treatment of Overweight and Obesity in Adults—The Evidence
Report.
National Institutes of Health. Obes Res
1998,
2(suppl):
51S–209S.
37. Williams IL, Wheatcroft SB, Shah AM, Kearney MT:
Obesity,
atherosclerosis and the vascular endothelium: mechanisms
of reduced nitric oxide bioavailability in obese humans.
Int J Obes Relat Metab Disord
2002,
26:
754–764.
38. McGill HC:
Fatty streaks in the coronary arteries and aorta.
Lab Invest
1968,
18:
560–564.
39. Skalen K, Gustafsson M, Rydberg EK,
et al.
:
Subendothelial
retention of atherogenic lipoproteins in early atherosclero-
sis. Nature
2002,
417:
750–754.
40. McGill HC Jr, McMahan CA, Herderick EE,
et al.
:
Origin of
atherosclerosis in childhood and adolescence. Am J Clin Nutr
2000,
72:
1307S–1315S.
41. Berenson GS:
Bogalusa Heart Study: a long-term community
study of a rural biracial (Black/White) population. Am J Med
Sci
2001,
322:
293–300.
Obesity and Cardiovascular Disease • Poirier and Eckel 453
42. Enos WF, Holmes RH, Beyer J:
Coronary disease among
United States soldiers killed in action in Korea.
JAMA
1953,
152:
1090–1093.
43. McGill HC, McMahan CA, Malcom GT, Oalmann MC,
Strong JP:
Relation of glycohemoglobin and adiposity to
atherosclerosis in youth. Pathobiological Determinants
of Atherosclerosis in Youth (PDAY) Research Group.
Arterioscler Thromb Vasc Biol
1995,
15:
431–440.
44.• Zieske AW, Malcom GT, Strong JP:
Natural history and risk
factors of atherosclerosis in children and youth: the PDAY
study. Pediatr Pathol Mol Med
2002,
21 :
213–237.
An overview of the main data generated from the Pathobiological
Determinants of Atherosclerosis in Youth (PDAY) study.
45.•• McGill HC Jr, McMahan CA, Herderick EE,
et al.
:
Obesity
accelerates the progression of coronary atherosclerosis
in young men. Circulation
2002,
105:
2712–2718.
The Pathobiological Determinants of Atherosclerosis in Youth study
collected arteries, blood, and other tissue from approximately 3000
persons aged 15 to 34 years who died of external causes and were
autopsied in forensic laboratories. The investigators measured gross
atherosclerotic lesions in the right coronary artery, American Heart
Association lesion grade in the left anterior descending coronary
artery, serum lipid concentrations, serum thiocyanate (for smoking),
intimal thickness of renal arteries (for hypertension), glycohemo-
globin (for hyperglycemia), and adiposity by body mass index
and thickness of the panniculus adiposus.
46. McGill HC, McMahan CA, Zieske AW,
et al.
:
Association
of coronary heart disease risk factors with microscopic
qualities of coronary atherosclerosis in youth. Circulation
2000,
102:
374–379.
47. Hubert HB, Feinleib M, McNamara PM, Castelli WP:
Obesity
as an independent risk factor for cardiovascular disease:
a 26-year follow-up of participants in the Framingham Heart
Study. Circulation
1983,
67:
968–977.
48. Eckel RH:
Obesity and heart disease: a statement for
healthcare professionals from the Nutrition Committee,
American Heart Association. Circulation
1997,
96:
3248–3250.
49. Deckelbaum RJ, Williams CL:
Childhood obesity: the
health issue. Obes Res
2001,
9(suppl 4):
239S–243S.
50. James PT, Leach R, Kalamara E, Shayeghi M:
The worldwide
obesity epidemic. Obes Res
2001,
9(suppl 4):
228S–233S.
51. Freedman DS, Khan LK, Dietz WH, Srinivasan SR, Berenson GS:
Relationship of childhood obesity to coronary heart disease
risk factors in adulthood: the Bogalusa Heart Study. Pediatrics
2001,
108:
712–718.
52. Holman RL:
Atherosclerosis—a pediatric nutrition problem?
Am J Clin Nutr
1961,
9:
565–569.
53. Poirier P, Després JP:
Exercise in weight management
of obesity. Cardiol Clin
2001,
19:
459–470.
54.•• Morrison JA, James FW, Sprecher DL, Khoury PR, Daniels SR:
Sex and race differences in cardiovascular disease risk factor
changes in schoolchildren, 1975–1990: the Princeton
School Study. Am J Public Health
1999,
89:
1708–1714.
Study undertaken to assess changes in obesity and risk factors
for cardiovascular disease in black and white children from
1975 through 1990.
55. Morrison JA, Barton BA, Biro FM, Daniels SR, Sprecher DL:
Overweight, fat patterning, and cardiovascular disease risk
factors in black and white boys. J Pediatr
1999,
135:
451–457.
56. Otsuka Y, Miyazaki S, Okumura H,
et al.
:
Abnormal glucose
tolerance, not small vessel diameter, is a determinant
of long-term prognosis in patients treated with balloon
coronary angioplasty. Eur Heart J
2000,
21 :
1790–1796.
57. Korpilahti K, Syvanne M, Engblom E,
et al.
:
Components
of the insulin resistance syndrome are associated with
progression of atherosclerosis in non-grafted arteries
5 years after coronary artery bypass surgery. Eur Heart J
1998,
19:
711–719.
58. Eisenstein EL, Shaw LK, Nelson CL,
et al.
:
Obesity and
long-term clinical and economic outcomes in coronary
artery disease patients. Obes Res
2002,
10:
83–91.
59. Gruberg L, Weissman NJ, Waksman R,
et al.
:
The impact
of obesity on the short-term and long-term outcomes after
percutaneous coronary intervention: the obesity paradox?
J Am Coll Cardiol
2002,
39:
578–584.
60. Marik P, Varon J:
The obese patient in the ICU. Chest
1998,
113:
492–498.
61. Moulton MJ, Creswell LL, Mackey ME, Cox JL, Rosenbloom M:
Obesity is not a risk factor for significant adverse outcomes
after cardiac surgery. Circulation
1996,
94:
II87–II92.
62. Birkmeyer NJ, Charlesworth DC, Hernandez F,
et al.
:
Obesity
and risk of adverse outcomes associated with coronary artery
bypass surgery. Northern New England Cardiovascular
Disease Study Group. Circulation
1998,
97:
1689–1694.
63. Tenkanen L, Manttari M, Manninen V:
Some coronary risk fac-
tors related to the insulin resistance syndrome and treatment
with gemfibrozil. Experience from the Helsinki Heart Study.
Circulation
1995,
92:
1779–1785.
64. Bloomfield Rubins H, Davenport J, Babikian V,
et al
.:
Reduction
in stroke with gemfibrozil in men with coronary heart
disease and low HDL cholesterol: The Veterans Affairs HDL
Intervention Trial (VA-HIT). Circulation
2001,
103:
2828–2833.
65. Gu K, Cowie CC, Harris MI:
Diabetes and decline in heart
disease mortality in US adults. JAMA
1999,
281:
1291–1297.
66. Knowler WC, Barrett-Connor E, Fowler SE,
et al.
:
Reduction
in the incidence of type 2 diabetes with lifestyle intervention
or metformin. N Engl J Med
2002,
346:
393–403.
67. Tuomilehto J, Lindstrom J, Eriksson JG,
et al.
:
Prevention
of type 2 diabetes mellitus by changes in lifestyle among
subjects with impaired glucose tolerance. N Engl J Med
2001,
344:
1343–1350.
68. Ziccardi P, Nappo F, Giugliano G,
et al.
:
Reduction of
inflammatory cytokine concentrations and improvement
of endothelial functions in obese women after weight loss
over one year. Circulation
2002,
105:
804–809.
69. Tchernof A, Nolan A, Sites CK, Ades PA, Poehlman ET:
Weight loss reduces C-reactive protein levels in obese
postmenopausal women. Circulation
2002,
105:
564–569.
70. Heilbronn LK, Noakes M, Clifton PM:
Energy restriction
and weight loss on very-low-fat diets reduce C- reactive
protein concentrations in obese, healthy women. Arterioscler
ThrombVasc Biol
2001,
21 :
968–970.
... existing data suggest that it has reached an alarming rate (1,34). It presents a major challenge to physicians and public health agencies (24). Obesity plays a central role in metabolic syndrome and leads to the development of chronic diseases (2). a recent study in tehran showed an estimated prevalence of more than 30% in adults. ...
... In our study, the Ms-related factors of blood lipid composition were not affected. Obesity and Ms have been known to be common and important clinical markers for early detection of cV disease and type 2 diabetes (12); Risk factors for Ms include higher tg levels (R150 mg/dl), lower HDL levels (<50 mg/dl for women), high blood pressure (R130/80 mm Hg), high fasting blood glucose levels (R100 mg/dl), and a large Wc (R88cm for women) (24). several previous studies have reported that aerobic exercise significantly improves Ms-related factors of blood lipid composition (25,26). ...
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To the Editor: In a recent article, Pyorala et al1 have stated that hyperinsulinemia/area under the plasma insulin response curve (AUC insulin) during an oral glucose tolerance test (OGTT) was a statistically significant predictor of coronary heart disease (CHD) risk over the 22-year follow-up in the Helsinki Policemen Study. In addition, the authors had another interesting observation that AUC glucose also predicted CHD risk in the first 5 years of follow-up. However, subjects with diabetes mellitus were excluded, and it would seem that subjects with impaired glucose tolerance (IGT) might have been involved in the study. Besides plasma cholesterol level, AUC glucose was the only significant independent predictor of CHD risk during this period. To assess major risk factors and to provide secondary prevention for patients with recent myocardial infarction, we performed OGTTs in 28 patients free of diabetes who had a fasting plasma glucose level <6.1 mmol/L (23 males, 5 females). Thirteen patients had IGT based on the 2-hour postload glucose level (≥7.8 mmol/L). Fifteen patients had normal glucose tolerance (NGT) according to World Health Organization and American Diabetes …
Article
Context.— Obesity is a well-established risk factor for coronary heart disease (CHD), but whether regional fat distribution contributes independently to risk remains unclear.Objective.— To compare waist-hip ratio (WHR) and waist circumference in determining risk of CHD in women.Design and Setting.— Prospective cohort study among US female registered nurses participating in the Nurses' Health Study conducted between 1986, when the nurses completed a questionnaire, and follow-up in June 1994.Participants.— A total of 44,702 women aged 40 to 65 years who provided waist and hip circumferences and were free of prior CHD, stroke, or cancer in 1986.Main Outcome Measures.— Incidence of CHD (nonfatal myocardial infarction or CHD death).Results.— During 8 years of follow-up 320 CHD events (251 myocardial infarctions and 69 CHD deaths) were documented. Higher WHR and greater waist circumference were independently associated with a significantly increased age-adjusted risk of CHD. After adjusting for body mass index (BMI) (defined as weight in kilograms divided by the square of height in meters) and other cardiac risk factors, women with a WHR of 0.88 or higher had a relative risk (RR) of 3.25 (95% confidence interval [CI], 1.78-5.95) for CHD compared with women with a WHR of less than 0.72. A waist circumference of 96.5 cm (38 in) or more was associated with an RR of 3.06 (95% CI, 1.54-6.10). The WHR and waist circumference were independently strongly associated with increased risk of CHD also among women with a BMI of 25 kg/m2 or less. After adjustment for reported hypertension, diabetes, and high cholesterol level, a WHR of 0.76 or higher or waist circumference of 76.2 cm (30 in) or more was associated with more than a 2-fold higher risk of CHD.Conclusions.— The WHR and waist circumference are independently associated with risk of CHD in women.
Article
Context Mortality from coronary heart disease has declined substantially in the United States during the past 30 years. However, it is unknown whether patients with diabetes have also experienced a decline in heart disease mortality. Objective To compare adults with diabetes with those without diabetes for time trends in mortality from all causes, heart disease, and ischemic heart disease. Design, Setting, and Participants Representative cohorts of subjects with and without diabetes were derived from the First National Health and Nutrition Examination Survey (NHANES I) conducted between 1971 and 1975 (n=9639) and the NHANES I Epidemiologic Follow-up Survey conducted between 1982 and 1984 (n=8463). The cohorts were followed up prospectively for mortality for an average of 8 to 9 years. Main Outcome Measure Changes in mortality rates per 1000 person-years for all causes, heart disease, and ischemic heart disease for the 1982-1984 cohort compared with the 1971-1975 cohort. Results For the 2 periods, nondiabetic men experienced a 36.4% decline in age-adjusted heart disease mortality compared with a 13.1% decline for diabetic men. Age-adjusted heart disease mortality declined 27% in nondiabetic women but increased 23% in diabetic women. These patterns were also found for all-cause mortality and ischemic heart disease mortality. Conclusions The decline in heart disease mortality in the general US population has been attributed to reduction in cardiovascular risk factors and improvement in treatment of heart disease. The smaller declines in mortality for diabetic subjects in the present study indicate that these changes may have been less effective for people with diabetes, particularly women.
Article
In a cooperative multicenter study (Pathobiological Determinants of Atherosclerosis in Youth, PDAY) of 1532 young persons 15 through 34 years of age who died of external causes and were autopsied in medical examiners’ laboratories, we quantified atherosclerosis of the aorta and the right coronary artery. We analyzed postmortem blood cells for glycohemoglobin and postmortem serum for lipoprotein cholesterol and thiocyanate (as an indicator for smoking). We measured the thickness of the panniculus adiposus and the body mass index (weight per height squared) as indicators of adiposity. Glycohemoglobin levels exceeding 8% were associated with substantially more extensive fatty streaks and raised lesions in the right coronary artery in persons more than 25 years of age and with more extensive raised lesions in the aorta in persons more than 30 years of age. Both thickness of the panniculus adiposus and body mass index were associated with more extensive fatty streaks and raised lesions in the right coronary artery. The associations of atherosclerotic lesions with glycohemoglobin and adiposity were not explained by a less favorable lipoprotein profile or smoking. The results show that atherosclerosis in young adults is associated with the prediabetic or early diabetic state, as indicated by elevated glycohemoglobin levels, and with obesity.
Article
Context The Third Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (ATP III) highlights the importance of treating patients with the metabolic syndrome to prevent cardiovascular disease. Limited information is available about the prevalence of the metabolic syndrome in the United States, however.Objective To estimate the prevalence of the metabolic syndrome in the United States as defined by the ATP III report.Design, Setting, and Participants Analysis of data on 8814 men and women aged 20 years or older from the Third National Health and Nutrition Examination Survey (1988-1994), a cross-sectional health survey of a nationally representative sample of the noninstitutionalized civilian US population.Main Outcome Measures Prevalence of the metabolic syndrome as defined by ATP III (≥3 of the following abnormalities): waist circumference greater than 102 cm in men and 88 cm in women; serum triglycerides level of at least 150 mg/dL (1.69 mmol/L); high-density lipoprotein cholesterol level of less than 40 mg/dL (1.04 mmol/L) in men and 50 mg/dL (1.29 mmol/L) in women; blood pressure of at least 130/85 mm Hg; or serum glucose level of at least 110 mg/dL (6.1 mmol/L).Results The unadjusted and age-adjusted prevalences of the metabolic syndrome were 21.8% and 23.7%, respectively. The prevalence increased from 6.7% among participants aged 20 through 29 years to 43.5% and 42.0% for participants aged 60 through 69 years and aged at least 70 years, respectively. Mexican Americans had the highest age-adjusted prevalence of the metabolic syndrome (31.9%). The age-adjusted prevalence was similar for men (24.0%) and women (23.4%). However, among African Americans, women had about a 57% higher prevalence than men did and among Mexican Americans, women had about a 26% higher prevalence than men did. Using 2000 census data, about 47 million US residents have the metabolic syndrome.Conclusions These results from a representative sample of US adults show that the metabolic syndrome is highly prevalent. The large numbers of US residents with the metabolic syndrome may have important implications for the health care sector.
Article
Background— Obesity is a risk factor for adult coronary heart disease and is increasing in prevalence among youths as well as adults. Results regarding the association of obesity with atherosclerosis are conflicting, particularly when analyses account for other risk factors. Methods and Results— The Pathobiological Determinants of Atherosclerosis in Youth (PDAY) study collected arteries, blood, and other tissue from ≈3000 persons aged 15 to 34 years dying of external causes and autopsied in forensic laboratories. We measured gross atherosclerotic lesions in the right coronary artery (RCA), American Heart Association (AHA) lesion grade in the left anterior descending coronary artery (LAD), serum lipid concentrations, serum thiocyanate (for smoking), intimal thickness of renal arteries (for hypertension), glycohemoglobin (for hyperglycemia), and adiposity by body mass index (BMI) and thickness of the panniculus adiposus. BMI in young men was associated with both fatty streaks and raised lesions in the RCA and with AHA grade and stenosis in the LAD. The effect of obesity (BMI>30 kg/m²) on RCA raised lesions was greater in young men with a thick panniculus adiposus. Obesity was associated with non-HDL and HDL (inversely) cholesterol concentrations, smoking (inversely), hypertension, and glycohemoglobin concentration, and these variables accounted for ≈15% of the effect of obesity on coronary atherosclerosis in young men. BMI was not associated with coronary atherosclerosis in young women although there was trend among those with a thick panniculus adiposus. Conclusions— Obesity is associated with accelerated coronary atherosclerosis in adolescent and young adult men. These observations support the current emphasis on controlling obesity to prevent adult coronary heart disease.
Article
Objective. —To test the hypothesis that both body mass index (expressed as the ratio of weight in kilograms per height in meters squared) and the ratio of waist circumference to hip circumference are positively associated with mortality risk in older women. Design. —Prospective cohort study with a 5-year follow-up period. Setting. —General community. Participants. —Random sample of 41 837 Iowa women aged 55 to 69 years. Main Outcome Measure. —Total mortality (1504 deaths). Main Results. —Body mass index, an index of relative weight, was associated with mortality in a J-shaped fashion: rates were elevated in the leanest as well as in the most obese women. In contrast, waist/hip circumference ratio was strongly and positively associated with mortality in a dose-response manner. Adjusted for age, body mass index, smoking, education level, marital status, estrogen use, and alcohol use, a 0.15-unit increase in waist/hip circumference ratio (eg, a 15-cm [6-in] increase in waist measurement in a woman with 100-cm [40-in] hips) was associated with a 60% greater relative risk of death. The observed associations were not explained to any great degree by bias from weight loss prior to baseline or higher early deaths among lean participants. Conclusions. —Waist/hip circumference ratio is a better marker than body mass index of risk of death in older women. Waist/hip circumference ratio should be measured as part of routine surveillance and risk monitoring in medical practice.JAMA. 1993;269:483-487)
Article
The purpose of this paper is to describe and analyze the gross lesions found in the coronary arteries of United States soldiers killed in action in Korea. The histology will be discussed in detail in a subsequent paper as will such pertinent data as race, body build, and personal habits.MATERIAL Recently 300 autopsies were performed on United States battle casualties in Korea. Most of these soldiers were killed in action or suffered accidental death in front line areas. The coronary arteries were carefully dissected in all cases. No case in which there was known clinical evidence of coronary disease was included in this series. The average age in 200 cases was 22.1 years. The ages in the first 98 cases were not recorded except that the oldest patient was 33. In the entire series, the youngest recorded age was 18 and the oldest 48.