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At least 19 recordsLinked to original sources

PubMed1992

Inheritability of atherosclerosis and the role of lipoproteins as risk factors in the development of atherosclerosis in WHHL rabbits: risk factors related to coronary atherosclerosis are different from those related to aortic atherosclerosis.

Inheritability of atherosclerosis and the influences of serum lipids on atherosclerosis were examined by following its progression in selectively bred WHHL rabbits. Our studies indicate (1) coronary atherosclerosis is clearly inherited from parents by offspring whereas inheritability of aortic atherosclerosis is uncertain; (2) coronary stenosis is positively correlated to serum cholesterol level, although the correlation coefficient is markedly low: in contrast, no relationship between serum lipid levels and aortic atherosclerosis was observed; (3) cholesterol-rich VLDL showed atherogenicity in aorta, but not in coronary arteries; (4) an unknown lipoprotein detected by 3.6% polyacrylamide gel electrophoresis was related to coronary atherosclerosis, although no relationship between the unknown lipoprotein and aortic atherosclerosis was observed. These findings suggest that there are two types of genetic factors involved in atherosclerosis, one of which is unique to coronary atherosclerosis whereas the other is related to only aortic atherosclerosis.

Animals↗

PubMed1995

Reversibility of atherosclerosis--evolving perspectives from two arterial imaging clinical trials: the cholesterol lowering atherosclerosis regression study and the monitored atherosclerosis regression study.

The Cholesterol Lowering Atherosclerosis Study (CLAS) and the Monitored Atherosclerosis Regression Study (MARS) are serial arterial imaging clinical trials that have explored the reversibility of atherosclerosis with lipid-lowering therapy in native coronary, carotid, and femoral arterial beds, as well as in coronary artery bypass grafts. Results demonstrate that progression of atherosclerosis can be reduced in all these vascular beds. Evolving data indicate that coronary lesions > or = 50% diameter stenosis (%S) at baseline respond more readily to lipid-lowering therapy than lesions <50%S. In addition, lipoproteins may have a differential effect on coronary lesion progression according to lesion size, with triglyceride-rich lipoproteins playing an important role in the progression of lesions <50%S. Limited data indicate that progression of atherosclerosis in women may be more responsive to lipid-lowering therapy than in men, and that estrogen replacement may enhance the anti-atherosclerosis effects of lipid lowering. Longitudinal measurements of carotid artery far wall intima-media thickness (IMT) with B-mode ultrasonography in CLAS and MARS indicate that carotid atherosclerosis at a stage before lesions intrude into the vessel lumen can be reduced by lipid-lowering therapy. Together, CLAS and MARS data indicate that the spectrum from very early lesions confined to the arterial wall to established lesions late in the atherosclerotic process can be reversed with lipid-lowering therapy.

Angiography↗

PubMed1982

Effect of cholesterol feeding on serum lipoproteins and atherosclerosis in atherosclerosis-susceptible and atherosclerosis-resistant Japanese quail.

Male and female Japanese quail from two strains bred for differing susceptibility to induction of atherosclerosis by dietary cholesterol (RES = resistant, SUS = susceptible) were fed a control diet or control diet + .5% USP cholesterol. The diets were fed for 20 weeks beginning when the quail were 7 weeks old. Only quail fed cholesterol developed atherosclerosis. Atherosclerosis (incidence and severity) was higher in males than females and higher in SUS than RES. Cholesterol feeding increased aortic, liver, and serum cholesterol concentrations and liver total fat content. There were high positive correlations between serum cholesterol and liver cholesterol in all cholesterol-fed groups but not in control groups. Diet, sex, and strain differences in cholesterol distribution among the various serum lipoproteins and ratios of beta/alpha lipoproteins were observed. These differences are discussed in terms of their usefulness in predicting atherosclerosis in quail as compared with humans.

Animals↗

PubMedDate not supplied

[Prevention of coronary atherosclerosis: (IV): Prevalence of aortic atherosclerosis in Mexico, D.F. Its relation to coronary atherosclerosis].

The severity and prevalence of coronary and aortic atherosclerosis was studied in 174 subjects who died from violent causes in Mexico City. As in other geographic areas, fatty streaks were found early in life (12 years old). Fibrolipid plaques were present in the thoracic aorta at age 15 and at age 19 in the abdominal segment. Complicated lesions were detected in the aorta after age 25. Because of the obvious clinical significance we looked for severe aortic lesions in the abdominal bifurcation. The prevalence of severe lesions in the bifurcation was 0 between 15 to 24 years and raised to 23.3% in the 45-54 age group. A moderate correlation was found between the severity of coronary and aortic lesions. The discordance most often found was the presence of severe coronary lesions without severe aortic involvement.

Adolescent↗

PubMed1995

Age-related differences in the distribution of peripheral atherosclerosis: when is atherosclerosis truly premature?

BACKGROUND: The natural history of peripheral atherosclerosis in young adults appears to be unfavorable compared with that in older patients. No universally accepted definition of "premature" atherosclerosis exists, however, making comparison of clinical studies difficult. This study examined age-related differences in distribution of atherosclerotic lesions and determined an age threshold at which such differences became apparent. Such a threshold may provide a definition of premature atherosclerosis. METHODS: Arteriograms of all patients 49 years of age and younger undergoing evaluation of lower extremity ischemia during the past 5 years were reviewed and the findings were tabulated. Medical records were reviewed to obtain demographic data, assess risk factors, and confirm disease etiology. Exclusion criteria included normal arteriograms (three patients), history of acute or remote trauma (six patients), unclear cause of ischemic symptoms (three patients), arteritis (four patients), aneurysmal disease (one patient), and acute ischemia without prior chronic symptoms (12 patients). For comparison we also reviewed arteriograms performed during the same period in 140 patients older than 50 years of age who had chronic lower extremity ischemia caused by atherosclerosis. RESULTS: The mean age of the 59 study patients was 43.4 +/- 5.8 years (median age, 46 years; range, 25 to 49 years). Arteriograms were available in all cases; medical records were available in 54 (92%). Atherosclerosis involved only the aortoiliac segment in 25 patients (42%), the femoropopliteal-tibial arteries alone in 21 (36%), and both levels in 13 (22%). Patients with distal atherosclerosis had a higher prevalence of diabetes than those with proximal atherosclerosis (p = 0.004). Ninety-two (66%) of the 140 patients older than 50 years of age had atherosclerosis confined to a single arterial segment, which was not significantly different from the prevalence of single-level disease in the study group. However, 25 (54%) of the 46 study patients with single-level atherosclerosis had aortoiliac disease compared with only 15 (16%) of 92 patients older than 50 years of age with single-level disease (p < 0.001). CONCLUSIONS: In contrast to the pattern of disease in older adults, atherosclerosis in young, nondiabetic patients most commonly involves the aortoiliac segment. Differences in lesion distribution become increasingly apparent with age but are most striking between those 49 years of age and younger and those 50 years of age and older. Accordingly, we propose that premature peripheral atherosclerosis be defined as beginning at or before the age of 49 years.

Adult↗

PubMed2002

Is insulin sensitivity a causal intermediate in the relationship between alcohol consumption and carotid atherosclerosis?: the insulin resistance and atherosclerosis study.

OBJECTIVE: A J-shaped association has been demonstrated between alcohol consumption and atherosclerosis. Insulin resistance, also a risk factor for atherosclerosis, has been shown to have a similar J-shaped association with alcohol intake. This raises the question of whether insulin sensitivity (S(I)) is a causal intermediate in the alcohol-atherosclerosis relationship. RESEARCH DESIGN AND METHODS: The Insulin Resistance Atherosclerosis Study was a multicenter cohort study designed to investigate relationships among S(I), risk factors for cardiovascular disease, and carotid artery atherosclerosis. Using regression analysis, we tested whether adjustment for S(I) attenuated the alcohol-atherosclerosis relationship observed at baseline. RESULTS: A J-shaped association was observed between alcohol consumption and common carotid artery intimal medial thickness. The protective aspect of the alcohol-atherosclerosis relationship was attenuated by 25% after the adjustment for S(I). However, an interaction was observed between alcohol consumption and glucose tolerance (GT) status. In comparison with never drinkers, all levels of alcohol consumption were associated with less atherosclerosis in participants with normal GT status. Participants with impaired GT status (but not diabetes) demonstrated a J-shaped alcohol-atherosclerosis association. All levels of alcohol consumption were associated with more atherosclerosis in participants with diabetes. CONCLUSIONS: S(I) may be a causal intermediate at protective levels of alcohol intake, but an alcohol-GT interaction precluded a definitive conclusion. Moderate alcohol consumption may increase the risk of atherosclerosis in people with diabetes. These findings contrast with previous reports and do not support current recommendations regarding moderate alcohol consumption in people with diabetes. More research is needed to clarify this issue.

Adult↗

PubMed1982

Pulmonary artery atherosclerosis: correlation with systemic atherosclerosis and hypertensive pulmonary vascular disease.

Atherosclerosis of the pulmonary arteries is a common autopsy finding and is associated with a variety of clinical conditions. To delineate the morphologic changes associated with pulmonary artery atherosclerosis, autopsies of 337 consecutive adults (greater than 15 years of age) were studied. For each, 35 features were studied, including age, coronary vascular disease, cardiac chamber hypertrophy and dilation, pulmonary artery and aortic atherosclerosis, and pulmonary thromboemboli and emphysema. These were compared using correlation coefficients and forward and backward stepwise regression procedures for selected variables. Pulmonary artery atherosclerosis correlated significantly with age, right ventricular dilation and hypertrophy, pulmonary emphysema, and aortic atherosclerosis. Regional evaluations of systemic and pulmonary atherosclerosis showed highly significant internal correlations. In the ligamentum arteriosum, the intensity of atherosclerosis over the aortic insertion correlated with the severity of a similar atheroma at the pulmonary artery insertion. With the multiple-regression procedure, pulmonary artery atherosclerosis was a significant predictor of aortic atherosclerosis, right ventricular hypertrophy, and pulmonary embolization. Our study shows that pulmonary embolization. Our study shows that pulmonary embolization. Our study shows that pulmonary artery atherosclerosis is accelerated in patients with atherosclerosis of the systemic arteries and the pathologic lesions associated with hypertensive pulmonary vascular disease.

Adolescent↗

PubMed1998

Cigarette smoking and progression of atherosclerosis: The Atherosclerosis Risk in Communities (ARIC) Study.

CONTEXT: Cigarette smoking is a powerful risk factor for incident heart disease and stroke, but the relationship of active and passive smoking with the progression of atherosclerosis has not been described. OBJECTIVE: To examine the impact of active smoking and exposure to environmental tobacco smoke (ETS) on the progression of atherosclerosis. DESIGN: A longitudinal assessment of the relationship between smoking exposure evaluated at the initial visit and the 3-year change in atherosclerosis. SETTING: A population-based cohort of middle-aged adults from 4 communities in the United States. PARTICIPANTS: A total of 10914 participants from the Atherosclerosis Risk in Communities (ARIC) study enrolled between 1987 and 1989. MAIN OUTCOME MEASURE: Change in atherosclerosis from baseline to the 3-year follow-up as indexed by intimal-medial thickness of the carotid artery assessed by ultrasound and adjusted for demographic characteristics, cardiovascular risk factors, and lifestyle variables. RESULTS: Exposure to cigarette smoke was associated with progression of atherosclerosis. Relative to never smokers and after adjustment for demographic characteristics, cardiovascular risk factors, and lifestyle variables, current cigarette smoking was associated with a 50% increase in the progression of atherosclerosis (mean progression rate over 3 years, 43.0 microm for current and 28.7 microm for never smokers, regardless of ETS exposure), and past smoking was associated with a 25% increase (mean progression rate over 3 years, 35.8 microm for past smokers and 28.7 microm for never smokers). Relative to those not exposed to ETS, exposure to ETS was associated with a 20% increase (35.2 microm for those exposed to ETS vs 29.3 microm for those not exposed). The impact of smoking on atherosclerosis progression was greater for subjects with diabetes and hypertension. Although more pack-years of exposure was independently associated with faster progression (P<.001), after controlling for the number of pack-years, the progression rates of current and past smokers did not differ (P=.11). CONCLUSIONS: Both active smoking and ETS exposure are associated with the progression of an index of atherosclerosis. Smoking is of particular concern for patients with diabetes and hypertension. The fact that pack-years of smoking but not current vs past smoking was associated with progression of atherosclerosis suggests that some adverse effects of smoking may be cumulative and irreversible.

Arteriosclerosis↗

PubMed1997

Interaction of family history of atherosclerosis with atherogenic lipid traits in men with non-coronary atherosclerosis.

Family history of atherosclerosis has been recognised as an nonmodifiable cardiovascular risk factor. Lipid levels, together with hypertension and diabetes, appear to have an inheritable component. The aim of the study was to ascertain whether lipoprotein abnormalities of 169 adult patients with non-coronary atherosclerosis were associated with a family history of atherosclerosis. Besides intermediate density lipopoprotein composition and Lp(a) levels, we focused on apo(a) and apo E phenotypes, LDL cholesterol/apo B ratio, VLDL triglyceride/HDL cholesterol ratio, and environmental factors. We found that patients with a family history of atherosclerosis had a higher prevalence of VLDL triglyceride/HDL cholesterol ratio above 1.8 (51.3% vs 34.7%) than patients without. Similarly, there was a significant inverse correlation between both considered ratios (r = -0.24, p < 0.05). The odds ratio of the presence of both abnormal ratios (4.60, 95% CI, 1.41-15.00) and low molecular weight apo(a) isoforms (3.30, 95% CI, 1.05-10.30 and family history of atherosclerosis was independent of smoking and hypertension. Apo(a) isoform size seems to be more important than Lp(a) concentrations in the family history of atherosclerosis risk determination. Subsequent analysis showed that patients with a family history of atherosclerosis had a greater-than-fourfold increased risk of having one or both abnormal ratios reflecting metabolic disturbances which probably constitute a combined trait. Family history of atherosclerosis may constitute a specific lipoprotein-related marker of atherosclerosis. Such a marker often precedes the onset of overt disease and may contribute to identifying patients with an atherogenic lipoprotein profile even in the absence of classical lipid risk factors.

Adult↗

PubMed1995

Effects of androgens on coronary artery atherosclerosis and atherosclerosis-related impairment of vascular responsiveness.

The factors responsible for the marked gender differences in risk of coronary heart disease and atherosclerosis severity remain largely undetermined. While some clinical and experimental evidence supports a protective effect of endogenous estrogen on the initiation and progression of atherosclerosis and incidence of coronary heart disease, much of the epidemiological data do not support this conclusion. The possibility that endogenous androgens may have adverse effects on atherosclerosis progression and coronary risk has received little attention. We investigated the effects of experimentally induced hyperandrogenism in female cynomolgus monkeys with diet-induced atherosclerosis. Animals were assigned randomly to one of four treatment groups: (1) untreated controls, (2) ovariectomized (sex hormone-deficient) controls, (3) treated with androstenedione and estrone (mild hyperandrogenism), or (4) treated with testosterone (male plasma androgen pattern). At necropsy, coronary atherosclerosis was approximately twice as extensive (P < .05) in testosterone-treated animals relative to untreated controls, while treatment with androstenedione and estrone had no effect on atherosclerosis extent. Coronary plaque size was positively correlated with lumen size in intact and ovariectomized controls; however, there was no evidence of a similar relation between animals in either androgen treatment group. The atherogenic effects of testosterone were independent of variations in plasma lipoprotein and nonlipoprotein risk variables. Although chronic hyperandrogenism had adverse effects on atherosclerosis progression, it reversed (P < .03) atherosclerosis-related impairment of endothelium-dependent vasodilator responses. We conclude that an experimentally induced male plasma androgen pattern results in exacerbation of diet-induced atherosclerosis-related arterial remodeling in female monkeys.(ABSTRACT TRUNCATED AT 250 WORDS)

Androgens↗

PubMed1950

The effect of alloxan diabetes on experimental cholesterol atherosclerosis in the rabbit. III. The mechanism of the inhibition of experimental cholesterol atherosclerosis in alloxan-diabetic rabbits.

A study of the serum lipids in normal and alloxan-diabetic rabbits during the course of cholesterol feeding is presented, particular attention being paid to the factors considered to be responsible for the stability of the serum lipids; namely, (1) their interrelations and (2) their association with the serum proteins. As far as the interrelations of the lipids were concerned a definite correlation was found between the development of atherosclerosis and an increase of serum cholesterol that was out of all proportion to the increase of serum lipid phosphorus and neutral fat. When these last two lipid constituents rose almost parallel with the serum cholesterol (as they did in some alloxan-diabetic rabbits), then the development of atherosclerosis was inhibited. This correlation was independent of the diabetic state, per se. It appeared likely that the marked elevation of serum neutral fat and lipid phosphorus in the diabetic animals was due to mobilization of body fat because of the disturbed carbohydrate metabolism. Because of their hydrophilic and emulsifying properties, it was thought probable that the elevation of the phospholipids was the important factor responsible for the stability of serum cholesterol. That neutral fat played a role, however, could not be denied. In normal rabbit sera, as we have previously shown, only small proportions of the lipid phosphorus and cholesterol are "readily extractable" (i.e., unattached or only loosely attached to protein). On the other hand, in every case in which the serum lipids were elevated, the greater proportion of the lipid phosphorus and cholesterol was "readily extractable," irrespective of whether atherosclerosis developed or was inhibited. Analysis of the lipid content of the aorta of rabbits not fed cholesterol, whether diabetic or non-diabetic, and from alloxan-diabetic rabbits fed cholesterol but protected from the development of atherosclerosis, showed that there was no significant difference in lipid content or composition among the animals of these groups. When atherosclerosis developed following cholesterol feeding, the lipid composition of the aortas was essentially the same in both control and diabetic animals. The deposited lipid consisted predominantly of cholesterol with small and fairly constant proportions of other lipids that did not vary significantly regardless of the quantities of these other lipids present in the circulating blood. In the less severe lesions the proportion of ester cholesterol was greater than that of free cholesterol, but in advanced lesions the reverse was true. The following conclusions are drawn concerning the pathogenesis of experimental cholesterol atherosclerosis in the rabbit: 1. Instability of cholesterol in the blood rather than hypercholesterolemia, per se, is the general condition responsible for the deposition of this substance in the arterial walls. 2. Of the two factors considered to be responsible for the stability of the lipids in the blood, the interrelations of the lipids appear to be more important than their relation to the serum proteins, at least in so far as the development of experimental cholesterol atherosclerosis is concerned. The importance of these conclusions in relation to the pathogenesis of human atherosclerosis is discussed.

Alloxan↗

PubMed2000

Steroid sex hormones for lower limb atherosclerosis.

BACKGROUND: There is accumulating evidence that steroid sex hormones have a beneficial effect on a number of risk factors for peripheral arterial disease. OBJECTIVES: The objective of this review was to determine whether exogenous steroid sex hormones are an effective treatment for patients with lower limb atherosclerosis. SEARCH STRATEGY: The Cochrane Peripheral Vascular Diseases Group trials register was searched, together with reference lists from relevant articles and reviews obtained through searches of Embase and Medline. SELECTION CRITERIA: Randomised controlled trials of steroid sex hormones in patients with lower limb atherosclerosis were selected. DATA COLLECTION AND ANALYSIS: Both reviewers extracted data and assessed trial quality independently. Whenever possible investigators were contacted to obtain information needed for the review that could not be found in published reports. MAIN RESULTS: Four trials appeared to meet the inclusion criteria, but one was excluded because of poor methodology and another is awaiting translation into English. The two remaining trials compared testosterone treatment with placebo in a total of 83 men with intermittent claudication. No trials were available which investigated the potentially beneficial effects of oestrogenic hormones in women with lower limb atherosclerosis. Testosterone therapy produced no improvement in tests of walking distance or in a variety of other objective tests for peripheral arterial disease, including venous filling time, muscle blood flow and plethysmography. The odds ratio for subjective improvement in symptoms using the combined trial results was also non-significant (odds ratio 1.28, 95% confidence interval 0.61 to 2.65). REVIEWER'S CONCLUSIONS: There is no evidence to date that short-term testosterone treatment is beneficial in male subjects with lower limb atherosclerosis. However, this might reflect limited data rather than the lack of a real effect.

Arteriosclerosis↗

PubMed1993

Past infection by Chlamydia pneumoniae strain TWAR and asymptomatic carotid atherosclerosis. Atherosclerosis Risk in Communities (ARIC) Study Investigators.

PURPOSE: To determine whether past infection by Chlamydia pneumoniae strain TWAR is associated with asymptomatic atherosclerosis. Previous studies have linked this organism with symptomatic coronary heart disease. SUBJECTS AND METHODS: Between 1986 and 1989, 15,800 men and women aged 45 to 64 years were examined as part of the Atherosclerosis Risk in Communities Study, a prospective cohort study of atherosclerosis being conducted in 4 United States communities. The examination included B-mode ultrasonography of the carotid arteries and an assessment of cardiovascular disease risk factors. Carotid wall thickening (blood-intima to medial-adventitial interface) in the absence of clinical cardiovascular disease was considered evidence of asymptomatic atherosclerosis. In 1991, IgG antibody titers to TWAR were assayed by microimmunofluorescence in stored sera from 326 case-control pairs matched by age group, race, sex, examination period, and field center. A titer of 1:8 or higher was considered a positive TWAR antibody response. RESULTS: Seventy-three percent of atherosclerosis cases had serologic evidence of past TWAR infection versus 63% of controls (matched odds ratio 1.76; 95% confidence interval, 1.21 to 2.57). After adjustment for age, hypertension, diabetes, cigarette smoking, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, and education, the odds ratio for atherosclerosis was essentially unchanged at 2.00 (95% confidence interval, 1.19 to 3.35). The association was stronger for individuals aged 45 to 54 years than for those aged 55 to 64 years. CONCLUSION: There was a significant cross-sectional association between past TWAR infection and asymptomatic atherosclerosis. This organism may be a contributor to the pathogenesis of atherosclerosis.

Age Factors↗

PubMed2002

Atherosclerosis imaging methods: assessing cardiovascular disease and evaluating the role of estrogen in the prevention of atherosclerosis.

Various interventions for cardiovascular disease (CVD) slow or reverse the progression of atherosclerosis and reduce the risk of clinical coronary events. Although the cardiovascular benefits of hormone replacement therapy have been demonstrated in observational studies in predominantly healthy women, no benefit has been found in a randomized clinical trial conducted in older women with established CVD. It is possible that the benefit of hormone therapy occurs when it is used relatively early in the progression of atherosclerosis. Techniques are now available to monitor the various stages of atherosclerosis. Quantitative coronary angiography, a technique used to evaluate relatively late-stage atherosclerosis, has been shown to predict the risk of subsequent clinical coronary events. B-mode ultrasonography of the intima-media wall thickness (IMT) of the carotid artery can assess the earlier stages of atherosclerosis and correlates with atherosclerosis risk factors, as well as with clinical cardiovascular and cerebrovascular outcome. This technique offers a relatively rapid and cost-effective method to test therapies for CVD and to screen for individuals who are at high risk for cardiovascular events. As an example of the use of atherosclerosis imaging to evaluate possible therapeutic interventions, measurements of IMT were performed in a randomized, controlled trial comparing oral 17beta-estradiol with placebo. The results demonstrated that 17beta-estradiol significantly reduces the progression of subclinical atherosclerosis in healthy, postmenopausal women when compared with placebo.

Coronary Angiography↗

PubMed2005

Analysis of intimal proteoglycans in atherosclerosis-prone and atherosclerosis-resistant human arteries by mass spectrometry.

The propensity to develop atherosclerosis varies markedly among different sites in the human vasculature. To determine a possible cause for such differences in atherosclerosis susceptibility, a proteomics-based approach was used to assess the extracellular proteoglycan core protein composition of intimal hyperplasia from both the atherosclerosis-prone internal carotid artery and the atherosclerosis-resistant internal thoracic artery. The intimal proteoglycan composition in these preatherosclerotic lesions was found to be more complex than previously appreciated with up to eight distinct core proteins present, including the large extracellular proteoglycans versican and aggrecan, the basement membrane proteoglycan perlecan, the class I small leucine-rich proteoglycans biglycan and decorin, and the class II small leucine-rich proteoglycans lumican, fibromodulin, and prolargin/PRELP (proline arginine-rich end leucine-rich repeat protein). Although most of these proteoglycans seem to be present in similar amounts at the two locations, there was a selective enhanced deposition of lumican in the intima of the atherosclerosis-prone internal carotid artery compared with the intima of the atherosclerosis-resistant internal thoracic artery. The enhanced deposition of lumican in the intima of an atherosclerosis prone artery has important implications for the pathogenesis of atherosclerosis.

Adult↗

PubMed1997

Does the association of risk factors and atherosclerosis change with age? An analysis of the combined ARIC and CHS cohorts. The Atherosclerosis Risk in Communities (ARIC) and Cardiovascular Health Study (CHS) investigators.

INTRODUCTION: A decrease in the estimated relative risk of cerebrovascular and cardiovascular diseases associated with known disease risk factors has been observed among elderly cohorts, perhaps suggesting that continued risk factor management in the elderly may not be as efficacious as with younger age groups. In this paper, the differential magnitude of the association of risk factors with atherosclerosis across the age spectrum from 45 years to older than 75 years is presented. METHODS: Subclinical atherosclerosis as measured by carotid ultrasonography and risk factor prevalence were assessed using similar methods among participants aged 45 to 64 years in the Atherosclerosis Risk in Communities (ARIC) study and among participants 65 years and older in the Cardiovascular Health Study (CHS). Pooling these two cohorts provided data on the relationship of risk factors and atherosclerosis on nearly 19,000 participants over a broad age range. Regression analyses were used to assess the consistency of the magnitude of the association of risk factors with atherosclerosis across the age spectrum separately for black and white participants in cross-sectional analyses. RESULTS: As expected, each of the risk factors was globally (across all ages) associated with increased atherosclerosis. However, the magnitude of the association did not differ across the age spectrum for hypertension, low density lipoprotein cholesterol (LDL-c), fibrinogen, or body mass index (BMI). For whites, there was a significantly greater impact of smoking and HDL-C among older age strata but a smaller impact of diabetes. For black women, the impact of HDL-C decreased among the older age strata. CONCLUSIONS: These data suggest that most risk factors continue to be associated with increased atherosclerosis at older ages, possibly suggesting a continued value in investigation of strategies to reduce atherosclerosis by controlling risk factors at older ages.

Black or African American↗

PubMed1996

How to study the role of hypertension in atherosclerosis. Lessons from MIDAS. Multicentre Isradipine Diuretic Atherosclerosis Study.

The development of atherosclerosis is clearly linked to the level of blood pressure. This is illustrated by the difference of atheroma formation in arteries as compared to veins, the development of atherosclerosis in veins transplanted to the arterial circulation or the finding of atherosclerosis also in the pulmonary circulation as an effect of pulmonary hypertension. Several experimental studies have also illuminated the strong link between high blood pressure and the development of atherosclerosis. From a therapeutic point of view it is worth noting that the lowering of blood pressure per se has a positive effect on the development of atherosclerosis. In particular, calcium antagonists have been shown, in numerous experimental studies, to have an antiatherosclerotic effect. The positive results in animal studies led to studies in man, the first of which was the MIDAS Study. The Multicentre Isradipine Diuretic Atherosclerosis (MIDAS) Study was a comparison between the dihydropyridine-derived calcium antagonist isradipine and hydrochlorothiazide in 883 hypertensive patients. B-mode ultrasonography of the carotid artery was used in order to evaluate changes in wall thickness and the development of atherosclerotic plaques during a 3-year period. The final publication has yet to appear in a medical journal. However, the study and its main findings have been presented at several international scientific meetings. In brief, isradipine was significantly more effective than hydrochlorothiazide in preventing an increase in intima-media thickness at several points of measurement in the carotid artery in spite of the fact that systolic blood pressure was not lowered as effectively by isradipine as by the diuretic therapy. There are numerous lessons to be learnt from MIDAS for future studies of this kind. A good example of this is the European Lacidipine Study of Atherosclerosis (ELSA) which is currently in progress in several European countries. By careful analysis of MIDAS an improved study design has been created, which should result in a definitive and irrefutable answer to the issue of the clinical importance of calcium antagonist treatment in the prevention of atherosclerosis.

Arteriosclerosis↗

PubMed2007

Autoimmunity and atherosclerosis: functional polymorphism of PTPN22 is associated with phenotypes related to the risk of atherosclerosis. The Cardiovascular Risk in Young Finns Study.

There is a growing body of evidence attesting the significance of inflammation in the pathogenesis of atherosclerosis. Protein tyrosine phosphate PTPN22 C/T single nucleotide polymorphism (SNP) at + 1858 has been identified recently as a susceptibility factor for various inflammatory autoimmune diseases. We hypothesized that data on the genetic polymorphism of the PTPN22 enzyme associated with an increased risk of autoimmunity could also provide insight into the possible role of autoimmunity in the pathogenesis of atherosclerosis. Therefore we analysed the PTPN22 + 1858 C/T polymorphism in a population of young Finnish adults (n = 2268) for whom data on carotid artery intima-media thickness (IMT), a presymptomatic predictor of atherosclerosis, and risk factors for atherosclerosis were available. In males carriage of the T allele of PTPN22 + 1858 was associated significantly with IMT in univariate and multivariate analyses, while in females it was associated with several risk factors for atherosclerosis (BMI, waist circumference, waist-to-hip ratio, serum concentrations of C-reactive protein and triglycerides) but not with IMT. Our results indicate that the genetic polymorphism of PTPN22 + 1858 known to predispose to autoimmunity also enhances the development of atherosclerosis and thereby links the genetics of autoimmunity and atherosclerosis.

Adult↗