Incidence of coronary heart disease in a population insured for medical care (HIP): myocardial infarction, angina pectoris, and possible myocardial infarction.

Shapiro, Sam; Weinblatt, Eve; Frank, Charles W.; Sager, Robert V.

doi:10.2105/ajph.59.suppl_6.1

Cited by 108 publications

(10 citation statements)

References 39 publications

(11 reference statements)

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“…1 -6 The potential for developing coronary heart disease in male cigarette smokers is approximately two times greater than in male nonsmokers. 7 Large epidemiological surveys have shown that the incidence of morbidity and mortality from coronary heart disease increases progressively with the number of cigarettes smoked. 68 Smoking cessation has been demonstrated to be associated with a decline in cardiovascular death.…”

mentioning

confidence: 99%

Long-term nicotine exposure increases aortic endothelial cell death and enhances transendothelial macromolecular transport in rats.

Lin

Hong

Chang

et al. 1992

Arterioscler Thromb

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Repeated endothelial cell injury has been suggested as an initiating factor in atherogenesis. Dying or dead endothelial cells have been shown to make significant contributions to the local enhancement of transendothelial macromolecular transport. Since cigarette smoking is one of the major risk factors for atherosclerosis, we examined the hypothesis that smoking accelerates atherogenesis by increasing the frequency of endothelial cell death and hence transendothelial macromolecular transport. Sixteen male Sprague-Dawley rats were given nicotine at a weight-adjusted dose of 5 mg/kg body wt per day in their drinking water over a period of 6 weeks. A group of 16 age-matched male Sprague-Dawley rats not exposed to nicotine and maintained over the same time period served as the control group. In en face preparations of thoracic aorta, immunoglobulin G-containing dying or dead endothelial cells were identified by the indirect immunoperoxidase method, and endothelial leakage to Evans blue-albumin (EBA) complexes (5 minutes after intravenous injection) was visualized by fluorescence microscopy. The results showed that in nicotine-treated rats, 51% of dead endothelial cells were associated with EBA leakage, which was responsible for 57% of total EBA leaky foci. C igarette smoking is generally accepted to be one of the major risk factors for coronary heart disease. 1 -6 The potential for developing coronary heart disease in male cigarette smokers is approximately two times greater than in male nonsmokers. 7Large epidemiological surveys have shown that the incidence of morbidity and mortality from coronary heart disease increases progressively with the number of cigarettes smoked. 68 Smoking cessation has been demonstrated to be associated with a decline in cardiovascular death.9 Autopsy studies have also revealed the increased occurrence of advanced atherosclerotic le-

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mentioning

confidence: 99%

Long-term nicotine exposure increases aortic endothelial cell death and enhances transendothelial macromolecular transport in rats.

Lin

Hong

Chang

et al. 1992

Arterioscler Thromb

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“…It has been shown that weight gain after reaching adulthood is a more sensitive predictor of subsequent coronary heart disease than actual weight 1 and that fat accumulated in adulthood tends to be distributed more centrally than peripherally. 2 - 3 Several studies indicate that a central pattern of fat deposition is associated with disorders of carbohydrate metabolism, 45 hypertension, 6 lipid metabolism, 2 ' 5~8 and risk of coronary heart disease morbidity and mortality.…”

mentioning

confidence: 99%

Body fat distribution as a risk factor for coronary artery atherosclerosis in female cynomolgus monkeys.

Shively¹,

Clarkson²,

Miller³

et al. 1987

Arteriosclerosis

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Central fat deposition Is associated with Increased risk of coronary heart disease morbidity and mortality In women. Subcutaneous fat distribution was Investigated as a potential factor that might exacerbate diet-Induced coronary artery atherosclerosis (CAA) in female cynomolgus monkeys (Macaca fasclcularls) which share with North American Caucasian women a gender-related protection against CAA. In a retrospective necropsy study (n = 36), the distribution of the antemortem ratio of subscapular/ triceps sklnfold thickness was divided at the mean and the two resulting groups were designated high and low for this variable. CAA was quantified as the mean crosssectional Intlmal area based on nine coronary artery sections. The extent of CAA was significantly greater In the high sklnfold ratio group as compared to the low sklnfold ratio group. Ponderosity was closely associated with the sklnfold ratio but was not a useful predictor of CAA. These findings suggest that female cynomolgus macaques may provide a primate model of the health consequences of regional fat distribution in women. (Arteriosclerosis 7:226-231, May/June 1987) T here is an emerging interest in body fat distribution, rather than quantity, as a risk factor for coronary artery' atherosclerosis (CAA). It has been shown that weight gain after reaching adulthood is a more sensitive predictor of subsequent coronary heart disease than actual weight 1 and that fat accumulated in adulthood tends to be distributed more centrally than peripherally.2 -3 Several studies indicate that a central pattern of fat deposition is associated with disorders of carbohydrate metabolism, 45 hypertension, 6 lipid metabolism, 2 ' 5~8 and risk of coronary heart disease morbidity and mortality. 8 The distribution of fat has a stronger relationship with coronary heart disease than obesity. 8 -9 The interaction between obesity and fat distribution as risk factors for coronary heart disease and death from all causes in women appears to be a paradoxical effect in need of further study. 8 In view of the potential insight to be gained from further investigation of fat distribution as a cardiovascular risk factor, it would be helpful to have an animal model in which to study this phenomenon. Female cynomolgus macaques (Macaca fascicularis) share with Caucasian North American women protection against CAA.10 However, some of these monkeys, like some women, are not protected. Specifically, it is known that female Macaca fascicularis that are socially subordinate 10 ' 11 and those that have poorFrom the Arteriosclerosis Research Center, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, North Carolina.This work was supported in part by Nonhuman Primate Models Contract #N01 HV 72978 from the National Heart, Lung and Blood Institute.Address for reprints: Dr. Carol A. Shivery, Arteriosclerosis Research Center, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, North Carolina 27103. Received December 5,1985; revision accepted December 29, 1986. ...

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“…Third, patients' knowledge and attitude toward the intervention might differ by race and ethnicity. For example, some studies suggest that African Americans are more risk averse (Shapiro et al 1969;Oddone et al 1998) and more concerned about being experimented upon by physicians without their knowledge or consent than whites (Corbie-Smith, Thomas, and St George 2002). Fourth, unconscious provider bias may affect delivery of care so that a provider may be more likely to vaccinate a white rather than a minority patient.…”

Section: Potential Causes Of Disparitiesmentioning

confidence: 99%

“…Previous studies have focused primarily on racial differences in risk aversion, (Shapiro et al 1969;Oddone et al 1998;Ayanian et al 1999) but have largely ignored the role of patient initiative or demand for care. Attitudes toward medical interventions may represent a continuum ranging from active resistance to active demand.…”

Section: Improved Understandingmentioning

confidence: 99%

Commentary—Anatomy of Racial Disparity in Influenza Vaccination

Fiscella¹

2005

Health Services Research

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Incidence of coronary heart disease in a population insured for medical care (HIP): myocardial infarction, angina pectoris, and possible myocardial infarction.

Cited by 108 publications

References 39 publications

Long-term nicotine exposure increases aortic endothelial cell death and enhances transendothelial macromolecular transport in rats.

Long-term nicotine exposure increases aortic endothelial cell death and enhances transendothelial macromolecular transport in rats.

Body fat distribution as a risk factor for coronary artery atherosclerosis in female cynomolgus monkeys.

Commentary—Anatomy of Racial Disparity in Influenza Vaccination

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