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M H Criqui

Publications and source records attributed to M H Criqui.

At least 91 records · Page 5Linked to original sources

Postmenopausal estrogen use and mortality. Results from a prospective study in a defined, homogeneous community.

The authors studied the association between postmenopausal estrogen use and mortality from cardiovascular disease, coronary heart disease, cancer, and all causes in a cohort of 1,868 women aged 50-79 years residing in a planned community. After 12 years, the age-adjusted all-cause mortality rate was lower in the 734 postmenopausal estrogen users (14.9/100 women) compared with the 1,134 nonusers (21.5/100 women) (relative risk (RR) = 0.69, 95% confidence interval (Cl) 0.55-0.87). After adjustment for age, systolic blood pressure, social class, fasting plasma cholesterol, fasting plasma glucose, Quetelet index (weight (lbs)/height (in)2 x 100), and cigarette smoking by the Cox model, the relative risk increased to 0.79 (95% Cl 0.62-1.01). Because a postmenopausal estrogen-smoking interaction term was significant (p = 0.025), separate Cox models were run for never, past, and current smokers. In never and current smokers, estrogen was protective for all-cause mortality, with relative risks of 0.67 (95% Cl 0.45-0.99) and 0.62 (95% Cl 0.39-0.98), respectively. However, past smokers were not protected by postmenopausal estrogen use (RR = 1.32, 95% Cl 0.84-2.08). Cause-specific models revealed differences in the association of postmenopausal estrogen use with cardiovascular disease mortality and coronary heart disease mortality that were dependent on smoking status. Postmenopausal estrogen use was strongly protective in current smokers but was associated with increased risk in past smokers. As expected, cancer mortality was increased in smokers. The confidence intervals for the relative risk estimate of postmenopausal estrogen use for cancer mortality in each smoking category included one. Finally, a separate analysis of subsequent three-year mortality in women surviving the first nine years of follow-up revealed reduced death rates only for women using estrogen at both baseline and nine years of follow-up, suggesting both a conservative bias in our data introduced by the large reduction in postmenopausal estrogen use during the study period and the possibility of a stronger protective effect for recent postmenopausal estrogen use.

Aged↗

IgE and cardiovascular disease. Results from a population-based study.

Because previous reports have suggested that IgE-mediated events may lead to both platelet activation and arterial spasm, a population-based study of 262 men and 315 women, aged 38 to 82, was conducted to investigate the association of serum IgE levels with myocardial infarction, stroke, and noninvasively diagnosed large-vessel peripheral arterial disease. In men with previous myocardial infarction, previous stroke, or current large-vessel peripheral arterial disease, geometric mean serum IgE levels were increased 119 percent, 164 percent, and 78 percent, respectively. These associations were statistically significant (p less than 0.05). Because IgE was positively or inversely correlated with several traditional cardiovascular disease risk factors, logistic regression was used to evaluate the independent association of IgE with any cardiovascular disease (myocardial infarction, stroke, or large-vessel peripheral arterial disease). In a model including age, cigarette smoking, fasting plasma glucose level, diastolic blood pressure, and low-density lipoprotein cholesterol level as covariates, IgE was positively and independently associated with any cardiovascular disease (p = 0.03). Similar evaluations in women revealed no correlation between IgE and cardiovascular disease by either univariate or multivariable analysis. These data indicate that IgE may be an independent marker for cardiovascular disease in men, and thus suggest IgE-mediated events may play a role in the pathogenesis of cardiovascular disease.

Adult↗

Alcohol and hypertension: new insights from population studies.

The link between alcohol and blood pressure is now well established. Certain subsets, such as older persons, whites and perhaps men may be at increased susceptibility to an alcohol pressor effect, although considerable interindividual variation in the pressor response probably exists. A threshold may exist at around two drinks per day, but several studies report either different thresholds or more linear relationships. The evidence to date suggests that ethanol, rather than some other constituent of alcoholic beverages or an associated behavior, raises blood pressure. The data available to date are perhaps most compatible with a withdrawal hypothesis, but a straightforward pressor effect cannot be excluded at this time. Whatever the mechanism, the pressor effect appears to be fully reversible. Finally, the available evidence suggests that alcohol induced hypertension will indeed lead to the usual hypertensive sequelae.

Alcohol Drinking↗

Lipoproteins as mediators for the effects of alcohol consumption and cigarette smoking on cardiovascular mortality: results form the Lipid Research Clinics Follow-up Study.

Because alcohol consumption is associated with increased high density lipoprotein (HDL) cholesterol and decreased low density lipoprotein (LDL) cholesterol, and cigarette smoking is associated with lower HDL cholesterol and higher LDL cholesterol, there has been speculation that the protective effect of moderate alcohol consumption and/or the noxious effect of cigarette smoking for cardiovascular disease might be mediated in large part by a lipoprotein mechanism. The authors examined this question in a prospective study of 7,461 men and women in 10 North American populations initially seen in 1972-1976 and followed for an average of 8.5 years. Moderate alcohol consumption was weakly protective for cardiovascular disease, while cigarette smoking was strongly and significantly associated with cardiovascular disease mortality. As expected, LDL cholesterol was positively related and HDL cholesterol was inversely related to cardiovascular disease mortality. However, multivariable analysis of cardiovascular disease mortality alternately excluding and including HDL cholesterol and LDL cholesterol as covariates indicated that the effect of alcohol consumption on cardiovascular disease mortality was independent of an LDL cholesterol pathway and only partially mediated by an HDL cholesterol pathway, while the effect of cigarette smoking was independent of both the HDL cholesterol and LDL cholesterol pathways, suggesting alternative biologic mechanisms of action for both alcohol consumption and cigarette smoking on cardiovascular disease.

Adult↗

The roles of alcohol in the epidemiology of cardiovascular diseases.

Alcohol, both alone and in concert with deficiencies or excesses of other substances, can produce cardiomyopathy. In addition, alcohol can directly affect the cardiac conduction system and produce arrhythmias. Alcohol also affects known risk factors for stroke and coronary heart disease (CHD). Alcohol increases blood pressure, which may lead to hypertension and thus increase the risk of stroke. HDL cholesterol, which is inversely related to CHD risk, increases with alcohol, and LDL cholesterol, which is positively related to CHD risk, may decrease with alcohol, a potentially dually protective effect. However, both case-control and population based studies indicate only moderate levels of consumption, defined as two drinks per day or less, may be of benefit. Preliminary data from the Lipid Research Clinics Follow-up Study suggest that the beneficial effect of moderate amounts of alcohol may be mediated in part by increased HDL cholesterol and in part by another factor, possibly reduced coagulation. Clinical and laboratory data, in addition to epidemiologic data, suggest alcohol intake above two drinks per day leads to excess cardiovascular disease (CVD), probably reflecting hypercoagulability as well as hypertension at higher levels of intake. Because alcohol can lead to excess morbidity and mortality from CVD as well as several other diseases and conditions, public health policy should continue to discourage the drinking of alcohol, especially non-moderate consumption.

Adult↗

Cardiovascular mortality and noncontraceptive use of estrogen in women: results from the Lipid Research Clinics Program Follow-up Study.

A cohort of 2270 white women, aged 40-69 years at baseline, were followed for an average of 8.5 years in the Lipid Research Clinics Program Follow-up Study. There were 44 deaths due to cardiovascular disease among the 1677 nonusers of estrogens and six cardiovascular disease deaths among the 593 estrogen users. The age-adjusted relative risk (RR) of cardiovascular disease deaths in users compared with nonusers was 0.34 (95% confidence limits 0.12 to 0.81). After multivariable adjustment for potential confounding factors (age, blood pressure, and smoking), the estimated RR for estrogen use was 0.37 (95% confidence limits 0.16 to 0.88). Analyses were done to explore whether these results could be due to selection bias for estrogen use. However, the prevalence of cardiovascular disease at baseline was slightly higher in estrogen users (12%) than in nonusers (10%); furthermore, the exclusion of all women with prevalent cardiovascular disease at baseline did not alter the apparent protective effect of estrogen use on cardiovascular disease mortality (RR = 0.42, 95% confidence limits 0.13 to 1.10). Additional analyses examining the complex association between estrogen use, lipoprotein levels, and cardiovascular disease mortality suggest that the protective effect of estrogen is substantially mediated through increased high-density lipoprotein levels.

Adult↗

Epidemiology of atherosclerosis: an updated overview.

Ongoing epidemiologic research continues to provide new insight into the multifactorial etiology of atherosclerosis and coronary artery disease (CAD). Cigarette smoking remains a primary risk factor; low tar and nicotine cigarettes have apparently not contributed to a reduced incidence of CAD and cardiovascular death. The stepwise risk of increasing levels of diastolic blood pressure to cardiovascular death is well known; however, elevated systolic blood pressure may be a more potent risk factor. The benefits of treating diastolic blood pressure greater than or equal to 115 mm Hg are indisputable; the benefits of treating milder hypertension, i.e., diastolic blood pressure between 90 and 114 mm Hg, probably outweigh the risks, but controversy persists. Low-density lipoprotein cholesterol, which comprises approximately 70% of total cholesterol, is strongly associated with CAD. Studies continue to relate hypercholesterolemia and CAD, showing approximately a 2% reduction in disease for each 1% reduction in total cholesterol. The influences of diabetes mellitus, thrombosis and psychosocial factors in the genesis of CAD are reviewed, as well as the evidence supporting the synergistic hazard presented by risk-factor clusters. High-density lipoprotein cholesterol bears an inverse, protective relation to CAD. Factors affecting high-density lipoprotein levels, e.g., obesity/exercise, cigarette smoking, alcohol consumption and postmenopausal use of estrogen in women, are also reviewed in light of recent findings. Additional investigation is necessary to clarify the benefits and risks associated with the treatment or modification of known risk factors and to identify others.

Adult↗

Correlates of change in postmenopausal estrogen use in a population-based study.

During the late 1970s, there was a dramatic reduction in postmenopausal estrogen use in the United States, which may have reflected concern over a well-publicized postmenopausal estrogen-endometrial cancer link. The authors studied 310 postmenopausal women in a defined population over the period 1974-1981 to evaluate whether hysterectomy and certain other characteristics predicted change in postmenopausal estrogen use status during this period and, as a secondary issue, whether women who subsequently began postmenopausal estrogen use had different characteristics prior to use, an important question in the evaluation of the relation of postmenopausal estrogen use to morbidity and mortality from cancer, cardiovascular disease, or other diseases in observational studies. The only strong predictor of whether postmenopausal estrogen use would be discontinued was the presence of an intact uterus. Women who discontinued postmenopausal estrogen use were also somewhat older and heavier than those who continued, but were otherwise quite similar on a wide range of variables, including risk factors for and the presence of various chronic diseases. Similarly, the absence of a uterus was the only strong predictor of the initiation of postmenopausal estrogen use. Thus, concern about a possible postmenopausal estrogen-endometrial cancer link appeared to have been the major determinant of change in postmenopausal estrogen use in this time period. In the secondary analysis, variables other than hysterectomy did not discriminate between women who initiated postmenopausal estrogen use versus those who did not report use of postmenopausal estrogens, suggesting that a broad range of other characteristics was not a priori different in these two groups.

Aged↗

Alcohol consumption, blood pressure, lipids, and cardiovascular mortality.

Interest in the effects of alcohol on cardiovascular risk factors and disease has increased sharply with reports of complex and previously unsuspected associations. The present report focuses on the associations of alcohol with blood pressure, lipids, and cardiovascular disease mortality. The epidemiological evidence to date appears to support the idea that moderate alcohol consumption, defined as two drinks a day or less, may offer some protection for coronary heart disease, but that higher levels of alcohol promote hypertension and are directly toxic to the heart, leading to stroke, arrhythmias, cardiomyopathy, and perhaps even coronary heart disease.

Alcohol Drinking↗

The association of dyslipoproteinemia with symptoms and signs of peripheral arterial disease. The Lipid Research Clinics Program Prevalence Study.

Intermittent claudication, leg pain during a graded exercise test (GXT), and resting systolic pressures in the upper and lower extremities were recorded as indicators of peripheral arterial disease at visit 2 of the Lipid Research Clinics (LRC) Prevalence Study. Systolic pressures of the upper and lower extremities were measured in a subsample of participants. We compared lipid levels of persons with and without claudication and with or without GXT-induced leg pain. We also compared lipid levels between groups with high and low arm:ankle systolic blood pressure ratios. Twenty-one (1.0%) men, 10 (1.0%) female nonusers and six (1.0%) female users of gonadal hormones had intermittent claudication determined by standardized questionnaire. Men with claudication had lower high-density lipoprotein (HDL)-cholesterol (35.6 vs 46.4 mg/dl), and their mean triglyceride level and cigarette consumption were higher and regular exercise less frequent. Men with type IIb dyslipoproteinemia were more likely to report claudication. One hundred sixty-nine (4.0%) men, 101 (3.8%) female nonusers, and 47 (4.1%) female users of hormones stopped the GXT because of leg pain. Mean HDL-cholesterol levels were lower for those with GXT-induced leg pain in all three sex-hormone usage groups (42.0 vs 46.9, p less than .001; 53.9 vs 59.4, p less than .001; 65.3 vs 67.2, p = NS) and mean low-density lipoprotein cholesterol levels were higher in those with leg pain on GXT in two of three groups (146.4 vs 146.2, p = NS; 155.7 vs 144.6, p less than .01; 144.4 vs 133.5, p less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Patterns of dyslipoproteinemia in selected North American populations. The Lipid Research Clinics Program Prevalence Study.

This article describes the assignment of dyslipoproteinemia (DLP) in several free-living North American populations and presents mean lipid and lipoprotein levels for each type. Dyslipoproteinemic phenotypes were assigned by a modified version of the National Institutes of Health (Fredrickson) phenotyping system. Criteria for assigning phenotypes included age- and sex-specific 5th and 95th percentiles for low-density lipoprotein and high-density lipoprotein cholesterol and total triglyceride, as well as other qualitative and quantitative criteria. Phenotypes IIb, III, I, and V were uncommon, confirming clinical impressions of their frequency. Lipid and lipoprotein levels in specific phenotypes were generally as expected. In the type III phenotype, however, mean cholesterol and triglyceride levels were surprisingly low. Gonadal hormone use, in the form of both oral contraceptives and postmenopausal estrogens, was reported in approximately 30% of women in these populations and was associated with dramatic differences in the frequency of DLP when compared with women not taking hormones. In general, these differences reflected the previously described effects of estrogen and progestins on lipoprotein levels. These data gathered in free-living populations: confirm clinical impressions of the rarity of some phenotypes, focus attention on those phenotypes in which diminished rather than elevated lipoproteins are found, and provide further evidence of the effect of hormones on lipid and lipoprotein levels.

Adolescent↗

Frequency and clustering of nonlipid coronary risk factors in dyslipoproteinemia. The Lipid Research Clinics Program Prevalence Study.

In a defined population of 4349 men and 3398 women, we evaluated the frequency and clustering of five nonlipid coronary heart disease risk factors--obesity, hypertension, sedentary lifestyle, cigarette smoking, and alcohol consumption--in nine categorical lipoprotein phenotypes--normal, types I or V, IIA, IIB, III, IV, hypoHDL (high-density lipoprotein), hypoLDL (low-density lipoprotein), and hyperHDL. This analysis indicated that compared with the normal phenotype, nonlipid coronary risk factors tend to be more frequent and thus cluster in individuals with "high risk" phenotypes, and occur somewhat less frequently in those with "low risk" phenotypes. Thus, identification of a high-risk phenotype suggests the presence of nonlipid risk factors as well, and the clinician should be alert to this possibility. A multivariable analysis of the independent associations of each of the risk factors with the lipid and lipoprotein components that define the phenotypes suggested that several behavioral risk factors may directly affect lipid and lipoprotein levels. This observation raises the possibility that certain intervention strategies, such as weight loss, smoking cessation, and regular exercise, may favorably influence dyslipoproteinemia.

Adult↗

Dietary vitamin D and calcium and risk of colorectal cancer: a 19-year prospective study in men.

Mortality rates from colon cancer in the USA are highest in populations exposed to the least amounts of natural sunlight; differences in endogenous vitamin D production and calcium absorption could be responsible. To investigate this possibility, the association of dietary vitamin D and calcium with 19-year risk of colorectal cancer was examined in 1954 men who had completed detailed, 28-day dietary histories in the period 1957-59. Risk of colorectal cancer was inversely correlated with dietary vitamin D and calcium. In the quartiles of a combined index of dietary vitamin D and calcium, from lowest to highest, observed risks of colorectal cancer were 38.9, 24.5, 22.5, and 14.3/1000 population. This association remained significant after adjustment for age, daily cigarette consumption, body mass index, ethanol consumption, and percentage of calories obtained from fat.

Adult↗

High- and low-density lipoprotein cholesterol: correlates in an older population.

A predominantly upper-middle-class white population of 279 men and 345 women with an average age of 66 years was evaluated to determine correlates of high- and low-density lipoprotein cholesterol (HDL and LDL), since these may be the only cholesterol measurements predictive of cardiovascular disease after age 50. Associations of HDL and LDL with age, alcohol use, obesity, smoking, diet, exercise, and medication use were examined using multiple linear regression. Alcohol, average and above-average exercise, postmenopausal estrogen use (women), B vitamin intake, and corticosteroid use were all positively related to HDL levels, and obesity (men only), cigarette smoking, and thyroid hormone use were inversely related. The only statistically significant correlates of LDL were an increase with age (women only) and lower levels in women using thyroid hormone. However, the associations of several behavioral variables with LDL, although not statistically significant, were in the expected direction. These results may suggest the continuing potential for preventive intervention even in an elderly population.

Age Factors↗

Effects of passive smoking on ischemic heart disease mortality of nonsmokers. A prospective study.

The mortality attributable to ischemic heart disease as a result of cigarette smoking is greater of a community of older adults in southern California, the authors tested the hypothesis that nonsmoking women exposed to their husband's cigarette smoke would have an elevated risk of fatal ischemic heart disease. Married women aged 50-79 years who had never smoked cigarettes (n = 695) were classified according to the husband's self-reported smoking status at entry into the study: never, former, or current smoker. After 10 years, nonsmoking wives of current or former cigarette smokers had a higher total (p less than or equal to 0.05) and age-adjusted (p less than or equal to 0.10) death rate from ischemic heart disease than women whose husbands never smoked. After adjustment for differences in risk factors for heart disease, the relative risk for death from ischemic heart disease in nonsmoking women married to current or former cigarette smokers was 14.9 (p less than or equal to 0.10). These data are compatible with the hypothesis that passive cigarette smoking carries an excess risk of fatal ischemic heart disease.

Aged↗