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Objectives: This study sought to evaluate long-term predictors of coronary events in men and women with arteriographically defined coronary artery disease (CAD)., Background: There is conflicting evidence of the role of triglycerides (TGs) as a prognosticator of CAD, and no studies have examined the long-term outcome of "normal" levels in predicting new coronary events., Methods: This was a retrospective cohort study that evaluated 740 consecutive patients presenting for diagnostic coronary arteriography between 1977 and 1978. Beginning in 1988, patients with arteriographic CAD (n=350) were recontacted and asked to complete detailed medical questionnaires. Case and control patients were stratified by development of new coronary events, including death from ischemic heart disease, nonfatal myocardial infarction and revascularization., Results: There were 199 events during the 18-year follow-up period. The mean high density lipoprotein cholesterol (HDL-C) was significantly lower (35 vs. 39 mg/dl; p=0.002) and TGs higher (160 vs. 137 mg/dl; p=0.03) in case patients than in control patients; After adjusting for age, gender and beta-adrenergic blocking agent use, multiple logistic regression analysis revealed the following independent predictors of CAD events: diabetes mellitus (relative risk [RR] 2.1, 95% confidence interval [CI] 1.4% to 3.1%), HDL-C <35 mg/dl (RR 1.5, 95% CI 1.1% to 2.00) and TGs >100 mg/dl (RR 1.5, 95% CI 1.1% to 2.1%). A Kaplan-Meier analysis revealed significantly reduced survival from CAD events in patients with baseline TG levels > or = 100 mg/dl compared with TG levels <100 mg/dl (p=0.008)., Conclusions: TG levels previously considered "normal" are predictive of new CAD events. The cutpoints established by the National Cholesterol Education Program for elevated TGs (>200 mg/dl) may need to be refined.

Discussion of potential strategies to modify lipids and lipoproteins other than low density lipoproteins (LDLs) should first recognize the convincing evidence in favour of the identification and aggressive treatment of elevated LDL cholesterol (LDL-C) levels in patients with established cardiovascular disease. Elevated LDL-C level is one of the few risk factors for which there is evidence of involvement in every pathophysiological step of the development of cardiovascular disease. Longitudinal studies have established the role of LDL-C as a risk factor for cardiovascular disease incidence, recurrence and fatal outcome. Clinical trials and economic analyses have proven that aggressive treatment of elevated LDL-C in patients at high risk can prevent cardiac events with excellent cost effectiveness.

Dehydroepiandrosterone, an adrenal steroid, has many purported roles in the body and has been used as an oral supplement in the treatment of various illnesses. Because little is known about normal changes over time in dehydroepiandrosterone concentrations, we studied the 5-year change in plasma dehydroepiandrosterone concentrations in 614 free-living adults. Two hundred seventy-three males and 341 females had dehydroepiandrosterone and dehydroepiandrosterone sulfate concentrations measured in 1989 and 1994. Demographic data were also obtained. Dehydroepiandrosterone concentrations differed significantly by sex and 5-year age group. The average decline in dehydroepiandrosterone was 5.6%/year, and the rate of decline was directly related to age but not to sex, measures of adiposity, or serum glucose. Dehydroepiandrosterone sulfate concentrations differed significantly by sex and age group. The average decline in the sulfated hormone was 2.0%/year and was not related to age, sex, measures of adiposity, or serum glucose. Knowledge of the natural course of age-related changes in dehydroepiandrosterone and dehydroepiandrosterone sulfate concentrations is essential to our understanding of the relationship of dehydroepiandrosterone to chronic diseases.

Recent studies have suggested that variations in apoE genotypes may influence the magnitude of plasma lipid changes in response to dietary interventions. We examined the ability of apoE genotype to predict plasma lipid response to reductions in percent of calories from total fat (TF) and saturated fat (SF) in a normolipidemic study population (n = 103) heterogeneous with respect to age, gender, race, and menopausal status. Three diets, an average American diet (34.3% TF, 15.0% SF), an AHA Step 1 diet (28.6% TF, 9.0% SF), and a low saturated fat (Low-Sat) diet (25.3% TF, 6.1% SF) were each fed for a period of 8 weeks in a three-way crossover design. Cholesterol was kept constant at 275 mg/d; monounsaturated and polyunsaturated fat were kept constant at approximately 13% and 6.5% of calories, respectively. Fasting lipid levels were measured during each of the final 4 weeks of each diet period. Participants were grouped by apoE genotype: E2 (E2/2, E2/3, E2/4); E3 (E3/3); E4 (E3/4, E4/4). Relative to the average American diet, both the Step 1 and Low-Sat diets significantly reduced total cholesterol, LDL cholesterol, and HDL cholesterol in all three apoE genotype groups. No evidence of a significant diet by genotype interaction, however, could be identified for any of the measured lipid and lipoprotein end points. Additional analysis of the data within individual population subgroup (men and women, blacks and whites) likewise provided no evidence of a significant diet by genotype interaction. Thus, in a heterogeneous, normolipidemic study population, apoE genotype does not predict the magnitude of lipid response to reductions in dietary saturated fat.

Progress in vascular biology, epidemiology, clinical trials, and cost-effectiveness analyses have allowed development of guidelines for risk reduction in patients with vascular disease and congestive heart failure. However, these advances appear necessary but not sufficient to promote implementation of these guidelines for treating coronary artery disease (CAD) and congestive heart failure (CHF). Evidence from the United Kingdom and Europe, and estimates from the United States, suggest that a large "treatment gap" exists between recommended therapies for patients with cardiovascular disease and the care that they are actually receiving. Despite known interventions with proven efficacy to reduce disease recurrence and death from CAD and CHF, only a minority of patients are receiving any intervention whatsoever. A second problem is that, among those receiving care, many are undertreated resulting in a very small number of patients reaching goals and recommended levels of therapy. Third, the levels of intervention and the proportion of patients at goal that should be attainable (i.e., community standards) are not known. A variety of barriers exist for implementation of preventive cardiology services. Although the patient has a chain of opportunities for risk reduction, it is not clear which of the links in this chain (inpatient/hospital programs, specialist/generalist communication, ambulatory care, or patient compliance) is the major reason for the treatment gap. An ongoing project, the American College of Cardiology Evaluation of Preventive Therapeutics (ACCEPT), will attempt to quantify the treatment gap in coronary disease patients in the United States and will try to identify those barriers playing the greatest role in limiting the optimal care of the coronary disease patient.

A number of pharmacologic interventions are now recommended for the prevention of cardiovascular disease, based on the results of randomized controlled trials. These include antihypertensive drugs, lipid-lowering agents, antiplatelet and anticoagulant drugs, estrogen replacement therapy, beta-blockers, and angiotensin converting enzyme (ACE) inhibitors. It is likely that additional pharmacologic interactions will soon be proven efficacious. Despite the strength of this evidence and the development of clinical guidelines incorporating their use, a surprisingly low proportion of patients are actively treated with these agents. There may be a variety of explanations for this, including barriers at the level of the patient, health care provider, and health care institution. Finally, a number of questions remain as to the optimal combination of interventions, both behavioral and pharmacologic, which will yield maximal reduction in risk. The description of factors which reduce the effectiveness of pharmacologic interventions below the efficacy demonstrated in randomized clinical trials should be a fertile area for epidemiologic and behavioral research.

At present a large number of patients with atherosclerotic disease are not receiving aggressive cholesterol-lowering therapy. Consequently they are being deprived of a cost-effective, risk-reducing treatment. Every physician who treats patients with clinical atherosclerotic disease should become fully informed about the results of cholesterol-lowering trials in patients at high risk. All physicians who care for high-risk patients should take responsibility for cholesterol management, including primary care physicians and cardiovascular specialists. Highly effective and generally safe drugs for cholesterol lowering are available. The benefits of therapy for reducing recurrent CHD and prolonging life are considerable. There is no justification for unduly delaying institution of therapy for the majority of patients. The many advantages of nonpharmaceutical therapy call for its use in almost all patients, but drug treatment should not be postponed if the target for LDL cholesterol lowering (< or = 100 mg/dL) is unlikely to be achieved in the near term by a nonpharmaceutical approach alone. The view that patients with CHD or other forms of atherosclerotic disease do not receive substantial clinical benefits from aggressive cholesterol-lowering therapy is no longer warranted. Intensive cholesterol reduction, initiated immediately, has the potential to significantly reduce both morbidity and mortality. Cholesterol-lowering therapy thus should become a routine part of clinical management to reduce risk of future coronary events and to prolong life in patients with CHD or other forms of atherosclerotic disease.

Studies with animal models suggest that saturated fatty acids raise low density lipoprotein (LDL)-cholesterol levels by reducing LDL receptor-mediated clearance. To examine this directly in humans, we studied the effects of lowering dietary saturated fat on LDL-receptor abundance in peripheral mononuclear cells which reflects hepatic LDL-receptor status. Healthy males and females (n = 25) participating in the DELTA (Dietary Effects on Lipoproteins and Thrombogenic Activity) Study consumed three experimental diets in a randomized cross-over design. Diets provided 34% fat, 15% saturated fatty acids (Average American Diet); 29% fat, 9% saturated fatty acids (Step-One Diet); and 25% fat, 6% saturated fatty acids (Low SAT Diet). Peripheral mononuclear cells were isolated from blood samples collected after 6 and 8 wk. An ELISA was used to quantify LDL-receptor protein in total cell membranes. LDL-receptor abundance increased by 10.5% after the Low SAT Diet (P < 0.05). This was associated with an 11.8% decrease in serum LDL-cholesterol (P < 0.05). A linear inverse relationship was observed between the percentage change in LDL-cholesterol and the percentage change in LDL-receptor abundance (r = -0.59; P < 0.01). In addition, LDL-receptor abundance also was correlated inversely (P < 0.001) with serum levels of LDL-cholesterol (r = -0.747) and apoB (r = -0.593). In summary, reducing dietary saturated fat is associated with an increase in LDL-receptor abundance of magnitude similar to the decrease in serum LDL-cholesterol. Thus, an important mechanism by which reductions in dietary saturated fatty acids decrease LDL-cholesterol in humans is through an increase in LDL-receptor number.

Background: Osteoarthritis is associated with obesity, sedentary behavior and poor fitness. This study was conducted to test the hypothesis that risk factors for coronary heart disease (CHD) are more prevalent among patients with osteoarthritis than among non-arthritic adults of the same age and sex., Methods: Forty-six patients with osteoarthritis of the hip and/or knee were evaluated; 23 non-arthritic subjects served as control group. A panel of metabolic risk factors were measured including body mass index (BMI), waist-hip ratio (WHR), blood pressure, fasting blood glucose, and serum lipids and apoproteins., Results: Measures of arthritis severity confirmed marked disability and deformity in the arthritis group. Patients reported the performance of less aerobic exercise than controls. Compared with controls, patients were noted to have greater mean BMI (31.2 +/0- 5.9 versus 24.6 +/- 3.2 kg/m2, P < 0.000005), WHR (0.88 +/- 0.07 versus 0.83 +/- 0.08, P < 0.05), systolic blood pressure (140.8 +/- 17.9 versus 131.3 +/- 15.3 mmHg, P < 0.05) and fasting blood glucose (105.0 +/- 24.6 versus 93.2 +/- 7.0 mg/dl, P < 0.01), and lower mean high-density-lipoprotein cholesterol (47.9 +/- 10.9 versus 56.7 +/- 17.1 mg/dl, P < 0.05). Nonsignificant trends for higher mean diastolic blood pressure and serum triglycerides were also noted in the arthritic group. Mean estimated risk for development of CHD within 10 years of evaluation was greater in the arthritic than in the control group (21.6 +/- 14.4% versus 15.2 +/- 11.7%, P < 0.05)., Conclusion: Patients with moderately severe to end-stage lower extremity osteoarthritis may be at advanced risk for the development of CHD by virtue of their unfavorable risk factor profile.

Seasonal variation in the plasma lipids and lipoproteins is reported in the literature. Whether this variation is the result of changes in diet or other factors has not been adequately addressed. We investigated the effects of a controlled diet on the seasonal variation in the levels of plasma lipids and apolipoproteins and also on the excretion of urine metabolites of TXA2 and PGI2 in healthy males. Two well-controlled diet studies were conducted to evaluate effects of dietary fatty acids on plasma lipids (Studies 1 and 2; n = 33) and eicosanoid excretion (Study 2 only; n = 15). Participants consumed whole-food test diets in a randomized, four-period crossover design during each 26-day experimental period. A non-intervention control group also participated in each study (Study 1, n = 12; Study 2, n = 11). Blood was collected monthly and analyzed for plasma lipids and apolipoproteins A-1 (Apo A-1) and B100 (Apo B). Twenty-four hour urine samples were collected monthly only in Study 2 and analyzed for TXB2 and 6-keto-PGF1 alpha by RIA. Seasonal fluctuations were observed in all subjects in plasma Apo A-1 (zenith = July, with 95% CI June-July; P < 0.05) and Apo B (zenith = October, 95% CI September-November, P < 0.05). Although there was no significant variation in plasma cholesterol levels, the increase in Apo B is consistent with an increase in LDL particle number during the fall/winter. Additionally, excretion of both eicosanoid metabolites and the ratio of 6-keto-PGF1 alpha/TXB2 was markedly elevated in July (95% CI June-July, P < 0.001). Three seasonal fluctuations were observed both in participants who consumed a highly-controlled experimental diet and in the non-intervention controls. Thus, these results suggest a diet-independent seasonal variation in parameters thought to be involved in coronary heart disease risk status. An understanding of these variations is important not oly for clinical evaluation and metabolic study design issues, but more importantly, to clarify their clinical significance with the seasonal incidence of CHD events.

The authors previously studied the validity of self-reported cardiovascular disease (CVD) risk factors assessed by telephone surveys, and found the validity low, especially for self-reported hypertension and hypercholesterolemia. One way to improve validity is to combine repeated measurements (dual response) into a single measure. The authors explored this and the reliability of self-reported CVD data collected by the Behavioral Risk Factor Survey in three New York counties from January 1989 to May 1990. Nine hundred and eleven subjects were interviewed by telephone to collect CVD risk factor and health behavior information. Interviewees were offered physical examination and laboratory testing to verify self-reported CVD risk factors; 628 participated. Subjects were also reinterviewed to assess the test-retest reliability of the survey, and to study how validity of self-reported CVD data changes by dual response. Reliability coefficients for CVD risk factors, preventive health practices, and knowledge of risk factor levels ranged from 0.42 to 0.99. Minimal improvement in sensitivity of self-reported risk factors was found using dual response, and it did not improve specificity. Also, for prevalence of risk factors, dual response minimally improved self-reported rates compared to objective estimates. Combining self-reported measurements causes minimal changes in the validity of these variables. Physiological assessment for hypertension and hypercholesterolemia, or correction for misclassification, is needed for valid individual measurement and for community prevalence estimates from telephone surveys. Self-reported cigarette smoking, obesity, and diabetes mellitus have better validity, but physiological assessment or correction for misclassification may supplement these self-reported risk factors.

The rationale for the identification and aggressive treatment of lipid disorders in the patient with established vascular disease is thoroughly convincing. Elevated LDL cholesterol level is one of the few risk factors for which there is evidence of involvement in endothelial dysfunction, smooth-muscle proliferation, plaque destabilization, and thrombosis. Longitudinal studies have identified the role of elevated LDL cholesterol and low HDL cholesterol levels in the natural history of coronary artery disease. Clinical trials have successfully tested the feasibility of preventing coronary events using diet therapy or cholesterol-lowering drugs. These experiments have used a variety of end points, including myocardial infarction, cardiac death, total mortality rate, progression and regression of coronary artery stenoses, and progression of extracardiac atherosclerotic disease. The results are strikingly consistent. Economic analyses of the cost-benefit ratios also support these interventions in high-risk patients. These analyses also suggest that patients at high risk for coronary disease prior to its symptomatic presentation may be identified and treated to provide additional avenues for cost-effective primary prevention of this disease. The cardiologic community cannot ignore these results while embracing interventions such as angioplasty, coronary artery disease, antiarrhythmic therapy, and so forth. The scientific basis of cardiology demands the integration of techniques to control the atherosclerotic disease process itself, rather than merely the symptoms that it produces. Cardiology practices must reorganize to allow these proven interventions to become an integral part of comprehensive cardiologic care.

Health care reform in the United States will likely attempt to expand the health insurance coverage to uninsured groups, control costs, enhance quality, and expand access to care. Preventive services will be assigned to the medical care system, while new roles and responsibilities will be defined for public health agencies. The clinical preventive services likely required are examined in a population of 44,565 persons residing in Otsego County, New York. Expansion of preventive services to Medicaid requests and the uninsured will require considerable resource expenditure to correct the current deficit in preventive services received by these groups. Moreover, the uninsured and Medicaid recipients have high levels of risk behaviors, identifying a need for health education services effective to that population subgroup. The transfer of responsibilities for clinical preventive services to the medical care system may free up resources for public health agencies to focus on other initiatives such as disease surveillance, health education, and quality assurance. New interrelationships, some cooperative and some adversarial, are likely to emerge, due to a closer working relationship between the medical care system and public health agencies than previously seen in American health care.

We describe the use of a central laboratory to identify patients who may be candidates for a hypercholesterolemia treatment program and to direct their referral into this program. The laboratory, providing service for 16 medical practices in a rural area of upstate New York, served as the entry point to the treatment program for those patients with serum cholesterol > or = 5.18 mmol/L. This treatment program, designed to follow the National Cholesterol Education Program Adult Treatment Panel Guidelines, was provided by the lipid referral center staff, including a registered dietitian and a lipid specialist. After introduction of this program, 52% of eligible patients received nutritional counseling for hypercholesterolemia, compared with only 29% in usual care settings. This program represents an enhanced role for laboratories in the implementation of treatment protocols typical of those adopted by managed care networks.

1. An imbalance between generalists and cardiovascular subspecialists exists that will require decades to correct. We question the validity of the 50:50 generalist/specialist ratio in view of current practice patterns for cardiology. 2. There has been a large increase in the number of cardiovascular specialists in the past 30 years that will continue if training programs remain at their current size. 3. Cardiovascular specialists provide a substantial amount of inpatient care, care to older patients and care to those with cardiovascular symptoms, although generalists actually provide the majority of office-based cardiovascular care. 4. A significant portion of cardiovascular specialist care can be classified as comprehensive care to patients with and without cardiovascular disease. 5. Most generalists and cardiovascular specialists do not perceive a need for additional cardiovascular specialists. 6. Many providers perform cardiovascular procedures at levels below the recommended threshold for maintenance of clinical competence. 7. Managed care may result in a reduced demand for cardiovascular specialists. 8. If cardiovascular specialists provide general care, it may not be assumed that previous training prepares them for generalist practice. 9. The appropriate boundaries of cardiovascular care between generalists and cardiovascular specialists are indistinct. They are defined somewhat by the training programs from which the generalists graduate. 10. Many generalists have deficiencies in basic skills in clinical cardiology. 11. Desirable interactions between generalists and cardiovascular specialists involve referral of patients in both directions to the provider who can give care to a given patient, at a given time, with the best outcome and lowest cost.(ABSTRACT TRUNCATED AT 250 WORDS)

In case-control studies in which cases are ascertained from hospitals, controls are frequently chosen from among patients with other diseases at the same hospitals. This study was undertaken to examine the extent to which a hospital control group is representative of the population to which inferences are made. A hypothetical hospital control group was assembled consisting of 233 men and women aged 40-74 years who were surgical inpatients at the two hospitals in Otsego County, New York, in 1990. The characteristics of this group were compared with the characteristics of 15,563 men and women aged 40-74 years who participated in a privately conducted health census in the same county in 1989 with the use of health-related data collected in the census. In this rural setting, only small differences were found between the hospital control group and the census population on most of the measures considered, including demographic characteristics, certain health behaviors, and the prevalence of common conditions. However, the female hospital controls were more likely to be overweight than the females enumerated in the census, and the men were more likely to have ever smoked cigarettes. These differences were large enough to lead to different interpretations about the strength of the associations between these variables and case-control status.

Objectives: Few studies have described physical activity in rural populations. This study describes the frequency, types, and correlates of physical activity in 29,304 free-living adults in a rural county in New York State., Methods: Self-reported responses about regular physical activity (maintained long enough to work up a sweat) were analyzed from a private household census of Otsego County with an 86.6% response rate., Results: This survey categorized 46.2% of county residents as sedentary. Walking, the most frequent choice of activity (62% of the women, 36% of the men), increased in frequency with age of respondents whereas cycling, jogging, aerobics, team sports, and swimming (listed in rank order of frequency) generally tended to decrease in frequency with age. Farmers demonstrated an increased amount of "sweat activity" compared with persons in most other occupations., Conclusions: This descriptive study of physical activity in a rural county shows that sedentary lifestyle is of high prevalence. The high frequency of walking and the gender differences in both the levels and choice of activity suggest that further research and public policy recommendations focus on these issues.

Heterozygous familial hypercholesterolemia (hFH) is known to be associated with a high risk for development of coronary disease. However, several issues still remain as to whether this condition merits a special approach to diagnosis and case finding. It appears that hFH meets the World Health Organization criteria as a condition worthy of a screening program. However, none of several current strategies appears to be successful in the identification of even a majority of hFH cases. These strategies include community-wide programs to test everyone for total serum cholesterol levels, the testing of first degree family members of hFH patients or family members of patients with coronary disease at age < or = 55 years, or even the screening of patients with premature vascular events. The barriers for patients and physicians to carry out screening recommendations need to be identified and removed, including the need to sensitize primary care providers about the importance of identifying those with hFH.

To determine the accuracy of self-reported risk factors in 78 physicians, self-reported information was compared to findings on a standardized examination. Measured weight (r = 0.98), height (r = 0.95), body mass index (r = 0.96), systolic blood pressure (SBP) (r = 0.72), and diastolic blood pressure (DBP) (r = 0.60) were highly correlated with self-reported values (all P < 0.0001). Mean self-reported SBP and DBP did not differ from measured values; measured weight was 1.5 kg greater and measured height 1.4 cm less than self-reported values (both p < 0.0001). Regression of measured on self-reported values indicated excellent agreement except for DBP and heart rate. Differences between measured and self-reported values were not associated with a variety of variables except for a greater difference in SBP at higher levels of SBP. None of the 60 self-reported nonsmokers had expired carbon monoxide levels greater than 10 ppm. These results indicate that physicians' self-reports of height, body mass index, SBP, and smoking are extremely accurate and suitable for research purposes.