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Biomedical subjects

T A Pearson

Publications and source records attributed to T A Pearson.

At least 91 records · Page 5Linked to original sources
PubMed1997

Epidemiology of thrombotic-hemostatic factors and their associations with cardiovascular disease.

Abundant evidence proves that thrombosis is involved in the acute presentation of coronary, cerebrovascular, and peripheral vascular diseases. However, the role of thrombotic factors in the development of the atherosclerotic lesions themselves has been more difficult to prove. This difficulty has been due, at least in part, to several methodologic issues in the study of hemostatic factors and cardiovascular disease (CVD). These include the possibility that associations between CVD and hemostatic factors may not be causal but rather due to confounding by other factors, acting as part of an extended causal pathway or requiring interaction with other risk factors or atherosclerotic disease, or may result from disease rather than causing the disease. In addition, several challenges remain in the measurement of hemostatic factors. Nonetheless, a growing number of studies have examined the association of CVD with coagulation factors (fibrinogen, factor VII, factor VIII, and platelet aggregability) and fibrinolytic factors [tissue plasminogen activator, plasminogen activator inhibitor 1, lipoprotein(a), and plasminogen or global fibrinolytic activity]. Of these, only for fibrinogen is there significant, strong, and consistent evidence of a causal association. Given the preliminary nature of these associations, any association between dietary factors and hemostatic factors other than fibrinogen is difficult to invoke as evidence for a deleterious effect of diet on CVD risk via thrombogenic mechanisms.

Blood Coagulation↗
PubMed1997

ApoE genotype does not predict lipid response to changes in dietary saturated fatty acids in a heterogeneous normolipidemic population. The DELTA Research Group. Dietary Effects on Lipoproteins and Thrombogenic Activity.

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.

Adult↗
PubMed1997

Reducing saturated fat intake is associated with increased levels of LDL receptors on mononuclear cells in healthy men and women.

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.

Adult↗
PubMed1996

Seasonal variation in parameters related to coronary heart disease risk in young men.

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.

6-Ketoprostaglandin F1 alpha↗
PubMed1996

Reliability and changes in validity of self-reported cardiovascular disease risk factors using dual response: the behavioral risk factor survey.

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.

Adult↗
PubMed1996

Lipid lowering: the case for identifying and treating the high-risk patient.

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.

Clinical Trials as Topic↗
PubMed1996

Osteoarthritis as a determinant of an adverse coronary heart disease risk profile.

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.

Aged↗
PubMed1995

Who will provide preventive services? The changing relationships between medical care systems and public health agencies in health care reform.

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.

Delivery of Health Care↗
PubMed1995

Role of a central laboratory in implementing national cholesterol education panel guidelines in rural practices: model system for managed 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.

Counseling↗