Principles for national and regional guidelines on cardiovascular disease prevention: a scientific statement from the World Heart and Stroke Forum.
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Biomedical subjects
Publications and source records attributed to Thomas A Pearson.
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STUDY OBJECTIVES: We determine the relative risk and severity of traumatic brain injury among occupants of lateral impacts compared with occupants of nonlateral impacts. METHODS: This was a secondary analysis of the National Highway Traffic Safety Administration's National Automotive Sampling System, Crashworthiness Data Systems for 2000. Analysis was restricted to occupants of vehicles in which at least 1 person experienced an injury with Abbreviated Injury Scale score greater than 2. Traumatic brain injury was defined as an injury to the head or skull with an Abbreviated Injury Scale score greater than 2. Outcomes were analyzed using the chi2 test and multivariate logistic regression, with adjustment of variance to account for weighted probability sampling. RESULTS: Of the 1,115 occupants available for analysis, impact direction was lateral for 230 (18.42%) occupants and nonlateral for 885 (81.58%) occupants. One hundred eighty-seven (16.07%) occupants experienced a traumatic brain injury, 14.63% after lateral and 16.39% after nonlateral impact. The unadjusted relative risk of traumatic brain injury after lateral impact was 0.89 (95% confidence interval [CI] 0.51 to 1.56). After adjusting for several important crash-related variables, the relative risk of traumatic brain injury was 2.60 (95% CI 1.1 to 6.0). Traumatic brain injuries were more severe after lateral impact according to Abbreviated Injury Scale and Glasgow Coma Scale scores. The proportion of fatal or critical crash-related traumatic brain injuries attributable to lateral impact was 23.5%. CONCLUSION: Lateral impact is an important independent risk factor for the development of traumatic brain injury after a serious motor vehicle crash. Traumatic brain injuries incurred after lateral impact are more severe than those resulting from nonlateral impact. Vehicle modifications that increase head protection could reduce crash-related severe traumatic brain injuries by up to 61% and prevent up to 2,230 fatal or critical traumatic brain injuries each year in the United States.
BACKGROUND: Little evidence of the effects of moderate-fat (from monounsaturated fat) weight-loss diets on risk factors for cardiovascular disease exists because low-fat diets are typically recommended. Previous studies in weight-stable persons showed that a moderate-fat diet results in a more favorable lipid and lipoprotein profile (ie, lower serum triacylglycerol and higher HDL cholesterol) than does a low-fat diet. OBJECTIVE: We evaluated the effects of energy-controlled, low-fat and moderate-fat diets on changes in lipids and lipoproteins during weight loss and subsequent weight maintenance. DESIGN: We conducted a parallel-arm study design in overweight and obese [body mass index (in kg/m(2)): 29.8 +/- 2.4] healthy men and women (n = 53) assigned to consume a low-fat (18% of energy) or moderate-fat (33% of energy) diet for 6 wk to achieve weight loss, which was followed by 4 wk of weight maintenance. All foods were provided and body weight was monitored to ensure equal weight loss between groups. RESULTS: The moderate-fat diet elicited favorable changes in the lipoprotein profile. Compared with baseline, HDL cholesterol was unchanged, whereas triacylglycerol and the ratios of total and non-HDL cholesterol to HDL cholesterol were lower at the end of the weight-maintenance period in the moderate-fat diet group. Despite similar weight loss, triacylglycerol rebounded, HDL cholesterol decreased, and the ratios of total and non-HDL cholesterol to HDL cholesterol did not change during the 10-wk interval in the low-fat diet group. CONCLUSIONS: A moderate-fat weight-loss and weight-maintenance diet improves the cardiovascular disease risk profile on the basis of favorable changes in lipids and lipoproteins. There is merit in recommending a moderate-fat weight-loss diet.
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OBJECTIVES: This study was designed to assess prospectively changes in serum lipid profile and myocardial perfusion with serial radionuclide single photon emission computed tomography (SPECT) myocardial perfusion imaging (MPI) during the first six months of pravastatin therapy. BACKGROUND: Morbid coronary events occur despite statin therapy and lipid-lowering in patients with coronary artery disease (CAD). A reliable strategy to identify responders with effective treatment from nonresponders on statin therapy before clinical events is needed. METHODS: Rest and stress SPECT MPI and lipids were assessed serially in 25 patients (36% women) with CAD and dyslipidemia during the first six months of pravastatin therapy. RESULTS: Total cholesterol, low-density lipoprotein cholesterol, and triglycerides declined (26%, 32%, and 30%, respectively) by six weeks and remained reduced at six months. Mean stress perfusion defect (summed stress score [SSS]) was severe (13.3 +/- 6.0) at baseline, showed no change at six weeks, and improved significantly at six months (10.3 +/- 7.3, p < 0.01). The six-month study SSS improved in 11 (48%) patients, was unchanged in 10 (43%) patients, and worsened in 2 (9%) patients. Changes in lipid levels did not reliably predict changes in myocardial perfusion at six weeks or six months in this small pilot study. CONCLUSIONS: Serial SPECT MPI demonstrated improved stress myocardial perfusion in 48% of patients treated for six months with pravastatin. Time course of improved myocardial perfusion during pravastatin therapy is delayed compared to lipids. Direction and magnitude of changes in the myocardial perfusion vary and do not correlate closely with improvements in lipids.
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BACKGROUND: Comparing the dose-response of a new drug to that of a previously studied drug can aid in understanding their relative potencies. Two dose-finding studies addressed the effect of a new drug, rosuvastatin, on its ability to decrease low-density lipoprotein cholesterol (LDL-C) levels. One of these studies included 2 doses of atorvastatin, and substantial additional information is available in the literature about the effect of atorvastatin on LDL-C level lowering. METHODS: The 2 dose-finding studies of rosuvastatin considered otherwise healthy patients who had hypercholesterolemia. Comparable studies of atorvastatin were identified via a MEDLINE search in December 1999. Multiple reviewer consensus identified 15 of 41 studies on atorvastatin published since 1996 that met these selection criteria: reporting of LDL-C level change from baseline at least 6 weeks after treatment initiation, doses administered, and treatment group sizes. Eligible populations had clinical evidence of hypercholesterolemia. We excluded studies with patients who had severe illness or a previous history of transplantation. Data extraction of the mean, sample sizes, and SDs (or CIs) by dose was carried out independently by multiple reviewers. We combined the results from the various studies with Bayesian hierarchical modeling and analyzed them with Markov chain Monte Carlo techniques. RESULTS: Combining this study and literature results substantially increased the power to compare the dose-response relationships of rosuvastatin and atorvastatin. Rosuvastatin reduced LDL-C level by an estimated 10 to 17 percentage points more than atorvastatin when both were given at the same dose. Approximately one quarter of the dose of rosuvastatin achieved about the same magnitude of LDL-C level reduction as atorvastatin at dosages as high as 80 mg. This finding does not imply a 4-fold difference in efficacy overall and specifically does not describe the results at higher dosage levels. CONCLUSIONS: Bayesian meta-analysis of results from related studies allows the comparison of the dose-response relationships of 2 drugs, better estimates of a particular dose-response relationship within an individual study, and the expression of relative benefits (of dose and drug) in terms of probabilities. Explicitly comparing a study's results with historical data using Bayesian meta-analysis allows clinicians to view the study in the larger context of medical research.
This article describes the pilot testing of the Case-Based Series in Population-Oriented Prevention (C-POP) and accompanying evaluation instruments in a problem-based medical curriculum at the University of Rochester Medical Center. Several of the cases were successfully taught in the curriculum, but the evaluation instruments revealed no change in population-oriented skills or orientation. Issues of implementation and evaluation of the C-POP curriculum are discussed.
The 2002 World Health Report warns that the allies of poverty and ignorance are joining forces with the new formidable enemies of health. This describes the epidemiologic transition of burden of disease from infectious and parasitic diseases to that of noncommunicable diseases. All parts of the world, with the possible exception of sub-Saharan Africa, have well-established epidemics of coronary heart disease and stroke. Hypertension contributes significantly to mortality everywhere and is a leading global problem. Education and wealth have strong influences on the epidemiologic transition and might serve as a double-edged sword of benefit and risk. While improved education and enhanced resources are necessary to reduce infectious, parasitic, and perinatal diseases, these factors are also associated with adoption of deleterious health behaviors, which lead to the atherosclerotic diseases. The diffusion of innovation theory describes the early adoption of unhealthy lifestyles in the educated and wealthy, who soon recognize the costs to their community and modify these lifestyles. The uneducated poor may adopt these unhealthy lifestyles later, but, once that occurs, are left with higher risk and burden of cardiovascular disease. One possible reason for this is that discretionary income and the desire for modern conveniences quickly attract unhealthy products (tobacco, high fat/high salt foods) and unhealthy behaviors (sedentary entertainment transportation without physical exertion). The commercial interests of these products have been efficient and effective in delivering their messages to developing societies. Heart health organizations must be more aggressive in their assessment of needs for programs, education of people over a broad range of education levels, assurance of access to heart health services, alteration of the environment to facilitate heart health, and the development of policies and laws to limit deleterious products and behaviors. These late-adopter communities are assumed to require additional efforts and services to counterbalance deleterious influences. Sub-Saharan Africa is the only WHO region in which cardiovascular disease is not the leading cause of death. There is no precedent to support the notion that Africa will, without special efforts, avoid progression to later stages of the epidemiologic transition. The goal of improved education and eradication of poverty in Africa should not and need not carry the unhappy consequence of a cardiovascular disease epidemic.
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The concept of risk assessment and reduction, introduced initially by the Framingham Heart Study and refined in other models, forms the cornerstone of preventive cardiology. Risk factor assessment determines the therapeutic strategy, because the intensity of preventive intervention is tailored to the patient's risk of coronary heart disease. The conventional risk factors for coronary heart disease include elevated serum total cholesterol and LDL cholesterol, low HDL cholesterol, elevated blood pressure, cigarette smoking, diabetes, vascular disease, menopausal status (women only), and age. Aggressive risk factor reduction, formerly used exclusively in secondary prevention, may be pivotal to optimal patient management in high-risk primary prevention. A number of noninvasive imaging modalities have the potential to measure and to monitor atherosclerosis in asymptomatic individuals and include exercise ECG testing, electron beam computed tomography, magnetic resonance coronary angiography, positron emission tomography, ankle-brachial index, and B-mode ultrasound. Novel serum markers, including C-reactive protein and homocysteine, have the ability to gauge risk in the individual patient. Systemic therapy for risk reduction in primary prevention may be preferable to local therapy (eg, angioplasty and bypass) and may more effectively prevent acute coronary events than these more invasive approaches.
Plasma lipoprotein [a] (Lp[a]) concentrations are inversely associated with, and largely determined by, apolipoprotein [a] (apo[a]) gene size, a highly polymorphic trait. We studied if, within an individual, the smaller apo[a] isoform always dominated, whether there was interaction between the two alleles, and whether these features differed between Caucasians and African Americans. We determined apo[a] gene sizes, apo[a] protein sizes and relative amounts, and plasma Lp[a] levels in 430 individuals (263 Caucasians and 167 African Americans). Of the 397 heterozygotes with at least one detectable apo[a] isoform (238 Caucasians and 159 African Americans), the larger allele dominated in 28% of Caucasians and 23% of African Americans, while the smaller allele dominated in 56% of Caucasians and 45% of African Americans. In Caucasians, dominance of the smaller allele increased with Lp[a] levels, from 44% at Lp[a] < or = 30 nM to 81% at Lp[a] >100 nM (P < 0.0001). Dominance by the smaller allele increased with increasing size of the larger allele in both groups but with the smaller allele only in African Americans. There was no interaction between apo[a] alleles within genotypes; one apo[a] isoform level was not associated with the other isoform level, and isoform levels were not affected by the difference in size. More of the dominance pattern was explained by Lp[a] level and apo[a] genotype in African Americans than in Caucasians (29% vs. 13%). Thus, genotype influences isoform-specific Lp[a] levels and dominance patterns differently in African Americans and in Caucasians.
OBJECTIVE: To observe the experience of 9 practice sites in implementing provider-defined disease management programs for coronary heart disease patients. STUDY DESIGN: Observational study of provider-defined practice improvement programs. METHODS: Practices chose from a variety of interventions that included provider- and patient-based disease management tools. Data were collected at baseline, 6, and 12 months. RESULTS: Complete baseline, 6-month, and 12-month data were available for 586 patients (58% of the 1013 patients enrolled). Compared with baseline, 6-month data showed more patients whose total cholesterol was less than 200 mg/dL (56% to 76%; P < or = .001), whose low-density lipoprotein (LDL) cholesterol was less than 100 mg/dL (30% to 54%; P < or = .001), and whose high-density lipoprotein cholesterol was at least 35 mg/dL (75% to 81%; P < or = .001); who exercised rigorously for 30 minutes, 3 times a week (40% to 53%; P < or = .001); who used lipid medication (74% to 80%; P < or = .01); and who used aspirin (84% to 92%; P < or = .001). There were no significant improvements in triglyceride levels, blood pressure control, glycemic control among diabetes patients, smoking cessation, body mass index, and beta-blocker use. The 12-month results were similar to the 6-month results. Sites with a practice coordinator had the highest number of patients achieving their LDL goal (72% to 89%). CONCLUSIONS: There may be an opportunity to improve patient care by applying disease management principles with a variety of interventions. Dedicated personnel to help coordinate disease management programs may be critical to the success of such programs.
Despite reductions in cardiovascular disease (CVD) mortality, current evidence suggests that CVD is not being prevented but, rather, is being made less lethal. Evidence-based guidelines have been developed for secondary, primary, and community-based prevention. To improve compliance with secondary prevention guidelines, programs must better organize and monitor care. Primary prevention requires assessment of risk in asymptomatic people, to yield cost-effective benefits. CVD prevention at the societal level should target deleterious behavior in community settings, using effective public health interventions. Policy options that involve multiple preventive approaches offer the best opportunity to minimize the economic and social burdens of CVD.