Effectiveness of a community health worker cardiovascular risk reduction program in public health and health care settings.

OBJECTIVES: We evaluated whether a program to prevent coronary heart disease (CHD) with community health workers (CHWs) would improve CHD risk in public health and health care settings. METHODS: The CHWs provided point-of-service screening, education, and care coordination to residents in 34 primarily rural Colorado counties. The CHWs utilized motivational interviewing and navigated those at risk for CHD into medical care and lifestyle resources. A software application generated a real-time 10-year Framingham Risk Score (FRS) and guideline-based health recommendations while supporting longitudinal caseload tracking. We used multiple linear regression analysis to determine factors associated with changes in FRS. RESULTS: From 2010 to 2011, among 4743 participants at risk for CHD, 53.5% received medical or lifestyle referrals and 698 were retested 3 or more months after screening. We observed statistically significant improvements in diet, weight, blood pressure, lipids, and FRS with the greatest effects among those with uncontrolled risk factors. Successful phone interaction by the CHW led to lower FRS at retests (P = .04). CONCLUSIONS: A CHW-based program within public health and health care settings improved CHD risk. Further exploration of factors related to improved outcomes is needed.

Impact of a nurse telephone intervention among high-cardiovascular-risk, health fair participants.

BACKGROUND AND OBJECTIVES: Cardiovascular disease (CVD) is the leading cause of death in the United States, yet most individuals remain unaware of their risk. Current health fair models assess individual risk factors but miss the opportunity to assess, counsel, and follow-up with participants regarding global CVD risk. Objectives of this nurse telephone intervention were to (1) describe high-CVD-risk participants' healthcare-seeking behavior after the health fair and following a nurse telephone intervention and (2) describe CVD risk-reducing therapies provided to high-risk participants after the health fair and following a nurse telephone intervention. SUBJECTS AND METHODS: Five hundred twenty-nine of 4,489 health fair participants who completed an interactive Framingham risk assessment in 2006 were identified with high CVD risk. These participants received a nurse telephone intervention approximately 1 month after the health fair, during which the risk message was reinforced, principles of motivational interviewing were applied, and follow-up care was assessed. We evaluated the proportion of high-CVD-risk participants who obtained healthcare before and after intervention, and we compared the care received before and after intervention. RESULTS AND CONCLUSION: Among 447 contacted high-CVD-risk participants, 59% (n = 262) saw a healthcare provider, and 86% of those discussed CVD risk at their healthcare visit. A greater proportion of participants were started on a cardioprotective drug (41% vs 20%; P < .01), and more participants discussed "heart health" (96% vs 75%; P < .001) after receiving the nurse telephone intervention. Our findings suggest that a nurse intervention may improve individuals' CVD risk awareness as well as activate providers to implement CVD risk reduction strategies.

A founder mutation of the MSH2 gene and hereditary nonpolyposis colorectal cancer in the United States.

CONTEXT: Hereditary nonpolyposis colorectal cancer (HNPCC), also known as Lynch syndrome, is caused by mutations in the mismatch repair genes and confers an extraordinarily high risk of colorectal, endometrial, and other cancers. However, while carriers of these mutations should be identified, counseled, and offered clinical surveillance, at present the mutations are not tested for in mutation analyses. OBJECTIVE: To describe the prevalence of a large genomic deletion encompassing exons 1 to 6 of the MSH2 gene that is widespread in the US population as a result of a founder effect. DESIGN, SETTING, AND PATIENTS: Ongoing genealogical and historical study conducted to assess the origin and spread of an MSH2 mutation previously identified in 9 apparently unrelated families with putative HNPCC and living in widely different geographic locations in the United States. MAIN OUTCOME MEASURES: Classification of family members as carriers or noncarriers of the MSH2 mutation; spread of the mutation across the continental United States. RESULTS: To date, 566 family members of the 9 probands have been identified to be at risk and counseled; 137 of these have been tested, and 61 carry the founder mutation. Three families have been genealogically shown to descend from a German immigrant family that arrived and first settled in Pennsylvania in the early 1700s. Movements of branches of the family from Pennsylvania through North Carolina, Alabama, Kentucky, Missouri, Iowa, Nebraska, Utah, Texas, and California have been documented, and carriers of the mutation have already been diagnosed in 14 states. In contrast, the deletion was not found among 407 European and Australian families with HNPCC. CONCLUSION: The postulated high frequency and continent-wide geographic distribution of a cancer-predisposing founder mutation of the MSH2 gene in a large, outbred (as opposed to genetically isolated) population, and the ease with which the mutation can be detected, suggest that the routine testing of individuals at risk for HNPCC in the United States should include an assay for this mutation until more is learned about its occurrence.

State consensus guideline for the prevention of cardiovascular disease in primary care settings.

Cardiovascular disease (CVD) is the leading cause of death in the United States and is often attributable to poorly controlled yet modifiable risk factors. All national guidelines strongly recommend performing global CVD risk assessments to inform therapeutic intensity, but only a minority of clinicians regularly quantitate their patient's CVD risk. Not surprisingly, many patients are not at goal with regard to blood pressure, lipids, and the appropriate receipt of antiplatelet therapy. Given this background, the Colorado Clinical Guidelines Committee partnered with the Colorado Prevention Center to craft a simple algorithm for CVD risk reduction that emphasizes risk quantification and aggressive treatment for established CVD. The Colorado Clinical Guidelines Committee assembled a multidisciplinary team of health professionals with the goal of creating a comprehensive primary and secondary prevention framework that targets primary care physicians. We described the rationale, methods, and ultimate deployment of this guideline statewide in Colorado and hope this process may be a resource to other states interested in harmonizing a public health approach to CVD risk reduction.

Hereditary nonpolyposis colorectal carcinoma (HNPCC) and HNPCC-like families: Problems in diagnosis, surveillance, and management.

BACKGROUND: To the authors' knowledge, hereditary nonpolyposis colorectal carcinoma (HNPCC) is the most commonly occurring hereditary disorder that predisposes to colorectal carcinoma (CRC), accounting for approximately 2-7% of all CRC cases diagnosed in the U.S each year. Its diagnosis is wholly dependent on a meticulously obtained family history of cancer of all anatomic sites, with particular attention to the pattern of cancer distribution within the family. METHODS: The objective of the current study was to illustrate various vexing problems that can deter the diagnosis of HNPCC and, ultimately, its management. This was an observational cohort study. Sixteen HNPCC and HNPCC-like families were selected from a large resource of highly extended HNPCC families. High-risk patients were selected from these HNPCC families. An ascertainment bias was imposed by the lack of a population-based data set. Personal interviews and questionnaires were used for data collection. RESULTS: There was an array of difficulties highlighted by limitations in compliance, lack of a clinical or molecular basis for an HNPCC diagnosis, ambiguous DNA findings, problems in genetic counseling, failure to meet Amsterdam or Bethesda criteria, small families, lack of medical and pathologic documentation, poor cooperation of family members and/or their physicians, cultural barriers, economic stress, frequent patient fear and anxiety, perception of insurance discrimination, and limited patient and/or physician knowledge regarding hereditary cancer. CONCLUSIONS: The diagnosis and management of HNPCC is predicated on physician knowledge of its phenotypic and genotypic heterogeneity, in concert with the multifaceted problems that impact on patient compliance.