Cost-effectiveness of a statewide public health intervention to reduce cardiovascular disease risk.

BACKGROUND: The cost-effectiveness of community health worker (CHW)-based cardiovascular disease (CVD) risk-reduction interventions is not well established. Colorado Heart Healthy Solutions is a CHW-based intervention designed to reduce modifiable CVD risk factors. This program has previously demonstrated success, but the cost-effectiveness is unknown. CHW-based interventions are potentially attractive complements to healthcare delivery because laypersons implement the intervention at a lower cost relative to medical care and may be attractive in rural settings with limited clinical resources. METHODS: CHWs performed screenings and provided ongoing participant support within predominantly rural communities. A point-of-service software tool was used to generate 10-year Framingham CVD risk scores and assist CHWs to make medical referrals and provide ongoing individualized support for lifestyle changes. A sample of program participants returned for reassessment of risk factors. We calculated quality-adjusted life years (QALYs) gained and program costs using a Markov model. Transition probabilities were calculated using Framingham risk equations or derived from the literature using the observed mean reduction in 10-year CVD risk score over of 37- months follow-up. Program cost-effectiveness was calculated for both at-risk (abnormal baseline CVD risk factors) and overall program populations. RESULTS: The base-case scenario evaluating a 52-year-old male participant revealed an incremental cost savings of $3576 and a gain of 0.16 QALYs associated with the intervention. Cost savings were greater in at-risk populations. The economic dominance of the model was robust in multiple sensitivity analyses. CONCLUSIONS: A community-based CVD intervention demonstrated to reduce CVD risk is cost-effective. This suggests that population-based public health programs may have the potential to complement primary care preventative services to improve health and reduce the burden of traditional medical care.

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.

The I1307K APC polymorphism in Ashkenazi Jews with colorectal cancer: clinical and pathologic features.

Colorectal cancer is common in Ashkenazi Jews. The I1307K APC mutation occurs in 6-7% of Ashkenazi Jews and increases the risk of colorectal cancer. This study aimed to describe the clinical, pathologic and epidemiologic features of colorectal cancer in I1307K carriers to determine whether there were any features which might warrant individual screening for the mutation. In all, 215 Ashkenazi Jews with a personal history of colorectal cancer were enrolled. Clinical and family history, pathology reports, and slides were obtained and blood drawn for I1307K determination. The presence of the mutation was determined by PCR from white blood cell DNA. Colorectal cancer pathology slides were read in a blinded fashion. Of the 215 enrolled patients, 26 (12.1%) tested positive for I1307K. There was no difference in the pathologic features between colorectal cancers in Ashkenazi carriers compared to noncarriers. There was no difference in the age at diagnosis or history of second or other primaries. Carriers had an increased likelihood of having a first-degree relative with colorectal cancer (50%) compared to noncarriers (28%, P < 0.04). We could find no distinguishing feature other than family history that characterizes I1307K positive colorectal cancers. We could find no group of Ashkenazi Jews with colorectal cancer for whom screening for I1307K would be clinically useful.

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.

American founder mutation for Lynch syndrome. Prevalence estimates and implications.

BACKGROUND: Recently, a new founder mutation, an exon 1-6 deletion in a mismatch repair gene (MMR), MSH2, in nine kindreds with Lynch syndrome was reported. In 3 of the kindreds this mutation was traced by genealogy through 11-12 generations to a common founder, and thus termed the American Founder Mutation (AFM). Since then, 13 additional 'unrelated' kindreds with AFM were detected by a recently designed single polymerase chain reaction. This test might serve as first-line screening for Lynch syndrome mutations, provided AFM was prevalent, which is assessed in the current study. METHODS: The number of current AFM carriers and the incidence of Lynch syndrome caused by AFM were estimated based on population growth of mutation carriers derived from genealogy data. For cross-checking, its annual incidence was also estimated based on published epidemiology data. RESULTS: There are 18,981 (5th and 95th percentiles, 6038 and 34,466, respectively) expected current AFM carriers, or 160 (range 51-290) Lynch syndrome cases diagnosed per year due to AFM estimated based on genealogy data. The incidence estimate closely overlaps with that based on published epidemiology data, which is 114-400 cases per year. CONCLUSIONS: A large number of AFM carriers are likely to exist in the U.S., which harbors significant implications for cancer control. Given the ease of detection, testing for AFM not only among members of the existing AFM families, but also among all patients with Lynch syndrome in the U.S. is proposed.

Increasing evidence for a human breast carcinoma virus with geographic differences.

BACKGROUND: An early immunologic study suggesting that a virus similar to the mouse mammary tumor virus (MMTV) was associated highly with breast carcinoma in Tunisian patients, compared with patients in the United States, led the authors to examine different breast carcinoma populations by using more current molecular techniques. METHODS: Thirty-nine paraffin blocks were selected for sequencing of the 250-base pair segment of the MMTV from patients with breast carcinoma who were seen and treated at the Institut Salah Azaiz in Tunisia. Fifteen of those blocks were examined under code by a second laboratory, which used a different methodology and was blinded to the results of the first laboratory, and 14 blocks were analyzed successfully. RESULTS: The comparison of Tunisian patients and patients from other countries clearly showed a significantly higher proportion of tumors with MMTV-like sequences in the Tunisian series of patients. There was complete reproducibility of data between the two laboratories. Using the results from the first laboratory and similar studies from the literature, detection of the MMTV-like env gene sequence showed an important geographic pattern with a significantly higher percentage of positive patients with breast carcinoma in Tunisia (74%) compared with patients with breast carcinoma in the United States (36%), Italy (38%), Australia (42%), Argentina (31%), and Vietnam (0.8%) CONCLUSIONS: The findings provided increased evidence for a human breast carcinoma virus with geographic differences in prevalence. The geographic differences were compatible with studies of MMTV in wild mice; thus, the data were plausible biologically.

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.