Clinical and Educational Outcomes of an Integrated Inpatient Quality Improvement Curriculum for Internal Medicine Residents.

BACKGROUND: Integrating teaching and hands-on experience in quality improvement (QI) may increase the learning and the impact of resident QI work. OBJECTIVE: We sought to determine the clinical and educational impact of an integrated QI curriculum. METHODS: This clustered, randomized trial with early and late intervention groups used mixed methods evaluation. For almost 2 years, internal medicine residents from Dartmouth-Hitchcock Medical Center on the inpatient teams at the White River Junction VA participated in the QI curriculum. QI project effectiveness was assessed using statistical process control. Learning outcomes were assessed with the Quality Improvement Knowledge Application Tool-Revised (QIKAT-R) and through self-efficacy, interprofessional care attitudes, and satisfaction of learners. Free text responses by residents and a focus group of nurses who worked with the residents provided information about the acceptability of the intervention. RESULTS: The QI projects improved many clinical processes and outcomes, but not all led to improvements. Educational outcome response rates were 65% (68 of 105) at baseline, 50% (18 of 36) for the early intervention group at midpoint, 67% (24 of 36) for the control group at midpoint, and 53% (42 of 80) for the late intervention group. Composite QIKAT-R scores (range, 0-27) increased from 13.3 at baseline to 15.3 at end point (P < .01), as did the self-efficacy composite score (P < .05). Satisfaction with the curriculum was rated highly by all participants. CONCLUSIONS: Learning and participating in hands-on QI can be integrated into the usual inpatient work of resident physicians.

Educational system factors that engage resident physicians in an integrated quality improvement curriculum at a VA hospital: a realist evaluation.

PURPOSE: Learning about quality improvement (QI) in resident physician training is often relegated to elective or noncore clinical activities. The authors integrated teaching, learning, and doing QI into the routine clinical work of inpatient internal medicine teams at a Veterans Affairs (VA) hospital. This study describes the design factors that facilitated and inhibited the integration of a QI curriculum-including real QI work-into the routine work of inpatient internal medicine teams. METHOD: A realist evaluation framework used three data sources: field notes from QI faculty; semistructured interviews with resident physicians; and a group interview with QI faculty and staff. From April 2011 to July 2012, resident physician teams at the White River Junction VA Medical Center used the Model for Improvement for their QI work and analyzed data using statistical process control charts. RESULTS: Three domains affected the delivery of the QI curriculum and engagement of residents in QI work: setting, learner, and teacher. The constant presence of the QI material on a public space in the team workroom was a facilitating mechanism in the setting. Explicit sign-out of QI work to the next resident team formalized the handoff in the learner domain. QI teachers who were respected clinical leaders with QI expertise provided role modeling and local system knowledge. CONCLUSIONS: Integrating QI teaching into the routine clinical and educational systems of an inpatient service is challenging. Identifiable, concrete strategies in the setting, learner, and teacher domains helped integrate QI into the clinical and educational systems.

Palliative care in medical school curricula: a survey of United States medical schools.

OBJECTIVE: To provide an updated estimate of the extent and manner in which palliative care is incorporated in the curricula of U.S. medical schools. METHODS: Data were obtained from two sources: a 40-item written survey sent directly to deans of all 128 medical schools and corresponding information was obtained from the Curriculum Management and Information Tool (CurrMIT) national database of the Association of American Medical Colleges. RESULTS: Information was obtained from 47 of 128 (37%) medical schools; 30 through the survey and 17 through the CurrMIT database. "Palliative and Hospice Care" is a required course in 30% (n = 14) of responding medical schools and a required rotation in 19% (n = 9); 15% (n = 7) offer an elective course and 29% (n = 14) an elective rotation; and 53% (n = 25) integrate this subject into a required course. Of responding schools, 49% (n = 23) believe medical students should be evaluated in the care patients with advanced, incurable conditions during the clerkships; 30% (14) currently do so. CONCLUSIONS: A minority of U.S. medical schools from which information was obtained requires training in palliative care and evaluates students in their care of patients with advanced, incurable conditions. Most medical schools have chosen to include palliative care topics within existing courses. AAMC's existing database does not assess the scope or extent of coursework and rotations in palliative care. Guidelines are needed that address palliative care education and training of medical students.

Relative risk for cardiovascular atherosclerotic events after smoking cessation: 6-9 years excess risk in individuals with familial hypercholesterolemia.

BACKGROUND: Smoking history is often di- or trichotomized into for example "never, ever or current smoking". However, smoking must be treated as a time-dependent covariate when lifetime data is available. In particular, individuals do not smoke at birth, there is usually a wide variation with respect to smoking history, and smoking cessation must also be considered. METHODS: Therefore we analyzed smoking as a time-dependent risk factor for cardiovascular atherosclerotic events in a cohort of 2400 individuals with familial hypercholesterolemia who were followed from birth until 2004. Excess risk after smoking-cessation was modelled in a Cox regression model with linear and exponential decaying trends. The model with the highest likelihood value was used to estimate the decay of the excess risk of smoking. RESULTS: Atherosclerotic events were observed in 779 patients with familial hypercholesterolemia and 1569 individuals had a smoking history. In the model with the highest likelihood value the risk reduction of smoking after cessation follows a linear pattern with time and it appears to take 6 to 9 years before the excess risk is reduced to zero. The risk of atherosclerotic events due to smoking was estimated as 2.1 (95% confidence interval 1.5; 2.9). CONCLUSION: It was concluded that excess risk due to smoking declined linearly after cessation in at least six to nine years.

Diagnosing familial hypercholesterolaemia: the relevance of genetic testing.

AIMS: We assembled a cohort of patients with familial hypercholesterolaemia (FH) for both basic and clinical research. We used a set of established diagnostic criteria to define FH. Some put forward that a definite diagnosis of FH is made when a mutation in the LDL-receptor (LDLR) gene is identified. We therefore set out to determine in these patients whether patients with a DNA diagnosis would differ significantly from those diagnosed clinically. METHODS AND RESULTS: We randomly selected 4000 hypercholesterolaemic patients from the Dutch Lipid Clinic network database. Phenotypical data were acquired by reviewing medical records. After review of medical records, 2400 patients could be defined as having FH. An LDLR mutation was identified in 52.3% of these patients. Patients with and without an LDLR mutation demonstrated different clinical and laboratory characteristics. Low-density lipoprotein cholesterol was higher in patients with an LDLR mutation, whereas triglycerides were higher in patients without an LDLR mutation. The phenotypic differences between the groups remained even after stratification for the presence or absence of tendon xanthomas. CONCLUSION: Despite the use of stringent clinical criteria to define FH patients, two cohorts could be identified within our study population, namely those patients with and those without an LDLR mutation. Our findings suggest that among those without an LDLR mutation, patients with other causes of dyslipidaemia may be present. These observations underline the relevance of genetic testing in FH for clinical practice, for screening purposes, and for research involving these patients.

Genetic determinants of plasma HDL-cholesterol levels in familial hypercholesterolemia.

The objective of this study was to determine the extent to which common genetic variants can explain the variation of high-density lipoprotein cholesterol (HDL-C) plasma levels in familial hypercholesterolemia (FH). FH is characterized by elevated low-density lipoprotein cholesterol levels and premature cardiovascular disease (CVD). Although low HDL-C levels have been shown to affect the severity of the clinical phenotype, little is known about the factors that determine HDL-C levels in these patients. A cohort of 1002 heterozygous FH patients was genotyped for polymorphisms in the genes encoding for ATP-binding cassette transporter A1, apolipoprotein (apo) AIV, apoCIII, apoE, cholesteryl transfer ester protein, hepatic lipase, lipoprotein lipase, and two paraoxonases. Multiple linear regression showed that, together, these polymorphisms explain only 3.9% of the variation of HDL-C plasma levels. When significant two-way interactions between the polymorphisms were also taken into account, the explained variation rose to 12.5%. In a regression model that also incorporated sex, smoking, alcohol use, body mass index, and concomitant beta-blocker use as covariates, the explained variation of HDL-C plasma levels even increased to 32.5%. This study provides direct evidence that multiple, modestly penetrant, but highly prevalent, polymorphisms can explain a substantial part of the variation of HDL-C plasma levels in a representative large cohort of heterozygous FH patients.

Genetic determinants of cardiovascular disease risk in familial hypercholesterolemia.

OBJECTIVE: To investigate the contribution of polymorphisms in multiple candidate genes to cardiovascular disease (CVD) risk in a large cohort of patients with heterozygous familial hypercholesterolemia (FH). METHODS AND RESULTS: We genotyped 1940 FH patients for 65 polymorphisms in 36 candidate genes. During 91.451 person-years, 643 (33.1%) patients had at least 1 cardiovascular event. Multifactorial Cox survival analysis revealed that the G20210A polymorphism in the prothrombin gene was strongly associated with a significantly increased CVD risk (GA versus GG; P<0.001). CONCLUSIONS: In a large cohort of FH patients, we found that the G20210A polymorphism in the prothrombin gene is strongly associated with CVD risk. Our results constitute a step forward in the unraveling of the hereditary propensity toward CVD in FH and might lead to better risk stratification and hence to more tailored therapy for CVD prevention.

Guidelines were developed for data collection from medical records for use in retrospective analyses.

OBJECTIVE: To construct a set of guidelines for data collection from medical records. STUDY DESIGN AND SETTING: Retrospective analysis of clinical data is often performed by physician-scientists. In such research, the source of clinical data is the patient's medical record; however, medical records are intended for patient care and the data are not systematically recorded for research purposes. We drew on recommendations in the literature and our own experience with a retrospective cohort study that uses a DNA bank to construct guidelines for data collection from medical records. RESULTS: The guidelines incorporate a number of strategies for accurate data collection, which are discussed and illustrated by application. CONCLUSION: With guidelines for data collection, the quality of research data is enhanced. A well-designed case record form and a handbook for standardized data collection are essential for training the data collectors and for ensuring fastidious searching of the record; however, certain kinds of information are not always well documented in patient records. Consequently, it is essential to perform a pilot study to assess the study design and to use additional questionnaires. Correct interpretation of clinical outcomes documented in the medical records often necessitates an independent adjudication committee to prevent bias in outcome definition.

Clinical, diagnostic, and therapeutic aspects of familial hypercholesterolemia.

Heterozygous familial hypercholesterolemia (FH) is a common inherited disorder of lipoprotein metabolism. FH is characterized by elevated levels of low-density lipoprotein cholesterol, the presence of tendon xanthomas, and premature cardiovascular disease. The underlying molecular defect of FH consists of mutations in the gene coding for the low-density-lipoprotein-receptor protein, detection of which provides the only unequivocal diagnosis. Although the cause of FH is monogenic, there is wide variation in the onset and severity of atherosclerotic disease in these patients. Additional atherogenic risk factors of environmental, metabolic, and genetic origin are presumed to influence the clinical phenotype in FH. Criteria used to identify individuals with FH include a combination of clinical characteristics, personal and family history of early coronary artery disease, and biochemical parameters. Since the introduction in 1989 of statins, which have been shown to be effective and to delay or prevent the onset of cardiovascular disease, drug treatment of FH has greatly improved. New lipid-lowering agents are presently being developed for clinical use. This review provides an update on the clinical, diagnostic, and therapeutic aspects of heterozygous familial hypercholesterolemia.