Does a lipid clinic increase compliance with National Cholesterol Education Program Treatment Guidelines? Report of a case-matched controlled study

Despite a national effort to promote measurement of cholesterol levels in adults, previous studies have shown that poor control is the norm. We sought to determine the effects of implementation of a structured lipid treatment program. Forty-one clinic-managed patients were matched with similar control patients. Clinic patients had more risk factors overall and therefore lower low-density lipoprotein (LDL) goals. They had significantly greater LDL reduction after the 6-month visit, resulting in a lower final LDL level. The percentage of patients reaching the LDL goal recommended by the National Cholesterol Education Program (NCEP) was the primary endpoint of the study. The NCEP guidelines were followed more frequently within the clinic, and significantly more clinic patients were treated to NCEP LDL goal than control patients. When indicated, medication was more frequently used and titrated in clinic patients. This study shows the efficacy of an organized lipid treatment clinic in management of dyslipidemia.     

Can we apply the European surveillance program of nosocomial infections (HELICS) to pediatric intensive care units?

Objective To evaluate the applicability of the HELICS program [part of the “Improving Patient Safety in Europe” program aiming at controlling nosocomial infections (NI) through surveillance] in European pediatric ICUs. Design and setting A comparison of HELICS and pediatric definitions of the main NI was performed. The adaptability of the HELICS questionnaire for pediatric patients was examined. Then a European survey was carried out by e-mail questionnaire to analyze NI surveillance programs. Participants Units affiliated with the European Society of Paediatric and Neonatal Intensive Care or the French Groupe Francophone de Réanimation et Urgences Pédiatriques. Measurements and results The main differences between adult and pediatric ICUs were the definition of ICU-acquired pneumonia, severity scores at admission, and scores of risk for NI. A total of 65 answers from 23 countries were collected. Among them 56 had a NI surveillance program that was of local origin for 64%. The most frequently collected NI were blood stream infections (91% of the units), catheter-related infections (88%), acquired pneumonia (86%), and urinary tract infections (77%). Definitions of NI had a local-based origin in 18% of cases, a regional-based or nation-wide origin in 21%, came from the Centers for Disease Control and Prevention in 38% and had multiple origins in 20%. Seventy-five percent of the units declared an interest in joining a European pediatric working group on NI within the European Society of Paediatric and Neonatal Intensive Care. Conclusions The adaptation of the HELICS protocol for pediatric ICUs is necessary. Its application is largely wished and may be easily performed. Electronic supplementary material The online version of this article (doi:) contains supplementary material, which is available to authorized users.     

Is visceral obesity the cause of the metabolic syndrome?

Despite the fact that controversy remains around the underlying pathophysiological processes leading to the development of the metabolic syndrome (insulin resistance and/or hyperinsulinemia versus abdominal obesity), there is increased recognition that abdominal obesity is the most prevalent form of the metabolic syndrome. Although it has been well established that there is a greater prevalence of chronic metabolic diseases such as diabetes and cardiovascular diseases in obese patients than among normal weight individuals, obesity is a remarkably heterogeneous condition and not every obese patient is characterized by co-morbidities. In this regard, body fat distribution, especially visceral adipose tissue accumulation, has been found to be a major correlate of a cluster of diabetogenic, atherogenic, prothrombotic and proinflammatory metabolic abnormalities referred to as the metabolic syndrome. Due to its anatomic location and peculiar metabolic, hyperlipolytic activity, the expanded visceral adipose depot is a key correlate of the altered cardiometabolic risk profile observed among individuals with a high-risk abdominal obesity phenotype. Evidence suggests that this dysmetabolic profile is predictive of a substantially increased risk of coronary heart disease even in the absence of classical risk factors. Finally, a moderate weight loss in initially abdominally obese patients is associated with a preferential mobilization of visceral adipose tissue, which in turn leads to substantial improvements in the metabolic risk profile predictive of a reduced risk of coronary heart disease and of type 2 diabetes.     

Metabolically Healthy Obesity and Risk of Mortality: Does the definition of metabolic health matter?

OBJECTIVE

To assess the association of a “metabolically healthy obese” phenotype with mortality using five definitions of metabolic health.

RESEARCH DESIGN AND METHODS

Adults (n = 5,269; 71.7% men) aged 39–62 years in 1991 through 1993 provided data on BMI and metabolic health, defined using data from the Adult Treatment Panel-III (ATP-III); criteria from two studies; and the Matsuda and homeostasis model assessment (HOMA) indices. Cross-classification of BMI categories and metabolic status (healthy/unhealthy) created six groups. Cox proportional hazards regression models were used to analyze associations with all-cause and cardiovascular disease (CVD) mortality during a median follow-up of 17.7 years.

RESULTS

A total of 638 individuals (12.1% of the cohort) were obese, of whom 9–41% were metabolically healthy, depending on the definition. Regardless of the definition, compared with metabolically healthy, normal-weight individuals, both the metabolically healthy obese (hazard ratios [HRs] ranged from 1.81 [95% CI 1.16–2.84] for ATP-III to 2.30 [1.13–4.70] for the Matsuda index) and the metabolically abnormal obese (HRs ranged from 1.57 [1.08–2.28] for the Matsuda index to 2.05 [1.44–2.92] for criteria defined in a separate study) had an increased risk of mortality. The only exception was the lack of excess risk using the HOMA criterion for the metabolically healthy obese (1.08; 0.67–1.74). Among the obese, the risk of mortality did not vary as a function of metabolic health apart from when using the HOMA criterion (1.93; 1.15–3.22). Similar results were obtained for cardiovascular mortality.

CONCLUSIONS

For most definitions of metabolic health, both metabolically healthy and unhealthy obese patients carry an elevated risk of mortality.Obesity is a major public health problem that has reached epidemic proportions worldwide (1). It is associated with numerous metabolic and cardiovascular disturbances such as insulin resistance, type 2 diabetes, hypertension, and dyslipidemia (2–5). However, these cardiometabolic abnormalities are not found in all obese people (6,7), as evidenced by the occurrence of a subset of apparently healthy obese subjects referred to as metabolically healthy obese (MHO) (8,9). Several studies have confirmed the existence of MHO individuals (10–16), accounting for as much as 40% of the obese population. MHO individuals display a favorable metabolic profile, characterized by high levels of insulin sensitivity, a low prevalence of hypertension, and a favorable lipid and inflammation profile.The long-term health consequences of obesity among those who are metabolically healthy remain unclear. Obesity is known to carry an elevated risk of mortality (17), but few studies have examined associations of the MHO phenotype with mortality, and the evidence from these studies is mixed. In general population samples from Scotland and England, MHO individuals were not at increased risk of all-cause and cardiovascular disease (CVD) mortality compared with healthy nonobese individuals (18), a finding replicated in an Italian study of obesity and insulin sensitivity (19). However, overweight and obese individuals without the metabolic syndrome had an increased risk of mortality compared with normal-weight individuals without the metabolic syndrome in a Swedish cohort of middle-aged men (20). Furthermore, in the U.S. National Health and Nutrition Examination Survey III (21), metabolically healthy and abnormal obese individuals had similar elevations in mortality risk compared with metabolically healthy, normal-weight subjects. Several factors may have contributed to these inconsistencies. The comparison group varies when estimating risk of mortality in the MHO phenotype; risk is compared either with metabolically healthy nonobese (18,19) or metabolically healthy, normal-weight people (20,21). Another difference between the studies is that metabolic health is defined in different ways, with little consensus on how best to define it. Therefore, the objective of the current study is to assess whether there is consistency in the association of the MHO phenotype with all-cause and CVD mortality using different definitions of metabolic health and reference groups.     

What Does Teaching Declaratives Tell Us About the Criteria by Which we Can Judge the Developmental Importance of Treatment Outcomes?

This paper uses examples of treatment research on declaratives to illustrate criteria for determining whether a taught behavior is a "skill", not just a context-bound behavior and whether the taught skill has associations with other theoretically linked skills as one type of validation evidence. The paper uses data from three treatment studies to illustrate the issues and proposed criteria. The paper concludes with a call to consumers and producers of treatment research to use the criteria to judge the developmental importance of treatment outcomes.     

Does the association of habitual physical activity with the metabolic syndrome differ by level of cardiorespiratory fitness?

OBJECTIVE: Cardiovascular fitness (VO(2max)) and physical activity are both related to risk of metabolic disease. It is unclear, however, whether the metabolic effects of sedentary living are the same in fit and unfit individuals. The purpose of this study was, therefore, to describe the association between physical activity and the metabolic syndrome and to test whether fitness level modifies this relationship. RESEARCH DESIGN AND METHODS: Physical activity was measured objectively using individually calibrated heart rate against energy expenditure. VO(2max) was predicted from a submaximal exercise stress test. Fat mass and fat-free mass (FFM) were calculated using impedance biometry. A metabolic syndrome score was computed by summing the standardized values for obesity, hypertension, hyperglycemia, insulin resistance, hypertriglyceridemia, and the inverse level of HDL cholesterol and was expressed as a continuously distributed outcome. To correct for exposure measurement error, a random subsample (22% of cohort) re-attended for three repeat measurements in the year following the first assessment. RESULTS: The relationship of VO(2max) (ml O2.kg(FFM)(-1).min(-1)) and the metabolic syndrome score was of borderline significance after adjusting for age, sex, physical activity, and measurement error (beta = -0.58, P = 0.06). The magnitude of the association between physical activity (kJ.d(-1).kg(FFM)(-1)) and the metabolic syndrome was more than three times greater than for VO(2max) (standardized beta = -1.83, P = 0.0042). VO(2max), however, modified the relationship between physical activity energy expenditure and metabolic syndrome (P = 0.036). CONCLUSIONS: This study demonstrates a strong inverse association between physical activity and metabolic syndrome, an association that is much steeper in unfit individuals. Thus, prevention of metabolic disease may be most effective in the subset of unfit inactive people.