The Impact of Tobacco Smoke Exposure on Childhood Asthma in a Medicaid Managed Care Plan.

BACKGROUND: Tobacco smoke exposure increases breathing problems of children. Texas Children's Health Plan is a Managed Medicaid and Children's Health Insurance Program (CHIP) managed care provider. The aim of this study is to determine associations among tobacco smoke exposure, asthma prevalence, and asthma health-care utilization. METHODS: Texas Children's Health Plan conducts an annual survey of members who have a physician visit. Questions were added to the survey in March 2010 about asthma and tobacco smoke exposure. Survey results for children < 18 years of age were matched to health plan claims data for the 12 months following the date of the physician visit. RESULTS: A total of 22,470 parents of unique members/patients from birth to < 18 years of age participated in the survey. More whites than African Americans or Hispanics report that the child's mother is a smoker (19.5% vs 9.1% and vs 2.3%, respectively; P < .001). Compared with children whose mother does not smoke, parent report of asthma diagnosis and claims for dispensing of short-acting beta agonist medication are greater if the mother is a smoker (adjusted OR, 1.20 [95% CI, 1.03-1.40] and 1.24 [95% CI, 1.08-1.42], respectively). In contrast to Medicaid, in which there are no out-of-pocket costs, the CHIP line of business requires copays for ED visits. ED visits are influenced by maternal smoking only in the CHIP line of business (adjusted OR, 4.40; 95% CI, 1.69-11.44). CONCLUSION: Maternal smoking increases risk for asthma diagnosis and prescription of asthma quick relief medication. Maternal smoking predicted asthma-related ED visits only for the CHIP line of business.

Lipoprotein-associated phospholipase A2 mass is significantly reduced in dyslipidemic patients treated with lifestyle modification and combination lipid-modifying drug therapy.

Lipoprotein-associated phospholipase A2 (Lp-PLA(2)) mass is a novel inflammatory biomarker. In human blood, Lp-PLA(2) is predominately associated with low-density lipoprotein (LDL). This study examines the ability of lifestyle modification (diet and exercise) and combination lipid therapy to reduce Lp-PLA(2) levels while also determining the relationship between changes in LDL cholesterol and Lp-PLA(2). Thirty dyslipidemic patients who received lifestyle intervention and combination lipid therapy for an average of 6 months were included in these analyses (mean age, 60.9 years); 40% had stable angiographically established coronary artery disease, 40% had the metabolic syndrome, and 70% were men. Drug therapy included omega-3 fish oil, extended-release niacin, colesevelam hydrochloride, and a fixed combination of 10-mg ezetimibe and 40-mg simvastatin. The study revealed a 33% reduction in mean Lp-PLA(2) values (baseline 224.9+/-47.5 vs posttreatment 149.5+/-35.5 ng/mL; P<.001). Significant changes in mean LDL cholesterol from baseline (127.9+/-49.3 vs posttreatment 65.2+/-32.1 mg/dL; P<.001) were also observed. However, regression analysis revealed only a weak positive relationship between changes in LDL cholesterol and Lp-PLA(2) mass (R(2)=0.29; P<.01). Thus, Lp-PLA(2) mass is significantly reduced with lifestyle and combination lipid therapy. Changes in Lp-PLA(2) were only partially explained by the changes observed for LDL cholesterol.

The role of insulin resistance in the pathogenesis of atherosclerotic cardiovascular disease: an updated review.

Insulin resistance is the main pathologic mechanism that links the constellation of clinical, metabolic and anthropometric traits with increased risk for cardiovascular disease and type II diabetes mellitus. These traits include hyperinsulinemia, impaired glucose intolerance, endothelial dysfunction, dyslipidemia, hypertension, and generalized and upper body fat redistribution. This cluster is often referred to as insulin resistance syndrome. The progression of insulin resistance to diabetes mellitus parallels the progression of endothelial dysfunction to atherosclerosis leading to cardiovascular disease and its complications. In fact, insulin resistance assessed by homeostasis model assessment (HOMA) has shown to be independently predictive of cardiovascular disease in several studies and one unit increase in insulin resistance is associated with a 5.4% increase in cardiovascular disease risk. This review article addresses the role of insulin resistance as a main causal factor in the development of metabolic syndrome and endothelial dysfunction, and its relationship with cardiovascular disease. In addition to this, we review the type of lifestyle modification and pharmacotherapy that could possibly ameliorate the effect of insulin resistance and reverse the disturbances in insulin, glucose and lipid metabolism.

Efficacy of combination drug pulse therapy in maintaining lipid levels in patients intolerant of daily statin use.

The objective of this study was to evaluate the efficacy of combination drug pulse therapy in maintaining lipid levels in patients intolerant of a daily dose of statins. Twenty-three patients, previously receiving aggressive statin therapy, were treated twice weekly with rosuvastatin or atorvastatin in different dosages along with ezetimibe as well as daily doses of bile acid sequestrant for a mean period of 4.5 months. The recommended National Cholesterol Education Program Adult Treatment Panel III goals had already been achieved in 78% of patients (n=18) before starting combination pulse therapy. This combination therapy significantly increased high-density lipoprotein cholesterol values by 5.82% (t=2.138, P=.044), while the increases in total cholesterol, low-density lipoprotein cholesterol, triglyceride, and apolipoprotein B levels compared with baseline were not statistically significant. Overall, 3 of 23 patients (13%) discontinued the combination therapy because of muscle-related symptoms over a mean course of 4.5 months of treatment.

The role of lipoprotein-associated phospholipase A2 on cardiovascular disease risk assessment and plaque rupture: a clinical review.

During the last several last decades, reduction in lipids has been the main focus to decrease the risk of coronary heart disease (CHD). Several lines of evidence, however, have indicated that lipids account only for the <50% of variability in cardiovascular risk in the United States. Therefore, for better identification of people at high cardiovascular risk, a more effective and complete approach is required. Our understanding of atherosclerosis has shifted from a focal disease resulting in symptoms caused by severe stenosis to a systemic disease distinguished by plaque inflammation with a potential to rupture and thrombosis, turning a substenotic atherosclerotic lesion into a complete occlusive lesion. Lipoprotein-associated phospholipase A(2) (Lp-PLA(2)) is a novel inflammatory biomarker that can provide much needed information about plaque inflammation and plaque stability. Lp-PLA(2) is among the multiple biomarkers that have been associated with increased CHD risk. In this present work, we review the evidence from previous studies addressing the effect of different therapies on decreasing Lp-PLA(2) and the role of direct Lp-PLA(2) inhibitors. This work also briefly reviews the evidence of Lp-PLA(2) clinical utility as a potential marker of vascular inflammation and formation of rupture prone plaques. Additionally, we also discuss the implication of available evidence in context of current cardiovascular inflammatory biomarkers recommendations and the evidence from epidemiologic studies addressing the relationship of Lp-PLA(2) and risk of cardiovascular disease.

Effects of lifestyle counseling and combination lipid-modifying therapy on lipoprotein-associated phospholipase A2 mass concentration.

BACKGROUND: Lipoprotein-associated phospholipase A2 (Lp-PLA(2)) is a novel inflammatory biomarker that is associated with increased cardiovascular disease risk independent of and additive to traditional risk factors. Lp-PLA(2) activity is correlated with the degree of inflammation in the atherosclerotic plaque. In human blood, approximately 80% of Lp-PLA(2) is associated with low-density lipoproteins (LDL). Thus, it is hypothesized that changes in Lp-PLA(2) should imitate the changes in the LDL cholesterol. OBJECTIVE: In this present study, we examined the efficacy of lifestyle intervention and combination lipid-lowering therapy on reducing the Lp-PLA(2) levels and determined the relationship between changes in LDL-C and Lp-PLA(2). METHODS: This retrospective chart review study includes two hundred forty eight patients (58% men and 42% women) who completed the life style intervention in combination with pharmacologic therapy for an average period of 10.5 months. Life style modification included diet and exercise counseling. Combination therapy included omega 3 fish oil (2000mg/d), extended-release niacin (500-1000mg/d), ezetimibe (10mg/d), fenofibrate 160mg/d and colesevelam HCI (1850mg/d), as well as statins. The statins used were either simvastatin (20-40mg/d) or rosuvastatin (5-20mg/d). Sixty five percent (n=161) received low to medium doses of simvastatin, whereas 35% (n=87) received low to medium doses of rosuvastatin. RESULTS: The study revealed a 32.5% reduction in mean Lp-PLA(2) values (baseline 181.1±41.5 vs 122.1±28.1 ng/mL after treatment; P<.001). The change observed in LDL-C was 41%, (baseline 126.2±43 vs 73.9±37.7mg/dL after treatment), which also was significant (P < .001). However, a Pearson correlation test analysis revealed only a weak positive association between changes in Lp-PLA(2) and LDL-C (r(2)=0.052, P < .001). CONCLUSION: Lp-PLA(2) is reduced with the use of life style counseling and combination lipid lowering therapy. Results also revealed that changes in Lp-PLA(2) may be partially explained by the changes in LDL-C.