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Michael Wegner - One of the best experts on this subject based on the ideXlab platform.
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abstract 3531 lipoprotein associated phospholipase a2 mass is significantly reduced in dysLipidemic patients treated with lifestyle counseling and combination Lipid Modifying Drug therapy
Circulation, 2007Co-Authors: Joey Banjit, Kota J. Reddy, Miseah Zaheer, Arsalan Kahn, Carol Cockerham, Rick Lanman, Michael WegnerAbstract:Background: Lipoprotein-associated phospholipase A 2 (Lp-PLA 2 ) mass is a novel inflammatory biomarker and independent predictor for cardiovascular disease. In human blood, Lp-PLA 2 is predominately associated with low-density lipoprotein (LDL). Thus, it is hypothesized that changes in Lp-PLA 2 should mirror changes in levels of LDL. To our knowledge, no studies exist which have examined the efficacy of lifestyle intervention and Lipid Drug therapy on reducing levels of Lp-PLA 2 while also determining the relationship between changes in LDL and Lp-PLA 2 . Therefore, the primary purpose of this study was to assess the ability of lifestyle and combination Lipid Drug therapy to reduce levels of Lp-PLA 2 among patients treated for mixed dysLipidemia. The secondary purpose was to examine the relationship between changes observed in Lp-PLA 2 and LDL cholesterol (LDL-C). Methods: Thirty dysLipidemic patients who received lifestyle intervention and combination Lipid altering Drug therapy for an average period of 6 months were included in these analyses (mean age=60.9, 40% with stable angiographically established CAD, 40% metabolic syndrome, 70% male). Lifestyle intervention included diet and exercise counseling. Drug therapy included omega-3 fish oil, extended release niacin, colesevelam HCl and a fixed combination of 10 mg ezetimibe and 40 mg simvastatin. Measures of Lp-PLA 2 were determined by an FDA approved ELISA assay (PLAC ™ test, diaDexus, Inc.), whereas LDL-C was calculated with the Friedewald equation using overnight fasting blood samples. Results: The study revealed a 34% reduction in median Lp-PLA 2 values (baseline 230.5 3 47.4 vs. post-treatment 151.0 ± 35.5 ng/mL; p 2 mass (R 2 =0.29; p Conclusion: Lp-PLA 2 mass is significantly reduced with the use of lifestyle and combination Lipid lowering Drug therapy. Changes in Lp-PLA 2 were only partially explained by the changes observed for LDL-C.
Kota J. Reddy - One of the best experts on this subject based on the ideXlab platform.
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Lipoprotein-associated phospholipase A2 mass is significantly reduced in dysLipidemic patients treated with lifestyle modification and combination Lipid-Modifying Drug therapy.
Preventive Cardiology, 2009Co-Authors: Kota J. Reddy, Richard R. Batsell, Joey R. Bangit, Rekha A. Miraskar, Manmeet Singh, Misbah S. ZaheerAbstract:Lipoprotein-associated phospholipase A2 (Lp-PLA2) mass is a novel inflammatory biomarker. In human blood, Lp-PLA2 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-PLA2 levels while also determining the relationship between changes in LDL cholesterol and Lp-PLA2. 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-PLA2 values (baseline 224.9±47.5 vs posttreatment 149.5±35.5 ng/mL; P
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lipoprotein associated phospholipase a2 mass is significantly reduced in dysLipidemic patients treated with lifestyle modification and combination Lipid Modifying Drug therapy
Preventive Cardiology, 2009Co-Authors: Kota J. Reddy, Richard R. Batsell, Joey R. Bangit, Rekha A. Miraskar, Manmeet Singh, Misbah S. ZaheerAbstract:Lipoprotein-associated phospholipase A2 (Lp-PLA2) mass is a novel inflammatory biomarker. In human blood, Lp-PLA2 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-PLA2 levels while also determining the relationship between changes in LDL cholesterol and Lp-PLA2. 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-PLA2 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-PLA2 mass (R2=0.29; P<.01).Thus, Lp-PLA2 mass is significantly reduced with lifestyle and combination Lipid therapy. Changes in Lp-PLA2 were only partially explained by the changes observed for LDL cholesterol. Prev Cardiol. 2010;13:130–134.©2009 Wiley Periodicals, Inc.
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abstract 3531 lipoprotein associated phospholipase a2 mass is significantly reduced in dysLipidemic patients treated with lifestyle counseling and combination Lipid Modifying Drug therapy
Circulation, 2007Co-Authors: Joey Banjit, Kota J. Reddy, Miseah Zaheer, Arsalan Kahn, Carol Cockerham, Rick Lanman, Michael WegnerAbstract:Background: Lipoprotein-associated phospholipase A 2 (Lp-PLA 2 ) mass is a novel inflammatory biomarker and independent predictor for cardiovascular disease. In human blood, Lp-PLA 2 is predominately associated with low-density lipoprotein (LDL). Thus, it is hypothesized that changes in Lp-PLA 2 should mirror changes in levels of LDL. To our knowledge, no studies exist which have examined the efficacy of lifestyle intervention and Lipid Drug therapy on reducing levels of Lp-PLA 2 while also determining the relationship between changes in LDL and Lp-PLA 2 . Therefore, the primary purpose of this study was to assess the ability of lifestyle and combination Lipid Drug therapy to reduce levels of Lp-PLA 2 among patients treated for mixed dysLipidemia. The secondary purpose was to examine the relationship between changes observed in Lp-PLA 2 and LDL cholesterol (LDL-C). Methods: Thirty dysLipidemic patients who received lifestyle intervention and combination Lipid altering Drug therapy for an average period of 6 months were included in these analyses (mean age=60.9, 40% with stable angiographically established CAD, 40% metabolic syndrome, 70% male). Lifestyle intervention included diet and exercise counseling. Drug therapy included omega-3 fish oil, extended release niacin, colesevelam HCl and a fixed combination of 10 mg ezetimibe and 40 mg simvastatin. Measures of Lp-PLA 2 were determined by an FDA approved ELISA assay (PLAC ™ test, diaDexus, Inc.), whereas LDL-C was calculated with the Friedewald equation using overnight fasting blood samples. Results: The study revealed a 34% reduction in median Lp-PLA 2 values (baseline 230.5 3 47.4 vs. post-treatment 151.0 ± 35.5 ng/mL; p 2 mass (R 2 =0.29; p Conclusion: Lp-PLA 2 mass is significantly reduced with the use of lifestyle and combination Lipid lowering Drug therapy. Changes in Lp-PLA 2 were only partially explained by the changes observed for LDL-C.
Joey Banjit - One of the best experts on this subject based on the ideXlab platform.
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abstract 3531 lipoprotein associated phospholipase a2 mass is significantly reduced in dysLipidemic patients treated with lifestyle counseling and combination Lipid Modifying Drug therapy
Circulation, 2007Co-Authors: Joey Banjit, Kota J. Reddy, Miseah Zaheer, Arsalan Kahn, Carol Cockerham, Rick Lanman, Michael WegnerAbstract:Background: Lipoprotein-associated phospholipase A 2 (Lp-PLA 2 ) mass is a novel inflammatory biomarker and independent predictor for cardiovascular disease. In human blood, Lp-PLA 2 is predominately associated with low-density lipoprotein (LDL). Thus, it is hypothesized that changes in Lp-PLA 2 should mirror changes in levels of LDL. To our knowledge, no studies exist which have examined the efficacy of lifestyle intervention and Lipid Drug therapy on reducing levels of Lp-PLA 2 while also determining the relationship between changes in LDL and Lp-PLA 2 . Therefore, the primary purpose of this study was to assess the ability of lifestyle and combination Lipid Drug therapy to reduce levels of Lp-PLA 2 among patients treated for mixed dysLipidemia. The secondary purpose was to examine the relationship between changes observed in Lp-PLA 2 and LDL cholesterol (LDL-C). Methods: Thirty dysLipidemic patients who received lifestyle intervention and combination Lipid altering Drug therapy for an average period of 6 months were included in these analyses (mean age=60.9, 40% with stable angiographically established CAD, 40% metabolic syndrome, 70% male). Lifestyle intervention included diet and exercise counseling. Drug therapy included omega-3 fish oil, extended release niacin, colesevelam HCl and a fixed combination of 10 mg ezetimibe and 40 mg simvastatin. Measures of Lp-PLA 2 were determined by an FDA approved ELISA assay (PLAC ™ test, diaDexus, Inc.), whereas LDL-C was calculated with the Friedewald equation using overnight fasting blood samples. Results: The study revealed a 34% reduction in median Lp-PLA 2 values (baseline 230.5 3 47.4 vs. post-treatment 151.0 ± 35.5 ng/mL; p 2 mass (R 2 =0.29; p Conclusion: Lp-PLA 2 mass is significantly reduced with the use of lifestyle and combination Lipid lowering Drug therapy. Changes in Lp-PLA 2 were only partially explained by the changes observed for LDL-C.
Gillian M. Keating - One of the best experts on this subject based on the ideXlab platform.
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Prolonged-Release Nicotinic Acid
Drugs, 2005Co-Authors: Paul L. Mccormack, Gillian M. KeatingAbstract:Prolonged-release (PR) nicotinic acid (niacin) [Niaspan®] is an oral, once-daily formulation of the Lipid-Modifying Drug designed to produce less vasodilatory flushing than crystalline immediate-release (IR) nicotinic acid and less hepatotoxicity than previous sustained-release formulations of nicotinic acid. PR nicotinic acid appears to retain the same level of efficacy as crystalline IR nicotinic acid and be better tolerated than older nicotinic acid formulations. Nicotinic acid has beneficial effects on all traditional blood Lipid and lipoprotein fractions and is the most effective agent for increasing high-density lipoprotein (HDL)-cholesterol (HDL-C) and reducing lipoprotein(a). The effects of PR nicotinic acid are often additive when used in combination with HMG-CoA reductase inhibitors (statins), making it a useful addition when Lipid goals are not achieved with the usual statin monotherapy or when additional correction of a specific Lipid abnormality is required. PR nicotinic acid also slows atherosclerotic progression and even appears to produce regression of atherosclerosis in patients on stable statin therapy. PR nicotinic acid is a logical Drug choice for treating atherogenic dysLipidaemia commonly associated with type 2 diabetes mellitus and the metabolic syndrome, and has been shown to be effective in patients with diabetes without adversely affecting glycaemic control in the majority of patients. The incidence of vasodilatory flushing with PR nicotinic acid is lower than with IR nicotinic acid and it decreases substantially over time as tolerance develops. To date, there has been no clinically significant hepatotoxicity observed with PR nicotinic acid. Therefore, once-daily PR nicotinic acid appears to maximise the potential benefits of nicotinic acid, while minimising any historical tolerability or safety concerns. Pharmacological Properties PR nicotinic acid appears to increase HDL-C levels by selectively blocking hepatic catabolic uptake of HDL particles containing apolipoprotein A-I and thereby augmenting reverse cholesterol transport. It selectively increases the proportion of larger HDL particles resulting in an overall increase in HDL particle size. The increase in HDL-C in patients with coronary artery disease was shown to correlate with improved endothelium-dependent vasodilation. PR nicotinic acid also reduces triglycerides and very low-density lipoprotein (VLDL) particles by decreasing the mobilisation of free fatty acids from peripheral adipose tissue to the liver. PR nicotinic acid decreases the number of low-density lipoprotein (LDL) particles and increases the mean LDL particle size. Oral PR nicotinic acid is rapidly absorbed and undergoes extensive first-pass metabolism. The time to peak plasma concentration was 4–5 hours. Approximately 60–76% of the dose was recovered in the urine as unchanged nicotinic acid or metabolites. The ratio of non-conjugative to conjugative metabolites decreased with increasing dosage of PR nicotinic acid between 1000 (7.2) and 3000 (1.4) mg/day. Therapeutic Efficacy PR nicotinic acid beneficially altered all serum Lipid components relative to placebo in patients with primary dysLipidaemia. The response was dose-proportional in the range 500–2000 mg/day. In two studies, PR nicotinic acid 2000 mg/ day increased HDL-C by 23% and 26% from baseline and decreased triglycerides by 29% and 35%, lipoprotein(a) by 24% and 27%, LDL-cholesterol (LDL-C) by 14% and 17%, apolipoprotein B by 16% and total cholesterol by 10% and 12%, respectively. PR nicotinic acid maintained full efficacy for at least 2 years in open-label extension studies. In a head-to-head comparison in patients with hyperLipidaemia, the efficacy of PR nicotinic acid was similar to that of IR nicotinic acid when administered at the same daily dosage (1500 mg/day). PR nicotinic acid 1500–2000 mg/day increased HDL-C and reduced lipoprotein(a) to a greater extent than did gemfibrozil 1200 mg/day in patients with low HDL-C, while gemfibrozil reduced triglycerides to a greater extent than did PR nicotinic acid. PR nicotinic acid tended to increase HDL-C more than lovastatin and to reduce lipoprotein(a) more than lovastatin or rosuvastatin in patients with hyperLipidaemia or mixed dysLipidaemia. Lovastatin and rosuvastatin each tended to reduce total cholesterol and LDL-C to a greater extent than PR nicotinic acid. The combinations of PR nicotinic acid/lovastatin 1500mg/20mg and 2000mg/ 40mg produced generally additive responses. Combinations of PR nicotinic acid and rosuvastatin were generally superior to rosuvastatin alone only with respect to improvements in HDL-C, lipoprotein(a) or apolipoprotein A-I. PR nicotinic acid in combination with a statin reduced the progression of carotid intima-media thickness compared with placebo, but the difference did not reach statistical significance. Atherosclerotic progression at 12 months in placebo recipients was statistically significant, while progression in recipients of PR nicotinic acid was not significant. Preliminary results from an open-label, 12-month extension study suggest that PR nicotinic acid added to a statin produces significant regression of atherosclerosis over 12–24 months. PR nicotinic acid 1500 mg/day effectively increased HDL-C and decreased triglycerides and LDL-C in patients with dysLipidaemia and type 2 diabetes. Tolerability PR nicotinic acid is generally well tolerated with most adverse events being mild-to-moderate in intensity and transient in nature. Flushing was the most frequent adverse event, followed by gastrointestinal symptoms and other cutaneous reactions. PR nicotinic acid-induced flushing decreased over time and was associated with a low incidence of treatment discontinuation. The incidence of flushing with PR nicotinic acid was initially significantly lower than that with IR nicotinic acid. PR nicotinic acid produced small, reversible elevations in liver transaminases, but there was no clinically significant hepatotoxicity. Similarly, elevated uric acid levels associated with recommended dosages of PR nicotinic acid did not result in any instances of clinical gout. PR nicotinic acid therapy in patients with type 2 diabetes and dysLipidaemia was associated with a small, but statistically significant, increase in glycosylated haemoglobin levels. However, fasting blood glucose levels were well controlled over the course of the 16-week study in most patients. The incidence of adverse events and treatment discontinuation was higher with PR nicotinic acid than with lovastatin or rosuvastatin, predominantly as a result of flushing with PR nicotinic acid, while the overall tolerability of PR nicotinic acid was similar to that of gemfibrozil. No instances of myopathy or new adverse events occurred when PR nicotinic acid was given in combination with statins.
Misbah S. Zaheer - One of the best experts on this subject based on the ideXlab platform.
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Lipoprotein-associated phospholipase A2 mass is significantly reduced in dysLipidemic patients treated with lifestyle modification and combination Lipid-Modifying Drug therapy.
Preventive Cardiology, 2009Co-Authors: Kota J. Reddy, Richard R. Batsell, Joey R. Bangit, Rekha A. Miraskar, Manmeet Singh, Misbah S. ZaheerAbstract:Lipoprotein-associated phospholipase A2 (Lp-PLA2) mass is a novel inflammatory biomarker. In human blood, Lp-PLA2 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-PLA2 levels while also determining the relationship between changes in LDL cholesterol and Lp-PLA2. 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-PLA2 values (baseline 224.9±47.5 vs posttreatment 149.5±35.5 ng/mL; P
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lipoprotein associated phospholipase a2 mass is significantly reduced in dysLipidemic patients treated with lifestyle modification and combination Lipid Modifying Drug therapy
Preventive Cardiology, 2009Co-Authors: Kota J. Reddy, Richard R. Batsell, Joey R. Bangit, Rekha A. Miraskar, Manmeet Singh, Misbah S. ZaheerAbstract:Lipoprotein-associated phospholipase A2 (Lp-PLA2) mass is a novel inflammatory biomarker. In human blood, Lp-PLA2 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-PLA2 levels while also determining the relationship between changes in LDL cholesterol and Lp-PLA2. 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-PLA2 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-PLA2 mass (R2=0.29; P<.01).Thus, Lp-PLA2 mass is significantly reduced with lifestyle and combination Lipid therapy. Changes in Lp-PLA2 were only partially explained by the changes observed for LDL cholesterol. Prev Cardiol. 2010;13:130–134.©2009 Wiley Periodicals, Inc.