Relationship between Dietary Habits and Control of Lipid Profiles in Patients with Dyslipidemia Using Pravastatin
Seo Young KangTae Hee JeonKeun‐Sang YumSung SunwooHyun‐Young ShinDae Hyun KimKi-duk KimJong Lull YoonJaekyung ChoiYoung Sik Kim
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Abstract:
We investigated the association between dietary habits, evaluated using the modified Mini Dietary Assessment Index for Koreans (MDA), and lipid control among patients aged ≥20 years who had used pravastatin for dyslipidemia for 6 months. Participants were administered questionnaires regarding sociodemographic characteristics and lifestyle factors. Odds ratios and 95% confidence intervals for the control of low-density lipoprotein cholesterol (LDL-C), triglyceride (TG), and total cholesterol (TC) at 6 months for each category of the modified MDA items were calculated through multivariate logistic regression analysis. The odds for controlled LDL-C was higher among those who consumed cholesterol-rich foods <1 time/week (3.27, 1.25-8.57) than for those who did so ≥4 times/week. The odds for controlled TG was higher among those who always consumed dairy products (2.96, 1.36-6.44), ate protein-rich foods three times/day (2.94, 1.06-8.10), and had a regular eating schedule (3.02, 1.30-7.00) than among those who did not have any of these. The odds for controlled TC was higher among those with a regular eating schedule (3.47, 1.55-7.76) than among their counterparts. Patients with dyslipidemia should consume less cholesterols, consume more dairy and protein-rich foods, and follow a regular eating schedule to control lipid profiles.Keywords:
Dyslipidemia
Secondary Prevention
Cardiovascular event
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To study the effect of the beneficial influence of early Pravastatin therapy with large dose on baroreflex sensitivity(BRS) and chemoreflex sensitivity(ChRS) after acute myocardial infarction(AMI), 84 patients were divided randomly into control,pravastatin 20mg/d and Pravastatin 40mg/d groups.Blood lipid were measured on the first day and after 4 weeks, BRS,ChRS were measured on the fifth day and after 4 weeks. Total harmful responses were followed by for three weeks.Results:After 4 weeks the levels of cholesterol,HDL-c ,LDL-c,triglyceride in Pravastatin 20mg/d and 40mg/d group had significant difference compared to those before therapy;the difference between control and treatment group was significant(P0.05),but between two treatment groups was not significant(P0.05). After 4 weeks the levels of BRS and ChRS in three groups were significantly better than those on the fifth day,but between control and treatment group was significant(7.34±2.26,6.87±0.53 vs 5.66±1.34;7.83±3.36,6.38±1.25 vs 5.28±1.12;all P0.05).After 4 weeks the levels of BRS and ChRS in Pravastatin 40mg/d group were significantly better than those in Pravastatin 20mg/d group(P0.05).Conclusion:The early intensive pravastatin therapy is effective and safe,it can improve the levels of BRS and ChRS after AMI.
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Conventional lipid-lowering agents displayed only limited efficacy in lowering total and LDL cholesterol and a high incidence of side effects. Pravastatin is a new potent cholesterol-lowering agent, which selectively inhibits hepatic HMG-CoA-reductase. In a double-blind, placebo-controlled Swiss multicenter study with determination of lipids and lipoprotein in a central laboratory, the efficacy and safety of 6 months' therapy with pravastatin was evaluated in 50 patients with mild hypercholesterolemia and additional coronary risk factors. Compared to baseline and after 26 weeks' therapy, pravastatin significantly reduced total cholesterol (pravastatin vs placebo, -17% vs +7%, p < 0.0001) and LDL cholesterol (-26 vs +2%, p < 0.0001). The total/HDL cholesterol ratio ( = "atherogenic index") was comparable in the two groups at baseline (5.9 +/- 1.1 vs 6.3 +/- 0.9), and was distinctly lowered by pravastatin but not placebo (-20 vs 0%, p < 0.0001). In 11 patients in whom the reduction of serum total cholesterol after 13 weeks' treatment with 20 mg pravastatin was still below target (on average -9.1%), doubling of the dose produced a further decrease of 4.3%. Serum HDL cholesterol and serum triglyceride levels did not change significantly during pravastatin treatment as compared to baseline and placebo. Pravastatin was well tolerated during the 26 weeks without relevant subjective side-effects. There were 5 dropouts during the study, 2 patients in the pravastatin group and 3 in the placebo group. These findings document that pravastatin, administered in a single daily dose of 20 to 40 mg, effectively lowers serum cholesterol and total-/HDL-cholesterol improving action and is well tolerated.
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Pravastatin is an inhibitor of HMG-CoA reductase inhibitor which is used as a hypolipidemic agent to reduce cholesterol level. Chemically, 9-Fluoro-11β,17-dihydroxy-16α-methyl-3,20-dioxopregna-1,4-dien21-yl disodium phosphate. Pravastatin is a drug of choice for the cardiovascular disease. It reduces the coronary and cerebrovascular morbidity and mortality in middle aged individual. Elevated plasma concentration of C-reactive protein are associated with protein increased cardiovascular disease, long term therapy with pravastatin an agent that reduces cardiovascular risk, might alter levels of this inflammatory parameter. This review consist of various analytical methods for the determination of pravastatin in various marketed pharmaceutical formulation of biological fluid. Analytical methods consist of various chromatographic methods, spectrophotometer methods and electrical methods reported for determination of pravastatin.
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AIM: To observe and compare the antihyperlipidemia efficacy of fluvastatin vs pravasatin. METHODS: Fluvastatin group( n =41,M 22, F 19; age 60 a± s 8 a) was treated with fluvastatin 20 40 mg, po , qn for 4 wk. Pravastatin group( n =35, M 20, F 15; age 60 a±6 a) was treated with pravastatin 10 mg, po , qn for 4 wk. RESULTS: The total effective rate of fluvastatin for reducing TC was 92 %, it was higher than that of pravastatin 70 %( P 0.05). The total effective rates of flavastatin for reducing TG and raising HDL C were 61 % and 61 %, were similar to that of pravastatin 73 % and 69 %( P 0.05). Adverse reactions occurred in 8 patients of fluvastatin(20 %) and in 7 patients of pravastatin(20 %), but were mild in both groups. CONCLUSION: Fluvastatin is a safe and effective antihyperlipidemic drug, and fluvastatin is more effective than pravastatin in decreasing total cholesterol.
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Objective:To compare the lipid - regulating effects of fluvastatin and pravastatin. Methods:40 patients in fluvastatin group received 40mg of fluvastatin a day and 38 patients in pravastatin group received 20mg of pravastatin a day. All the two groups were treated for four weeks. Results: The fluvastatin and pravastatin lowered serum total cholesterol by 87 % and 87 % , triglyceride, 60% and 61 % , while they elevated high-density lipoprotein- cholesterol by 65 % and 63 % . Conclusion: Both drugs have similar lipid-regulating effect.
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42 patients with acute cerebral stroke (average age 70, 83ą9, 95 years) were examined for fluctuations in the level of serum triglyceride, total cholesterol, HDL-cholesterot and LDL-cholesterol within 24 hours after the acute event and on the eight day after the onset of symptoms. Patients did not receive specific hipolipemic drugs during the treatment. On the first day average values of serum triglyceride were 1, 97ą0, 94 ; of total cholesterol 5, 99 ą1, 91 ; of HDL-cholesterol 0, 86ą0, 35 and of LDL-cholesterol 3, 91ą1, 63 mmol/L. On the eight day average values of triglyceride were 2, 26ą2, 31 ; of total cholesterol 4, 59ą1, 49 ; of HDL-cholesterol 1, 2ą0, 54 and of LDL-cholesterol 2, 91ą1, 17 mmol/L. The results revealed a statistically significant (p<0, 05) decrease in total cholesterol and LDL-cholesterol and statistically significaiit increase in HDL-cholesterol, while there was no statistically significant difference between levels of triglyceride. We. conclude that in patients with acute cerebral stroke, triglyceride, total cholesterol and LDL cholesterol is increased, due to stress and increased secretion of catecholamines. On the eight day there is decrease in serum levels of triglyceride, total cholesterol and LDL-cholesterol, while HDL-cholesterol is increased. These changes are probably due to dietary changes after stroke, besides the fact that stress inducing catecholamines overproduction is no long acting.
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To assess the effects of pravastatin on all-cause mortality and cause-specific mortality and to compare the effects for patients with prior coronary heart disease with those for patients without, using pooled data from the Long-Term Intervention with Pravastatin in Ischaemic Disease (LIPID) study, the Cholesterol and Recurrent Events (CARE) study, and the West of Scotland Coronary Prevention Study (WOSCOPS).13 173 patients with coronary heart disease and 6595 men with elevated cholesterol and no prior coronary disease received pravastatin, 40 mg daily, or placebo for an average of 5 to 6 years. Data were analysed according to a pre-specified, published protocol. For all three trials combined, the mortality among patients assigned pravastatin was significantly lower, at 7.9%, than the 9.8% among those assigned placebo, a relative risk reduction of 20% (95% confidence interval (CI) 12-27%, P<0.0001). Active treatment was associated with a reduction in coronary mortality (24%, 95% CI 14-33%). Larger reductions in absolute risk were estimated in those with prior coronary heart disease than in those without.Treatment with pravastatin over 5 years reduces all-cause mortality and coronary mortality in patients with and those without a history of coronary heart disease. The size of the benefit was related principally to the baseline risk.
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