This significant effect was derived by the use of fibrates ( RR 0.80 , 95 % CI 0.73–0.87 , P < 0.001 , I2 = 22 % ) and meta-regression analysis showed that this benefit was consistent with an absolute reduction in low-density lipoprotein cholesterol .
Meta-regression analyses failed to demonstrate a significant association of pharmacologically increased high-density lipoprotein cholesterol with key endpoints .
Conclusion The use of high-density lipoprotein cholesterol modifying treatments had no significant effect on cardiovascular mortality , stroke or all-cause mortality .
The beneficial effect on myocardial infa rct ion was lost when drugs were used with statin therapy
Background The effects of increasing high-density lipoprotein cholesterol on cardiovascular outcomes remain uncertain .
Design We conducted a meta- analysis to investigate the effects of high-density lipoprotein cholesterol modifiers ( niacin , fibrates and cholesteryl ester transfer protein inhibitors ) on cardiovascular outcomes .
Helsinki Heart Study: primary-prevention trial with gemfibrozil in middle-aged men with dyslipidemia. Safety of treatment, changes in risk factors, and incidence of coronary heart disease.
In a r and omized , double-blind five-year trial , we tested the efficacy of simultaneously elevating serum levels of high-density lipoprotein ( HDL ) cholesterol and lowering levels of non-HDL cholesterol with gemfibrozil in reducing the risk of coronary heart disease in 4081 asymptomatic middle-aged men ( 40 to 55 years of age ) with primary dyslipidemia ( non-HDL cholesterol greater than or equal to 200 mg per deciliter [ 5.2 mmol per liter ] in two consecutive pretreatment measurements ) . One group ( 2051 men ) received 600 mg of gemfibrozil twice daily , and the other ( 2030 men ) received placebo . Gemfibrozil caused a marked increase in HDL cholesterol and persistent reductions in serum levels of total , low-density lipoprotein ( LDL ) , and non-HDL cholesterol and triglycerides . There were minimal changes in serum lipid levels in the placebo group . The cumulative rate of cardiac end points at five years was 27.3 per 1,000 in the gemfibrozil group and 41.4 per 1,000 in the placebo group -- a reduction of 34.0 percent in the incidence of coronary heart disease ( 95 percent confidence interval , 8.2 to 52.6 ; P less than 0.02 ; two-tailed test ) . The decline in incidence in the gemfibrozil group became evident in the second year and continued throughout the study . There was no difference between the groups in the total death rate , nor did the treatment influence the cancer rates . The results are in accord with two previous trials with different pharmacologic agents and indicate that modification of lipoprotein levels with gemfibrozil reduces the incidence of coronary heart disease in men with dyslipidemia
This significant effect was derived by the use of fibrates ( RR 0.80 , 95 % CI 0.73–0.87 , P < 0.001 , I2 = 22 % ) and meta-regression analysis showed that this benefit was consistent with an absolute reduction in low-density lipoprotein cholesterol .
Meta-regression analyses failed to demonstrate a significant association of pharmacologically increased high-density lipoprotein cholesterol with key endpoints .
Conclusion The use of high-density lipoprotein cholesterol modifying treatments had no significant effect on cardiovascular mortality , stroke or all-cause mortality .
The beneficial effect on myocardial infa rct ion was lost when drugs were used with statin therapy
Background The effects of increasing high-density lipoprotein cholesterol on cardiovascular outcomes remain uncertain .
Design We conducted a meta- analysis to investigate the effects of high-density lipoprotein cholesterol modifiers ( niacin , fibrates and cholesteryl ester transfer protein inhibitors ) on cardiovascular outcomes .