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 .
A co-operative trial in the primary prevention of ischaemic heart disease using clofibrate. Report from the Committee of Principal Investigators.
A double-blind intervention trial was started in 1965 to test the hypothesis that the incidence of ischaemic heart disease in middle-aged men can be reduced by lowering raised serum cholesterol levels . It was carried out in 3 European centres-Edinburgh , Budapest , and Prague . Serum cholesterol was to be lowered by the drug clofibrate ( ethyl chlorophenoxyisobutyrate ) which was considered to be free from serious side effects . Studies were carried out on 15 745 males , aged 30 to 59 at entry , for an average of 5 - 3 years , accumulating 83 534 years of experience . The treatment group , of about 5000 , Group I , was a r and omly chosen half of the men in the upper third of the serum cholesterol distribution in some 30 000 volunteers . The comparable control group , Group II , comprised the other 5000 men of the upper third of the cholesterol distribution , and these were given a placebo . A further control group , Group III , of 5000 men , was selected r and omly from the lower third of the cholesterol distribution . These numbers were chosen in order to be 90 per cent certain of detecting a 30 per cent reduction in the incidence of ischaemic heart disease should this occur . Subjects with manifest heart or other major disease were excluded from the trial . No attempt was made to correct other ' risk factors ' for IHD , but their presence was monitored and considered in the analysis . Investigators and participants in the trial were unaware of the groups to which individual men belonged . A mean reduction of approximately 9 per cent of the initial serum cholesterol levels was achieved in the treatment group ( ranging from 7 to 11 % in the 3 centres ) ; this was less than the 15 per cent fall expected . In Edinburgh , during treatment , serum triglyceride concentrations in Group I resembled those naturally occurring in Group III . The incidence ofIHO was lower by 20 per cent in the clofibrate group compared with the high cholesterol controls ( P < 0.05 ) ; this fall was confined to non-fatal myocardial infa rcts which were reduced by 25 per cent . The incidence offatal heart attacks was similar in the 2 high cholesterol groups and there was no significant difference in the incidence of angina . Group III showed substantially lower rates of ischaemic heart disease . The reduction of myocardial infa rct ion in the clofibrate-treated group was greatest in men with the highest levels , and greatest reduction in serum cholesterol . Men with a substantial reduction of cholesterol concentration , who smoked , and also had above average blood pressure levels showed the most benefit . The numbers of deaths , and crude mortality rates from all causes in the clofibrate-treated group significantly exceeded those in the high cholesterol control group ( P < 0.05 ) , though the age-st and ardised mortality rates did not differ significantly between the 3 groups . The numbers of deaths from '
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 .