Meta-analysis: no evidence that raising HDL lowers CV events
The Observational HDL Hypothesis: A Useful Therapeutic Target? a Meta Analysis of 117,411 Patients in Randomised Controlled Trials
News - June 18, 2014Keene D, Shun-Shin M, Price C, Francis D
Heart 2014;100:A62-A63
A meta-analysis presented at the British Cardiovascular Society Annual Conference 2014 shows that there are no HDL-raising agents that reduce all-cause mortality, coronary heart disease (CHD), myocardial infarction (MI) or stroke in statin-treated patients.
Epidemiological studies have identified HDL as a prognostic marker, which has led to the hypothesis that pharmacological intervention to raise HDL levels may be beneficial for CV outcomes.
A meta-analysis was conducted to evaluate the benefit of HDL-raising agents niacin, fibrates and cholesteryl ester transfer protein inhibitors (CETP-I) on all-cause mortality, CHD mortality, non-fatal myocardial infarction (MI) and stroke. 39 trials were included, with information on 117.411 patients who were randomised to HDL-raising therapy or control therapy.
Thus, the results of this meta-analysis do not support the observational hypothesis that raising HDL-levels reduces CV events.
This abstract was published in Heart
Heart 2014;100:A62-A63
A meta-analysis presented at the British Cardiovascular Society Annual Conference 2014 shows that there are no HDL-raising agents that reduce all-cause mortality, coronary heart disease (CHD), myocardial infarction (MI) or stroke in statin-treated patients.
Epidemiological studies have identified HDL as a prognostic marker, which has led to the hypothesis that pharmacological intervention to raise HDL levels may be beneficial for CV outcomes.
A meta-analysis was conducted to evaluate the benefit of HDL-raising agents niacin, fibrates and cholesteryl ester transfer protein inhibitors (CETP-I) on all-cause mortality, CHD mortality, non-fatal myocardial infarction (MI) and stroke. 39 trials were included, with information on 117.411 patients who were randomised to HDL-raising therapy or control therapy.
- All-cause mortality was not significantly affected by any of the pharmacotherapies (OR(niacin): 1.03, 95%CI: 0.92-1.15 (P=0.59), OR(fibrates): 0.98, 95%CI: 0.89-1.08 (P=0.66) and OR(CETP-I): 1.16, 95%CI: 0.93-1.44, (P=0.19)).
- Nor was there a significant effect of any of the HDL-raising therapies on CHD mortality (OR(niacin): 0.93, 95%CI: 0.76-1.12 (P=0.44), OR(fibrates): 0.92, 95%CI: 0.81-1.04 (P=0.19) and OR(CETP-I): 1.00, 95%CI: 0.80-1.24, (P=0.99)).
- Stroke risk was not affected by raising HDL-levels (OR(niacin): 0.96, 95%CI: 0.75-1.22 (P=0.72), OR(fibrates): 1.01, 95%CI: 0.90-1.13 (P=0.84) and OR(CETP-I): 1.14, 95%CI: 0.90-1.45, (P=0.29)).
- Only niacin trials that were conducted prior to routine statin therapy showed a significant reduction of non-fatal MI (OR: 0.69, 95%CI: 0.56-0.85, P=0.0004). Niacin with background statin therapy did not show a significant risk reduction (OR: 0.96, 95%CI: 0.85-1.09, P=0.52).
- Fibrates showed a similar difference in effect with or without background statin therapy (without statins: OR for non-fatal MI: 0.78, 95%CI: 0.71-0.86, P<0.00001), with background statins (OR: 0.83, 95%CI: 0.69-1.01, P=0.07).
Thus, the results of this meta-analysis do not support the observational hypothesis that raising HDL-levels reduces CV events.
This abstract was published in Heart
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