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Editor’s Note
Welcome to “What Matters,” a blog about the clinical research that is most likely to affect your practice, patient outcomes, and your bottom line. We know you have too much to read; there are simply too many studies and often too much buzz generated about them to really make sense of it all in a practical, systematic way. Dr. Jon O. Ebbert, professor of medicine at the Mayo Clinic in Rochester, Minn., offers an authoritative view on recent key clinical developments and what they may mean for you. Follow him every week to stay informed and on top of your world.
Elevated LDL cholesterol is an independent risk factor for cardiovascular disease (CVD) and the evidence supporting treatment to lower LDL is clear. Low HDL also is an independent risk factor for CVD. However, guidance is mixed and practice heterogeneous on how clinicians should address low HDL when LDL goals are achieved with statin therapy.
The AIM-HIGH trial recently published evidence on the effect of extended-release niacin among patients with established CVD with low baseline HDL (less than 40 mg/dL) (N. Engl. J. Med. 2011;365:2255-67). Subjects in the experimental group received niacin 1,500-2,000 mg per day plus simvastatin while subjects in the placebo group received a matching subtherapeutic control (50 mg immediate-release niacin) in addition to simvastatin to maintain blinding. Doses of simvastatin were adjusted to achieve a target LDL of 40-80 mg/dL. Subjects could receive ezetimibe to achieve target LDL cholesterol as needed. A very large sample size of 3,414 subjects was randomized. At 2 years, the mean HDL level had increased by 25% to 42 mg/dL in the niacin group and by about 10% to 38 mg/dL in the placebo group. Triglycerides also improved more in the niacin group. Study drug was discontinued in 25% of patients in the niacin group and 20% in the placebo group. No differences were observed in the first event of the composite of death from CVD, nonfatal myocardial infarction, ischemic stroke, hospitalization for acute coronary syndrome, or symptom-driven coronary or cerebral revascularization.
Many clinicians treat HDL as a “secondary target” for reduction of CVD events when LDL goals have already been achieved. Data from this study would suggest that exposing patients to additional risk and cost in an attempt to raise HDL in this setting is not warranted. In light of present data, we are once again reminded to “treat the patient, not a number.”
Editor’s Note
Welcome to “What Matters,” a blog about the clinical research that is most likely to affect your practice, patient outcomes, and your bottom line. We know you have too much to read; there are simply too many studies and often too much buzz generated about them to really make sense of it all in a practical, systematic way. Dr. Jon O. Ebbert, professor of medicine at the Mayo Clinic in Rochester, Minn., offers an authoritative view on recent key clinical developments and what they may mean for you. Follow him every week to stay informed and on top of your world.
Elevated LDL cholesterol is an independent risk factor for cardiovascular disease (CVD) and the evidence supporting treatment to lower LDL is clear. Low HDL also is an independent risk factor for CVD. However, guidance is mixed and practice heterogeneous on how clinicians should address low HDL when LDL goals are achieved with statin therapy.
The AIM-HIGH trial recently published evidence on the effect of extended-release niacin among patients with established CVD with low baseline HDL (less than 40 mg/dL) (N. Engl. J. Med. 2011;365:2255-67). Subjects in the experimental group received niacin 1,500-2,000 mg per day plus simvastatin while subjects in the placebo group received a matching subtherapeutic control (50 mg immediate-release niacin) in addition to simvastatin to maintain blinding. Doses of simvastatin were adjusted to achieve a target LDL of 40-80 mg/dL. Subjects could receive ezetimibe to achieve target LDL cholesterol as needed. A very large sample size of 3,414 subjects was randomized. At 2 years, the mean HDL level had increased by 25% to 42 mg/dL in the niacin group and by about 10% to 38 mg/dL in the placebo group. Triglycerides also improved more in the niacin group. Study drug was discontinued in 25% of patients in the niacin group and 20% in the placebo group. No differences were observed in the first event of the composite of death from CVD, nonfatal myocardial infarction, ischemic stroke, hospitalization for acute coronary syndrome, or symptom-driven coronary or cerebral revascularization.
Many clinicians treat HDL as a “secondary target” for reduction of CVD events when LDL goals have already been achieved. Data from this study would suggest that exposing patients to additional risk and cost in an attempt to raise HDL in this setting is not warranted. In light of present data, we are once again reminded to “treat the patient, not a number.”
Editor’s Note
Welcome to “What Matters,” a blog about the clinical research that is most likely to affect your practice, patient outcomes, and your bottom line. We know you have too much to read; there are simply too many studies and often too much buzz generated about them to really make sense of it all in a practical, systematic way. Dr. Jon O. Ebbert, professor of medicine at the Mayo Clinic in Rochester, Minn., offers an authoritative view on recent key clinical developments and what they may mean for you. Follow him every week to stay informed and on top of your world.
Elevated LDL cholesterol is an independent risk factor for cardiovascular disease (CVD) and the evidence supporting treatment to lower LDL is clear. Low HDL also is an independent risk factor for CVD. However, guidance is mixed and practice heterogeneous on how clinicians should address low HDL when LDL goals are achieved with statin therapy.
The AIM-HIGH trial recently published evidence on the effect of extended-release niacin among patients with established CVD with low baseline HDL (less than 40 mg/dL) (N. Engl. J. Med. 2011;365:2255-67). Subjects in the experimental group received niacin 1,500-2,000 mg per day plus simvastatin while subjects in the placebo group received a matching subtherapeutic control (50 mg immediate-release niacin) in addition to simvastatin to maintain blinding. Doses of simvastatin were adjusted to achieve a target LDL of 40-80 mg/dL. Subjects could receive ezetimibe to achieve target LDL cholesterol as needed. A very large sample size of 3,414 subjects was randomized. At 2 years, the mean HDL level had increased by 25% to 42 mg/dL in the niacin group and by about 10% to 38 mg/dL in the placebo group. Triglycerides also improved more in the niacin group. Study drug was discontinued in 25% of patients in the niacin group and 20% in the placebo group. No differences were observed in the first event of the composite of death from CVD, nonfatal myocardial infarction, ischemic stroke, hospitalization for acute coronary syndrome, or symptom-driven coronary or cerebral revascularization.
Many clinicians treat HDL as a “secondary target” for reduction of CVD events when LDL goals have already been achieved. Data from this study would suggest that exposing patients to additional risk and cost in an attempt to raise HDL in this setting is not warranted. In light of present data, we are once again reminded to “treat the patient, not a number.”