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Take home message:

In the AIM-HIGH trial, the mean LDL-c was already quite excellent at 71 mg/dl, prior to adding Niaspan. Intravascular ultrasound of the plaque (IVUS Trials shown above) has consistently shown that after 24 months of intensive statin therapy where LDL-c levels were maintained at around 70 mg/dl, plaque regression has already occurred. At this level of intensive LDL-c therapy, the incremental benefits of the addition of Niaspan when the mean HDL-c was only mildly reduced (34.6 mg/dl) may be hard to observe if any.

This apparent lack of benefits applies only to the specific patient group in this study. It does not apply to patients with higher risk, patients with on-treatment LDL over 100 mg/dl, patients with HDL-c below 30 mg/dl or patients with high Lp(a).

The conclusion of the AIM-HIGH trial supports what NJPCCC advocates - personalized preventive care. Not every patient with low HDL-c benefits by the addition of Niaspan to statin therapy. NJPCCC customizes therapy according to each patient's level of cardiovascular risk, focusing first and foremost to lowering LDL-c to less than 70 and when the test is covered by the patient's insurance, lowering LDL-Particle number to less than 1,000 for those at the highest risk, while at the same time, mentoring patients about healthier lifestyle.

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AIM-HIGH tries to answer the question raised by HPS (Heart Protection Study) 10 years ago about residual risk. Does raising HDL-c with niacin eliminate the residual risk the remains after simvastatin 40mg? If it is not from low HDL-c, what is it due to?

The Heart Protection Study is a large (20,536 high risk patients) placebo-controlled clinical outcomes trial with simvastatin 40 mg. The study showed a significant large event reduction with simvastatin compared to placebo. But a residual risk was identified after simvastatin therapy. The above slide from the Heart Protection Study shows the event rates in three simvastatin patient groups based on their HDL-c levels. Those with HDL-c < 35 mg/dl had a event rate of 10.2%; whereas those with HDL-c ≥ 43 mg/dl had a lower event rate of 7.3%. Based on the AIM-HIGH trial, raising HDL-c with niacin may not be the way to eliminate the residual risk. Many patients with low HDL-c also have higher LDL-P in relation to LDL-c (upward discordant).

My usual approach in eliminating the residual risk in this patient group is to reduce LDL-P to less than 1,000 nmol/L with more intensive statin therapy, adding ezetamibe or both. Then, depending upon the level cardiovascular risk and how low HDL-c remains after statin therapy and positive lifestyle changes, consider adding niacin to raise HDL-c.