Ask The Doctors: August 2013
I’ve read conflicting information about HDL-cholesterol in the last few years, with some experts saying you should raise it and others saying it might not be that important. What do we know for sure about HDL and how aggressively should we treat it?
Your question is very timely, and addresses a hotly-debated subject in the medical community. High-density lipoprotein (HDL) is a microscopic, spherical particle, that can be thought of as a package for sending cholesterol from the arteries and other distant tissues back to the liver. This pathway is known as reverse cholesterol transport. For many years it has been known that people with lower levels of HDL-cholesterol (HDL-C) are at higher risk for coronary artery disease (CAD) and myocardial infarction (MI or heart attack), and those with higher levels are at lower risk. In the past it has been suggested that HDL might serve a protective function against heart disease, in contrast to low-density lipoprotein (LDL), which is a known risk factor. This theory, while reasonable, was difficult to prove. For LDL-C, we had tools which caused huge drops in its level: statin drugs. Medications which raised HDL-C, on the other hand, generally had major effects on other lipid populations as well. For example, nicotinic acid or niacin lowers LDL-C and lowers triglycerides, in addition to raising HDL-C. Thus far, a safe and powerful agent that primarily raises HDL-C is not available.
Two recently-published studies, called AIM-HIGH and HPS2-THRIVE, have dampened enthusiasm about the benefits of raising HDL-C. In both trials, patients were first placed on a statin (plus ezetimibe if needed) in order to achieve a low LDL-C level. Then, they were given either niacin or placebo. Although HDL-C was raised on average from 14-20%, there was no significant reduction in cardiovascular events such as MI or stroke. In the AIM-HIGH trial, more strokes were seen in the niacin treatment group, but the difference was not statistically significant. In the HPS2-THRIVE study, more new cases of diabetes were seen in the niacin-treated group, which was a concerning finding. What most cardiologists take away from these results is that our focus of cholesterol treatment should be to lower LDL-C. While HDL probably does have a beneficial role, raising the amount of HDL-C in circulation does not appear to reduce risk of MI. Future research will focus on better understanding the process of reverse cholesterol transport, and the role HDL plays.
Several years ago I was diagnosed with chronic atrial fibrillation and was treated with radiofrequency ablation. Recently symptoms resumed. A neighbor had the same treatment and hasn’t had an episode in more than three years. Was my procedure was done poorly or does it only work in half the cases? Can it be repeated?
I would certainly not infer from your experience that there was anything deficient about the procedure you underwent. Studies suggest that for persistent atrial fibrillation (when episodes tend to last >7 days), only about 20 percent of people are in normal sinus rhythm after a single catheter-based ablation procedure. The chance of success rises to near 50 percent after multiple ablations. The longer someone is in a-fib, the more the heart becomes “entrained” in that rhythm, and the more difficult it is to restore normal rhythm. Chronic a-fib also causes the upper chambers of the heart, the atria, to dilate, and this tends to perpetuate the abnormal rhythm, as well. I would suggest that you go back to the cardiologist who performed the ablation, and discuss your options for future therapy. Medications which help control cardiac rhythm could potentially be utilized. And additional attempts at ablation would certainly be very reasonable to consider, especially considering the initial symptomatic benefit that you experienced.