Author + information
- Dennis T. Ko, MD, MSc∗ ( and )
- Jack V. Tu, MD, PhD
- ↵∗Institute for Clinical Evaluative Sciences (ICES), G106-2075 Bayview Avenue, Toronto, Ontario, M4N 3M5, Canada
We appreciate the insights of Dr. Onat and colleagues regarding the potential role of inflammation in explaining the results of our study. Indeed, Dr. Onat’s group previously documented a lack of beneficial association of high-density lipoprotein cholesterol (HDL-C) in men with diabetes and suggested that subclinical inflammation may be responsible (1).
In our study (2), individuals with lower HDL-C levels had progressively higher rates of lower income, poor lifestyle habits (less physical activity, less fruit and vegetable consumption), and more comorbidities (hypertension, diabetes, smoking, and chronic obstructive pulmonary disease). Even after adjusting for these potential confounding factors, there was an increased hazard associated with lower HDL-C with cardiovascular deaths, cancer deaths, and noncardiovascular noncancer deaths. In addition, individuals with very high HDL levels had an increased hazard of noncardiac or noncancer death.
Given the lack of availability of data on inflammatory markers and the fact that we observed similar relationships between HDL-C and cause-specific mortality rates in both statin users and nonstatin users, it is difficult for us to hypothesize whether the lack of a protective effect of HDL-C was the result of the inflammation or whether, an alternative possibility, HDL-C levels were simply not protective. Nevertheless, we agree with Dr. Onat and colleagues that it may be the appropriate time to shift away from a preoccupation with HDL-C levels alone to understand the role of HDL function in cardiovascular disease more clearly.
Please note: Both authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- 2017 American College of Cardiology Foundation