Author + information
- Istvan Reiber, PhD, MD⁎ (, )
- Izabella Mezo, MD,
- Laszlo Mark, PhD, MD and
- Gyorgy Paragh, DSc, MD
- ↵⁎Department of Internal Medicine, Szent Gyorgy Hospital, 4th Department Internal Medicine, Seregelyesi u. 3, Szekesfehervar, Fejer 8000, Hungary
The history of the diagnostics and therapy (management) of atherosclerosis and, in close connection with it, dyslipidemia, has reached an important stage. In the 1950s, we used the word hypercholesterinemia, but later on we began using the correct term: dyslipidemia. Today, it is clear that the process of atherosclerosis, which leads to cardiovascular diseases, is initiated or augmented not only by quantitative changes of the molecules taking part in the lipid metabolism, but also by their qualitative or functional changes. Dysfunctional high-density lipoprotein cholesterol (HDL-C), small, dense low-density lipoprotein cholesterol (LDL-C), and the various enzyme defects are only a couple of examples supporting this statement. With the concept of pre-diabetes serving as a model, in the everyday prevention way of thinking, the term impaired lipid metabolism may be preferable.
The question of the priority of LDL-C and non-HDL-C is fundamental in a different way of thinking. In their paper, Ramjee et al. (1) carefully and thoroughly investigated the significance of non–HDL-C and also the question of apolipoprotein B. We agree with the final conclusion, that non–HDL-C should be taken more into consideration as a risk factor and as a therapeutic target. It should be applied much more extensively in daily medical practice, especially in light of the worldwide spread of obesity, hypertension, diabetes mellitus, and metabolic syndrome.
What makes a good risk marker? It is easily measured and calculated with a low-cost procedure, not to increase healthcare expenses. Non–HDL-C is ideal in almost every aspect, except for its name. Our opinion is that the term atherogenic cholesterol (AC) illustrates its significance more effectively and can be kept in mind much more easily than non–HDL-C. Everything that is not HDL-C is atherogenic; therefore, non–HDL-C = AC. In everyday usage, it may be helpful to speak about good cholesterol (i.e., HDL-C, to date exclusively), bad cholesterol (i.e., LDL-C), and besides these, AC.
To shed some light on the question, we prepared a table that demonstrates the contradictions between AC and LDL-C calculated by the Friedewald formula (Table 1). The table shows the distortions caused by fasting triglycerides within the normal (<400 mg/dl) triglyceride level. We would like to raise attention to the significance of different HDL-C levels measured beside matching triglyceride levels. It is clearly shown that there can be a 40 to 60 mg/dl difference in the LDL-C levels at a certain AC (non–HDL-C) value, according to the actual metabolic state. The table shows that, regarding high cardiovascular risk patients, the true risk is more reliably represented by a 150 to 160 mg/dl AC (non–HDL-C) value than by taking only the LDL-C value into account.
In daily medical practice, it is strongly recommended that AC values be taken into consideration in addition to determining total cholesterol and HDL-C levels. If the values minimally required to determine the AC value are not measured in a fasting state (postprandial state), then we may be able to catch a glimpse of the cardiometabolic risk decades in advance.
- American College of Cardiology Foundation