LETTER TO THE EDITOR

Abstract

I read with interest the editorial by John LaRosa, MD, concerning the newest NCEP guidelines.1 I concur that the guidelines have gotten more complex, and said so in a letter to the editor of JAMA.2 I have published a (global) risk-factor graph that accurately predicts the population at risk for atherothrombotic disease (ATD) (Figure). The lipid predictor balances the proatherogenic lipids (mainly low-density lipoprotein [LDL]) and antiatherogenic lipids (mainly high-density lipoprotein [HDL]) in the form of a fraction, the cholesterol retention fraction (CRF, or [LDL - HDL]/LDL), which is placed on the ordinate of the graph. The systolic blood pressure (SBP) in mm Hg is placed on the abscissa. A threshold line has been drawn, with loci at CRF-SBP plots (0.74, 100) and (0.49, 140). In the Bowling Green Study (BGS) database, 85% of all ATD patients will have CRF-SBP plots above the threshold line. Of the 15% of ATD patients who develop ATD despite a CRF-SBP plot below the threshold line, most are cigarette smokers. This leaves only 6% of all ATD patients in the BGS database that could not be predicted by a CRF-SBP plot above the threshold line and/or cigarette smoking status.3 The Bowling Green Study graph. CRF=cholesterol retention fraction ([low-density lipoprotein {LDL} - high-density lipoprotein]/LDL). Reproduced with permission from J Cardiovasc Risk. 2000;7:415–423. In a meta-analysis of eight published angiographic regression trials (over 2000 angiograms), involving all the usual treatments for dyslipidemia, any therapy that brought the patient's CRF-SBP plot below the threshold line resulted in angiographic stabilization or reversal of coronary plaque in a minimum average of 75% of cases. (Had the Program on Surgical Control of Hyperlipidemia [POSCH] been structured to control blood pressure, many more patients' CRF-SBP plots would have come below the threshold line and the average rate of plaque stabilization or regression would have approached 95%.3) I have shown a graph that plots the percentage of people's CRF-SBP plots per age group that transgress the threshold line vs. the percentage of people per age group, in that same population, who develop some form of clinical ATD. The curves, both for men and women, more or less run parallel, with a 40-year gap between the curves for men and a 20-year gap between the curves for women.4 Hence, the graph also tells the physician when the clock starts to tick. The people who develop ATD despite a CRF-SBP plot below the threshold line, in the absence of any history of cigarette smoking, are quite old when that ATD event occurs—at an average age of 78 years for men and 75 years for women. Moreover, the men don't die until an average age of 94 years, and the women don't die until an average age of 84 years.4 A CRF-SBP plot position below the threshold line, in the absence of any history of cigarette smoking, implies virtual invulnerability to ATD, and hence should be the goal of ATD treatment. I should like to note that HDL is unable to compensate for unlimited LDL. In our regional lab, the breakpoint of LDL above which HDL begins to lose its compensatory ability is 170 mg/dL (or 4.4 mmol/L). The more that LDL exceeds this breakpoint, the less that HDL can compensate. At LDL levels of 250 mg/dL (6.5 mmol/L), HDL is virtually unable to compensate. Even so, the lower the CRF, the older the person will be when the ATD event occurs. This scenario is much more likely to occur in women than in men. Hence, I also treat any LDL level ≥170 mg/dL to bring it below this level, regardless of CRF value. The BGS graph was initially presented to the medical community at the 1983 Annual Scientific Assembly of the American Academy of Family Physicians, was modified in 1988 to include an initial threshold line for primary prevention, and finally modified (threshold line lowered) to include secondary prevention in 2000. The BGS graph is simple to use and utilizes a global risk factor approach. It provides support for early screening for ATD risk factors, and gives the physician and patient an easy means of guiding therapy to maximally stabilize or reverse coronary (and by extension, cerebral, and peripheral vascular) plaque. The author does not intend to further modify the BGS graph.