I may be able to shed some light on the quandary concerning the role of triglycerides in the pathogenesis of atherothrombotic disease, as voiced by Dr. Ginsberg in his recent editorial [1]. I am the chief investigator for the Bowling Green Study of the primary and secondary prevention of atherothrombotic disease [2, 3]. To date, I have compiled an age and sex registry of 668 patients who developed some form of the disease between 4 November 1974 and 1 January 1997.

The Bowling Green Study uses as its lipid predictor the cholesterol retention fraction ([low-density lipoprotein (LDL) –highdensity lipoprotein (HDL)]/LDL). Abnormal fractions are 0.70 or higher; another indicator of abnormality is an LDL cholesterol level of 170 mg/dL (4.4 mmol/L) or greater. According to the Framingham Heart Study guidelines and with a triglyceride level of 150 mg/dL (1.7 mmol/L) or greater, pure hypertriglyceridemia would occur if the cholesterol reduction fraction is 0.69 or less, the LDL cholesterol level is 169 mg/dL or less, and the triglyceride level is 50 mg/dL or greater. (In the early days of the Bowling Green Study [from 1974 to 1978], data on LDL and HDL cholesterol were not available; thus, a cholesterol disorder was considered to be present if the total cholesterol level was 250 mg/dL [6.5 mmol/L] or more. The 250 mg/dL level was chosen because at this level the LDL cholesterol level is almost always elevated; below this level, no abnormality could be inferred with certainty.)

Given the above, 267 male patients with atherothrombotic disease and 229 female patients with the disease had sufficient lipid data with which to determine cholesterol and triglyceride disorders. Pure hypertriglyceridemia was seen in only 9% of the men and 17% of the women. Of the men with pure hypertriglyceridemia, only 20% had never smoked cigarettes; the respective Figure for women was 47%. The mean age at disease onset was 71 years for these men and 76 years for these women.

Twenty-two percent of male patients and 25% of female patients were normolipidemic according to the criteria I described. Of the normolipidemic men, only 19% had never smoked cigarettes; the respective percentage for women was 65%. The mean age at disease onset was 79 years for these men and 77 years for these women.

The point I wish to make is that pure hypertriglyceridemia is uncommon in patients with atherothrombotic disease. When the disease occurs in this scenario, it does so late in life. There may be some disadvantage to the pure hypertriglyceride state in men with the disease, but not in women. Unfortunately, even this conclusion is subject to question because most patients in our registry with atherothrombotic disease and pure triglyceridemia who never smoked cigarettes were also hypertensive, with variable degrees of glucose tolerance. I therefore conclude that pure hypertriglyceridemia does not warrant treatment.