Plasma Triglyceride Level and Mortality from Coronary Heart Disease
Michael H. Criqui, Gerardo Heiss, Richard Cohn, Linda D. Cowan, Chirayath M. Suchindran, Shrikant Bangdiwala, Steven Kritchevsky, David R. Jacobs, Haesook Kim O'Grady, and C.E. Davis
Background Whether the plasma triglyceride level is a risk factorfor coronary heart disease has been controversial, and evaluationof the triglyceride level as a risk factor is fraught with methodologicdifficulties.
Methods We studied the association between plasma triglyceridelevels and the 12-year incidence of death from coronary heartdisease in 10 North American populations participating in theLipid Research Clinics Follow-up Study, while adjusting forthe potential confounding effects of other risk factors forcardiovascular disease, including the level of high-densitylipoprotein (HDL) cholesterol. All analyses were sex-specific,and separate analyses were performed in high and low strataof HDL cholesterol, low-density lipoprotein (LDL) cholesterol,fasting plasma glucose, and age.
Results The rates of coronary death in both men and women increasedwith the triglyceride level. In Cox proportional-hazards modelsadjusted for age, in which the natural log of the triglyceridelevels was used to give a normal distribution, the relativerisk per natural-log unit of triglyceride (e.g., a triglyceridelevel of 150 mg per deciliter vs. a level of 55 mg per deciliter)was 1.54 (95 percent confidence interval, 1.19 to 1.98; P<0.001)in men and 1.88 (95 percent confidence interval, 1.19 to 2.98;P = 0.007) in women. After an adjustment for potential covariates,however, these relative risks were not statistically significant.Analyses based on lipoprotein cholesterol levels revealed apositive association between the triglyceride level and coronarymortality in the lower stratum of both HDL and LDL cholesterol,but not in the higher stratum. Conversely, the HDL cholesterollevel was unrelated to coronary mortality in the lower stratumof LDL cholesterol, but was strongly inversely associated withcoronary death in the higher stratum of LDL cholesterol. Therelative risk of coronary death associated with triglyceridelevel was higher at younger ages. The associations between thetriglyceride level and coronary mortality in the lower HDL cholesterol,LDL cholesterol, and age strata were small and were furtherreduced by an adjustment for the fasting plasma glucose level.
Conclusions Overall, the plasma triglyceride level showed noindependent association with coronary mortality. However, insubgroups of subjects with lower HDL and LDL cholesterol levelsand in younger subjects, defined a priori, an association betweenthe triglyceride level and coronary mortality was observed,although this association was small and was not statisticallysignificant after an adjustment for the plasma glucose level.
Despite decades of interest and numerous clinical and epidemiologicinvestigations, the status of the plasma triglyceride levelas a risk factor for coronary heart disease remains unsettled1,2,3.In many prospective studies the triglyceride level has beena strong risk factor for coronary heart disease in univariateanalyses, but an adjustment in multivariate analyses for thetotal or high-density lipoprotein (HDL) cholesterol level oftendiminished the association1,4,5,6,7. Nonetheless, the triglyceridelevel has been reported to be an independent and statisticallysignificant risk factor in multivariate analyses in severalstudies8,9,10,11,12,13,14,15.
The formulation of multivariate models that include the triglyceridelevel as an independent variable is complex and associated withseveral problems. First, the conventional adjustment for thetotal cholesterol level, which is used as a surrogate for thelevel of low-density lipoprotein (LDL) cholesterol, is inappropriate.In patients with very high triglyceride levels, a large portionof the total cholesterol will consist of very-low-density lipoprotein(VLDL) cholesterol, which is reflected in the total triglyceridelevel3. Thus, in this instance, the total triglyceride levelis, in effect, being adjusted for the VLDL triglyceride level.
Second, the distribution of triglyceride levels is markedlyskewed16. Thus, only categorical or normalizing transformationsare appropriate for distribution-dependent analyses, such asstandard regression techniques.
Third, there is considerable individual variation in triglyceridelevels, and this variability increases with the level of triglyceride17.Thus, when a covariate such as HDL cholesterol appears to explainthe effect of triglyceride in multivariate analysis, this couldbe because of true confounding or because HDL cholesterol issimply measured more precisely.
Fourth, the levels of HDL cholesterol and apolipoprotein A-Iare strongly and inversely correlated with triglyceride levels,18as is consistent with the active metabolic link between triglyceride-richlipoproteins and the lipoprotein particles in the high-densityrange. The levels of HDL cholesterol (or apolipoprotein A-I)may be indicators of efficient metabolism of triglyceride-richparticles in the fasting and postprandial states19. Consequently,adjusting the effects of triglyceride for HDL cholesterol levelsin a multivariate model may not provide an appropriate representationof the underlying biologic process.
Fifth, some studies suggest that the triglyceride level maybe a risk factor only in certain subjects, such as women,20,21those with low total cholesterol levels,6 or diabetics22,23,24.These relations can be obscured by an analysis of all subgroupstogether. Finally, elevated triglyceride levels often accompanyglucose intolerance, and previous studies have not consideredthe full range of glucose levels as a covariate.
With the above considerations in mind, we analyzed the statusof triglyceride as an independent risk factor for death dueto coronary heart disease in 7505 men and women 30 years ofage or older who were followed for an average of 12.2 yearsin the Lipid Research Clinics Follow-up Study.
Methods
The methods used in the Lipid Research Clinics Follow-up Studyhave been reported elsewhere25,26. The subjects were from 10North American populations and were initially studied between1972 and 1976. The base-line examination for this report wasconsidered the second visit and included a random sample of15 percent of the original study population (seen on the firstvisit) and all patients who had hyperlipidemia on the firstvisit26. As a result, 43.3 percent of the subjects in the Follow-upStudy had hyperlipidemia. Table 1 shows the number of men andwomen in the Follow-up Study and the number excluded from theseanalyses. A total of 8825 subjects who were at least 30 yearsof age on the second visit, 4704 men and 4121 women, were eligiblefor the Follow-up Study. We excluded 323 men and 365 women withclinically manifest coronary heart disease at base line, definedas a finding of any one of the following: angina or the useof anginal medications; use of antiarrhythmic agents, digitalis,or propranolol; congestive heart failure; arrhythmias at restduring electrocardiography; and electrocardiographic evidenceof myocardial infarction at rest. Because of their small numbers,222 men and 342 women who were nonwhite were excluded. Othersubjects were excluded because they had fasted for less than12 hours before the study began, they were pregnant, or theyhad missing values for the triglyceride level or one or morecovariables. Thus, a total of 4129 men and 3376 women remainedin the study.
Table 1. The Number of Subjects in the Lipid Research Clinics Follow-up Study and the Number Excluded.
Participants underwent an extensive base-line interview andphysical examination. Plasma cholesterol and triglyceride levelswere determined in each laboratory with the Technicon AutoAnalyzerI or II analytical system adapted for the Lipid Research ClinicsProgram. Triglycerides were analyzed fluorometrically in allsamples, and the same method of analysis was used with bothinstruments. The HDL cholesterol level was estimated in plasmaafter precipitation of the apolipoprotein B-containing lipoproteinby heparin and manganese chloride. Lipoproteins were separatedby centrifugation in a saline density gradient (1.006 g permilliliter) to yield a supernatant fraction containing VLDLcholesterol and an infranatant fraction containing both LDLcholesterol and HDL cholesterol. Total cholesterol was measuredin the infranatant fraction, and the LDL cholesterol level wascalculated by subtracting the HDL cholesterol level from thetotal infranatant cholesterol level. These measurements arestandard methods used by the Lipid Research Clinics Program26,27.
In addition to HDL and LDL cholesterol levels, other potentialconfounding variables considered for this analysis were age,cigarette-smoking status, systolic blood pressure, body-massindex (expressed as the weight in kilograms divided by the squareof the height in meters), fasting plasma glucose level, andpostmenopausal estrogen use in women, all of which were potentiallyassociated with both the triglyceride level and coronary heartdisease. These variables were assessed with the standard methodsused by the Lipid Research Clinics Program25. Alcohol was notanalyzed as a covariate because it showed no significant independentassociation with the triglyceride level in earlier analyses16,28.
Vital status was determined annually with a mailed questionnaire.As of the last follow-up date for these analyses, November 14,1987, vital status had been determined for over 99 percent ofthe subjects. When a participant was identified as deceased,a death certificate was forwarded to the central patient registryof the Lipid Research Clinics. If there was any mention of cardiovasculardisease on the death certificate, the cause of death was reviewedby a formal mortality-classification panel, which consideredvarious materials in such decisions, including narratives providedby the next of kin, physicians' records, and hospital records,in addition to the death certificate. Discrepancies were adjudicatedby the panel. Details of this protocol have been published previously29.In these analyses, deaths listed as definitely due to coronaryheart disease or as suspected to be due to it were included.Previous analyses of HDL and LDL cholesterol levels and mortalityfrom coronary heart disease have shown similar relations forthe end points of definite as compared with definite or suspectedcoronary heart disease,29 and use of the latter category maximizesthe number of events. These analyses were based on an averageof 12.2 years of follow-up.
Sex-specific rates of mortality due to coronary heart diseaseadjusted directly for age were calculated according to the quintileof triglyceride level. The cutoff points were calculated fromthe random sample examined on the second visit. In an attemptto reduce the effects of the large intraindividual variabilityin triglyceride level, the mean of the triglyceride measurementson visits 1 and 2 -- values that were obtained an average ofthree months apart -- were calculated and employed in theseanalyses. The rates derived from these mean values were comparedwith the rates derived from the values obtained on visit 2 alone.The rates were also calculated for phenotype IV and for phenotypesI and V combined (the phenotypes refer to different patternsof hypertriglyceridemia)30.
The Cox proportional-hazards model31 was employed for multivariateanalysis, with the length of time to the occurrence of deathfrom coronary heart disease as the dependent variable. The naturallog of the triglyceride levels was used as the independent variablein order to normalize the distribution of triglyceride levels(a requirement for the Cox model). Separate models were runthat considered age alone and age plus the usual covariatesfor coronary heart disease, and a third set of models also includedthe fasting plasma glucose level as a covariate. Models withoutas well as with the plasma glucose level as a covariate arereported for comparison with earlier studies, which generallydid not include glucose as a covariate. Separate models wererun for men and women, and to explore the possibility that theplasma triglyceride level might have a different associationwith mortality from coronary heart disease at different levelsof other lipoproteins or glucose, or at different ages, sex-specificmodels were run separately for subjects whose values were belowor above selected cutoff points for the HDL cholesterol level,LDL cholesterol level, glucose level, and age. These cutoffpoints were 35 mg per deciliter (0.90 mmol per liter) for HDLcholesterol and 160 mg per deciliter (4.13 mmol per liter) forLDL cholesterol, on the basis of the National Cholesterol EducationProgram guidelines, and 110 mg per deciliter (6.11 mmol perliter) for glucose, the standard upper limit of normal in mostlaboratories. Too few women had HDL cholesterol levels below35 mg per deciliter (n = 72), so a level of 45 mg per deciliter(1.16 mmol per liter) was used as the cutoff point. The base-linecutoff point for age was 70 years. No adjustments were madefor multiple comparisons, but individual P values are reported.All P values are two-tailed.
Results
The age-adjusted rates of death from coronary heart diseaseper 1000 person-years, according to the quintile of the meanof the triglyceride levels on visits 1 and 2, are shown formen in Figure 1 and Figure for women in Figure 2. The triglyceridecutoff points are also shown. In men, no clear association betweentriglyceride levels and death from coronary heart disease appeareduntil the fourth and fifth quintiles, in which the mortalityrates were higher. In women, the increase in risk began at thethird quintile and continued through the fifth quintile. Theanalysis of dyslipoproteinemia phenotypes showed an increasedrisk for phenotype IV, but not for phenotypes I and V combined,although the number of subjects with phenotype I or V was verysmall (n = 39). In addition to its association with mortalityfrom coronary heart disease, an elevated triglyceride levelwas also associated with total mortality. The age-adjusted totaldeath rates per 1000 person-years of follow-up for triglyceridequintiles 1 through 5 were 8.6, 10.4, 10.9, 11.6, and 12.2 inmen and 4.9, 5.5, 7.1, 8.2, and 8.9 in women.
Figure 2. Age-Adjusted Rates of Mortality Due to Coronary Heart Disease in Women, According to Quintile of Triglyceride.
The cutoff points are shown below the figure.
Table 2 shows the results of the multivariate Cox regressionanalyses. The use of the natural-log unit of triglyceride asthe independent variable results in different increments oftriglyceride per natural-log unit at different levels of triglyceride.The following are examples of typical differences in triglycerideof 1 natural-log unit: 100 mg per deciliter as compared with37 mg per deciliter (63 mg per deciliter), 150 mg per deciliteras compared with 55 mg per deciliter (95 mg per deciliter),and 200 mg per deciliter as compared with 74 mg per deciliter(126 mg per deciliter). In men there was a 54 percent increase(P<0.001) in the risk of death from coronary heart diseaseper natural-log unit of triglyceride, and in women there wasan 88 percent increase (P = 0.007), after an adjustment forage alone. After an additional adjustment for HDL and LDL cholesterollevels, smoking status, systolic blood pressure, body-mass index,and postmenopausal estrogen use in women, the excess risk decreasedto 31 percent in men and 19 percent in women, and neither excesswas statistically significant, indicating substantial confoundingby these covariates. Further adjustment for the plasma glucoselevel reduced the excess risk to 9 percent in men and to 4 percentin women, values that were also not statistically significant.
Table 2. Relative Risk of Death from Coronary Heart Disease per Natural-Log Unit of Triglyceride.
Table 3 shows the results of the multivariate stratified analyses.As in Table 2, multivariate relative risks were estimated withand without the fasting plasma glucose level as a covariate.Separate analysis of the risk of death from coronary heart diseaseand the triglyceride level at higher and lower levels of HDLand LDL cholesterol indicated that the elevated risk associatedwith triglyceride levels was confined in men to HDL cholesterollevels of less than 35 mg per deciliter (relative risk, 1.86;P = 0.05) and to LDL cholesterol levels of less than 160 mgper deciliter (relative risk, 1.86; P = 0.02). After an adjustmentfor the glucose level, however, these relative risks were 1.44(P = 0.24) and 1.60 (P = 0.08), respectively. The findings inwomen showed a less pronounced trend, and the smaller numbersof events precluded nominal levels of statistical significancefrom being achieved. We also evaluated the relative risks posedby each increase of 10 mg per deciliter (0.26 mmol per liter)in the HDL cholesterol level with respect to the LDL cholesterolstrata. In both men and women, the triglyceride level but notthe HDL cholesterol level (relative risk, 0.98 in men and 1.12in women; P not significant for both) was related to mortalityfrom coronary heart disease at lower LDL cholesterol levels,whereas at higher LDL cholesterol levels there was no associationwith the triglyceride level, but HDL cholesterol levels werestrongly inversely associated with mortality from coronary heartdisease (relative risk, 0.68 in men [P<0.001] and 0.67 inwomen [P = 0.006]).
Table 3. Relative Risk of Death from Coronary Heart Disease per Natural-Log Unit of Triglyceride, Stratified According to HDL and LDL Cholesterol Levels and Age at Base Line.
The relative risks did not differ according to the glucose level.The age stratification revealed higher relative risks with respectto the triglyceride level in men (relative risk, 1.41; P = 0.06)and women (relative risk, 1.85; P = 0.06) who were less than70 years of age. An additional adjustment for the glucose levelreduced the relative risk in men to 1.20 (P = 0.34) and in womento 1.61 (P = 0.17).
Discussion
Recent reviews of case-control studies and prospective studiesof the triglyceride level as a risk factor for coronary heartdisease indicate that the triglyceride level is, with rare exception,a univariate risk factor3,32. As Hulley et al. pointed out someyears ago, an adjustment for the total cholesterol level andthe HDL cholesterol level in particular usually markedly reducesthis association1. There are, however, several exceptions tothis observation8,9,10,11,12,13,14,15. Some studies have foundan association only for defined subgroups, such as women,20,21men with low total cholesterol levels,6 or diabetics22,23,24.
Our analyses were designed to avoid several pitfalls of earlierresearch. Models that adjust for the total cholesterol levelpartially adjust for high levels of VLDL cholesterol and triglyceridesin subjects with high levels of total triglyceride. We exploredsuch models in our data, and they "overadjusted" the data onmen to a moderate degree, but not the data on women. We thusadjusted for the HDL and LDL cholesterol levels. Furthermore,we used the natural-log transformation of the triglyceride levelto avoid the problem of the nonnormal distribution of triglyceridelevels. Finally, since we had two separate measurements of triglyceridelevel available from the first and second visits, we evaluatedthe mean of these two values to reduce the very large knownintraindividual variability of triglyceride levels17. In agreementwith theoretical expectation,33 the mean values gave a slightlymore precise estimate of risk than the values for the secondvisit alone.
The fasting plasma glucose level was a predictor of death fromcoronary heart disease in our population and was strongly correlatedwith the triglyceride level16. Previous epidemiologic studiesof the risk associated with the triglyceride level have generallynot considered the fasting glucose level as a covariate. Inour study, the relative risks associated with the triglyceridelevel were considerably reduced after the glucose level wasadded to the models, indicating that part of the risk of coronaryheart disease associated with the triglyceride level is dueto associated glucose intolerance.
Our analyses showed stronger associations between an elevatedtriglyceride level and the risk of coronary heart disease inthe presence of lower levels of HDL and LDL cholesterol. TheHDL cholesterol level was not related to the risk of coronaryheart disease in the presence of low levels of LDL cholesterol,but was strongly protective at higher levels. Although two recentreports have indicated that there is an inverse associationbetween the HDL cholesterol level and myocardial infarctionat lower levels of total cholesterol,34,35 neither of thesestudies was adjusted for the triglyceride level. A previousstudy has reported that the triglyceride level is significantlyassociated with coronary heart disease in men with a total cholesterollevel of 220 mg per deciliter ( 5.68 mmol per liter)6. Inthe presence of lower levels of LDL cholesterol and elevatedtriglyceride levels, LDL particles are cholesterol-poor andthe production of LDL may be impaired. Here, the triglyceridelevels appear to predict risk. With higher levels of LDL cholesterol,the reverse cholesterol-transfer function of HDL may assumegreater importance. For subjects over 70 years of age at baseline, the triglyceride level was unrelated to the risk of coronaryheart disease. This finding is concordant with that of the HonoluluHeart Study, in which the serum triglyceride level was a strongand independent risk factor for coronary heart disease beginningbefore the age of 60, but not at older ages36.
Two recent studies have indicated that there is an excess riskof coronary heart disease in the presence of triglyceride levelsof 204 mg per deciliter (2.3 mmol per liter) when the ratioof LDL cholesterol to HDL cholesterol exceeds 537,38. However,such stratified analyses are still confounded by the inversecorrelation between triglyceride levels and HDL cholesterollevels39.
There has been some speculation that the lipoprotein phenotypesI and V might not be associated with an increased risk of cardiovasculardisease despite the presence of elevated levels of triglyceride,whereas in clinical reports the type IV phenotype apparentlyis accompanied by an increased risk. Our data support this view.However, even in our large population, which included many subjectswith hyperlipidemia, there were only 39 subjects with phenotypeI or V (and only one death from coronary heart disease), indicatingthat this finding should be interpreted with caution. It islikely that triglyceride particles of different sizes differin prognostic importance. For example, a recent clinical trialindicated that the increase in triglyceride levels accompanyingpostmenopausal estrogen use in women resulted from the increasedproduction of large, triglyceride-rich VLDL, most of which wascleared directly from the circulation and not converted to smallVLDL or LDL40. Particle heterogeneity in our population-baseddata increases the generalizability of our results, but probablyis also responsible for an underestimation of the risk of coronaryheart disease in certain subgroups with elevated triglyceridelevels.
A case-control study and several experimental studies providerelevant information. Austin and colleagues showed that patientswith nonfatal myocardial infarctions had LDL levels similarto those of control subjects, but were three times as likelyto have a larger number of small, dense LDL particles, the so-calledpattern B41. Subjects with pattern B lipoproteins were alsomore obese and had higher triglyceride levels and lower HDLcholesterol levels. In a multivariate analysis, however, thetriglyceride level explained most of the risk associated withpattern B and was a better explanatory variable than any othercovariate, including the HDL cholesterol level. Although Austinet al.41 suggest that pattern B may have a strong genetic component,recent experimental evidence also suggests that exercise mayfavorably affect the levels of triglycerides, HDL cholesterol,apolipoprotein A, and apolipoprotein B and the size and densityof LDL particles42,43.
In the Stockholm Ischaemic Heart Disease Secondary PreventionStudy, the group treated with clofibrate and niacin had a sharpand significant reduction in the rate of mortality from coronaryheart disease, which was strongly and significantly correlatedwith the reduction in triglyceride levels but not with the reductionin cholesterol levels44. Hypertriglyceridemia was the most commonlipid abnormality in this study, occurring in 50 percent ofthe patients, whereas hypercholesterolemia was present in only13 percent. In the Helsinki Heart Study, the reduction in coronaryheart disease resulting from gemfibrozil therapy was largelylocalized to the previously noted subgroup with a triglyceridelevel of 204 mg per deciliter ( 2.3 mmol per liter) and aratio of LDL cholesterol to HDL cholesterol of more than 538.
Data from several sources now suggest that the fasting triglyceridelevel may contain information about the risk of coronary heartdisease, but the exact lipid metabolic pathways involved, andthe best way to intervene in those pathways, is still uncertain.Non-lipid pathways have been little explored -- for example,the association of hypertriglyceridemia with hypercoagulabilityhas been studied. Hypertriglyceridemia has been reported tobe associated with increased levels of both fibrinogen and clottingfactor X45 and with decreased fibrinolytic capacity due to increasedplasma levels of a rapid inhibitor to tissue-type plasminogenactivator46. The latter condition has been associated with increasedrates of reinfarction in young men47.
In conclusion, an elevated triglyceride level serves at a minimumas a univariate sentinel for persons at high risk of dying ofcoronary heart disease, and physicians should not ignore thissign. In our data, the triglyceride levels in subjects who were70 years of age or younger at base line remained a risk factorfor death from coronary heart disease after adjustment for thestandard covariates, including the HDL cholesterol level, andwas particularly important prognostically in a setting of lowerlevels of HDL and LDL cholesterol. Adjustment for the fastingglucose level reduced these associations, however, so that theresults were no longer statistically significant.
Supported by Lipid Research Clinics collaborative contractsfrom the National Institutes of Health (N01-HV12159, N01-HV12156,N01-HV32961, N01-HV12160, N01-HV22914, N01-HV22913, N01-HV12158,N01-HV12161, N01-HV22915, N01-HV12903, N01-HV12243, N01-HV22932,N01-HV22917, N01-HV12157, and Y01-HV30010).
We are indebted to Clydene Nee and Kristine Wilson for assistancein the preparation of the manuscript.
Source Information
From the Departments of Community and Family Medicine and Medicine, University of California, La Jolla (M.H.C.); the Departments of Epidemiology (G.H.) and Biostatistics (G.H., R.C., C.M.S., S.B., H.K.O., C.E.D.), University of North Carolina, Chapel Hill; the Department of Biostatistics and Epidemiology, College of Public Health, University of Oklahoma, Oklahoma City (L.D.C.); the Department of Biostatistics and Epidemiology, University of Tennessee, Memphis (S.K.); and the Division of Epidemiology, School of Public Health, University of Minnesota, Minneapolis (D.R.J.).
Address reprint requests to Dr. Basil M. Rifkind at the Lipid Metabolism-Atherogenesis Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892.
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Appendix
The following persons participated in the Lipid Research ClinicsFollow-up Study: Executives: H.A. Tyroler (Chairman), K. Bangdiwala,E. Barrett-Connor, C.E. Davis, M. Feinleib, W. Hazzard, D. Jacobs,L. Kirkland-Ellis, I. Mebane, R. Mowery, R. Prineas, B. Rifkind,C. Rubenstein, and W.J. Schull; Directors: E. Barrett-Connor,R. Bradford, B. Christensen, L. Cowan, M. Criqui, W. Haskell,J. Hoover, D. Jacobs, J.A. Little, J. Morrison, G. Owen, P.Van Natta, P. Wahl, and R. Wallace; Mortality-ClassificationPanel: A.S. Leon, R. Prineas, C. Rubenstein (Chairman), J. Ruwitch,and J. Wilson; and Directors Committee: F. Abboud, W.S. Agras,E. Bierman, R. Bradford, V. Brown, M. Buzzard, W. Connor, G.Cooper, J. Farquhar, I. Frantz, E. Gerasimova, A. Gotto, J.Grizzle, W.R. Hazzard, D. Hunninghake, F. Ibbott, W. Insull,A. Klimov, R. Knopp, P. Kwiterovich, J.C. LaRosa, J.A. Little,F. Mattson, M. Mishkel, B.M. Rifkind, G. Schonfeld, H. Schrott,Y. Stein, D. Steinberg, G. Steiner, and O.D. Williams.
Treatment of and Screening for Hyperlipidemia
Ornish D., Brown S. E., Kottke B. A., Shea S., Barth J. D., Bryan G. K., Hokanson J. E., Austin M. A., Ginsberg H. N., Tall A. R., Deckelbaum R. J., Hunninghake D. B., Criqui M. H., Heiss G., Sox H. C.
Extract |
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N Engl J Med 1993;
329:1124-1128, Oct 7, 1993.
Correspondence
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220 mg per deciliter ( 
204 mg per deciliter (2.3 mmol per liter) when the ratio of LDL cholesterol to HDL cholesterol exceeds 537,38. However, such stratified analyses are still confounded by the inverse correlation between triglyceride levels and HDL cholesterol levels39. 
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