THE ROLE OF TRIGLYCERIDES IN ATHEROTHROMBOTIC DISEASE
INTRODUCTION
Triglycerides (TG) have been linked to atherothrombotic disease (ATD) (1-5), but such a link is
controversial (6-10). It is common knowledge that TG do not form any significant portion of the
atherosclerotic plaque, and this in turn implies that the role of TG in ATD must be indirect. It is the
purpose of this paper to demonstrate that the link between TG and ATD occurs indirectly via one of two
mechanisms: an atherogenic link via the inverse relationship between TG and high-density lipoprotein
(HDL) cholesterol and a thrombotic link via a cigarette smoking. To this end the author will examine
data from the Bowling Green Study (BGS) of the Primary and Secondary Prevention of Atherothrombotic
Disease. (11-13)
MATERIALS AND METHODS
The background of the BGS has been described elsewhere. (11-13) In brief, when the author set up
his family practice of medicine in Bowling Green, the county seat of Wood County, in northwest Ohio, in
late 1974, he had as one of his objectives to learn as much as possible about the causes (risk factors) of
ATD. As a result, he set up his medical practice as an age-sex database. Every patient entering his
practice had his/her blood pressure, height, and weight determined, the latter two measures being
converted in a Body Mass Index. When the fundamental importance of cigarette smoking to ATD
became evident, the author began, in mid 1984, to survey his patients for their use of tobacco products,
initially only patients aged 15 years and older, but about ten years later he expanded his survey to all
patients aged 10 years and older. Finally, whenever the opportunity presented itself, the author
obtained blood for a lipid panel, thyroid, and fasting/two-hour postprandial blood sugar determination.
The lipid panel was obtained after a fast of at least 12 hours, and the postprandial blood sugar was
obtained precisely two hours after the ingestion of a standard meal. Since HDL was not available to the
BGS until 1 January 1978, all lipid panels obtained prior to that date consisted only of total cholesterol
(CT) and TG, whereas virtually all lipid panels obtained after that date also included HDL and low-density
lipoprotein (LDL) cholesterol, the latter being calculated by the Friedewald formula: LDL=CT-HDL-TG/5.
(14) Since LDL calculations are relatively accurate above the TG of 400 mg/dl limit (15), the author
accepted LDL calculations as long as TG<500 mg/dl. All of this data was entered into the General
Population database.
A comment must be made about the BGS lipid predictor. Since the risk factors for ATD were not
precisely known in the 1970’s, a number of the author’s patients sustained various ATD events. After 56 years of practice, enough of the author’s patients had sustained ATD events to enable the author to
separate an ATD database from the General Population database. Observations made on the ATD
database revealed, not unexpectedly, that some ATD patients had high LDL levels and others had low
HDL levels. However, some ATD patients had high HDL levels and others had low LDL levels. In 1981 a
paper was published entitled “Is the LDL:HDL Ratio the Best Lipid Predictor?” (This author regrets that
the paper is lost to him and therefore he cannot properly credit the author of the paper.) Review of this
paper caused, in turn, the author to review his ATD database. This review revealed that ATD patients
with low LDL generally had a very low HDL associated, whereas those ATD patients with high HDL
generally had a very high LDL associated. Where this was not the case, the younger ATD patients were
usually cigarette patients, whereas the older ATD patients were generally hypertensive, with/without
attendant diabetes mellitus. Thus the author concluded that indeed it was the ratio between LDL and
HDL that was critical for the lipid portion of ATD risk.
In 1983, it occurred to the author that what he really wanted to know was the amount of cholesterol
accumulating within the arterial wall. This, he reasoned, was best estimated as the difference between
the cholesterol entering the artery wall (primarily LDL) and the cholesterol exiting the artery wall by
reverse cholesterol transport (primarily HDL), expressed as a percentage of the cholesterol entering the
arterial wall. In other words, of the cholesterol entering the arterial wall, how much (what percentage)
remained there? Thus was born the concept of the Cholesterol Retention Fraction (CRF, or [LDL -HDL]/
LDL). The author then compared the CRF with the LDL:HDL ratio and found that comparing CRF of 0.70
or greater with LDL:HDL of 3.5 or greater, the CRF predicted 5% more ATD patients than did the
LDL:HDL. (Feeman, unpublished data) Hence, since 1983, the author has relied on the CRF as his lipid
predictor.
Review of the ATD database also revealed that if LDL levels were very high (170 mg/dl or greater, or
4.25 mmoles/L), then ATD events occurred even if HDL levels were also very high. However, despite
high LDL levels, the lower the CRF, the later was the average age of ATD onset. Thus, all LDL levels of
170 mg/dl or greater are treated even if the CRF is normal (0.69 or less). The combination of CRF of
0.70 or greater and/or LDL of 170 mg/dl or greater is termed the Cholesterol Threshold (C Thr). The
C Thr requires treatment.
Changes in laboratory methodology of measuring HDL will significantly impact the CRF. In the
author’s database and in all of the earlier trials that studied the epidemiology of ATD as well as the
pharmaceutical trials that examined the effects of various medications, procedures, etc . on ATD
outcomes (clinical and angiographic), in all those trials HDL measurement was done by the indirect
method. Within the last decade, a newer methodology has been used in many laboratories: the direct
method of HDL measurement. While the direct method is simpler and less error-prone, the HDL value
obtained by the direct method of HDL measurement is about 10 mg/dl (0.25 mmoles/L) higher than the
equivalent value obtained when the indirect method is used. Not only does this impact the use of HDL
in prediction of the population at risk of ATD and the use of HDL in guiding therapy of dyslipidemia, but
since LDL is generally calculated by the Friedewald formula , then the value of LDL obtained when HDL is
measured by the direct method is necessarily about 10 mg/dl (0.25 mmoles/L) lower than the equivalent
LDL calculated when HDL is measured by the indirect method. This point is not trivial. The author has
published a report of a 55 year old man with no other ATD risk factors, who sustained an acute
myocardial infarction. The author had been treating the patient for depression, and had no compelling
reason to test his lipids. When he sustained his acute infarct, he had a lipid panel drawn at the hospital.
The lipid panel revealed only a rather mild lipid disorder, based on direct HDL measurement. When the
lipid panel was converted to the equivalent panel, based on indirect HDL measurement, the lipid
disorder was more severe, and indeed the patient had his infarct when it would have been predicted.
(16)
The purpose of this data collection was to provide the basis for the prediction of the population at
risk of ATD. Therefore, clinical data were entered into the General Population database, from which
was separated out the ATD database, as previously noted. Many of these ATD events occurred while
the patient was a member of the author’s practice since as already indicated the predictive tools for ATD
were suboptimal in the 1970”s and 1980”s. A number of patients, on entering the author’s practice,
reported a past history of an ATD event, and having accepted such a history, the author also accepted
as evidence of ATD any test indicating evidence of ATD, such as a CAT scan showing an old stroke, an
EKG showing an old myocardial infarction, etc., including the occasional autopsy report.
This report will examine both the ATD and the General Population databases to determine the role of
TG elevations in ATD. Subsequent reports will examine the roles TG when linked to HDL (as in the
TG:HDL ratio) or to LDL (as in non-HDL cholesterol).
RESULTS
Table I reveals the TG distributions, according to sextiles, in the General Population and in the
ATD Population. It will be noted that the incidence of each sextile above the 150-199 mg/dl sextile is
higher in the ATD Population than in the General Population. The 100-149 mg/dl sextile has the same
incidence in the ATD Population and the General Population, and the 99 mg/dl and lower sextile is
more frequent in the General Population than in the ATD Population. This, the author interprets to
mean that TG levels worth treating begin at 150 mg/dl. (All statin-treated patients have been excluded
from this analysis.)
Table II reveals the distribution of TG in the ATD database. Table II reveals that 231/467 (49%) of
male and 189/404 (47%) of female ATD patients have normal TG levels (<150 Mg/dl). This compares
with 64% of males and 71% of females in the General Population database. (Data not shown.) Table II
gives the average age of ATD onset in each TG sextile and frequency distribution of each of those TG
sextiles. It is evident from Table II that the average age of ATD onset is younger as TG levels rise;
however, this trend is minimal in men, in whom no real change is seen till TG levels exceed 200 mg/dl,
whereas in women a significant fall in the average age of ATD onset can be seen when TG levels exceed
250 mg/dl. If the data for men and women are combined, then the averages of ATD onset are
significantly earlier when TG levels are 250 mg/dl or greater.
The role of TG in ATD can be clarified by dividing both TG and CRF into sextiles. This is shown in Table
III, which combines these sextiles for men and women. It will be noted that at any level of TG, the
average age of ATD onset is earlier when the CRF is higher and later if the CRF is lower. However, the
same relationship is much less clear when one stratifies CRF by TG. When one examines ATD patients
with elevated TG (150 mg/dl or higher), and when all ATD patients are considered, then 235/336 (70%)
of patients have an elevated CRF (0.70 or higher) and an additional 63/336 (19%) have a CRF=0.60-0.69,
which will require treatment in the seventh or eighth decade of life., and the other 38/336 (11%) have a
CRF of 0.59 or lower, which does not require treatment unless LDL levels are very high (170 mg/dl or
higher). The average age of ATD onset for the hypertriglyceridemia patients with a high CRF is 62 years,
with an intermediate CRF is 68 years, and with a low CRF (0.59 or less) is 72 years. (These average ages
of ATD onset are based on associated CRF alone; cigarette smoking status and blood pressure are not
included in this analysis.) Of the patients with normal TG (149 mg/dl or lower), 142/374 (38%) have a
CRF of 0.70 or higher, 111/374 (30%) have an intermediate CRF, and 121/374 (32%) have a low CRF. The
average ages of ATD onset are virtually the same in each CRF group, whether TG are elevated or not.
The role of TG in ATD can be further evaluated by stratifying TG sextile by cigarette smoking status.
This is seen in Table IV. Table IV does not take into account the influence of CRF, but it is clear that early
onset ATD is unquestionably associated with cigarette smoking, regardless of TG sextile. If current
cigarette smoking is excluded, lower TG sextiles tend to be associated with later onset ATD and higher
TG sextiles tend to be associated with early onset ATD.
If one stratifies TG levels by CRF and cigarette smoking status, then when the CRF is ideal (0,59 or
less) and there is no history of cigarette smoking, TG do not appear to play a role in ATD. Table V reveals
that when the CRF is ideal, the average age of ATD onset is the same in each cigarette smoking status
group, regardless of whether TG are elevated or not.
Table III indicates that the lower TG sextiles tend to be associated with the lower CRF sextiles.
Indeed, if the distribution of C Thr sextiles is plotted against the distribution TG sextiles , the distribution
curves are parallel. The author interprets this to mean that C Thr and TG distributions run in tandem.
(See Figure I).
The CRF and Systolic Blood Pressure (SBP) can be combined into a global risk factor graph with the
CRF on the ordinate and SBP on the abscissa, stratified by cigarette smoking. (13) This graph contains a
threshold line with loci (0.74,100) and (0.49,140). When the CRF-SBP plots of all the ATD patients in the
author’s practice are plotted onto the graph, 85% of those plots will lie above the threshold line. Of the
15% of ATD patients with CRF-SBP plots below the threshold line, most are cigarette smokers, current or
past. This leaves only 6% of all ATD patients who could not be predicted by CRF-SBP plot above the
threshold line and/or cigarette smoking status—and such patients are very old at time of ATD onset (78
years of age, on average, for men and 75 years of age, on average, for women), and they do not die, on
average, for an additional 10-15 years. The line co-ordinates are valid when the indirect measurement
of HDL is utilized, but if the direct measurement of HDL is utilized, then the line co-ordinates must be
lowered to (0.62,100) and (0.40,140). This graph is illustrated in Figure II. (This is the graph based on
lipid values obtained when the indirect measurement of HDL is used.)
The BGS graph has been validated against eight published angiographic regression trials. As with all
such trials, participants are selected on the basis of their likelihood of have an ATD event during the
timeframe of the trial, or in the case of the angiographic regression trials, the likelihood of their having
an ATD plaque that can be followed during the trial, so that response to therapy can be assessed. Such
patients tend to younger men with a moderate to severe lipid disorder. In the eight angiographic
regression trials, 95% of the participants had CRF-SBP plots above the threshold line. When the younger
BGS ATD patients were examined, 93% of them had CRF-SBP plots above the threshold line. (17)
DISCUSSION
Since TG are not part of the ATD plaque, it is clear the role of TG in ATD must be indirect, acting via
mechanisms related to elevated TG levels. The author has suggested two such mechanisms: a
dyslipidemic mechanism related to the well known inverse relationship between TG and HDL, and a
thrombotic mechanism related to the associated use of cigarette smoking.
Table II reveals , in the ATD population, that 51% (236/467) of men and 53% (215/404) women will
have elevated TG levels, assuming TG elevations beginning at 150 mg/dl. Hence hypertriglyceridemia is
common in ATD patients. However, when TG levels are 150 mg/dl or higher, CRF is 0.70 or greater in
70% (235/336) of cases, and borderline (CRF=0.60-0.69, levels requiring treatment later in life) in 19%
(63/336). Only 11% (38/336) have ideal CRF values (0.59 or less). This latter data is best seen in Table III
and in Figure II. Indeed, the author has shown that in the presence of an ideal cholesterol level ( defined
as a CRF of 0.59 or less) and in the absence of any history of cigarette smoking, TG are not associated
with early-onset ATD and hence do not warrant therapy—except, of course, the treatment of very high
TG levels to prevent pancreatitis.
The link between cigarette smoking and TG is most likely mediated by thrombosis. The author has
shown that act of quitting smoking for only six months is associated with a delay in the average age of
ATD by about 12 years. (18) This most certainly implies that cigarette smoking acts in an acute fashion
and that quitting smoking abolishes that acute effect. This acute effect could be mediated by an
inflammatory response in the fibrous cap of the ATD plaque, leading to plaque rupture, and massive
thrombosis, or could be mediated by activation of thrombosis on the surface of the fibrous cap, in the
presence of erosions, but without plaque rupture. ( 19-21 ) TG elevations are associated with activation
of plasminogen inhibitor, which interferes with the lysis of thromboses.( 22-23) Thus, the combination
of cigarette smoking and TG elevation creates a pro-coagulant state.
Table V clearly shows that when CRF is ideal ( 0.59 or less) and when cigarette smoking is excluded,
ATD events occur very late in life, on average, regardless of whether or not TG are elevated. The author
interprets this to mean that TG in and of themselves are relevant to ATD only via the associated
mechanisms noted above. The prevention of ATD and/or stabilization/regression of extant ATD should
be focused on C Thr, cigarette smoking and hypertension. (24)
CONCLUSIONS
The author has shown that TG are relevant to ATD, but only via the associated disorders of C Thr and
cigarette smoking. TG elevations, in and of themselves, therefore do not warrant treatment, except as
previously noted, to treat very high TG levels to prevent pancreatitis. The prevention of ATD, or if
extant, then the stabilization/regression of ATD plaque, should focus on C Thr, cigarette smoking and
elevations of SBP.
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Table 1
TG Frequency Distribution in General Population vs ATD Population
TG
Male
Gen Pop
Male
Female
Female
Total
Total
ATD Pop
Gen Pop
ATD Pop
Gen Pop
ATD Pop
> 300
135
1875
7%
53
467
11%
105
2044
5%
49
404
12%
240
3919
6%
102
871
12%
250-299
113
1875
6%
48
467
10%
65
2044
3%
18
404
4%
178
3919
5%
66
871
8%
200-249
161
1875
9%
51
467
11%
145
2044
7%
60
404
15%
306
3919
8%
111
871
13%
150-199
275
1875
15%
84
467
18%
272
2044
13%
88
404
22%
547
3919
14%
172
871
20%
100-149
484
1875
26%
124
467
27%
572
2044
28%
105
404
26%
1056
3919
27%
229
871
26%
< 99
707
1875
38%
107
467
23%
885
2044
43%
84
404
21%
1592
3919
41%
191
871
22%
TG means triglycerides
Gen Pop means General Population
ATD Pop means Atherothrombotic Disease Population
Table II
TG & Average Age of ATD
Onset: 1974-2003
TG (mg/dl)
Male
Ave Age of
ATD Onset
Male
Sextile
Incidence
Female
Ave Age of
ATD Onset
Female
Sextile
Incidence
∑
Ave Age of
ATD Onset
∑
Sextile
Incidence
> 300
53
3088
58
53
467
11%
49
3132
64
49
404
16%
102
6220
61
102
871
12%
250-299
48
2883
60
48
467
10%
18
1137
63
18
404
4%
66
4020
61
66
871
8%
200-249
51
3095
61
51
467
11%
60
4098
68
60
404
15%
111
7193
65
111
871
13%
150-199
84
5358
64
84
467
18%
88
6192
70
88
404
22%
172
11,550
67
172
871
20%
100-149
124
7892
64
124
467
27%
105
7295
69
105
404
26%
229
15,187
66
229
871
26%
< 99
107
6778
63
107
467
23%
84
5939
71
84
404
21%
191
12,717
67
191
871
22%
TG means triglycerides
ATD means atherothrombotic disease
Table III
CRF vs. TG
ATD: 1974-2003
TG (mg/dl)
Sextiles
> 0.80
0.75-.0.79
0.70-0.74
0.65-0.69
0.60-0.64
< 0.59
∑
> 300
16
833
52
15
888
59
10
663
66
6
384
64
6
360
60
6
418
70
59
3546
60
250-299
12
631
53
17
1107
65
12
735
61
6
404
67
-
4
259
65
51
3136
61
200-249
24
1381
58
17
1054
62
21
1415
67
9
605
67
4
331
83
6
436
73
81
5222
64
150-199
34
2137
63
25
1544
62
32
2148
67
21
1476
70
11
737
67
22
1612
73
145
9654
67
100-149
30
1737
58
31
1920
62
33
2230
68
31
2094
68
28
1999
71
45
3140
70
198
13,120
66
< 99
10
582
58
16
959
60
22
1471
67
28
1864
67
24
1522
63
76
5350
70
176
11,748
67
∑
126
7301
58
121
7472
62
130
8662
67
101
6827
68
73
4949
68
159
11,215
71
710
46,426
65
CRF means Cholesterol Retention Fraction ([LDL-HDL]/LDL)
TG means triglycerides
Table IV
Cigarettes Vs. TG
∑ ATD
1974-2003
Cigarettes
< 99
100-149
150-199
200-249
250-299
> 300
+
40
2101
53
53
2972
56
28
1539
55
21
1113
53
18
956
53
20
1016
51
Past
30
2090
70
44
2974
68
33
2245
68
19
1223
64
21
1370
65
22
1374
62
-
34
2390
70
26
1876
72
22
1488
68
11
756
69
8
497
62
12
758
63
+
19
1175
62
29
1841
63
14
828
59
14
855
61
8
427
53
13
735
57
Past
18
1330
74
15
992
66
26
1827
70
10
682
68
2
141
71
11
673
61
-
45
3305
73
59
4299
73
49
3622
74
34
2441
72
8
569
71
24
1653
69
Male
Female
TG means triglycerides
ATD means atherothrombotic disease
+ means current cigarette smoker
Past means has quit smoking at least 6 months
- means never smoked cigarettes, though non-cigarette tobacco may have been used
Table V
Average Age of ATD Onset When CRF > 0.59,
Stratified by Cigarette Smoking and TG Levels
All ATD: 1974-2003
TG
+
Cigarette Smoking
Status
Past
> 150 mg/dl
10
613
61
13
948
73
15
1164
78
< 149 mg/dl
38
2271
60
36
2641
73
46
3578
78
-
ATD means atherothrombotic disease
CRF means Cholesterol Retention Fraction ([LDL-HDL]/LDL)
TG means triglycerides
+ means current cigarette smoker
Past means has quit smoking at least 6 months
- means never smoked cigarettes, though non-cigarette tobacco may have been used