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PubMed2006

Serum triglycerides and colorectal adenoma in a case-control study among cancer screening examinees (Japan).

OBJECTIVE: Most epidemiologic studies have shown serum triglycerides to be associated with colorectal adenoma. However, whether the association can be modified by smoking is unknown. We cross-sectionally investigated the association of serum triglycerides with the risk of adenoma by smoking status. METHODS: We identified 782 newly diagnosed adenoma cases from the examinees of a colorectal cancer screening program. All cases were diagnosed by a magnifying colonoscopy with dye spreading. We determined 738 controls without present illness or past history of adenoma from among the examinees. They provided their lifestyle information and fasting blood samples to measure their serum triglycerides. We calculated odds ratios (OR) and 95% confidence intervals (CI) of colorectal adenoma for serum triglycerides. RESULTS: High serum triglycerides were associated with colorectal adenoma (OR 1.5; 95% CI 1.1-2.0 for the highest versus the lowest quartile, P (trend, )0.030). A stronger association was observed between three or more adenoma cases and study controls (OR 2.3; 95% CI 1.3-4.2, P (trend,) < 0.0010). After classifying the study subjects by smoking status, a significant linear risk trend was found in ever-smokers (P (trend), 0.0018) but not in never-smokers (P (trend), 0.94; P (interaction), 0.067). CONCLUSIONS: Our results suggested that a higher serum triglyceride level may be related to a larger number of adenomas. Adenoma development involving an elevated serum triglyceride level may be modified by smoking.

Adenoma↗
PubMed2000

Low erucic acid canola oil does not induce heart triglyceride accumulation in neonatal pigs fed formula.

Canola oil is not approved for use in infant formula largely because of concerns over possible accumulation of triglyceride in heart as a result of the small amounts of erucic acid (22:1n-9) in the oil. Therefore, the concentration and composition of heart triglyceride were determined in piglets fed from birth for 10 (n = 4-6) or 18 (n = 6) d with formula containing about 50% energy fat as 100% canola oil (0.5% 22:1n-9) or 100% soybean oil, or 26% canola oil or soy oil (blend) with palm, high-oleic sunflower and coconut oil, providing amounts of 16:0 and 18:1 closer to milk, or a mix of soy, high-oleic sunflower and flaxseed oils with C16 and C18 fatty acids similar to canola oil but without 22:1. Biochemical analysis found no differences in heart triglyceride concentrations among the groups at 10 or 18 d. Assessment of heart triglycerides using Oil Red O staining in select treatments confirmed no differences between 10-d-old piglets fed formula with 100% canola oil (n = 4), 100% soy oil (n = 4), or the soy oil blend (n = 2). Levels of 22:1n-9 in heart triglyceride and phospholipid, however, were higher (P<0.01) in piglets fed 100% canola oil or the canola oil blend, with higher levels found in triglycerides compared with phospholipids. The modest accumulation of 22:1n-9 associated with feeding canola oil was not associated with biochemical evidence of heart triglyceride accumulation at 10 and 18 d.

Animal Feed↗
PubMed1997

On the interrelationship between hepatic carnitine, fatty acid oxidation, and triglyceride biosynthesis in nephrosis.

The nephrotic syndrome is associated with disturbances in plasma lipid pattern and metabolism. However, the reason for these perturbations is poorly understood. In the present study, we have investigated hepatic triglyceride metabolism in puromycin aminonucleoside-induced nephrotic syndrome in rats. Nephrotic rats displayed a 70% increase in hepatic triglyceride levels compared to controls (16.9 +/- 1.6 vs. 9.8 +/- 0.6 mumol/g liver; means +/- SEM, P < 0.01). The capacity for hepatic mitochondrial beta-oxidation of fatty acids was substantially elevated (80%). This was associated with a rise in the liver content of the fatty acid carrier carnitine (1.24 +/- 0.06 vs. 0.85 +/- 0.07 mumol/g dry weight, P < 0.05). A positive correlation between the levels of acetylcarnitine and acetyl-CoA was found in normal as well as in nephrotic rats, implying that carnitine plays an important role as an acetyl group acceptor in the liver under normo- and hyperlipidemic conditions. Changes in carnitine levels seem to be tightly coupled to the rate of fatty acid oxidation. There was a significant elevation in the activity of phosphatidate phosphohydrolase (E.C. 3.1.3.4) in liver microsomes from nephrotic rats (1.07 +/- 0.09 vs. 0.81 +/- 0.04 nmol/min.mg protein, P < 0.02). Hepatic very low density lipoprotein (VLDL)-triglyceride secretion rate was 18% higher in nephrotic rats than in controls. The results demonstrate a deranged hepatic triglyceride metabolism in nephrosis, with an increased hepatic triglyceride biosynthesis, a sizable accumulation of hepatic triglycerides, and only a modest increase in VLDL triglyceride secretion. In addition, mitochondrial beta-oxidation of fatty acids was enhanced, associated with an increased availability of carnitine.

Acetyl Coenzyme A↗
PubMed1978

Serum triglycerides and serum uric acid in untreated and thiazide-treated patients with mild hypertension. The Oslo study.

Levels of serum lipids, uric acid and body weight are reported from a controlled trial of drug treatment of middle-aged men with uncomplicated mild hypertension. The results come from 300 men after three years of follow up; 150 men in the treatment group and 150 men in the control group. The treatment has been standardized starting with hydrochlorothiazide alone and adding alpha methyldopa when necessary. In case of side effects, alpha methyldopa was replaced with propranolol. Pretreatment results demonstrated a strong covariation among body weight, uric acid and triglycerides. In the entire treatment group, there was no significant change in triglycerides after three years (increase from 1.85 to 2.02 mM/liter, P greater than 0.05). Cholesterol was also unchanged. Further analysis showed that certain patients reacted with an increase in triglycerides during treatment: those prone to a distinct increase in uric acid and those gaining weight. Those who needed combination therapy (having the highest pretreatment blood pressure) showed most of the increase in triglyceride and uric acid. In the group treated with hydrochlorothiazide alone, the triglycerides were unchanged. However, those selected from this group with a distinct increase in uric acid also showed an increase in triglycerides. The treatment increased the pretreatment positive correlation between uric acid and triglycerides.

Adult↗
PubMed1982

Relation of serum total cholesterol and triglyceride levels to the amount and extent of coronary arterial narrowing by atherosclerotic plaque in coronary heart disease. Quantitative analysis of 2,037 five mm segments of 160 major epicardial coronary arteries in 40 necropsy patients.

The amount of cross-sectional area narrowing by atherosclerotic plaques was determined histologically in each 5 mm segment of the entire lengths of the right, left main, left anterior descending, and left circumflex coronary arteries in 40 patients with fatal coronary heart disease and known fasting serum total cholesterol and triglyceride levels. The patients were divided into four groups based upon the serum total cholesterol and triglyceride levels: group I, total cholesterol of 250 mg/dl or less, triglyceride of 170 mg/dl or less; group II, total cholesterol of 250 or less, triglyceride of more than 170; group III, total cholesterol of more than 250, triglyceride of 170 or less; group IV, total cholesterol of more than 250, triglyceride of more than 170. The number of 5 mm segments of coronary artery narrowed severely (76 to 100 percent in cross-sectional area) by atherosclerotic plaques in each group was as follows: 172 of 505 (34 percent) 5 mm segments from group I; 242 of 353 (69 percent) segments from group II; 120 of 295 (41 percent) from group III and 425 of 884 (48 percent) segments from group IV. The mean percentage of 5 mm segments narrowed severely was significantly greater in group II than in group I (p less than 0.005) or group III (p less than 0.01). Additionally, the mean number of four coronary arteries per subject severely narrowed and the number of subjects with severe narrowing of the left main coronary artery were significantly greater in groups II and III than in group I. The percentages of 5 mm segments narrowed severely correlated significantly with the serum triglyceride level (p less than 0.03). Although it correlated with the number of severely narrowed coronary arteries per subject, the serum total cholesterol level did not correlate with the percentage of 5 mm segments of coronary artery with severe narrowing.

Adult↗
PubMed1983

Norethindrone acetate inhibition of triglyceride synthesis and release by rat hepatocytes.

The progestin, norethindrone acetate has been widely administered to patients in the form of oral contraceptives; however, its hypolipemic action has received little study. This report describes the effects of conventional doses of norethindrone acetate (100 micrograms/day.kg body weight 0.75) on rat plasma lipid levels in vivo as well as the mechanism of action on triglyceride metabolism in isolated hepatocytes in vitro. Norethindrone acetate administration led to significant and proportional reductions of the concentrations of triglycerides, cholesterol and phospholipids of plasma lipoproteins of density less than 1.006 of rats fed a high carbohydrate diet. Norethindrone acetate (0.1 mM) also significantly inhibited the incorporation of both [9,10(-3)H] palmitate and [U-14C]glycerol into triglycerides of isolated hepatocytes from fed rats, by 11 to 16% (P less than 0.001). Release of labeled triglycerides from the isolated hepatocytes was similarly inhibited, 21% and 46%, respectively (P less than 0.05). At the higher concentration of 1.0 mM, norethindrone acetate inhibited the incorporation of [2(-3)H]glycerol into hepatocytic triglycerides by 35-39% (P less than 0.05). The present findings suggest that inhibition of hepatic triglyceride synthesis can account for the reduction of hepatic triglyceride secretion and for at least part of the lowering of plasma VLDL levels which occurs during administration of norethindrone acetate in the rat.

Animals↗
PubMed1992

Relationship of triglycerides and HDL cholesterol in hypertriglyceridemia.

Hypoalphalipoproteinemia (plasma HDL-cholesterol concentration at or below 35 mg/dl as reported in the National Cholesterol Education Program Guidelines) is a well known risk factor for premature coronary artery disease (CAD). In hypertriglyceridemic patients, hypoalphalipoproteinemia is commonly believed to be linked to the derangement of triglyceride metabolism. In this study the occurrence of primary hypoalphalipoproteinemia has been investigated in a cohort of hypertriglyceridemic patients whose plasma triglyceride concentration had been normalized either through diet or diet plus drug treatment. Following the initial visit, 115 hypertriglyceridemic patients received dietary advice and returned for the second visit four months later. Diet reduced plasma triglycerides in all the patients. HDL-cholesterol increased in 76 patients whereas in the others, it remained unchanged or even decreased. Plasma triglyceride concentration was normalized (less than 200 mg/dl) in 54 patients by diet alone, but among these 11 remained hypoalphalipoproteinemics. Patients in whom, despite dietary restrictions, triglycerides exceeded 200 mg/dl, were considered for pharmacological treatment with Bezafibrate (300 mg t.i.d.) for 4 months. Thirty-nine concluded the study. Treatment significantly decreased plasma triglyceride concentration in all the subjects. Normalization was achieved in 32 patients. Four of them, however, remained hypoalphalipoproteinemic. These results indicate that a subgroup of hypertriglyceridemic patients remained hypoalphalipoproteinemic even after normalization of triglyceride levels. In these patients hypertriglyceridemia and hypoalphalipoproteinemia may occur as expression of two distinct primary metabolic defects.

Adult↗
PubMed1995

Lipid-lowering activity of atorvastatin and lovastatin in rodent species: triglyceride-lowering in rats correlates with efficacy in LDL animal models.

Since inhibitors of HMG-CoA reductase lower plasma triglycerides rather than cholesterol in rats, we compared the triglyceride-lowering activity of lovastatin in rats to that of atorvastatin, a more potent synthetic inhibitor, prior to evaluating these drugs in established animal models in which low density lipoproteins (LDL) rather than high density lipoproteins (HDL) are the major transporters of plasma cholesterol. Atorvastatin was more efficacious than lovastatin in normal, chow-fed rats, and more potent in rats with endogenous hypertriglyceridemia (sucrose-fed). In hypertriglyceridemic rats plasma apoB concentrations decreased only with atorvastatin (30 mg/kg), and VLDL-triglyceride secretion (Triton method) was also decreased more by atorvastatin. The inactive enantiomer of atorvastatin did not lower plasma triglycerides. Thus, triglyceride-lowering was dependent upon inhibition of HMG-CoA reductase. Liver unesterified cholesterol and cholesteryl esters (mg/g) were increased by both drugs in normal rats but remained unchanged in hypertriglyceridemic rats. In normal, chow-fed guinea pigs atorvastatin was a more potent cholesterol-lowering drug, and unlike lovastatin, lowered plasma triglycerides and VLDL-cholesterol. In casein-fed rabbits with endogenous hypercholesterolemia and in chow-fed rabbits atorvastatin lowered LDL-cholesterol more potently than lovastatin, but in chow-fed rabbits neither drug had an effect on the in vivo rate of VLDL-lipid secretion, suggesting that efficacy was due to inhibition of direct LDL production and/or enhanced LDL clearance. We conclude that normal rats can be used as a preclinical tool to assess the efficacy of HMG-CoA reductase inhibitors since triglyceride-lowering correlates with cholesterol-lowering in LDL animal models. In this regard atorvastatin is a more potent hypolipidemic agent than lovastatin in animals. A common but not sole mechanism for these drugs may be direct inhibition of the hepatic production of the major apoB-containing lipoprotein in a given species, e.g. VLDL in rats and LDL in guinea pigs and rabbits.

Animals↗
PubMed1976

Stress-induced inhibition of triglyceride secretion in vivo sand rats (Psammomys obesus).

The effects of acute stress upon circulating triglyceride, glucose, insulin, free fatty acids, and glycerol were investigated in obese desert sand rats. Three groups of animals, designated "nonstress", "non-exertional stress", and "exertional stress", were studied. Acute stress, with or without accompanying exercise, was associated with significant decreases in circulating triglyceride; significant increases in circulating glucose, free fatty acids, and glycerol; and variable changes in circulating insulin. Since these data indicated that substrate availability and hepatic insulization were adequate and therefore could not explain the observed fall in circulating triglyceride, endogenous triglyceride secretion rates were examined by the Triton method. Compared to predicted rates based upon earlier studies, both nonexertional and exertional stress were associated with significantly decreased endogenous triglyceride secretion. Thus, acute stress in the sand rat, with or without accompanying exercise, appears to induce an immediate decrease in endogenous triglyceride secretion and circulating triglyceride.

Animals↗
PubMed1979

Metabolism of triglyceride in rabbit plasma low and high density lipoproteins: studies in vivo and in vitro.

The metabolism of triglyceride in the plasma low density lipoproteins (LDL) and high density lipoproteins (HDL) was studied in the normal-fed rabbit. Preparations of LDL and HDL la-eled with 3H in the triglyceride moiety were obtained from donor rabbits that had previously been injected with 3H-palmitic acid. These labeled lipoproteins were subsequently either reinjected into other rabbits or incubated in vitro with unlabeled lipoprotein fractions. In vivo, there were bidirectional transfers of 3H-triglyceride between the LDL and HDL, the rate of which considerably exceeded that of any irreversible removal from the plasma compartment. To a much lesser extent, there was also a transfer of 3H-triglyceride from both LDL and HDL to very low density lipoproteins (VLDL). In vitro, so long as the dialysed 1.21 g/ml infranate of serum was present there was a significant transfer of 3H-triglyceride from both LDL and HDL into each of the other lipoprotein fractions that in no case could be accounted for by a corresponding net transfer of triglyceride mass. It was concluded that the pools of triglyceride in LDL and HDL, and to a lesser extent in VLDL, comprise parts of a larger, progressively equilibrating pool.

Animals↗
PubMed1980

A selective decline of postheparin plasma hepatic triglyceride lipase in hypothyroid rats.

The present study aimed to define the effect of thyroid status on two postheparin plasma lipases, i.e., lipoprotein lipase and hepatic triglyceride lipase. Rats with hypo- and hyperthyroidism were used for this purpose. Separate measurement of these two lipases was done by an immunochemical method utilizing antiserum specific to hepatic triglyceride lipase. The 5-wk thyroidectomized, hypothyroid rats had normal plasma concentrations of both triglyceride and cholesterol. These rats showed a selective decline in the activity of postheparin plasma hepatic triglyceride lipase with normal lipoprotein lipase activity. The rats made thyrotoxic by thyroxine treatment had normal plasma levels of both triglyceride and cholesterol. These rats showed normal activities of both hepatic triglyceride lipase and lipoprotein lipase. The observed finding of a selective decline of hepatic triglyceride lipase in hypothyroid rats is discussed in connection with the possible function of this enzyme in lipoprotein metabolism.

Animals↗
PubMed1981

Lipid metabolism in pregnancy. VIII. Effects of dietary fat versus carbohydrate on lipoprotein and hepatic lipids and tissue triglyceride lipases.

UNLABELLED: We have asked, is hypertriglyceridemia in the fed state in pregnancy due to intolerance to exogenous fat, accumulation of endogenous triglycerides, or accumulation of remnants of d < 1.006 lipoprotein metabolism? To answer these questions, we fed fat-free diets high in starch or sucrose, or diets containing fat or fat plus cholesterol to pregnant and nonpregnant rats for 12 days until gestational day 21 (term = 22 days). Blood was obtained 0, 4, or 8 hr after removal of food from the cages. Lipid concentrations were determined in chylomicrons and very low, low, and high density lipoproteins. Hypertriglyceridemia in pregnancy exists on both starch and sucrose containing fat-free diets and is exaggerated 4 and 8 hr after food is removed from the cage. The triglyceride rise occurs in d < 1.006 lipoproteins. With fat feeding, chylomicron triglyceride concentrations are not significantly elevated in pregnant rats, 0 or 8 hr postabsorptively despite greater food intake in pregnancy. In contrast, very low density lipoprotein (VLDL) triglyceride concentrations are elevated at all times following fat feeding in pregnant compared to nonpregnant animals. A significant contribution of lipoprotein remnants to the triglyceride rise in d < 1.006 lipoproteins seems unlikely since an isolated increase in VLDL cholesterol is not observed. No statistically significant accumulation of hepatic triglycerides occurs on any diet in pregnancy. Diet induced shifts in adipose tissue and muscle lipoprotein lipase activity are exaggerated in pregnancy while hepatic lipase is unaffected. Fetal weight is similar on all diets except sucrose where weight is reduced. CONCLUSIONS: Hypertriglyceridemia in fed pregnant rats is due to an increase in endogenous triglycerides. Remnant lipid accumulation does not appear to contribute to the endogenous hypertriglyceridemia. There is no intolerance to exogenous (dietary) fat. The results are compatible with an unimpaired delivery of exogenous fat to fat oxidizing tissues thereby maximizing glucose availability for fetal growth.

Adipose Tissue↗
PubMed1983

A new model of human VLDL metabolism based on simultaneous studies of its APOB and triglyceride.

Previous studies which separately examined the behavior of the B apolipoprotein and of the triglyceride of VLDL had raised the possibility that each was metabolized in a different manner. The present studies have explored this possibility by simultaneously studying each of these VLDL constituents in thirteen humans. 125I-labeled Sf 60-400 lipoproteins were injected. The fate of their apo B (a reflection of the metabolism of the lipoprotein particle) was followed in this, and in the smaller Sf 12-60 lipoproteins. In everyone, the larger particle was catabolized to the smaller one. Furthermore, the smaller particle was derived exclusively from the larger one. The behavior of the lipoproteins' triglyceride was examined by following the specific activity of 3H-triglyceride which had been endogenously labelled by injecting 2-3H-glycerol. Some of the larger lipoproteins' triglyceride appeared in the smaller particles. However, in contrast to the apo B, the triglyceride in the smaller particle was not derived exclusively from that in the larger particle. In eleven subjects, the triglyceride specific activity curves above demonstrated that some of the triglyceride entered the smaller circulating particle from a source other than the large particle.

Adult↗
PubMed1985

Postprandial distribution of apolipoproteins C-II and C-III in normal subjects and patients with mild hypertriglyceridemia: comparison of meals containing corn oil and medium-chain triglyceride oil.

Five healthy male subjects and five patients with mild hypertriglyceridemia were studied following the administration of 800-kcal liquid meals containing 40% of energy from fat, 40% from carbohydrate, and 20% from protein. On the first day of the study, the fat source was corn oil (long-chain triglyceride), whereas medium-chain triglyceride (MCT) oil was used the second day. Meals were infused into the duodenum using a peristaltic pump. Plasma samples, obtained at hourly intervals for 8 hours, were analyzed for glucose, cholesterol, triglyceride, and apolipoproteins C-II and C-III. The distribution of apoC-II and apoC-III between ultracentrifugally-separated triglyceride-rich lipoproteins (TRL) and high-density lipoproteins (HDL) was also evaluated. The patient group had significantly elevated fasting levels of triglyceride, apoC-II and apoC-III, as well as much greater lipemic response to the meal containing corn oil. In both groups, TRL apoC-II and apoC-III levels were positively correlated with the triglyceride level as it increased following the corn oil meal. These correlations were also observed in the normal subjects when the MCT oil meal was administered, even though changes in plasma triglycerides were minimal. In normal subjects, whole plasma levels of apoC-II and apoC-III decreased significantly following the meal containing corn oil, whereas no net changes occurred following the MCT oil meal. In hypertriglyceridemic subjects, small decreases in plasma apoC-II and apoC-III levels occurred after both meals, although the changes in apoC-II were not statistically significant. The tendency for decreased plasma apoC levels following alimentary lipemia confirms previous reports, and provides further data to support the concept that some apoC is cleared from plasma in association with TRL remnants. The finding that mildly hypertriglyceridemic subjects responded similarly to both conventional fat and MCT may indicate that their rates of remnant clearance were similar following the two meals.

Adult↗
PubMed1991

Effects of dietary glucose or fructose on the secretion rate and particle size of triglyceride-rich lipoproteins in Zucker fatty rats.

Effects of dietary carbohydrate on the secretion rate and particle size of triglyceride-rich lipoproteins were examined in Zucker fatty rats fed fructose and glucose and were compared with those of Zucker lean rats. Carbohydrates were supplied as 10% drinking solutions for 14 days. As compared with lean rats, Zucker fatty rats had hyperinsulinemia and hypertriglyceridemia associated with an increased rate of triglyceride secretion into the circulation. Feeding fructose and glucose to fatty rats produced an increase in plasma glucose levels, whereas plasma insulin concentrations did not show significant changes. Neither fructose nor glucose supplementation produced significant changes in the rate of triglyceride secretion. Despite this, plasma triglyceride concentrations in fructose-fed fatty rats were twice as high as those in glucose-fed rats or those receiving no supplementary carbohydrate. Particle diameters of lipoproteins of density between 0.96 and 1.006 were larger in fructose-fed fatty rats than in those receiving no sugar. The results suggest that feeding fructose, but not glucose, into fatty rats is associated with an impairment of triglyceride removal and a resultant increase in plasma triglyceride concentration, the latter of which is accompanied by an increase in triglyceride contents in each particle.

Animals↗
PubMed1980

Hypertriglyceridemia associated with Trypanosoma brucei brucei infection in rabbits: role of defective triglyceride removal.

Rabbits infected with Trypanosoma brucei brucei develop a hypertriglyceridemia characterized by an increase in very low density lipoprotein and, to a lesser extent, low density lipoprotein, with a decrease in high density lipoprotein. Triglyceride production studies showed that the triglyceride production rate was not significantly different in trypanosome-infected rabbits from controls. Studies of triglyceride degradation using very low density lipoprotein triglyceride endogenously labelled with [3H]palmitate demonstrated a marked slowing of triglyceride removal in the infected rabbits when compared to controls. Lipase activity in post-heparin plasma was found to be deficient in trypanosome-infected animals. Furthermore, the greater the decrease in lipolytic activity, the greater the increase in serum triglyceride level. We conclude that the hypertriglyceridemia associated with T. b. brucei infection in rabbits results predominantly from a defect in triglyceride degradation.

Animals↗
PubMed2004

Decrease of plasma triglycerides during the acute phase of unstable angina or non-ST elevation myocardial infarction is a marker of recurrent ischemia.

Both increase and decrease of plasma triglycerides during acute coronary syndromes (ACS) are reported, however, a clinical relevance for these distinct metabolic responses is unclear. To test the association between distinct responses of lipid metabolism and cardiovascular risk, 39 subjects admitted with non-ST elevation ACS within 48 h of presentation had plasma lipids measured on the first and sixth days of hospitalization, and continuous electrocardiogram was performed during the first 2 days to quantify recurrent ischemia and heart rate variability. No lipid-lowering therapy was offered to the patients. During the first 5 days, half of them experimented a decrease in triglycerides (n=19, median: -18 mg/dl) and the other half presented triglyceride increase (n=20, median: +44 mg/dl). A higher incidence of recurrent ischemia (35% versus 5%, P=0.02) and greater ischemic burden/patient (123 +/- 286 mm min versus 47 +/- 212 mm min, P=0.02) were observed in subjects with triglyceride reduction, when compared with those with triglyceride increase. Individuals with heart rate variability below the median presented a median decrease in triglycerides during the 5-day period, as opposed to the counterparts (P=0.05). In conclusion, triglyceride reduction during ACS is associated with a greater incidence of recurrent ischemia and may constitute a sign of higher sympathetic activity.

Acute Disease↗
PubMed2000

Relation of serum triglyceride levels to survival after coronary artery bypass grafting.

We performed a prospective observational study on 6,602 subjects (94% for 5 years and 34% for 10 to 15 years) who underwent coronary artery bypass graft surgery (CABG) between 1982 and 1992. We examined whether triglyceride concentrations adjusted for other factors (total cholesterol, history of diabetes mellitus, systemic hypertension, left ventricular function, number of coronary arteries significantly narrowed, and use of the internal thoracic arteries) explained total and event-free survival. These analyses were duplicated within gender (1,354 women and 5,248 men). This approach allowed a determination of any gender-related disparities in lipid predictors. Triglycerides in the highest quartile were associated with an increased risk of mortality of 20% (confidence interval [CI] 1.0 to 1.4). Similar risk was seen for event-free survival. Although there was no evidence of gender differences in adjusted survival (p = 0.33), a gender by triglyceride interaction (p = 0.004) indicated that the response to high triglycerides as related to survival did differ by gender. Specifically, women had a dramatically higher risk (hazard ratio [HR] 1.5, CI 1.1 to 2.1) than men (HR 1.1, CI 0.9 to 1. 3). Both men and women did have triglyceride-associated risk with regard to event-free survival (HR in men 1.2, CI 1.1 to 1.4; HR in women 1.4, CI 1.1 to 1.8). Examination of high-density lipoprotein cholesterol in a subcohort did not eliminate the observed triglyceride effects. Thus, triglyceride baseline values are primary determinants (similar to baseline left ventricular function or extent of coronary disease) for long-term total and event-free mortality after CABG in women but not in men.

Aged↗