Plasma Triglyceride Level and Mortality from Coronary Heart Disease

Criqui, Michael H.; Heiss, Gerardo; Cohn, Richard D.; Cowan, Linda D.; Suchindran, Chirayath; Bangdiwala, Shrikant I.; Kritchevsky, S. B.; Jacobs, David R.; O'grady, Haesook Kim; Davis, C. E.

doi:10.1056/nejm199304293281702

Cited by 377 publications

(181 citation statements)

References 36 publications

Supporting

Mentioning

163

Contrasting

Unclassified

Order By: Relevance

“…e results of studies on the relationship between lipoproteins and angiographically evaluated coronary atherosclerosis lack consistency [7,16]. Many studies reported important effects of TC, LDL-C, and HDL, whereas others reported the in uence of TG.…”

Section: Discussionmentioning

confidence: 99%

“…Several studies have clearly shown a correlation between lipoprotein lipid fractions and CAD [7][8][9][10]. e results of two studies on the relationship between Lp(a) levels and CAD report con icting information [7,8].…”

mentioning

confidence: 99%

“…e results of two studies on the relationship between Lp(a) levels and CAD report con icting information [7,8].…”

mentioning

confidence: 99%

See 2 more Smart Citations

The relationship between lipoprotein(a) and coronary artery disease, as well as its variable nature following myocardial infarction

Örnek¹,

Murat²,

Duran³

et al. 2011

CIM

View full text Add to dashboard Cite

Turkeye relationship between lipoprotein(a) and coronary artery disease, as well as its variable nature following myocardial infarction AbstractPurpose: e present study aimed to investigate the relationship between the severity of coronary artery disease (CAD) and level of Lipoprotein (LP)(a).Methods: e study included 52 CAD patients and a control group consisting of 38 individuals. e patients were classi ed into three groups based on the clinical form of CAD (stable angina pectoris, SAP, unstable angina pectoris,UAP, and myocardial infarction,MI), and were further divided into three groups based on CAD severity (1-, 2-and 3-vessel). Serum Lp(a) levels were monitored 4, 8, and 24 h, 10 and 30 days following acute MI in 18 patients.Results: Based on regression analysis, Lp(a) was not correlated with other lipoproteins or with risk factors of CAD, such as body mass index, smoking, family history, diabetes, age, gender, and hypertension (r = 0.08-0.22). 72% of the patients in the CAD group and 24% of the control group had an Lp(a) level >30 mg dL -1 (P = 0.004), and Lp(a) levels were higher in 3-vessel patients than in 2-vessel and 1-vessel CAD patients (86% vs. 68%, P = 0.02 and 86% vs. 62%, P=0.01, respectively). Serum Lp(a) levels were higher in the UAP and MI groups than in the SAP group (48 ± 44.7 mg dL -1 , 49 ± 36.1 mg dL -1 and 31.2 ± 22.3 mg dL -1 , respectively,P=0.02). Lp(a) levels increased a er acute MI, and reached peak levels 10 days post-MI (41% increase, P=0.001) and remained considerably elevated (18%) 30 days post-MI (P=0.01).Conclusion: Serum Lp(a) was higher in the UAP and MI patients in comparison with the SAP patients, and was higher in 3-vessel CAD in comparison with 1-and 2-vessel CAD patients.

show abstract

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

The relationship between lipoprotein(a) and coronary artery disease, as well as its variable nature following myocardial infarction

Örnek¹,

Murat²,

Duran³

et al. 2011

CIM

View full text Add to dashboard Cite

show abstract

“…association of high TG and low HDL cholesterol was necessary to predict cardiovascular risk (8). This apparent discrepancy is probably related to the fact that it is quite difficult to match for duration and degree of cardiovascular disease in different populations, and, when cardiovascular disease is established, some factors might have lost their primary pathogenic significance.…”

mentioning

confidence: 99%

Myocardial insulin resistance associated with chronic hypertriglyceridemia and increased FFA levels in Type 2 diabetic patients

Monti¹,

Landoni²,

Setola³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

dial insulin resistance associated with chronic hypertriglyceridemia and increased FFA levels in Type 2 diabetic patients. Am J Physiol Heart Circ Physiol 287: H1225-H1231, 2004. First published May 6, 2004; 10.1152/ajpheart.00629.2003.-We evaluated the influence of chronic hypertriglyceridemia and endothelial dysfunction on myocardial glucose uptake (MGU) in Type 2 diabetic patients without coronary heart disease. Patients were divided into two groups according to fasting triglyceride (TG) levels: 5.4 Ϯ 1.1 and 1.5 Ϯ 0.3 mmol/l for high-and normal-TG groups, respectively. Five subjects were assigned to the high-TG group and 11 to the normal-TG group. Age, gender, body mass index, systolic and diastolic blood pressure, glucose, insulin, HbA1c, cholesterol, and HDL cholesterol were similar in the two groups, whereas free fatty acid (FFA) levels were higher in the high-TG group basally and at the end of the clamp. Furthermore, five healthy subjects were subjected to the same protocol and used as the control group. MGU was assessed by using 18 F-labeled 2-fluoro-2-deoxy-D-glucose under hyperglycemic-hyperinsulinemic conditions. Basal endothelin-1 and nitric oxide levels were significantly higher in the high-TG group than in the normal-TG and control groups, and cGMP and maximal postischemic vasodilation were significantly decreased in the high-TG group compared with the normal-TG and control groups. However, significant alterations were found in the same parameters in the normal-TG group compared with the control group. By the end of the hyperglycemic clamp, in the high-TG group, MGU was ϳ40 and 65% of that in the normal-TG and control groups. MGU negatively correlated with TG, FFA, and endothelin-1, whereas a positive correlation was found with cGMP and maximal postischemic vasodilation. In conclusion, increased TG and FFA levels are risks, in addition to Type 2 diabetes mellitus, for myocardial insulin resistance, endothelial dysfunction, and alteration of nitric oxide/cGMP levels. triglycerides; myocardial glucose uptake; positron emission tomography study; endothelium; free fatty acid FOR MANY YEARS, hypertriglyceridemia was considered a marker of cardiovascular disease only in certain subjects, such as women (5, 12) and patients with Type 2 diabetes (10). The association between triglycerides (TGs), independently of HDL cholesterol levels, and definite cardiovascular disease, such as myocardial infarction or angina, was found in some studies (5) and denied in others, in which the simultaneous association of high TG and low HDL cholesterol was necessary to predict cardiovascular risk (8). This apparent discrepancy is probably related to the fact that it is quite difficult to match for duration and degree of cardiovascular disease in different populations, and, when cardiovascular disease is established, some factors might have lost their primary pathogenic significance. Hypertriglyceridemia occurs frequently in patients with coronary heart disease (CHD) and in survivors of myocardial infarction (5), and, durin...

show abstract

“…N umerous studies have shown that plasma lipids and lipoproteins are associated with increased risk of cardiovascular disease (CVD), including smaller-size LDL particles, 1-3 elevated plasma triglyceride (TG), 4,5 and decreased levels of HDL cholesterol (HDL-C). 6 However, whether these associations with CVD are independent of one another remains controversial.…”

mentioning

confidence: 99%

Pleiotropic Genetic Effects on LDL Size, Plasma Triglyceride, and HDL Cholesterol in Families

Edwards

Mahaney

Motulsky

et al. 1999

ATVB

View full text Add to dashboard Cite

Abstract-The interrelationships among low density lipoprotein (LDL) particle size, plasma triglyceride (TG), and high density lipoprotein cholesterol (HDL-C) are well established and may involve underlying genetic influences. This study evaluated common genetic effects on LDL size, TG, and HDL-C by using data from 85 kindreds participating in the Genetic Epidemiology of Hypertriglyceridemia (GET) Study. A multivariate, maximum likelihood-based approach to quantitative genetic analysis was used to estimate the additive effects of shared genes and shared, unmeasured nongenetic factors on variation in LDL size and in plasma levels of TG and HDL-C. A significant (PϽ0.001) proportion of the variance in each trait was attributable to the additive effects of genes. Maximum-likelihood estimates of heritability were 0.34 for LDL size, 0.41 for TG, and 0.54 for HDL-C. Significant (PϽ0.001) additive genetic correlations ( G ), indicative of the shared additive effects of genes on pairs of traits, were estimated between all 3 trait pairs: for LDL size and TG G ϭϪ0.87, for LDL size and HDL-C G ϭ0.65, and for HDL-C and TG G ϭϪ0.54. A similar pattern of significant environmental correlations between the 3 trait pairs was also observed. These results suggest that a large proportion of the well-documented correlations in LDL size, TG, and HDL-C are likely attributable to the influence of the same gene(s) in these families. That is, the gene(s) that may contribute to decreases in LDL size also contribute significantly to higher plasma levels of TG and lower plasma levels of HDL-C. These relationships may be useful in identifying genes responsible for the associations between these phenotypes and susceptibility to cardiovascular disease in these families.

show abstract

Plasma Triglyceride Level and Mortality from Coronary Heart Disease

Cited by 377 publications

References 36 publications

The relationship between lipoprotein(a) and coronary artery disease, as well as its variable nature following myocardial infarction

The relationship between lipoprotein(a) and coronary artery disease, as well as its variable nature following myocardial infarction

Myocardial insulin resistance associated with chronic hypertriglyceridemia and increased FFA levels in Type 2 diabetic patients

Pleiotropic Genetic Effects on LDL Size, Plasma Triglyceride, and HDL Cholesterol in Families

Contact Info

Product

Resources

About