A study to determine the response of coronary atherosclerosis to raising low high density lipoprotein cholesterol with a fibric-acid derivative in men after coronary bypass surgery

Syvänne, Mikko; Taskinen, Marja‐Riitta; Nieminen, Markku S.; Manninen, Vesa; Ya, Kesäniemi; Pasternack, Amos; Nawrocki, J.W.; Haber, Harry; Frick, M. H.

doi:10.1016/s0197-2456(96)00091-8

Cited by 22 publications

(28 citation statements)

References 108 publications

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“…Fasting serum triglycerides, cholesterol, HDL and LDL cholesterol, and blood glucose were measured by methods described previously. 19,20 …”

Section: Patients and Study Protocolmentioning

confidence: 99%

“…Details of the entry criteria and screening process, clinical visits, and laboratory analyses have been described previously. 19,20 All patients provided written informed consent, and the study was approved by the ethics committees of the participating hospitals. All the patients underwent comprehensive clinical examinations, bicycle exercise tests, and received detailed dietary counseling at the baseline stage.…”

Section: Patients and Study Protocolmentioning

confidence: 99%

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Heart Rate Variability and Progression of Coronary Atherosclerosis

Huikuri

Jokinen

Syvänne

et al. 1999

ATVB

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Abstract-Low heart rate (HR) variability is associated with increased risk of cardiovascular morbidity and mortality, but the causes and mechanisms of this association are not well known. This prospective study was designed to test the hypothesis that reduced HR variability is related to progression of coronary atherosclerosis. Average HR and HR variability were analyzed in 12-hour ambulatory ECG recordings from 265 qualified patients participating in a multicenter study to evaluate the angiographic progression of coronary artery disease in patients with prior coronary artery bypass surgery and low high-density lipoprotein cholesterol concentrations (Ͻ1.1 mmol/L). Participants were randomized to receive a placebo or gemfibrozil therapy. The progression of coronary atherosclerosis was estimated by quantitative, computer-assisted analysis of coronary artery stenoses from the baseline angiograms and from repeated angiograms performed an average of 32 months later. The progression of focal coronary atherosclerosis of the patients randomized to placebo therapy was more marked in the tertile with the lowest standard deviation of all normal to normal R-R intervals ( Key Words: coronary artery disease Ⅲ lipids Ⅲ heart period Ⅲ angiography E levated heart rate (HR) and reduced HR variability are associated with an increased risk of cardiovascular morbidity and mortality in various populations, 1-8 but the pathophysiological link between these associations is not well understood. Experimental studies on monkeys fed an atherogenic diet have demonstrated a relationship between resting HR and progression of coronary atherosclerosis, 9 -11 and there is also a strong relationship between HR and arterial stiffness, 12 but there has been little evidence of any association between HR, or its variability, and human coronary atherosclerosis.Progression of coronary artery stenoses in repeated coronary angiograms increases the risk of adverse cardiac events, suggesting that rapid progression predisposes patients to acute complications of coronary artery plaques and serves as a surrogate end point for clinical events. 13,14 Lipid-modifying therapy has been shown to prevent the progression of coronary atherosclerosis, confirming that abnormalities in plasma lipid concentrations are strongly associated with the progression of coronary artery disease and the occurrence of adverse clinical events. 14 However, lipid theory may not explain all aspects of coronary artery disease, eg, the rapid progression of discrete stenoses in specific coronary arterial regions, which is thought to result from an interplay of hemodynamic, metabolic, and hemostatic factors. [15][16][17][18] To test the hypothesis that elevated HR and reduced HR variability are associated with the progression of human coronary atherosclerosis in patients with lipid abnormalities, we studied HR and its variability, measured by ambulatory ECG, and the angiographic progression of coronary artery disease in patients with reduced HDL cholesterol concentrations.

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“…Fasting serum triglycerides, cholesterol, HDL and LDL cholesterol, and blood glucose were measured by methods described previously. 19,20 …”

Section: Patients and Study Protocolmentioning

confidence: 99%

Section: Patients and Study Protocolmentioning

confidence: 99%

Heart Rate Variability and Progression of Coronary Atherosclerosis

Huikuri

Jokinen

Syvänne

et al. 1999

ATVB

Self Cite

251

144

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“…To examine the relationship between APOA5 gene variants and the metabolism of TG-rich particles in more Talmud et al APOA5 , lipoprotein distribution, and atherosclerosis detail, we determined the association between APOA5 Ϫ 1131T Ͼ C and S19W with lipids, lipoproteins, and apolipoproteins as well as ultracentrifuged lipoprotein subfractions in the Finnish Lopid Coronary Angiography Trial (LOCAT) study of postcoronary bypass men (13). To date, variations in the peroxisome proliferator-activated receptor ␣ gene, PPARA L162V and intron 7G Ͼ C (14), the stromelysin gene, MMP3 5A/6A (15), the platelet endothelial cell adhesion molecule-1 gene, PECAM1 53G Ͼ A (16), and the ␣ -1-antitrypsin gene, AAT V213A and 11478G Ͼ A (17), have all shown significant associations with the progression of atherosclerosis in LOCAT, with AAT V213A showing a pharmacogenetic interaction with the response to gemfibrozil treatment.…”

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confidence: 99%

APOA5 gene variants, lipoprotein particle distribution, and progression of coronary heart disease

Talmud

Martin

Taskinen

et al. 2004

Journal of Lipid Research

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Animal and human studies of the newly identified APOA5 gene are consistent in identifying APOA5 as a major determinant of plasma triglyceride (TG) levels (1). Thus, APOA5 , forming a cluster with APOA4-C3-A1 on chromosome 11q23, constitutes a locus involved in TG and HDL determination (2, 3). In both transgenic and knockout mouse models, it is clear that apolipoprotein A-V (apoA-V) is inversely associated with plasma TG levels. Transgenic mice overexpressing human APOA5 (1) or adenoviral vector-mediated transfer of APOA5 into mice (4) produce a 60-70% decrease in TG, whereas apoA5 knockout mice have 4-fold higher plasma TG than controls (1). The human APOA5 gene is fairly polymorphic, and in Caucasians, three common haplotypes have been identified: wild-type haplotype APOA5 * 1; APOA5 * 2, defined by rare alleles of Ϫ 1131T Ͼ C, c-3A Ͼ G, IVS3 ϩ 476G Ͼ T, and c1259T Ͼ C; and APOA5 * 3, defined by a rare allele of S19W (5) and thus genotyping for Ϫ 1131T Ͼ C or S19W, essentially acting as tagging single nucleotide polymorphisms (SNPs) (6). The Ϫ 1131C variants and to a lesser extent 19W have been associated with increased TG in healthy Caucasians (1, 5, 7-9) and in African Americans and Hispanics (5) and with higher relative risk of developing dyslipidemias (10, 11). The rare allele of Ϫ 1131T Ͼ C is more common in Japanese compared with Caucasians (0.34 versus 0.08, respectively) (12) and shows a strong association with TG levels, even in young school-age children. However, despite these consistent associations with TG levels, the function and role of apoA-V in TG metabolism remains unclear.To examine the relationship between APOA5 gene variants and the metabolism of TG-rich particles in more

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“…18,21 In the Post Coronary Artery Bypass Graft Trial (Post CABG trial), 15 aggressive lipid lowering using lovastatin with or without cholestipol suppressed the progression of atherosclerosis in the SVGs as well as in the native coronary arteries. In the Lopid Coronary Angiography Trial (LOCAT) 16,17 found that gemfibrozil retarded the progression of coronary atherosclerosis and formation of bypass graft lesions in post-CABG males with low HDL-C concentrations. The results of the present study support these previous demonstrations that lipid modification has the potential for delaying the progression of coronary atherosclerosis in Japanese post-CABG patients, too.…”

Section: Comparison With Previous Studiesmentioning

confidence: 99%

“…Although one of the inclusion criteria of the present study was having CABG within 1 year of beginning statin treatment, 67% of the patients had undergone surgery within 3 months. The patients enrolled in the previous studies included only those more than 3 months after CABG (CLAS), 18,21 3-48 months after CABG (LOCAT) 16 and 1-11 years after CABG (Post CABG). 15 No prior studies have specifically investigated the efficacy of early statin therapy on angiographic progression after CABG.…”

Section: Comparison With Previous Studiesmentioning

confidence: 99%