Skip to main content

Table 1 Summary of clinical studies links TG/TRLPs with CVD

From: Hypertriglyceridemia and atherosclerosis

Study

Study design

Sample size

Study population

Baseline lipid level (mgl/dL)

Follow-up

Key findings

[25] Faerge-Man et al. 2009

meta-analysis

(2 prospective, randomized, multicenter trials)

N = 15,779

with clinically evident coronary heart disease or a history of myocardial infarction

/

/

slightly increased TG levels are associated with higher risk of recurrence of CVEs in statin-treated patients

[24] Varbo et al. 2013

meta-analysis

(3 studies)

N = 73,513

white subjects of Danish descent from Copenhagen, of whom 11,984 had ischemic heart disease

/

/

the elevated nonfasting remnant cholesterol and TRLPs that are causally related to increased risk for ischemic heart disease

[32] Puri et al. 2016

meta-analysis

(9 clinical trials)

N = 4957

with coronary disease

/

/

Plaque progression overall was closely tied with changes in non-HDLC and appeared to associate with TG levels only

beyond 200 mg/dL

[33] DAIS 2001

multicenter, double-blind, placebo-controlled, randomized trial

Fen

(N = 207)

Pla

(N = 211)

with type 2 diabetes aged. 40–65 years, with or without previous coronary intervention

LDL(mean):

130.7(Fen)

132.6(Pla),

HDL(mean):

39.1(Fen)

40.6(Pla),

TG(median):

229.4(Fen)

214.3(Pla)

3 years

Fenofibrate could decreased significantly progression in minimum lumen diameter and percentage diameter stenosis (localised. coronary-artery disease)

[34] FIELD Study 2005

multicenter,

Controlled, randomized trial

Fen

(N = 4895, n = 944)

Pla

(N = 4900, n = 1776)

with type 2 diabetes

LDL(mean):

118.7(Fen)118.1(Pla),HDL(mean):

42.5(Fen)42.5(Pla),

TG(median):

152.8(Fen)

151.9 (Pla)

5 years

Fenofibrate did not significantly reduce the risk of the primary outcome of coronary events but reduce total cardiovascular events

[36] HATS Study 2007

double-blind placebo-controlled with

a two-by-two factorial design

N + S

(N = 33)

Antioxidant vitamins

(N = 39)

N-S + A

(N = 40)

all placebos

(N = 34)

with clinical coronary disease and at least three stenoses of at least 30% of the luminal diameter or one stenosis of at least 50%

LDL:127(P)132(N + S)117(A)124(N-S + A),

HDL: 32(P)31(N + S)

32(A)30(N-S + A),

TG:203(P)202(N + S)

207(A)236(N-S + A)

3 years

Niacin plus Simvastatin

provided marked clinical and angiographically measurable benefits in patiients with coronary disease and low HDL levels

[39] ACCORD Study 2010

multicenter, randomized trial

F + S

(N = 2765)

Pla + Sim

(N = 2753)

Subgroup:

F + S

(N = 485)

Pla + Sim

(N = 456)

with type 2 diabetes

LDL:100.0 ± 30.3(F + S)

101.1 ± 31.0(Pla),

HDL:38.0 ± 7.8(F + S) 38.2 ± 7.8(Pla),

TG(mean):164(F + S)160(Pla)

4.7 years

The use of combination fibrate–statin therapy,did not reduce cardiovascullar risk in the majority of patients with type 2 diabetes, rather than statin therapy alone, but can reduce the CVD risk in subgroup with elevated TG levels (≥204 mg/dL) and decreased HDL-C (≤ 34 mg/dL)

[37] AIM-HIGH Study 2011

randomized trial

N + S(or plus Eze)

(N = 1718)

Pla + Sim(or plus Eze)

(N = 1696)

with 45 years of age or older and established cardiovascular disease

LDL(mean):

74.0 ± 22.7(Nia)

74.2 ± 23.4(Pla),

HDL(mean):

34.9 ± 5.6(Nia)

34.5 ± 5.6(Pla),

TG(median):

163(Nia)167.5 (Pla)

36 months

No incremental benefit of niacin in reducing cardiovascular events, despite significant increases in HDL-C levels and decreases in triglyceride levels

[38] HPS2-THRIVE Study 2013

multicenter randomized trial

ERN/LRPT

(N = 12,838)

Pla

(N = 12,835)

with established cardiovascular disease

on the background of LDL-lowering therapy,

LDL(mean):63.4,

HDL(mean):44.1,

TG (median): 126.7

3.9 years

adding ERN/LRPT to simvastatin 40 mg daily (or plus ezetimibe) increased the risk of myopathy

[41] FIRST Study 2014

multicenter, double-blind, placebo-controlled

trial

FA135mg + Ato

(N = 340)

Pla + Ato

(N = 342)

with mixed dyslipidemia and a history of coronary heart disease or risk equivalent

LDL(mean):

84.0(F+A)84.5(Pla),HDL(mean):

40.1(F+A)39.6(Pla),TG(median):

205.0(F+A)

193.0 (Pla)

104 weeks

FA plus Atorvastatin did not decrease cIMT progression in high-risk patients with mixed dyslipidemia and may achieve a clinical benefit in patients with TG level of ≥175 mg /dL

  1. Abbreviations: CVEs cardiovascular events, TRLPs triglyceride-rich lipoproteins, LDL low-density lipoprotein, HDL high-density lipoprotein, TG triglyceride, Fen Fenofibrate, Pla Placebo, FA fenofibric acid, Ato Atorvastatin, Nia niacin, Eze ezetimib, ERN/LRPT Extended release niacin plus laropiprant, F+A fenofibric acid plus Atorvastatin, F+S Fenofibrate+Simvastatin, N+S Niacin+Simvastatin, N-S+A Niacin–Simvastatin+Antioxidants, n the sample size of starting other lipid-lowering therapy (statin) in both groups in FIELD study