Association of hypertensive status and its drug treatment with lipid and haemostatic factors in middle-aged men: the PRIME Study

Marques‐Vidal, Pedro; Montaye, Michèle; Haas, Bernadette; Bingham, Annie; Evans, Alun; Juhan‐Vague, I.; Ferrières, Jean; Luc, G.; Amouyel, Philippe; Arveiler, Dominique; McMaster, Dorothy; Ruidavets, J.B.; Bard, Jean‐Marie; Scarabin, P.Y.; Ducimetière, Pierre

doi:10.1038/sj.jhh.1001061

Cited by 13 publications

(4 citation statements)

References 36 publications

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“…Some reports have not demonstrated an increase with ACE inhibitors and others have. [39][40][41] Our data corroborate the fact that ACE inhibitors do reduce Lp(a) levels in people with renal insufficiency.…”

Section: Journal Of Human Hypertensionsupporting

confidence: 79%

Impact of an ACE inhibitor and calcium antagonist on microalbuminuria and lipid subfractions in type 2 diabetes: a randomised, multi-centre pilot study

Bakris¹,

Smith²,

Richardson³

et al. 2002

J Hum Hypertens

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Background: Microalbuminuria (MA) is associated with increased cardiovascular risk and lipid abnormalities in people with type 2 diabetes. ACE inhibitors and calcium channel blockers (CCBs) reduce MA and are neutral on total cholesterol and triglycerides. The effect of ACE inhibitors and CCBs on lipid subfractions such as Lp(a), apolipoprotein (apo) A1, apo B, and others, however, is unclear. The current study tests the hypothesis that a fixed-dose combination of an ACE inhibitor, benazepril (B) with the dihydropyridine CCB, amlodipine (A), will further reduce arterial pressure and reduce atherogenic lipid fractions compared to either agent alone. Design: A multicentre, randomised, open-label, parallel group design was used to study 27 participants with type 2 diabetes. Measurements for total cholesterol, high-and low-density lipoprotein (HDL and LDL), triglycerides, apo A1, apo B, Lp(a), MA, arterial pressure and creatinine clearance were obtained at baseline and at 12-week intervals during the 36 week study. Results: Arterial pressure was significantly reduced at 36 weeks in all three groups (P ‫؍‬ 0.0078 for A, P ‫؍‬

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Section: Journal Of Human Hypertensionsupporting

confidence: 79%

Impact of an ACE inhibitor and calcium antagonist on microalbuminuria and lipid subfractions in type 2 diabetes: a randomised, multi-centre pilot study

Bakris¹,

Smith²,

Richardson³

et al. 2002

J Hum Hypertens

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“…Blood pressure reduction with Ca-blockers also improves insulin sensitivi-ty in hypertensive patients (61). On the other hand, many studies have shown that diuretics and β-blockers decrease HDL levels (50,(62)(63)(64) and insulin sensitivity (65,66).…”

Section: Discussionmentioning

confidence: 99%

Effect of Antihypertensive Treatment on PlasmaFibrinogen and Serum HDL Levelsin Patients with Essential Hypertension

Papadakis

Mikhailidis

Vrentzos

et al. 2005

Clin Appl Thromb Hemost

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The influence of hypertension, and its treatment, on circulating lipid and fibrinogen (Fib) concentrations in patients with essential hypertension was investigated. The lipid profile and Fib levels were measured in 353 patients (131 men) with essential hypertension. Their median age was 60 years (range: 18-85 years). All patients had normal results from liver, renal, and thyroid function tests. There were 162 patients (45.9%) who were not receiving antihypertensive treatment. Of the remaining patients, 117 were taking 'lipid-hostile' beta-blockers, thiazide diuretics) antihypertensives and 74 were taking 'lipid-neutral' (angiotensin-converting enzyme inhibitors, calcium channel blockers, angiotensin-II receptor blockers) agents. Patients who were taking 'lipid-hostile' antihypertensive drugs had significantly higher plasma Fib concentrations when compared with those taking 'lipid-neutral' antihypertensives or those not receiving antihypertensive treatment. These differences were not attributable to established factors that influence plasma Fib levels, since when smokers and patients with diabetes mellitus and/or vascular disease were excluded, the difference remained significant. In addition, in these more homogeneous groups, patients receiving 'lipid-neutral' treatment had significantly higher serum high-density lipoprotein (HDL) cholesterol levels when compared with both those taking 'lipid-hostile' antihypertensives and untreated ones. There were no significant differences in the other lipid variables, independently of the presence/absence or the type of antihypertensives. These results suggest that antihypertensive drugs have additional effects, beyond lowering blood pressure, on other vascular risk factors, like Fib and HDL. These effects may depend on the type of drug used.

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“…Second, evidence involving the I/D variant of the ACE gene with lipid and lipoprotein levels comes from clinical trials using ACE inhibitors as antihypertensive drug. These drugs have considerable lowering effects, mostly on total and LDL‐C levels (46), and increasing effects on HDL‐C concentrations have also been reported (47). Third, an interaction between ACE I/D polymorphism and plasma lipoprotein/lipid response to fluvastatin (a lipid‐lowering agent) has been reported (7).…”

Section: Discussionmentioning

confidence: 99%

Influence of the angiotensin‐converting enzyme gene insertion/deletion polymorphism on lipoprotein/lipid response to gemfibrozil

Bossé¹,

Vohl

Dumont³

et al. 2002

Clinical Genetics

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Evidence suggests that fibrate therapy reduces the risk of recurrent coronary heart disease among men with low levels of high density lipoprotein cholesterol (HDL-C). Indirect observations and new possible biological pathways suggest that the angiotensin-converting enzyme (ACE) insertion/deletion (I/D) polymorphism might modulate the lipoprotein/lipid profile and its response to fibrate therapy. To assess the possible interaction between fibrate therapy and such variants on plasma lipid and lipoprotein levels, 65 dyslipidemic abdominally obese men were treated for 6 months with or without gemfibrozil (600 mg twice daily). No differences in baseline plasma lipid and lipoprotein levels were found between genotype groups except for the HDL(3)-C subfraction, which was higher in the DD group (p = 0.02). A two-way factorial ANOVA was used to evaluate the effect of the genotype (DD homozygotes vs I allele carriers), the treatment (placebo vs gemfibrozil), and the interaction between these two independent variables on changes observed in lipid and lipoprotein concentrations. A significant genotype-by-treatment interaction (p = 0.02) was found for the plasma HDL-C response to the intervention program. In fact, having the DD genotype and being treated with gemfibrozil had a synergical effect on HDL-C levels. The results of this study suggest that the ACE I/D polymorphism influences the effect of gemfibrozil on plasma HDL-C levels.

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Association of hypertensive status and its drug treatment with lipid and haemostatic factors in middle-aged men: the PRIME Study

Cited by 13 publications

References 36 publications

Impact of an ACE inhibitor and calcium antagonist on microalbuminuria and lipid subfractions in type 2 diabetes: a randomised, multi-centre pilot study

Impact of an ACE inhibitor and calcium antagonist on microalbuminuria and lipid subfractions in type 2 diabetes: a randomised, multi-centre pilot study

Effect of Antihypertensive Treatment on PlasmaFibrinogen and Serum HDL Levelsin Patients with Essential Hypertension

Influence of the angiotensin‐converting enzyme gene insertion/deletion polymorphism on lipoprotein/lipid response to gemfibrozil

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