No effects on myocardial ischaemia in patients with stable ischaemic heart disease after treatment with ramipril for 6 months

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

Objective

To assess the effects of a 6-month angiotensin-converting enzyme (ACE) inhibitor intervention on myocardial ischaemia.

Method

We randomized 389 patients with stable coronary artery disease to double-blind treatment with ramipril 5 mg/day ( n = 133), ramipril 1.25 mg/day ( n = 133), or placebo ( n = 123). Forty-eight-hour ambulatory electrocardiography was performed at baseline, and after 1 and 6 months.

Results

Relevant baseline variables were similar in all groups. Changes over 6 months in duration of ≥ 1 mm ST-segment depression (STD), total ischaemic burden and maximum STD did not differ significantly between the treatment groups. There was no difference in the frequency of adverse events between the groups.

Conclusion

ACE inhibitor treatment has little impact on incidence and severity of myocardial ischaemia in patients with stable ischaemic heart disease.

Related collections

Most cited references 48

Record: found
Abstract: found
Article: not found

Angiotensin-converting enzyme inhibition with quinapril improves endothelial vasomotor dysfunction in patients with coronary artery disease. The TREND (Trial on Reversing ENdothelial Dysfunction) Study.

G.B. Mancini, Gregory C. Henry, Carlos Macaya … (1996)

Angiotensin-converting enzyme (ACE) inhibitors may exert some of their benefits in the therapy of hypertension, congestive heart failure, and acute myocardial infarction by their improvement of endothelial dysfunction. TREND (Trial on Reversing ENdothelial Dysfunction) investigated whether quinapril might improve endothelial dysfunction in normotensive patients with coronary artery disease and no heart failure, cardiomyopathy, or major lipid abnormalities so that confounding variables that affect endothelial dysfunction could be minimized. Using a double-blind, randomized, placebo-controlled design, we measured the effects of quinapril (40 mg daily) on coronary artery diameter responses to acetylcholine using quantitative coronary angiography. The primary response variable was the net change in the acetylcholine-provoked constriction of target segments between the baseline (prerandomization) and 6-month follow-up angiograms. The constrictive responses to acetylcholine were comparable in the placebo (n = 54) and quinapril (n = 51) groups at baseline. After 6 months, only the quinapril group showed significant net improvement in response to incremental concentrations of acetylcholine (4.5 +/- 3.0% [mean +/- SEM] versus -0.1 +/- 2.8% at 10(-6) mol/L and 12.1 +/- 3.0% versus -0.8 +/- 2.9% at 10(-4) mol/L, quinapril versus placebo, respectively; overall P = .002). TREND shows that ACE inhibition with quinapril improved endothelial dysfunction in patients who were normotensive and who did not have severe hyperlipidemia or evidence of heart failure. These benefits of ACE inhibition are likely due to attenuation of the contractile effects and superoxide-generating effects of angiotensin II and to enhancement of endothelial cell release of nitric oxide secondary to diminished breakdown of bradykinin.

0 comments Cited 70 times – based on 0 reviews      Review now

Record: found
Abstract: found
Article: not found

Effects of statins on vascular wall: vasomotor function, inflammation, and plaque stability.

Jessie B K Koh (2000)

Clinical trials of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors or statin therapy demonstrate an improvement in cardiovascular end points and coronary stenosis. However, an improvement in cardiovascular end points and coronary stenosis is incompletely explained by the baseline or treated LDL cholesterol level. The beneficial effects of statins on clinical events may involve nonlipid mechanisms that modify endothelial function, smooth muscle cells, and monocyte-macrophage: vasomotor function, inflammatory responses, and plaque stability. Augmented bioactivity of NO by statin therapy either indirectly by its effect on lipoprotein levels and protection of LDL from oxidation, or directly by effects on NO synthesis and release, might account for enhancement of endothelium-dependent vasodilation. Recent experimental and animal studies have demonstrated that statins dose-dependently decrease smooth muscle cells migration and proliferation, independently of their ability to reduce plasma cholesterol. Moreover, statins are able to reduce the in vitro cholesterol accumulation in macrophages and expression of matrix metalloproteinase, resulting in plaque stability. These effects of statins were completely prevented by the addition of mevalonate and partially by all-trans farnesol and all-trans geranylgeraniol, confirming the specific role of isoprenoid metabolites, probably through prenylated proteins, in regulating these cellular events. Statins have been shown to prevent the activation of monocytes into macrophages, inhibit the production of pro-inflammatory cytokines, C-reactive protein, and cellular adhesion molecules. Statins decrease the adhesion of monocyte to endothelial cells. Accordingly, statins exert their cardiovascular benefits through a direct antiatherogenic properties in the arterial wall, beyond their effects on plasma lipids.

0 comments Cited 51 times – based on 0 reviews      Review now

Record: found
Abstract: not found
Article: not found

Extracellular matrix remodeling in heart failure: a role for de novo angiotensin II generation.

T Weber (1997)

0 comments Cited 47 times – based on 0 reviews      Review now

All references

Author and article information

Journal

Journal ID (nlm-ta): Curr Control Trials Cardiovasc Med

Title: Current Controlled Trials in Cardiovascular Medicine

Publisher: BioMed Central

ISSN (Print): 1468-6708

ISSN (Electronic): 1468-6694

Publication date (Print): 2001

Publication date (Electronic): 4 April 2001

Volume: 2

Issue: 2

Pages: 99-105

Affiliations

[1 ]Department of Cardiology, Malmö University Hospital, Lund University, Malmö, Sweden

Article

Publisher ID: cvm-2-2-099

DOI: 10.1186/cvm-2-2-099

PMC ID: 56204

PubMed ID: 11806779

SO-VID: ed470081-343b-4e1f-a9a1-a841a53b34c5

History

Date received : 23 January 2001

Date accepted : 20 March 2001

No effects on myocardial ischaemia in patients with stable ischaemic heart disease after treatment with ramipril for 6 months

Read this article at