Do All Patients With Coronary Artery Disease Benefit from Angiotensin Converting Enzyme Inhibitors?

Shah, Apurva D.; Arora, Rohit

doi:10.1177/107424840501000408

Cited by 4 publications

(2 citation statements)

References 6 publications

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“…The PEACE study population had a lower cardiovascular baseline risk (fewer patients with diabetes and high cardiovascular risk), lower arterial blood pressure, and LDL-cholesterol, and patients were treated more frequently with statins and antiplatelet drugs. Thus, as various editorials also pointed out, 125,126 what the PEACE study showed was that ACE inhibitors could be beneficial for patients with more risk factors (such as high serum lipids, diabetes mellitus) but may offer modest (to no) extra benefit for patients with low-risk factors or those that are already treated with statins and antiplatelet drugs. From the clinical studies, it can be concluded that aggressive risk factor modification in patients with atherosclerosis is still the primary goal and not all patients may need treatment with ACE inhibitors.…”

Section: Ace Inhibition In Patients With Coronary Artery Disease: CLImentioning

confidence: 99%

Angiotensin-Converting Enzyme and Vascular Remodeling

Heeneman

Sluimer

Daemen

2007

Circulation Research

187

132

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Abstract-Vascular remodeling is the result of a close interplay of changes in vascular tone and structure. In this review, the role of angiotension-converting enzyme (ACE) and the impact of ACE inhibition on vascular remodeling processes during vascular injury and restenosis, hypertension, atherosclerosis, and aneurysm formation are discussed. The role of ACE and angiotensin II (Ang II) in neointimal thickening has been firmly established by animal studies and is mediated by Ang II type 1 (AT 1 ) receptor signaling events via monocyte chemoattractant protein-1 and NAD(P)H oxidase. ACE and Ang II are involved in the remodeling of large and resistance arteries during hypertension; here, cell proliferation and matrix remodeling are also regulated by signaling events downstream of the AT 1 receptor. In atherosclerosis, Ang II is involved in the inflammatory and tissue response, mediated by various signaling pathways downstream of the AT 1 receptor. Although ACE inhibition has been shown to inhibit atherosclerotic processes in experimental animal models, results of large clinical trials with ACE inhibitors were not conclusive. Remodeling of vessel dimensions and structure during aneurysm formation is counteracted by ACE inhibition. Here, a direct effect of ACE inhibitors on matrix metalloproteinase activity has to be considered as part of the working mechanism. The role of ACE2 in vascular remodeling has yet to be established; however, ACE2 has been shown to be associated with vascular changes in hypertension and atherosclerosis. (Circ Res. 2007;101:441-454.)

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Section: Ace Inhibition In Patients With Coronary Artery Disease: CLImentioning

confidence: 99%

Angiotensin-Converting Enzyme and Vascular Remodeling

Heeneman

Sluimer

Daemen

2007

Circulation Research

187

132

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“…In addition, the limited/lack of success of these orally administered therapeutic agents may be related to the differential tissue distribution and drug-specific pharmacodynamics that could limit their therapeutic concentrations in lung tissue. [17][18][19] These observations, taken together with the well-established hypertrophic actions and emerging role of proinflammatory signaling by Ang II and Ang II type 1 (AT 1 ) receptors, 2,20,21 suggest that the involvement of the RAS in PH should be re-examined. This view takes on an added relevance since the discovery of ACE2 as a new member of the RAS.…”

mentioning

confidence: 99%

Prevention of Pulmonary Hypertension by Angiotensin-Converting Enzyme 2 Gene Transfer

Yamazato

Ferreira²,

Hong³

et al. 2009

Hypertension

138

109

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Abstract-In spite of recent advancements in the treatment of pulmonary hypertension, successful control has yet to be accomplished. The abundant presence of angiotensin-converting enzyme 2 (ACE2) in the lungs and its impressive effect in the prevention of acute lung injury led us to test the hypothesis that pulmonary overexpression of this enzyme could produce beneficial outcomes against pulmonary hypertension. Monocrotaline (MCT) treatment of mice for 8 weeks resulted in significant increases in right ventricular systolic pressure, right ventricle:left ventricle plus septal weight ratio, and muscularization of pulmonary vessels. Administration of a lentiviral vector containing ACE2, 7 days before MCT treatment prevented the increases in right ventricular systolic pressure (control: 25Ϯ1 mm Hg; MCT: 44Ϯ5 mm Hg; MCTϩACE2: 26Ϯ1 mm Hg; nϭ6; PϽ0.05) and right ventricle:left ventricle plus septal weight ratio (control: 0.25Ϯ0.01; MCT: 0.31Ϯ0.01; MCTϩACE2: 0.26Ϯ0.01; nϭ8; PϽ0.05). A significant attenuation in muscularization of pulmonary vessels induced by MCT was also observed in animals overexpressing ACE2. These beneficial effects were associated with an increase in the angiotensin II type 2 receptor:angiotensin II type 1 receptor mRNA ratio. Also, pulmonary hypertension-induced increases in proinflammatory cytokines were significantly attenuated by lentiviral vector-containing ACE2 treatment. Furthermore, ACE2 gene transfer in mice after 6 weeks of MCT treatment resulted in a significant reversal of right ventricular systolic pressure. These observations demonstrate that ACE2 overexpression prevents and reverses right ventricular systolic pressure and associated pathophysiology in MCT-induced pulmonary hypertension by a mechanism involving a shift from the vasoconstrictive, proliferative, and fibrotic axes to the vasoprotective axis of the renin-angiotensin system and inhibition of proinflammatory cytokines. (Hypertension. 2009;54:365-371.)

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