Fosinopril decreases levels of soluble vascular cell adhesion molecule-1 in borderline hypertensive type II diabetic patients with microalbuminuria

Gasić, S; Wagner, Oswald; Fasching, Peter; Ludwig, Christine; Veitl, Mario; Kapiotis, Stylianos; Jilma, Bernd

doi:10.1016/s0895-7061(98)00229-5

Cited by 48 publications

(29 citation statements)

References 48 publications

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“…The plasma levels of all of the target parameters did not differ significantly between hypertensive patients after ACE inhibitor treatment and the control group of healthy individuals. Failure to demonstrate significant decrease of E-selectin and ICAM-1 levels with ACE inhibitor therapy is in agreement with a previous study performed by Gasic et al 23 in borderline hypertensive patients with diabetes. On the contrary, Ferri et al 7 observed a significant 30-80% decrease of E-selectin and ICAM-1 levels in hypertensive patients treated with ACE inhibitors.…”

Section: Discussionsupporting

confidence: 92%

Circulating intercellular cell adhesion molecule-1, endothelin-1 and von Willebrand factor-markers of endothelial dysfunction in uncomplicated essential hypertension: the effect of treatment with ACE inhibitors

et al. 2002

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The aim of the study was to examine whether the circulating cell adhesion molecules, von Willebrand factor (vWf) and endothelin-1, are elevated in patients with essential hypertension with no other risk factors for atherosclerosis and thus may serve as a markers of endothelial dysfunction in uncomplicated hypertension. Furthermore, the effect of treatment with the ACE inhibitor, quinapril, on levels of endothelial dysfunction markers were studied. The levels of adhesion molecules (intercellular cell adhesion molecule-1 [ICAM-1], E-selectin, P-selectin), von Wilebrand factor (vWf) and endothelin-1 were measured in patients with hypertension without any other risk factors of atherosclerosis before and after treatment with quinapril (n = 22) and in normotensive controls (n = 22). Compared with normotensive subjects, the hypertensive patients had significantly higher levels of ICAM-1 (238 vs 208 ng/ml, P = 0.02), vWf (119 vs 105 IU/dl, P Ͻ 0.05) and endothelin-1 (5.76 vs 5.14 fmol/ml, P Ͻ 0.05). Three-month treatment of hyper-

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Section: Discussionsupporting

confidence: 92%

Circulating intercellular cell adhesion molecule-1, endothelin-1 and von Willebrand factor-markers of endothelial dysfunction in uncomplicated essential hypertension: the effect of treatment with ACE inhibitors

et al. 2002

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“…Gasic S et al (1999) [224] In microalbuminuric patients with NIDDM serum levels of cVCAM-1 decreased by -19%. Plasma levels of cE-selectin, cICAM-1, PAI-1 and TPA were unaffected.…”

Section: Fosinoprilmentioning

confidence: 99%

“…Analysing data provided by Gasic et al, [224] the ACEi fosinopril (10 mg/day) administered over 12 weeks to 11 microalbuminuric patients with non-insulin-dependent diabetes mellitus (NIDDM) provided the following actions: serum levels of cVCAM-1 decreased by -19% (CI: -25% to -13%) after treatment with fosinopril (P = .003) and were no longer different from those of the control group. In contrast, plasma levels of E-selectin, ICAM-1, plasminogen activator inhibitor (PAI-1) and tissue plasminogen activator (TPA) were unaffected.…”

Section: Part IV -Anti-inflammatory Effects Of Ace-imentioning

confidence: 99%

Effects of ACE-Inhibitors and Angiotensin Receptor Blockers on Inflammation

Raimondo¹,

Tuttolomondo²,

Buttà³

et al. 2012

CPD

112

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Abstract:The role of inflammation in cardiovascular disease and in hypertensive disease above all, is complex. Several studies confirm that activation of renin-angiotensin-aldosteron system (RAAS), through increase in the production of angiotensin II (Ang II), is closely related to local vascular inflammation. Over the BP lowering effects of anti-hypertensive treatments, several ancillary effects for every class may be found, distinguishing the various drugs from one another. Given the pro-inflammatory effects of Ang II and aldosterone, agents that interfere with the components of RAAS, such as ACE inhibitors, Angiotensin Recpetor Blockers (ARBs), and mineralocorticoid receptor antagonists (spironolactone or the more selective eplerenone), represent logical therapeutic tools to reduce vascular inflammation and cardiovascular risk, as suggested in large clinical trials in patients with hypertension and diabetes. Regarding ACE inhibitors, actually there is no convincing evidence indicating that ACEi's reduce plasma levels of major inflammatory markers in hypertension models. Lack of evidence concerns especially these inflammation markers, such as fibrinogen of CRP, which are less closely related to atherosclerotic disease and vascular damage and conversely are affected by several more aspecific factors. Results obtained by trials accomplished using ARBs seem to be more univocal to confirm, although to great extent, these is an anti-inflmmatory effect of drugs bocking AT1 receptor. In order to strictly study the effects of blockage of RAAS on inflammation, future studies may explore different strategies by, for example, simultaneously acting on the ACE and the AT1 angiotensin receptors.

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“…ACEIs possess pharmacological properties, which could delay the development of atherosclerosis and increase plaque stability. 5,6,49,50 In addition, ACEIs may shift the fibrinolytic balance from coagulation to lysis by reducing the angiotensin II-dependent production and secretion of plasminogen activator inhibitor-1. 5,6 Results of our overview support the hypothesis that for the same degree of BP lowering, ACEIs might be superior to CCBs in the protection against incident or recurrent CHD.…”

Section: Ancillary Properties Of Aceis and Ccbsmentioning

confidence: 99%

Angiotensin-Converting Enzyme Inhibitors and Calcium Channel Blockers for Coronary Heart Disease and Stroke Prevention

et al. 2005

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Abstract-We investigated whether protection from coronary heart disease (CHD) and stroke conferred by angiotensinconverting enzyme inhibitors (ACEIs) and calcium channel blockers (CCBs) in hypertensive or high-risk patients may be explained by the specific drug regimen. We extracted summary statistics regarding CHD and stroke from 28 outcome trials that compared either ACEIs or CCBs with diuretics, ␤-blockers, or placebo for a total of 179 122 patients, 9509 incident cases of CHD, and 5971 cases of stroke. CHD included myocardial infarction and coronary death. In placebo-controlled trials, ACEIs decreased the risk of CHD (PϽ0.001), and CCBs reduced stroke incidence (PϽ0.001).There were no significant differences in CHD risk between regimens based on diuretics/␤-blockers and regimens based on ACEIs (Pϭ0.46) or CCBs (Pϭ0.52). The risk of stroke was reduced by CCBs (Pϭ0.041) but not by ACEIs (Pϭ0.15) compared with diuretics/␤-blockers. Because heterogeneity between trials was significant, we investigated potential sources of heterogeneity by metaregression. Examined covariates were the reduction in systolic blood pressure (BP), drug treatment (ACEIs versus CCBs), their interaction term, sex, age at randomization, year of publication, and duration of treatment. Prevention of CHD was explained by systolic BP reduction (PϽ0.001) and use of ACEIs (Pϭ0.028), whereas prevention of stroke was explained by systolic BP reduction (Pϭ0.001) and use of CCBs (Pϭ0.042). These findings confirm that BP lowering is fundamental for prevention of CHD and stroke. However, over and beyond BP reduction, ACEIs appear superior to CCBs for prevention of CHD, whereas CCBs appear superior to ACEIs for prevention of stroke.

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Fosinopril decreases levels of soluble vascular cell adhesion molecule-1 in borderline hypertensive type II diabetic patients with microalbuminuria

Cited by 48 publications

References 48 publications

Circulating intercellular cell adhesion molecule-1, endothelin-1 and von Willebrand factor-markers of endothelial dysfunction in uncomplicated essential hypertension: the effect of treatment with ACE inhibitors

Circulating intercellular cell adhesion molecule-1, endothelin-1 and von Willebrand factor-markers of endothelial dysfunction in uncomplicated essential hypertension: the effect of treatment with ACE inhibitors

Effects of ACE-Inhibitors and Angiotensin Receptor Blockers on Inflammation

Angiotensin-Converting Enzyme Inhibitors and Calcium Channel Blockers for Coronary Heart Disease and Stroke Prevention

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