Isolated circulatory response to intravenous administration of the ACE inhibitor enalaprilat.

Boldt, Joachim; Knothe, Christoph; Schindler, Fernanda; Stertmann, W. A.; Hempelmann, G.

doi:10.1111/j.1365-2125.1994.tb04287.x

Cited by 11 publications

(2 citation statements)

References 21 publications

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“…This contrasts with data from several other studies that indicate that ACE inhibition decreases blood pressure 25 or increases vasoconstrictor requirement during and after CPB 26,27 but not with data from others. 28 The lack of apparent effect of ACE inhibition on MAP and vasoconstrictor requirements may relate to the short duration ACEI was stopped in the No-ACEI group.…”

Section: Pretorius Et Al Ace Inhibition Pai-1 and Cardiopulmonary Bcontrasting

confidence: 55%

Angiotensin-Converting Enzyme Inhibition Alters the Fibrinolytic Response to Cardiopulmonary Bypass

et al. 2003

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Background-Increased plasminogen activator inhibitor-1 (PAI-1) concentrations after coronary artery bypass grafting (CABG) are associated with increased risk of vein graft occlusion. Because angiotensin II stimulates PAI-1 expression, we tested the hypothesis that preoperative angiotensin-converting enzyme (ACE) inhibition decreases PAI-1 expression after CABG. Methods and Results-We measured the effects of cardiopulmonary bypass (CPB) on PAI-1 antigen and tissue-type plasminogen activator (tPA) antigen and activity in 31 patients taking an ACE inhibitor (ACEI) who were randomized to continue ACEI until the morning of surgery (ACEI group, nϭ19) or to discontinue it 48 hours before surgery (No-ACEI group, nϭ12). Arterial blood samples were taken at baseline before CPB, twice during CPB, after separation from CPB, and on postoperative day 1 (POD1). CPB caused an early decrease in PAI-1 antigen, followed by an increase in PAI-1 antigen on POD1 (PϽ0.001 for effect of time). ACE inhibition attenuated the increase in PAI-1 antigen such that both PAI-1 antigen on POD1 (Pϭ0.013) and the change in PAI-1 antigen from baseline to POD1 (Pϭ0.009) were higher in the No-ACEI group (from 17.0Ϯ5.0 to 48.7Ϯ8.8 ng/mL) versus the ACEI group (from 19.9Ϯ3.4 to 33.1Ϯ6.2 ng/mL). There was no significant difference between the 2 groups in intraoperative tPA activity (Pϭ0.259); however, the increase in tPA activity was significantly greater in the ACEI group than in the No-ACEI group (Pϭ0.030). Conclusions-Preoperative

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Section: Pretorius Et Al Ace Inhibition Pai-1 and Cardiopulmonary Bcontrasting

confidence: 55%

Angiotensin-Converting Enzyme Inhibition Alters the Fibrinolytic Response to Cardiopulmonary Bypass

et al. 2003

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“…It is reasonable to surmise that use of angiotensin coverting enzyme inhibitor (ACEI) that lowers that serum level of angiotensin II and the use of angiotensin II receptor type 1 blocker (ARB) will have possible antithrombotic effect. Second, RAS inhibitors have been shown to increase blood flow to both capillary and venous system [21] . Since venous stasis is an important risk factor for VTE, protective effect of RAS inhibition can be explained by the improvement of blood rheology.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Renin Angiotensin Axis May Be Associated with Reduced Risk of Developing Venous Thromboembolism in Patients with Atherosclerotic Disease

et al. 2014

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BackgroundArterial and venous thrombosis may share common pathophysiology involving the activation of platelets and inflammatory mediators. A growing body of evidence suggests prothrombotic effect of renin angiotensin system (RAS) including vascular inflammation and platelet activation. We hypothesized that the use of angiotensin converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs) plays a role in protecting against venous thromboembolism (VTE) in patients atherosclerosis.MethodsWe conducted a retrospective study, reviewing 1,100 consecutive patients admitted to a teaching hospital with a diagnosis of either myocardial infarction or ischemic stroke from 2005 to 2010. Patients who had been treated with anticoagulation therapy before or after the first visit were excluded. The occurrence of VTE during the follow up period, risk factors for VTE on admission, and the use of ACEIs or ARBs during the follow up period were recorded.ResultsThe mean age of the entire study population was 68.1 years. 52.0% of the patients were female and 76.5% were African American. 67.3% were on RAS inhibitorsThe overall incidence of VTE was 9.7% (n = 107). Among the RAS inhibitor users, the incidence of VTE events was 9.0% (54/603) for the ACEI only users, 7.1% (8/113) for the ARB only users, and 0% (0/24) for the patients taking combination of ACEI and ARB. Among patients on RAS inhibitors, 8.4% (62/740) developed a VTE, compared with 12.5% (45/360) in the nonuser group [HR (hazard ratio), 0.58; 95% CI (confidence interval), 0.39–0.84; P<0.01]. Even after controlling for factors related to VTE (smoking, history of cancer, and immobilization, hormone use) and diabetes, the use of RAS inhibitors was still associated with a significantly lower risk of developing VTE (AHR, 0.59; 95% CI, 0.40–0.88; P = 0.01).ConclusionsThe use of RAS inhibitors appears to be associated with a reduction in the risk of VTE.

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Do ACE Inhibitors have a Place in the Critically III?

Boldt¹,

Müller²,

Hempelmann³

1996

Yearbook of Intensive Care and Emergency Medicine

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Isolated circulatory response to intravenous administration of the ACE inhibitor enalaprilat.

Cited by 11 publications

References 21 publications

Angiotensin-Converting Enzyme Inhibition Alters the Fibrinolytic Response to Cardiopulmonary Bypass

Angiotensin-Converting Enzyme Inhibition Alters the Fibrinolytic Response to Cardiopulmonary Bypass

Inhibition of Renin Angiotensin Axis May Be Associated with Reduced Risk of Developing Venous Thromboembolism in Patients with Atherosclerotic Disease

Do ACE Inhibitors have a Place in the Critically III?

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