Inhibition of the Renin-Angiotensin System Reduces the Rise in Serum Aldosterone in Acute Coronary Syndrome Patients with Preserved Left Ventricular Function: Observations from the AVANT GARDE-TIMI 43 Trial

Udell, Jacob A.; Morrow, David A.; Braunwald, Eugene; Swedberg, Karl; Bode, Christoph; Rifai, Nader; Brunel, Patrick; Prescott, Margaret F.; Ren, Fang; Hoffman, Elaine; Scirica, Benjamin M.

doi:10.1373/clinchem.2012.199729

Cited by 9 publications

(13 citation statements)

References 35 publications

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“…Second, in this analysis aldosterone was measured in the subacute period after ACS, whereas in prior studies aldosterone had been measured at the time of presentation with ACS 13, 14, 24, 25. In the immediate period after ACS, left ventricular function, hemodynamics, manifestations of heart failure, and aldosterone levels themselves are in flux 12, 26. Moreover, many patients with ACS begin treatment with an angiotensin‐converting enzyme inhibitor or an angiotensin receptor blocker during hospitalization for ACS, and these drugs suppress aldosterone concentration 12.…”

Section: Discussionmentioning

confidence: 99%

“…18 In 3 important ways, the present analysis differs from and adds to prior studies that examined the relationship of aldosterone levels to outcomes after ACS. [12][13][14][24][25][26] First, the current analysis cohort is much larger and reflects a globally diverse population with broad application of evidence-based treatments. Second, in this analysis aldosterone was measured in the subacute period after ACS, whereas in prior studies aldosterone had been measured at the time of presentation with ACS.…”

Section: Discussionmentioning

confidence: 99%

“…[9][10][11] Plasma aldosterone concentrations are elevated in patients with acute myocardial infarction. 12,13 Prior small studies have associated elevated aldosterone at the time of acute myocardial infarction with increased short-and longterm risk of adverse cardiovascular outcomes. [13][14][15][16] However, these studies have had 2 principal limitations.…”

mentioning

confidence: 99%

“…[13][14][15][16] However, these studies have had 2 principal limitations. First, aldosterone levels are in flux during the early period after myocardial infarction, 12 affected by changing hemodynamic, neurohumoral, and pharmacologic conditions. Therefore, measurements of aldosterone immediately following myocardial infarction may not reflect the steady-state levels attained when patients are clinically stable and evidencebased treatments have been implemented.…”

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confidence: 99%

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Aldosterone Does Not Predict Cardiovascular Events Following Acute Coronary Syndrome in Patients Initially Without Heart Failure

Pitts

Gunzburger

Ballantyne

et al. 2017

JAHA

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BackgroundAldosterone may have adverse effects in the myocardium and vasculature. Treatment with an aldosterone antagonist reduces cardiovascular risk in patients with acute myocardial infarction complicated by heart failure (HF) and left ventricular systolic dysfunction. However, most patients with acute coronary syndrome do not have advanced HF. Among such patients, it is unknown whether aldosterone predicts cardiovascular risk.Methods and ResultsTo address this question, we examined data from the dal‐OUTCOMES trial that compared the cholesteryl ester transfer protein inhibitor dalcetrapib with placebo, beginning 4 to 12 weeks after an index acute coronary syndrome. Patients with New York Heart Association class II (with LVEF <40%), III, or IV HF were excluded. Aldosterone was measured at randomization in 4073 patients. The primary outcome was a composite of coronary heart disease death, nonfatal myocardial infarction, stroke, hospitalization for unstable angina, or resuscitated cardiac arrest. Hospitalization for HF was a secondary endpoint. Over a median follow‐up of 37 months, the primary outcome occurred in 366 patients (9.0%), and hospitalization for HF occurred in 72 patients (1.8%). There was no association between aldosterone and either the time to first occurrence of a primary outcome (hazard ratio for doubling of aldosterone 0.92, 95% confidence interval 0.78‐1.09, P=0.34) or hospitalization for HF (hazard ratio 1.38, 95% CI 0.96‐1.99, P=0.08) in Cox regression models adjusted for covariates.ConclusionsIn patients with recent acute coronary syndrome but without advanced HF, aldosterone does not predict major cardiovascular events.Clinical Trial Registration URL: http://www.clinicaltrials.gov. Unique identifier: NCT00658515.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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confidence: 99%

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Aldosterone Does Not Predict Cardiovascular Events Following Acute Coronary Syndrome in Patients Initially Without Heart Failure

Pitts

Gunzburger

Ballantyne

et al. 2017

JAHA

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“…CAP treatment of post-MI/R patients has been reported to decrease aldosterone levels. RAS inhibition by using ACE, ARB, or aldosterone inhibitors in acute coronary syndrome patients with large infarcts and decreased left ventricular function was indicated to increase survival rate and improve myocardial remodeling [37]. …”

Section: Discussionmentioning

confidence: 99%

Inhibition of Angiotensin-II Production Increases Susceptibility to Acute Ischemia/Reperfusion Arrhythmia

et al. 2016

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BackgroundMyocardial ischemia and reperfusion lead to impairment of electrolyte balance and, eventually, lethal arrhythmias. The aim of this study was to investigate the effects of pharmacological inhibition of angiotensin-II (Ang-II) production on heart tissue with ischemia-reperfusion damage, arrhythmia, and oxidative stress.Material/MethodsRats were divided into 4 groups: only ischemia/reperfusion (MI/R), captopril (CAP), aliskiren (AL), and CAP+AL. The drugs were given by gavage 30 min before anesthesia. Blood pressure and electrocardiography (ECG) were recorded during MI/R procedures. The heart tissue and plasma was kept so as to evaluate the total oxidant (TOS), antioxidant status (TAS), and creatine kinase-MB (CK-MB).ResultsCreatine kinase-MB was not different among the groups. Although TAS was not affected by inhibition of Ang-II production, TOS was significantly lower in the CAP and/or AL groups than in the MI/R group. Furthermore, oxidative stress index was significantly attenuated in the CAP and/or AL groups. Captopril significantly increased the duration of VT during ischemia; however, it did not have any effect on the incidence of arrhythmias. During reperfusion periods, aliskiren and its combinations with captopril significantly reduced the incidence of other types of arrhythmias. Captopril alone had no effect on the incidence of arrhythmias, but significantly increased arrhythmias score and durations of arrhythmias during reperfusion. MAP and heart rate did not show changes in any groups during ischemic and reperfusion periods.ConclusionsAngiotensin-II production appears to be associated with elevated levels of reactive oxygen species, but Ang-II inhibitions increases arrhythmia, mainly by initiating ventricular ectopic beats.

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Early eplerenone treatment in patients with acute ST-elevation myocardial infarction without heart failure: The Randomized Double-Blind Reminder Study

Montalescot¹,

Pitt²,

De³

et al. 2014

European Heart Journal

137

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Inhibition of the Renin-Angiotensin System Reduces the Rise in Serum Aldosterone in Acute Coronary Syndrome Patients with Preserved Left Ventricular Function: Observations from the AVANT GARDE-TIMI 43 Trial

Cited by 9 publications

References 35 publications

Aldosterone Does Not Predict Cardiovascular Events Following Acute Coronary Syndrome in Patients Initially Without Heart Failure

Aldosterone Does Not Predict Cardiovascular Events Following Acute Coronary Syndrome in Patients Initially Without Heart Failure

Inhibition of Angiotensin-II Production Increases Susceptibility to Acute Ischemia/Reperfusion Arrhythmia

Early eplerenone treatment in patients with acute ST-elevation myocardial infarction without heart failure: The Randomized Double-Blind Reminder Study

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