Impact of High-Dose N-Acetylcysteine Versus Placebo on Contrast-Induced Nephropathy and Myocardial Reperfusion Injury in Unselected Patients With ST-Segment Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention

Thiele, Holger; Hildebrand, Lysann; Schirdewahn, Carmen; Eitel, Ingo; Adams, Volker; Fuernau, Georg; Erbs, Sandra; Linke, Axel; Diederich, Klaus-Werner; Nowak, Marek; Desch, Steffen; Gutberlet, Matthias; Schuler, Gerhard

doi:10.1016/j.jacc.2009.08.091

Cited by 196 publications

(129 citation statements)

References 33 publications

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“…The volume of low-osmolar contrast agent administered (173 ± 42 mL) was lower than in older relevant trials or similar to recent trials [3,9,10]. MACD was exceeded in 3% of patients only.…”

Section: Discussionsupporting

confidence: 58%

“…STEMI patients treated by primary PCI represent a population at higher risk for AKI than those undergoing elective coronary angiography and/or PCI. Renal hypoperfusion caused by HF or prolonged hypotension, larger volume of contrast media, bleeding, and atheroembolic events during catheterisation are the most cited conditions that contribute to renal injury [3,9,10].…”

Section: Discussionmentioning

confidence: 99%

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Heart failure is the strongest predictor of acute kidney injury in patients undergoing primary percutaneous coronary intervention for ST-elevation myocardial infarction

Matejka

Varvařovský²,

Rozsíval³

et al. 2016

Kardiol Pol

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A b s t r a c tBackground: ST elevation myocardial infarction (STEMI) patients treated by primary percutaneous coronary intervention (PCI) are at higher risk of acute kidney injury (AKI) than patients undergoing PCI in stable clinical conditions. This fact suggests that mechanisms other than contrast nephrotoxicity are involved. Aim:To evaluate the incidence, risk factors, and consequences of AKI in patients undergoing primary PCI for STEMI in current daily practice. Methods:Analysis of all consecutive patients who underwent primary PCI over a one-year period. AKI was defined as an increase in serum creatinine ≥ 50% or 26.5 μmol/L (AKIN criteria) from the baseline within 48 h. Results:A total of 202 patients were included. AKI occurred in 25 (12.4%) subjects. Baseline characteristics and in-hospital complications of the patients with and without AKI did not differ significantly except for age (69 ± 13 vs. 62 ± 12; p = 0.003), female gender (48.0% vs. 26.6%; p = 0.035), hypertension (88.0% vs. 62.7%; p = 0.013), left ventricular ejection fraction (40% ± 12% vs. 49% ± 14%; p = 0.002), cardiogenic shock (44.0% vs. 5.1%; p < 0.0001), use of intravenous diuretics (76.0% vs. 26.0%; p < 0.0001), ventricular arrhythmias (24.0% vs. 3.4%; p = 0.001), and in-hospital mortality (24.0% vs. 3.4%; p = 0.001). In multivariate analysis heart failure remained the only independent correlate of AKI.Conclusions: AKI was an frequent and serious complication of STEMI in patients treated by primary PCI. Heart failure was the strongest predictor of AKI. Other risk factors including contrast medium volume, baseline renal function, diabetes, and age failed to predict AKI.

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Section: Discussionsupporting

confidence: 58%

Section: Discussionmentioning

confidence: 99%

Heart failure is the strongest predictor of acute kidney injury in patients undergoing primary percutaneous coronary intervention for ST-elevation myocardial infarction

Matejka

Varvařovský²,

Rozsíval³

et al. 2016

Kardiol Pol

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“…Supporting this notion, NAC as an exogenous thiol-providing ROS scavenger did not alter the functional state of postischemic Txnrd2ϩ/-control mice in our model. Consistently, in a recent clinical study, 49 NAC (2 x 1200 mg/d) did not increase the myocardial salvage of patients with ST elevation myocardial infarction, bona fide Txnrd2 carriers. Only in the instance of Txnrd2 deficiency did thiol supplementation by NAC attenuate I/R injury, enabling a functional improvement to the level of Txnrd2ϩ/-control mice ( Figure 6A and 6B).…”

Section: Discussionsupporting

confidence: 73%

Mitochondrial Thioredoxin Reductase Is Essential for Early Postischemic Myocardial Protection

et al. 2011

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Background— Excessive formation of reactive oxygen species contributes to tissue injury and functional deterioration after myocardial ischemia/reperfusion. Especially, mitochondrial reactive oxygen species are capable of opening the mitochondrial permeability transition pore, a harmful event in cardiac ischemia/reperfusion. Thioredoxins are key players in the cardiac defense against oxidative stress. Mutations in the mitochondrial thioredoxin reductase (thioredoxin reductase-2, Txnrd2) gene have been recently identified to cause dilated cardiomyopathy in patients. Here, we investigated whether mitochondrial thioredoxin reductase is protective against myocardial ischemia/reperfusion injury. Methods and Results— In mice, α-MHC-restricted Cre-mediated Txnrd2 deficiency, induced by tamoxifen ( Txnrd2-/-ic ), aggravated systolic dysfunction and cardiomyocyte cell death after ischemia (90 minutes) and reperfusion (24 hours). Txnrd2-/-ic was accompanied by a loss of mitochondrial integrity and function, which was resolved on pretreatment with the reactive oxygen species scavenger N-acetylcysteine and the mitochondrial permeability transition pore blocker cyclosporin A. Likewise, Txnrd2 deletion in embryonic endothelial precursor cells and embryonic stem cell-derived cardiomyocytes, as well as introduction of Txnrd2-shRNA into adult HL-1 cardiomyocytes, increased cell death on hypoxia and reoxygenation, unless N-acetylcysteine was coadministered. Conclusions— We report that Txnrd2 exerts a crucial function during postischemic reperfusion via thiol regeneration. The efficacy of cyclosporin A in cardiac Txnrd2 deficiency may indicate a role for Txnrd2 in reducing mitochondrial reactive oxygen species, thereby preventing opening of the mitochondrial permeability transition pore.

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“…A large number of drugs have been used to protect renal function after PCI, such as aminophylline (Shammas et al 2001;Rohani 2010), theophylline (Wang et al 2001), atrial natriuretic peptide (Chen 2009;Morikawa et al 2009), B-type natriuretic peptide (Zhang et al 2010), mannitol (Kelly et al 2008), prostaglandins (McCullough andTumlin 2009), N-acetylcysteine (Thiele et al 2010), sodium bicarbonate (Masuda 2008) and statins (Xinwei et al 2009); however, few of them (Kowalczyk et al 2007;Zoungas et al 2009) have shown exact protective effects.…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Anisodamine on Renal Function in Patients with ST-Segment Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention

Wang

et al. 2011

Tohoku J. Exp. Med.

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ST-segment elevation myocardial infarction (STEMI) is the most severe type of heart attack, and primary percutaneous coronary intervention (PCI) is the first line treatment for STEMI. However, these patients are at higher risk of contrast-induced nephropathy (CIN), which increases the length of hospital stay and mortality rate. Anisodamine, an alkaloid extracted from a Chinese herb, has been shown to exert protective effects on the renal function. The aim of this study was to investigate the protective effect of anisodamine on CIN in STEMI patients undergoing primary PCI. A total of 126 consecutive STEMI patients were randomly assigned to receive anisodamine (n = 60) or placebo (control, n = 66) from admission to 24 hours after PCI. The serum creatinine (SCr) concentrations, estimated glomerular filtration rate (eGFR) and incidence of CIN were measured on admission, and 24, 48 and 72 hours after PCI between the two groups. We found that the renal function of all patients after PCI underwent a course from injury to recovery. The incidence of CIN was 5.0%, 8.3%, and 6.7% at 24, 48 and 72 hours, respectively, after primary PCI in anisodamine group, while in control group it was 16.7%, 22.7%, and 19.7%, respectively. The incidence of CIN in anisodamine group was lower than that in control group during 72 hours after PCI (all P < 0.05). In conclusion, intravenous infusion of anisodamine before and after primary PCI may reduce the occurrence of CIN in STEMI patients undergoing primary PCI, without serious side effects.

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Impact of High-Dose N-Acetylcysteine Versus Placebo on Contrast-Induced Nephropathy and Myocardial Reperfusion Injury in Unselected Patients With ST-Segment Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention

Cited by 196 publications

References 33 publications

Heart failure is the strongest predictor of acute kidney injury in patients undergoing primary percutaneous coronary intervention for ST-elevation myocardial infarction

Heart failure is the strongest predictor of acute kidney injury in patients undergoing primary percutaneous coronary intervention for ST-elevation myocardial infarction

Mitochondrial Thioredoxin Reductase Is Essential for Early Postischemic Myocardial Protection

Protective Effects of Anisodamine on Renal Function in Patients with ST-Segment Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention

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