Original Article
Effect of Cyclosporine on Reperfusion Injury in Acute Myocardial Infarction
N Engl J Med 2008; 359:473-481July 31, 2008
- Abstract
Background
Experimental evidence suggests that cyclosporine, which inhibits the opening of mitochondrial permeability-transition pores, attenuates lethal myocardial injury that occurs at the time of reperfusion. In this pilot trial, we sought to determine whether the administration of cyclosporine at the time of percutaneous coronary intervention (PCI) would limit the size of the infarct during acute myocardial infarction.
Methods
We randomly assigned 58 patients who presented with acute ST-elevation myocardial infarction to receive either an intravenous bolus of 2.5 mg of cyclosporine per kilogram of body weight (cyclosporine group) or normal saline (control group) immediately before undergoing PCI. Infarct size was assessed in all patients by measuring the release of creatine kinase and troponin I and in a subgroup of 27 patients by performing magnetic resonance imaging (MRI) on day 5 after infarction.
Results
The cyclosporine and control groups were similar with respect to ischemia time, the size of the area at risk, and the ejection fraction before PCI. The release of creatine kinase was significantly reduced in the cyclosporine group as compared with the control group (P=0.04). The release of troponin I was not significantly reduced (P=0.15). On day 5, the absolute mass of the area of hyperenhancement (i.e., infarcted tissue) on MRI was significantly reduced in the cyclosporine group as compared with the control group, with a median of 37 g (interquartile range, 21 to 51) versus 46 g (interquartile range, 20 to 65; P=0.04). No adverse effects of cyclosporine administration were detected.
Conclusions
In our small, pilot trial, administration of cyclosporine at the time of reperfusion was associated with a smaller infarct by some measures than that seen with placebo. These data are preliminary and require confirmation in a larger clinical trial.
Media in This Article
Figure 1
Assessment of Infarct Size by Biomarker Measurement.Figure 2
Infarct Size as a Function of the Area at Risk.Article Activity
- Article
Myocardial infarction is a disabling disease that is common in the United States, with more than 1.5 million new cases diagnosed each year.1,2 Infarct size is a major determinant of mortality in myocardial infarction.3,4 Limitation of infarct size has therefore been an important objective of strategies to improve outcomes. Currently, the most effective way to limit infarct size is to reperfuse the jeopardized myocardium as soon as possible with the use of coronary angioplasty or thrombolysis and to prevent reocclusion of the coronary artery with the use of antiplatelet therapy.
Although reperfusion is undoubtedly beneficial, it has detrimental effects, including myocardial stunning, ventricular arrhythmias, and microvascular dysfunction.5-7 Accumulating evidence suggests that reperfusion may also cause irreversible myocardial injury, possibly through a form of mitochondrial dysfunction that has been designated permeability transition.8-12 The opening of a nonspecific high-conductance channel (called the mitochondrial permeability-transition pore) in the inner mitochondrial membrane results in the collapse of the membrane potential, the uncoupling of the respiratory chain, the efflux of cytochrome c and other proapoptotic factors, and the hydrolysis rather than synthesis of ATP; these metabolic alterations may lead to cardiomyocyte death.13,14 Calcium overload and excessive production of reactive oxygen species in the early minutes of reflow trigger the opening of the mitochondrial permeability-transition pore.10,12,14 Griffiths and Halestrap found that in the isolated rat heart, the permeability-transition pore remains closed during ischemia but opens at the time of reperfusion.15
In addition to its well-known immunosuppressive properties, cyclosporine is a potent inhibitor of mitochondrial permeability transition, and several reports indicate that it can limit ischemia−reperfusion injury under experimental conditions.8,15-21 The objective of the present study was to determine whether the administration of cyclosporine at the onset of reperfusion reduces the infarct size in patients with ongoing acute myocardial infarction.
Methods
Trial
This study was a prospective, multicenter, randomized, single-blind, controlled trial. The trial was designed, the data were collected and analyzed, and the manuscript was written solely by the authors. Cyclosporine for the trial was purchased with institutional grant support; the manufacturer had no role in the study. The trial was performed in accordance with the Declaration of Helsinki (revised version, 1996), the European Guidelines for Good Clinical Practice (version 11, July 1990), and French laws. In accordance with French law, the study protocol was approved by the ethics committee of the institution of the principal investigator (Dr. Ovize) acting on behalf of all the institutions involved in this trial. All subjects gave written informed consent before being included in the study.
Study Population
Men and women, 18 years of age or older, who presented within 12 hours after the onset of chest pain, who had ST-segment elevation of more than 0.1 mV in two contiguous leads, and for whom the clinical decision was made to treat with percutaneous coronary intervention (PCI) were eligible for enrollment. Patients were eligible for the study whether they were undergoing primary PCI or rescue PCI. Occlusion of the culprit coronary artery (Thrombolysis in Myocardial Infarction [TIMI] flow grade 0) at the time of admission was also a criterion for inclusion.22
Patients with cardiac arrest, ventricular fibrillation, cardiogenic shock, stent thrombosis, previous acute myocardial infarction, or angina within 48 hours before infarction were not included in the study. Patients with occlusion of the left main or left circumflex coronary artery or with evidence of coronary collaterals to the region at risk on initial coronary angiography (at the time of admission) were excluded.23 Patients with known hypersensitivity to cyclosporine, known renal failure or a serum creatinine level of 120 μmol per liter (1.36 mg per deciliter) or more at admission, liver failure, or uncontrolled hypertension and women who were pregnant or who were of childbearing age and were not using contraception were not included. Finally, patients who had any disorder that is associated with immunologic dysfunction (e.g., cancer, lymphoma, a positive serologic test for the human immunodeficiency virus, or hepatitis) more recently than 6 months before presentation were excluded.
Angiography and PCI
Left ventricular and coronary angiography was performed with the use of standard techniques, just before revascularization. The size of the area at risk, a major determinant of infarct size,24 was estimated for each patient by measuring the circumferential extent of abnormally contracting segments, according to the method of Feild et al.25 Revascularization was performed with the use of direct stenting.26
Experimental Protocol
After coronary angiography was performed but before the stent was implanted, patients who met the enrollment criteria were randomly assigned to either the control group or the cyclosporine group. Randomization was performed with the use of a computer-generated randomization sequence. Numbered, sealed envelopes that contained the study group assignment were distributed to each catheterization laboratory and were opened after informed consent had been obtained.
Less than 10 minutes before direct stenting, the patients in the cyclosporine group received an intravenous bolus injection of 2.5 mg of cyclosporine (Sandimmune, Novartis) per kilogram of body weight. Cyclosporine was dissolved in normal saline (final concentration, 25 mg per milliliter) and was injected through a catheter that was positioned within an antecubital vein. The patients in the control group received an equivalent volume of normal saline. The dose of cyclosporine was chosen arbitrarily, based on experimental data of Argaud et al.,17,27 as well as on our experience in the treatment of heart-transplant recipients, for whom this dose would be a typical loading dose.
Infarct Size
The primary end point was the size of the infarct as assessed by measurements of cardiac biomarkers. Blood samples were obtained at admission and repeatedly over the next 3 days. The area under the curve (AUC) (expressed in arbitrary units) for creatine kinase and troponin I release (Beckman kit) was measured in each patient by computerized planimetry (Image J1.32j).26,28,29
The principal secondary end point was the size of the infarct as measured by the area of delayed hyperenhancement that was seen on cardiac magnetic resonance imaging (MRI), assessed on day 5 after infarction.30-33 Because MRI facilities were available in only one of the three study centers, this estimation of infarct size could be performed in only a subgroup of patients. Imaging was performed on a 1.5-T whole-body MRI scanner (Magnetom Avanto, Siemens). For the late-enhancement analysis, 0.2 mmol of gadolinium–tetrazacyclododecanetetraacetic acid (DOTA) per kilogram was injected at a rate of 4 ml per second and was flushed with 15 ml of saline. Delayed hyperenhancement was evaluated 10 minutes after the injection of gadolinium–DOTA with the use of a three-dimensional inversion-recovery gradient−echo sequence. The images were analyzed in short-axis slices covering the entire left ventricle. Myocardial infarction was identified by delayed hyperenhancement within the myocardium, defined quantitatively by an intensity of the myocardial postcontrast signal that was more than 2 SD above that in a reference region of remote, noninfarcted myocardium within the same slice. For all slices, the absolute mass of the infarcted area was calculated according to the following formula: infarct mass (in grams of tissue)=Σ (hyperenhanced area [in square centimeters])×slice thickness (in centimeters)×myocardial specific density (1.05 g per cubic centimeter).
Other End Points
The whole-blood concentration of cyclosporine was measured at 1 and 20 minutes and at 3 and 12 hours after injection with the use of a radioimmunoassay kit (DiaSorin). Blood pressure and serum concentrations of creatinine and potassium were measured on admission and 24, 48, and 72 hours after PCI. Serum concentrations of bilirubin, γ-glutamyltransferase, and alkaline phosphatase, as well as white-cell counts, were measured on admission and 24 hours after PCI.
We recorded the cumulative incidence of major adverse events that occurred within the first 48 hours after reperfusion, including death, heart failure, acute myocardial infarction, stroke, recurrent ischemia, the need for repeat revascularization, renal or hepatic insufficiency, vascular complications, and bleeding. We also specifically assessed infarct-related adverse events, including heart failure and ventricular fibrillation. In addition, 3 months after acute myocardial infarction, cardiac events were recorded, and global left ventricular function was assessed by echocardiography (Vivid 7 systems; GE Vingmed).
Statistical Analysis
To calculate the target sample size for the present trial, we used the available database of the study of myocardial postconditioning by Staat et al.26 We hypothesized that cyclosporine would reduce the AUC for creatine kinase release by 30%. For a statistical power of 80% and a probability of a type I error of 0.05 using a two-sided test, we calculated that the sample size should be 62 subjects (31 per group).
All analyses were performed by independent experts who were unaware of the treatment-group assignments. Between-group comparisons of AUCs for serum creatine kinase or troponin I release, the time of ischemia, the area at risk, and the infarct size as assessed by MRI were performed with the use of the Wilcoxon rank-sum test. We performed an analysis of covariance to test for equality of the slopes of the regression of infarct size on the area at risk in the cyclosporine and control groups. A comparison of the incidence of cumulative adverse clinical events between the groups was performed by means of Fisher's exact test. All values are expressed as medians and interquartile ranges. All reported P values are two-sided.
Results
Characteristics of the Study Population
From July 2005 to October 2006, a total of 340 patients were hospitalized at the three study centers for management of acute myocardial infarction; 230 of these patients underwent PCI. Among these 230 patients, 24 were not evaluated for enrollment because study personnel were not available. Another 148 were evaluated and excluded for the following reasons: onset of chest pain more than 12 hours before presentation (20 patients), preadmission ventricular fibrillation (3), cardiac arrest before PCI (14), occlusion of the left main or circumflex coronary artery (27), stent thrombosis (16), previous myocardial infarction in the same territory (12), TIMI flow grade of more than 0 at admission (49), or evidence of coronary collaterals on initial angiography (7). Data are thus presented for 58 patients (28 in the control group and 30 in the cyclosporine group).
There was no significant difference between the two groups with respect to baseline characteristics (Table 1Table 1
Baseline Characteristics of the Study Population.). The mean age of the trial participants was 58 years, and almost 80% were men. The two study groups were similar with respect to ischemia time, the size of the area at risk, and the ejection fraction before PCI. Thrombolytic therapy before PCI failed in 13 patients (8 in the control group and 5 in the cyclosporine group).Stenting of the culprit lesion was performed in all patients (Table 1). No patient underwent PCI on arteries other than the infarct-related artery. In four patients, TIMI 2 flow was not achieved after PCI.
Infarct Size
The AUC for serum creatine kinase release after reperfusion was significantly reduced in the cyclosporine group as compared with the control group, with a median of 138,053 arbitrary units (interquartile range, 114,008 to 283,461) in the cyclosporine group versus 247,930 (interquartile range, 145,639 to 404,349) in the control group (P=0.04 for the difference), which represents a reduction in infarct size of approximately 40% (Figure 1AFigure 1
Assessment of Infarct Size by Biomarker Measurement.). The median AUC for troponin I release was 112,312 arbitrary units (interquartile range, 48,680 to 153,956) in the cyclosporine group and 129,320 arbitrary units (interquartile range, 65,019 to 224,116) in the control group. This difference was not significant (P=0.15) (Figure 1B).In the control group, there was a significant correlation between the AUC for serum creatine kinase release and the original area at risk (as defined by the circumferential extent of abnormally contracting segments on initial left ventricular angiography). As shown in Figure 2AFigure 2
Infarct Size as a Function of the Area at Risk., the regression line for the cyclosporine group had a smaller slope than the regression line for the control group, indicating that for any given size of area at risk, smaller infarcts developed in the cyclosporine-treated patients. This difference in the slope was significant by analysis of covariance (P=0.006). An analysis of the data for troponin I provided similar results, including a significant correlation between the AUC for troponin I release and the area at risk, with a smaller slope of the regression line for the cyclosporine group than for the control group (P=0.002 by analysis of covariance) (Figure 2B).In a subgroup of 27 patients, the absolute mass of the area of hyperenhancement on MRI was significantly reduced in the cyclosporine group as compared with the control group, with a median of 37 g (interquartile range, 21 to 51) versus 46 g (interquartile range, 20 to 65; P=0.04) (Figure 3Figure 3
Assessment of Infarct Size by Magnetic Resonance Imaging (MRI).). This 20% reduction in the area of hyperenhancement on MRI corresponded to the 26% and 36% reductions in AUCs for creatine kinase and troponin I release, respectively, that were observed in this subgroup of patients (baseline characteristics of the subgroup can be found in the Supplementary Appendix, available with the full text of this article at www.nejm.org).Other End Points
The whole-blood concentration of cyclosporine reached a peak level (mean ±SE, 6272±714 ng per milliliter) 1 minute after injection (Figure 4Figure 4
Blood Concentration of Cyclosporine during Reperfusion.). None of the treated patients had any clinical symptoms after the administration of cyclosporine. There were no significant changes in blood pressure; in serum concentrations of creatinine, potassium, bilirubin, γ-glutamyl-transpeptidase, or alkaline phosphatase; or in the white-cell count.During the first 48 hours after reperfusion, seven adverse clinical events were recorded in the control group: one episode of ventricular fibrillation and six episodes of heart failure. There were three adverse clinical events in the cyclosporine group: one episode of ventricular fibrillation, one episode of heart failure, and one episode of recurrent ischemia (P=0.11). When only infarct-related events were considered (i.e., ventricular fibrillation and heart failure), seven events were observed in the control group versus two in the cyclosporine group (P=0.05).
Three months after infarction, three patients in the control group and one in the cyclosporine group required rehospitalization for heart failure (P=0.28). These four patients were among those who had had heart failure within the first 2 days after acute myocardial infarction. There were no other adverse events during the interval from 48 hours to 3 months. At 3 months, the mean left ventricular ejection fraction as measured by echocardiography was 47±3% in the control group and 50±2% in the cyclosporine group (P=0.32).
Discussion
In our small, proof-of-concept trial, the administration of cyclosporine in patients with acute myocardial infarction at the time of reperfusion was associated with a smaller infarct size, as assessed by some measures, than that seen with placebo. Infarct size was assessed both by measuring the release of the cardiac biomarkers creatine kinase and troponin I and by measuring the area of late hyperenhancement of the reperfused myocardium on MRI on day 5. The AUC for the creatine kinase concentration suggests that the administration of cyclosporine was associated with a reduction in infarct size of approximately 40%. This finding was confirmed by a significant reduction in the area of late hyperenhancement on MRI in the cyclosporine-treated patients. However, the AUC for the troponin I concentration did not differ significantly between the two groups.
We investigated these observations further by comparing the infarct size, as measured by the release of cardiac biomarkers, with the size of the area at risk, as determined by left ventricular angiography. The slope of this relationship was not as steep in the cyclosporine group as in the control group, regardless of whether measurements of creatine kinase or of troponin I were used to assess infarct size.
The fact that cyclosporine reduced the infarct size, as estimated by the release of creatine kinase, when administered at the time of reperfusion suggests that lethal reperfusion injury occurs in humans.23,34,35 This observation supports the argument that reperfusion necrosis is a major component of infarct size after prolonged ischemia and reperfusion and raises the possibility that lethal reperfusion injury may be an important new pharmacologic target for the treatment of patients with ongoing acute myocardial infarction.26,34
The rationale for evaluating the ability of cyclosporine to reduce infarct size in patients with ongoing acute myocardial infarction was based on experimental evidence that indicated a crucial role of the opening of the mitochondrial permeability-transition pore in lethal reperfusion injury.9,10,14,17-20 Under physiologic conditions, the inner mitochondrial membrane is impermeable to almost all metabolites and ions, and the permeability-transition pore is in a closed conformation.9,10,12,36,37 At the time of reperfusion after prolonged ischemia, abrupt matrix accumulation of calcium and overproduction of reactive oxygen species trigger the opening of the pore.14,15,38 The resulting collapse of the membrane potential, uncoupling of the respiratory chain, efflux of proapoptotic factors, and hydrolysis of ATP may ultimately cause irreversible damage.
Cyclosporine probably inhibits the mitochondrial permeability transition by preventing the calcium-induced interaction of cyclophilin D with a pore component.14,39 Whether the reduction in infarct size that we observed by some measures in the present study is related to this mechanism is uncertain, since cyclosporine is not specific for mitochondrial cyclophilin D but has other intracellular effects as well.40-42 However, data from in vivo studies further support the hypothesis that specific inhibition of the opening of the permeability-transition pore may reduce infarct size. NIM811, a nonimmunosuppressive derivative of cyclosporine that also binds to the matrix cyclophilin D, significantly reduced infarct size when administered at the time of reperfusion in a rabbit model.43 Moreover, mice that lack cyclophilin D have an enhanced capacity to retain mitochondrial calcium and a delayed opening of the transition pore when calcium overload is present, and they have smaller infarcts after prolonged ischemia and reperfusion.44,45 The reduction in infarct size that was observed in the present study was similar to that seen with the use of ischemic postconditioning by means of angioplasty in patients with ongoing acute myocardial infarction, as described by Staat et al.26 Postconditioning, in which an angioplasty balloon is inflated repeatedly in the infarct-related artery after reperfusion has been achieved, is also believed to reduce the extent of reperfusion injury by inhibiting the opening of the permeability-transition pore.16,17
Cyclosporine is widely used as an immunosuppressive agent for the prevention of acute allograft rejection. Long-term use of cyclosporine has several potentially detrimental effects, including renal and hepatic toxicity and increased susceptibility to infections and cancers. In the present study, cyclosporine was administered as a single intravenous bolus. Although we cannot exclude the possibility of delayed toxicity, there was no evidence of acute renal or hepatic injury, hypertension, or other short-term adverse effects.
In summary, we evaluated the effect of cyclosporine in a small pilot study of patients with acute myocardial infarction who were undergoing PCI. The administration of cyclosporine at the time of reperfusion was associated with a reduction in infarct size as measured by the release of creatine kinase and delayed hyperenhancement on MRI. Release of troponin I, however, was not significantly reduced by the administration of cyclosporine. These data are preliminary and require confirmation in a larger clinical trial.
Supported by a Programme Hospitalier de Recherche Clinique 2004 grant from the French government.
Dr. Ovize reports serving as a consultant to Novartis. No other potential conflict of interest relevant to this article was reported.
We thank Valerie Prost and Alice Dubois for their excellent technical assistance in data monitoring.
Source Information
From Hôpital Arnaud de Villeneuve, Montpellier (C.P., T.T.C., C.M., F.R., C.S., G.G.); Hospices Civils de Lyon, Université Claude Bernard Lyon 1, Lyon (P.C., P.S., H.T., G.R., N.M., E.B., D.A., G.F., X.A.-F., D.R., G.K., G.D., M.O.); Service de Cardiologie, Mulhouse (R.E., J.-P.M.); and INSERM Unité 886, Lyon (H.T., G.R., D.A., G.F., G.D., M.O.) — all in France.
Address reprint requests to Dr. Ovize at Hôpital L. Pradel, Hospices Civils de Lyon, 59, Blvd. Pinel, 69394 Lyon CEDEX 03, France, or at ovize@sante.univ-lyon1.fr.
- References
References
1
Antman EM ,Anbe DT ,Armstrong PW , et al. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1999 Guidelines for the management of patients with acute myocardial infarction). J Am Coll Cardiol 2004;44:e1-e211
CrossRef | Medline2
Ergin A ,Muntner P ,Sherwin R ,He J . Secular trends in cardiovascular disease mortality, incidence, and case fatality rates in adults in the United States. Am J Med 2004;117:219-227
CrossRef | Web of Science | Medline3
Gibbons RJ ,Valeti US ,Araoz PA ,Jaffe AS . The quantification of infarct size. J Am Coll Cardiol 2004;44:1533-1542
CrossRef | Web of Science | Medline4
Burns RJ ,Gibbons RJ ,Yi Q , et al. The relationships of left ventricular ejection fraction, end-systolic volume index and infarct size to six-month mortality after hospital discharge following acute myocardial infarction treated by thrombolysis. J Am Coll Cardiol 2002;39:30-36
CrossRef | Web of Science | Medline5
Braunwald E ,Kloner RA . Myocardial reperfusion: a double-edged sword? J Clin Invest 1985;76:1713-1719
CrossRef | Web of Science | Medline6
Kloner RA ,Ganote CE ,Jennings RB . The “no-reflow” phenomenon following temporary coronary occlusion in the dog. J Clin Invest 1974;54:1496-1508
CrossRef | Web of Science | Medline7
Moens AL ,Claeys MJ ,Timmermans JP ,Vrints CJ . Myocardial ischemia/reperfusion injury: a clinical view on a complex pathophysiological process. Int J Cardiol 2005;100:179-190
CrossRef | Web of Science | Medline8
Nazareth W ,Yafei N ,Crompton M . Inhibition of anoxia-induced injury in heart myocytes by cyclosporin A. J Mol Cell Cardiol 1991;23:1351-1354
CrossRef | Web of Science | Medline9
Duchen MR ,McGuinness O ,Brown LA ,Crompton M . On the involvement of a cyclosporin A sensitive mitochondrial pore in myocardial reperfusion injury. Cardiovasc Res 1993;27:1790-1794
CrossRef | Web of Science | Medline10
Crompton M ,Costi A . A heart mitochondrial Ca2(+)-dependent pore of possible relevance to reperfusion-induced injury: evidence that ADP facilitates pore interconversion between the closed and open states. Biochem J 1990;266:33-39
Web of Science | Medline11
Di Lisa F ,Canton M ,Menabo R ,Dodoni G ,Bernardi P . Mitochondria and reperfusion injury: the role of permeability transition. Basic Res Cardiol 2003;98:235-241
Web of Science | Medline12
Hunter DR ,Haworth RA . The Ca-induced membrane transition in mitochondria. Arch Biochem Biophys 1979;195:468-477
CrossRef | Web of Science | Medline13
Bernardi P ,Petronilli V . The permeability transition pore as a mitochondrial calcium release channel: a critical appraisal. J Bioenerg Biomembr 1996;28:131-138
CrossRef | Web of Science | Medline14
Javadov S ,Karmazyn M . Mitochondrial permeability transition pore opening as an endpoint to initiate cell death and as a putative target for cardioprotection. Cell Physiol Biochem 2007;20:1-22
CrossRef | Web of Science | Medline15
Griffiths EJ ,Halestrap AP . Mitochondrial non-specific pores remain closed during cardiac ischaemia but open upon reperfusion. Biochem J 1995;307:93-98
Web of Science | Medline16
Hausenloy DJ ,Maddock HL ,Baxter GF ,Yellon DM . Inhibiting mitochondrial permeability transition pore opening: a new paradigm for myocardial preconditioning? Cardiovasc Res 2002;55:534-543
CrossRef | Web of Science | Medline17
Argaud L ,Gateau-Roesch O ,Raisky O ,Loufouat J ,Robert D ,Ovize M . Postconditioning inhibits mitochondrial permeability transition. Circulation 2005;111:194-197
CrossRef | Web of Science | Medline18
Di Lisa F ,Menabo R ,Canton M ,Barile M ,Bernardi P . Opening of the mitochondrial permeability transition pore causes depletion of mitochondrial and cytosolic NAD(+) and is a causative event in the death of myocytes in postischemic reperfusion of the heart. J Biol Chem 2001;276:2571-2575
CrossRef | Web of Science | Medline19
Qian T ,Nieminen AL ,Herman B ,Lemasters JJ . Mitochondrial permeability transition in pH-dependent reperfusion injury to rat hepatocytes. Am J Physiol 1997;273:C1783-C1792
Web of Science | Medline20
Kim JS ,Jin Y ,Lemasters JJ . Reactive oxygen species, but not Ca2+ overloading, trigger pH- and mitochondrial permeability transition-dependent death of adult rat myocytes after ischemia-reperfusion. Am J Physiol Heart Circ Physiol 2006;290:H2024-H2034
CrossRef | Web of Science | Medline21
Oka N ,Wang L ,Mi W ,Zhu W ,Honjo O ,Caldarone CA . Cyclosporine A prevents apoptosis-related mitochondrial dysfunction after neonatal cardiac arrest. J Thorac Cardiovasc Surg 2008;135:123-130
CrossRef | Web of Science | Medline22
Chesebro JH ,Knatterud G ,Roberts R , et al. Thrombolysis in Myocardial Infarction (TIMI) trial, phase 1: a comparison between intravenous tissue plasminogen activator and intravenous streptokinase. Circulation 1987;76:142-154
CrossRef | Web of Science | Medline23
Rentrop KP ,Cohen M ,Blanke H ,Phillips RA . Changes in collateral channel filling immediately after controlled coronary artery occlusion by an angioplasty balloon on human subjects. J Am Coll Cardiol 1985;5:587-592
CrossRef | Web of Science | Medline24
Reimer KA, Jennings RB. The “wavefront phenomenon” of myocardial ischemic cell death. II. Transmural progression of necrosis within the framework of ischemic bed size (myocardium at risk) and collateral flow. Lab Invest 1979;40633-44.
25
Feild BJ ,Russell RO Jr ,Dowling JT ,Rackley CE . Regional left ventricular performance in the year following myocardial infarction. Circulation 1972;46:679-689
Web of Science | Medline26
Staat P ,Rioufol G ,Piot C , et al. Postconditioning the human heart. Circulation 2005;112:2143-2148
CrossRef | Web of Science | Medline27
Argaud L ,Gateau-Roesch O ,Chalabreysse L , et al. Preconditioning delays Ca2+-induced mitochondrial permeability transition. Cardiovasc Res 2004;61:115-122
CrossRef | Web of Science | Medline28
Roberts R ,Henry PD ,Sobel BE . An improved basis for enzymatic estimation of infarct size. Circulation 1975;52:743-754
Web of Science | Medline29
Hackel DB ,Reimer KA ,Ideker RE , et al. Comparison of enzymatic and anatomic estimates of myocardial infarct size in man. Circulation 1984;70:824-835
CrossRef | Web of Science | Medline30
Mahrholdt H ,Wagner A ,Holly TA , et al. Reproducibility of chronic infarct size measurement by contrast-enhanced magnetic resonance imaging. Circulation 2002;106:2322-2327
CrossRef | Web of Science | Medline31
Kim RJ ,Fieno DS ,Parrish TB , et al. Relationship of MRI delayed contrast enhancement to irreversible injury, infarct age, and contractile function. Circulation 1999;100:1992-2002
Web of Science | Medline32
Rehwald WG ,Fieno DS ,Chen EL ,Kim RJ ,Judd RM . Myocardial magnetic resonance imaging contrast agent concentrations after reversible and irreversible ischemic injury. Circulation 2002;105:224-229
CrossRef | Web of Science | Medline33
Shan K ,Constantine G ,Sivananthan M ,Flamm SD . Role of cardiac magnetic resonance imaging in the assessment of myocardial viability. Circulation 2004;109:1328-1334
CrossRef | Web of Science | Medline34
Zhao ZQ ,Corvera JS ,Halkos ME , et al. Inhibition of myocardial injury by ischemic postconditioning during reperfusion: comparison with ischemic preconditioning. Am J Physiol Heart Circ Physiol 2003;285:H579-H588[Erratum, Am J Physiol Heart Circ Physiol 2004;286:H477.]
Web of Science | Medline35
Kloner RA . Does reperfusion injury exist in humans? J Am Coll Cardiol 1993;21:537-545
CrossRef | Web of Science | Medline36
Crompton M . The mitochondrial permeability transition pore and its role in cell death. Biochem J 1999;341:233-249
CrossRef | Web of Science | Medline37
Zoratti M ,Szabo I . The mitochondrial permeability transition. Biochim Biophys Acta 1995;1241:139-176
Web of Science | Medline38
Piper HM ,Garcia-Dorado D ,Ovize M . A fresh look at reperfusion injury. Cardiovasc Res 1998;38:291-300
CrossRef | Web of Science | Medline39
Woodfield K ,Ruck A ,Brdiczka D ,Halestrap AP . Direct demonstration of a specific interaction between cyclophilin-D and the adenine nucleotide translocase confirms their role in the mitochondrial permeability transition. Biochem J 1998;336:287-290
Web of Science | Medline40
Obasanjo-Blackshire K ,Mesquita R ,Jabr RI , et al. Calcineurin regulates NFAT-dependant iNOS expression and protection of cardiomyocytes: co-operation with Src tyrosine kinase. Cardiovasc Res 2006;71:672-683
CrossRef | Web of Science | Medline41
De Windt LJ ,Lim HW ,Taigen T , et al. Calcineurin-mediated hypertrophy protects cardiomyocytes from apoptosis in vitro and in vivo: an apoptosis-independent model of dilated heart failure. Circ Res 2000;86:255-263
Web of Science | Medline42
Bueno OF ,Lips DJ ,Kaiser RA , et al. Calcineurin Aβ gene targeting predisposes the myocardium to acute ischemia-induced apoptosis and dysfunction. Circ Res 2004;94:91-99
CrossRef | Web of Science | Medline43
Argaud L ,Gateau-Roesch O ,Muntean D , et al. Specific inhibition of the mitochondrial permeability transition prevents lethal reperfusion injury. J Mol Cell Cardiol 2005;38:367-374
CrossRef | Medline44
Nakagawa T ,Shimizu S ,Watanabe T , et al. Cyclophilin D-dependent mitochondrial permeability transition regulates some necrotic but not apoptotic cell death. Nature 2005;434:652-657
CrossRef | Web of Science | Medline45
Baines CP ,Kaiser RA ,Purcell NH , et al. Loss of cyclophilin D reveals a critical role for mitochondrial permeability transition in cell death. Nature 2005;434:658-662
CrossRef | Web of Science | Medline
- Citing Articles (195)
Citing Articles
1
J. Stumpner, M. Lange, A. Beck, T. M. Smul, C. A. Lotz, F. Kehl, N. Roewer, A. Redel. (2012) Desflurane-induced post-conditioning against myocardial infarction is mediated by calcium-activated potassium channels: role of the mitochondrial permeability transition pore. British Journal of Anaesthesia
CrossRef2
Henry Dube, David Selwood, Sylvanie Malouitre, Michela Capano, Michela I. Simone, Martin Crompton. (2012) A mitochondrial-targeted cyclosporin A with high binding affinity for cyclophilin D yields improved cytoprotection of cardiomyocytes. Biochemical Journal 441:3, 901-907
CrossRef3
X. Wen, Z. Peng, Y. Li, H. Wang, J. V. Bishop, L. R. Chedwick, K. Singbartl, J. A. Kellum. (2012) One dose of cyclosporine A is protective at initiation of folic acid-induced acute kidney injury in mice. Nephrology Dialysis Transplantation
CrossRef4
Julie Belliere, Flavien Devun, Cécile Cottet-Rousselle, Cécile Batandier, Xavier Leverve, Eric Fontaine. (2012) Prerequisites for ubiquinone analogs to prevent mitochondrial permeability transition-induced cell death. Journal of Bioenergetics and Biomembranes
CrossRef5
Dao-Fu Dai, Tony Chen, Simon Johnson, Hazel H. Szeto, Peter S. Rabinovitch. (2012) Cardiac Aging: From Molecular Mechanisms to Significance in Human Health and Disease. Antioxidants & Redox Signaling120109141037006
CrossRef6
X. Freixa, N. Bellera, J. T. Ortiz-Perez, M. Jimenez, C. Pare, X. Bosch, T. M. De Caralt, A. Betriu, M. Masotti. (2012) Ischaemic postconditioning revisited: lack of effects on infarct size following primary percutaneous coronary intervention. European Heart Journal 33:1, 103-112
CrossRef7
Qun Chen, Melanie Paillard, Ludovic Gomez, Heng Li, Ying Hu, Edward J. Lesnefsky. (2012) Postconditioning Modulates Ischemia-damaged Mitochondria During Reperfusion. Journal of Cardiovascular Pharmacology 59:1, 101-108
CrossRef8
Anna Onishi, Masami Miyamae, Kazuhiro Kaneda, Junichiro Kotani, Vincent M. Figueredo. (2012) Direct evidence for inhibition of mitochondrial permeability transition pore opening by sevoflurane preconditioning in cardiomyocytes: Comparison with cyclosporine A. European Journal of Pharmacology 675:1-3, 40-46
CrossRef9
Kazuhiro Niimi, Takahiro Yasui, Masahito Hirose, Shuzo Hamamoto, Yasunori Itoh, Atsushi Okada, Yasue Kubota, Yoshiyuki Kojima, Keiichi Tozawa, Shoichi Sasaki, Yutaro Hayashi, Kenjiro Kohri. (2012) Mitochondrial permeability transition pore opening induces the initial process of renal calcium crystallization. Free Radical Biology and Medicine
CrossRef10
Richdeep S. Gill, Namdar Manouchehri, Tze-Fun Lee, Woo Jung Cho, Aducio Thiesen, Thomas Churchill, David L. Bigam, Po-Yin Cheung. (2011) Cyclosporine treatment improves mesenteric perfusion and attenuates necrotizing enterocolitis (NEC)-like intestinal injury in asphyxiated newborn piglets during reoxygenation. Intensive Care Medicine
CrossRef11
Thomas Cuisset, Mathieu Pankert, Jacques Quilici. (2011) Synergy between pharmacological and mechanical reperfusion in ST-segment elevation myocardial infarction patients. Journal of Cardiovascular Medicine 12:12, 860-867
CrossRef12
M Chiong, Z V Wang, Z Pedrozo, D J Cao, R Troncoso, M Ibacache, A Criollo, A Nemchenko, J A Hill, S Lavandero. (2011) Cardiomyocyte death: mechanisms and translational implications. Cell Death and Disease 2:12, e244
CrossRef13
Yves Gouriou, Nicolas Demaurex, Philippe Bijlenga, Umberto De Marchi. (2011) Mitochondrial calcium handling during ischemia-induced cell death in neurons. Biochimie 93:12, 2060-2067
CrossRef14
Chien-Hua Huang, Min-Shan Tsai, Chiung-Yuan Hsu, Yu-Jen Su, Tzung-Dau Wang, Wei-Tien Chang, Wen-Jone Chen. (2011) Post-cardiac arrest myocardial dysfunction is improved with cyclosporine treatment at onset of resuscitation but not in the reperfusion phase. Resuscitation 82, S41-S47
CrossRef15
Tiago R. Figueira, Roger F. Castilho, Ângela Saito, Helena C.F. Oliveira, Anibal E. Vercesi. (2011) The higher susceptibility of congenital analbuminemic rats to Ca2+-induced mitochondrial permeability transition is associated with the increased expression of cyclophilin D and nitrosothiol depletion. Molecular Genetics and Metabolism 104:4, 521-528
CrossRef16
R. Tissier, B. Ghaleh, M. V. Cohen, J. M. Downey, A. Berdeaux. (2011) Myocardial protection with mild hypothermia. Cardiovascular Research
CrossRef17
T. Miura, M. Tanno. (2011) The mPTP and its regulatory proteins: final common targets of signalling pathways for protection against necrosis. Cardiovascular Research
CrossRef18
Holger K Eltzschig, Tobias Eckle. (2011) Ischemia and reperfusion—from mechanism to translation. Nature Medicine 17:11, 1391-1401
CrossRef19
Shiang Y. Lim, Derek J. Hausenloy, Sapna Arjun, Anthony N. Price, Sean M. Davidson, Mark F. Lythgoe, Derek M. Yellon. (2011) Mitochondrial cyclophilin-D as a potential therapeutic target for post-myocardial infarction heart failure. Journal of Cellular and Molecular Medicine 15:11, 2443-2451
CrossRef20
W.L. Wang, Y.J. Yuan, F.S. Xue, X. Liao, Q. Wang, J. Xiong, J.H. Liu. (2011) Extracellular cyclophilin A may be a potential target to protect against myocardial reperfusion injury. Medical Hypotheses 77:5, 734-738
CrossRef21
Ludovic Gomez, Melanie Paillard, Megan Price, Qun Chen, Geoffrey Teixeira, Sarah Spiegel, Edward J. Lesnefsky. (2011) A novel role for mitochondrial sphingosine-1-phosphate produced by sphingosine kinase-2 in PTP-mediated cell survival during cardioprotection. Basic Research in Cardiology 106:6, 1341-1353
CrossRef22
Xavier Marechal, David Montaigne, Camille Marciniak, Philippe Marchetti, Sidi Mohamed Hassoun, Jean Claude Beauvillain, Steve Lancel, Remi Neviere. (2011) Doxorubicin-induced cardiac dysfunction is attenuated by ciclosporin treatment in mice through improvements in mitochondrial bioenergetics. Clinical Science 121:9, 405-413
CrossRef23
Kayo Hirose, Yasuo M. Tsutsumi, Rie Tsutsumi, Masayuki Shono, Erika Katayama, Michiko Kinoshita, Katsuya Tanaka, Shuzo Oshita. (2011) Role of the O-linked β-N-acetylglucosamine in the Cardioprotection Induced by Isoflurane. Anesthesiology 115:5, 955-962
CrossRef24
Jérôme Thireau, Jean-Luc Pasquié, Eric Martel, Jean-Yves Le Guennec, Sylvain Richard. (2011) New drugs vs. old concepts: A fresh look at antiarrhythmics. Pharmacology & Therapeutics 132:2, 125-145
CrossRef25
Marisol Ruiz-Meana, Javier Inserte, Celia Fernandez-Sanz, Victor Hernando, Elisabet Miro-Casas, Ignasi Barba, David Garcia-Dorado. (2011) The role of mitochondrial permeability transition in reperfusion-induced cardiomyocyte death depends on the duration of ischemia. Basic Research in Cardiology 106:6, 1259-1268
CrossRef26
Yaser Abdallah, Sascha A. Kasseckert, Wisam Iraqi, Maher Said, Tayyab Shahzad, Ali Erdogan, Christiane Neuhof, Dürsün Gündüz, Klaus-Dieter Schlüter, Harald Tillmanns, H. Michael Piper, H. Peter Reusch, Yury Ladilov. (2011) Interplay between Ca2+ cycling and mitochondrial permeability transition pores promotes reperfusion-induced injury of cardiac myocytes. Journal of Cellular and Molecular Medicine 15:11, 2478-2485
CrossRef27
G. Heusch, P. Kleinbongard, A. Skyschally, B. Levkau, R. Schulz, R. Erbel. (2011) The coronary circulation in cardioprotection: more than just one confounder. Cardiovascular Research
CrossRef28
D. J. Hausenloy, D. M. Yellon. (2011) Taking lizard saliva to heart. European Heart Journal
CrossRef29
Michelle J. Butler, William Chan, Andrew J. Taylor, Anthony M. Dart, Stephen J. Duffy. (2011) Management of the no-reflow phenomenon. Pharmacology & Therapeutics 132:1, 72-85
CrossRef30
Arantxa González, Susana Ravassa, Javier Beaumont, Begoña López, Javier Díez. (2011) New Targets to Treat the Structural Remodeling of the Myocardium. Journal of the American College of Cardiology 58:18, 1833-1843
CrossRef31
J. Lonborg, N. Vejlstrup, H. Kelbaek, H. E. Botker, W. Y. Kim, A. B. Mathiasen, E. Jorgensen, S. Helqvist, K. Saunamaki, P. Clemmensen, L. Holmvang, L. Thuesen, L. R. Krusell, J. S. Jensen, L. Kober, M. Treiman, J. J. Holst, T. Engstrom. (2011) Exenatide reduces reperfusion injury in patients with ST-segment elevation myocardial infarction. European Heart Journal
CrossRef32
Matthias Götberg, Jesper Pals, Michael Götberg, Göran K. Olivecrona, Mikael Kanski, Sasha Koul, Andreas Otto, Henrik Engblom, Martin Ugander, Håkan Arheden, David Erlinge. (2011) Optimal timing of hypothermia in relation to myocardial reperfusion. Basic Research in Cardiology 106:5, 697-708
CrossRef33
Fadi G. Akar, Brian O'Rourke. (2011) Mitochondria are sources of metabolic sink and arrhythmias. Pharmacology & Therapeutics 131:3, 287-294
CrossRef34
Young-Ho Jang, June-Hong Kim, Changill Ban, Kyohan Ahn, Jae-Hun Cheong, Hyung-Hoi Kim, Jung-Soo Kim, Yong-Hyun Park, Jun Kim, Kook-Jin Chun, Gyeong- Ho Lee, Miju Kim, Cheolmin Kim, Zhelong Xu. (2011) Stromal Cell Derived Factor-1 (SDF-1) Targeting Reperfusion Reduces Myocardial Infarction in Isolated Rat Hearts. Cardiovascular Therapeuticsno-no
CrossRef35
DJ Hausenloy, EA Boston-Griffiths, DM Yellon. (2011) Cyclosporin A and cardioprotection: from investigative tool to therapeutic agent. British Journal of Pharmacologyno-no
CrossRef36
Ester Spagnolli, Warren M. Zapol. 2011. The Role of Reactive Oxygen and Nitrogen Species in Ischemia/Reperfusion Injury. , 63-77.
CrossRef37
J. Fauconnier, A. C. Meli, J. Thireau, S. Roberge, J. Shan, Y. Sassi, S. R. Reiken, J.-M. Rauzier, A. Marchand, D. Chauvier, C. Cassan, C. Crozier, P. Bideaux, A.-M. Lompre, E. Jacotot, A. R. Marks, A. Lacampagne. (2011) Ryanodine receptor leak mediated by caspase-8 activation leads to left ventricular injury after myocardial ischemia-reperfusion. Proceedings of the National Academy of Sciences 108:32, 13258-13263
CrossRef38
Borja Ibanez, Valentin Fuster, Jesús Jiménez-Borreguero, Juan J. Badimon. (2011) Lethal myocardial reperfusion injury: A necessary evil?. International Journal of Cardiology 151:1, 3-11
CrossRef39
G. S. Di Marco, S. Reuter, D. Kentrup, L. Ting, L. Ting, A. Grabner, A. M. Jacobi, H. Pavenstadt, H. A. Baba, K. Tiemann, M. Brand. (2011) Cardioprotective effect of calcineurin inhibition in an animal model of renal disease. European Heart Journal 32:15, 1935-1945
CrossRef40
D. Garcia-Dorado, I. Barba, J. Inserte. (2011) Twenty-five years of preconditioning: are we ready for ischaemia? From coronary occlusion to systems biology and back. Cardiovascular Research 91:3, 378-381
CrossRef41
Kerstin Boengler, Gerd Heusch, Rainer Schulz. (2011) Nuclear-encoded mitochondrial proteins and their role in cardioprotection. Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 1813:7, 1286-1294
CrossRef42
Ruenn Chai Lai, Tian Sheng Chen, Sai Kiang Lim. (2011) Mesenchymal stem cell exosome: a novel stem cell-based therapy for cardiovascular disease. Regenerative Medicine 6:4, 481-492
CrossRef43
Carlos Tarin, Begoña Lavin, Monica Gomez, Marta Saura, Antonio Diez-Juan, Carlos Zaragoza. (2011) The extracellular matrix metalloproteinase inducer EMMPRIN is a target of nitric oxide in myocardial ischemia/reperfusion. Free Radical Biology and Medicine 51:2, 387-395
CrossRef44
Ronit Lavi, Shahar Lavi. (2011) Melatonin and myocardial protection. International Journal of Cardiology 150:2, 207
CrossRef45
Fabio Di Lisa, Andrea Carpi, Valentina Giorgio, Paolo Bernardi. (2011) The mitochondrial permeability transition pore and cyclophilin D in cardioprotection. Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 1813:7, 1316-1322
CrossRef46
Elizabeth Murphy, Charles Steenbergen. (2011) What makes the mitochondria a killer? Can we condition them to be less destructive?. Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 1813:7, 1302-1308
CrossRef47
Derek J. Hausenloy, Derek M. Yellon. (2011) The therapeutic potential of ischemic conditioning: an update. Nature Reviews Cardiology 8:11, 619-629
CrossRef48
Ming-He Huang, Yewen Wu, Vincent Nguyen, Saurabh Rastogi, Bradley K. McConnell, Cori Wijaya, Barry F. Uretsky, Kian-Keong Poh, Huay-Cheem Tan, Kenichi Fujise. (2011) Heart Protection by Combination Therapy with Esmolol and Milrinone at Late-Ischemia and Early Reperfusion. Cardiovascular Drugs and Therapy 25:3, 223-232
CrossRef49
Gerd Heusch, Andreas Skyschally, Rainer Schulz. (2011) The in-situ pig heart with regional ischemia/reperfusion — Ready for translation. Journal of Molecular and Cellular Cardiology 50:6, 951-963
CrossRef50
G. Martinez-Palli, R. Hirose, T. Liu, F. Xu, K. Dang, J. Feiner, N. J. Serkova, C. U. Niemann. (2011) Donor pre-treatment with everolimus or cyclosporine does not reduce ischaemia-reperfusion injury in a rat kidney transplant model. Nephrology Dialysis Transplantation 26:6, 1813-1820
CrossRef51
M. I. Okorie, D. D. Bhavsar, D. Ridout, M. Charakida, J. E. Deanfield, S. P. Loukogeorgakis, R. J. MacAllister. (2011) Postconditioning protects against human endothelial ischaemia-reperfusion injury via subtype-specific KATP channel activation and is mimicked by inhibition of the mitochondrial permeability transition pore. European Heart Journal 32:10, 1266-1274
CrossRef52
L. LIU, J. ZHU, P. R. BRINK, P. S. A. GLASS, M. J. REBECCHI. (2011) Age-associated differences in the inhibition of mitochondrial permeability transition pore opening by cyclosporine A. Acta Anaesthesiologica Scandinavica 55:5, 622-630
CrossRef53
Sachiko Kanki, Diana E. Jaalouk, Samuel Lee, Alvin Y.C. Yu, Joseph Gannon, Richard T. Lee. (2011) Identification of targeting peptides for ischemic myocardium by in vivo phage display. Journal of Molecular and Cellular Cardiology 50:5, 841-848
CrossRef54
Jacob Lønborg, Thomas Engstrøm. (2011) Determining the optimal time to introduce ischemic postconditioning. Expert Review of Cardiovascular Therapy 9:5, 541-543
CrossRef55
Fernanda Ricchelli, Justina Šileikytė, Paolo Bernardi. (2011) Shedding light on the mitochondrial permeability transition. Biochimica et Biophysica Acta (BBA) - Bioenergetics 1807:5, 482-490
CrossRef56
PETER STEMPNIEWICZ, ALAN CHENG, ALLISON CONNOLLY, XIN YUAN WANG, HUGH CALKINS, GORDON F. TOMASELLI, RONALD D. BERGER, LARISA G. TERESHCHENKO. (2011) Appropriate and Inappropriate Electrical Therapies Delivered by an Implantable Cardioverter-Defibrillator: Effect on Intracardiac Electrogram. Journal of Cardiovascular Electrophysiology 22:5, 554-560
CrossRef57
Javier Inserte, Ignasi Barba, Marcos Poncelas-Nozal, Victor Hernando, Luís Agulló, Marisol Ruiz-Meana, David Garcia-Dorado. (2011) cGMP/PKG pathway mediates myocardial postconditioning protection in rat hearts by delaying normalization of intracellular acidosis during reperfusion. Journal of Molecular and Cellular Cardiology 50:5, 903-909
CrossRef58
Karin Przyklenk. (2011) Efficacy of Cardioprotective ‘Conditioning’ Strategies in Aging and Diabetic Cohorts. Drugs & Aging 28:5, 331-343
CrossRef59
Adelaide M. Arruda-Olson, Véronique L. Roger, Allan S. Jaffe, David O. Hodge, Raymond J. Gibbons, Todd D. Miller. (2011) Troponin T Levels and Infarct Size by SPECT Myocardial Perfusion Imaging. JACC: Cardiovascular Imaging 4:5, 523-533
CrossRef60
S. Benhabbouche, C. Crola da silva, M. Abrial, R. Ferrera. (2011) Base des phénomènes d’ischémie reperfusion et de la protection myocardique. Annales Françaises d'Anesthésie et de Réanimation 30, S2-S16
CrossRef61
Giampaolo Niccoli, Nicola Cosentino, Cristina Spaziani, Silvia Minelli, Francesco Fracassi, Filippo Crea. (2011) New strategies for the management of no-reflow after primary percutaneous coronary intervention. Expert Review of Cardiovascular Therapy 9:5, 615-630
CrossRef62
Xin Duan, Bingyang Ji, Kun Yu, Jinping Liu, Feilong Hei, Cun Long. (2011) Pharmacological Postconditioning Protects Isolated Rat Hearts Against Ischemia-Reperfusion Injury: The Role of Mitochondrial Permeability Transition Pore. ASAIO Journal 57:3, 197-202
CrossRef63
Melanie L. McEwen, Patrick G. Sullivan, Alexander G. Rabchevsky, Joe E. Springer. (2011) Targeting Mitochondrial Function for the Treatment of Acute Spinal Cord Injury. Neurotherapeutics 8:2, 168-179
CrossRef64
Nathan Mewton, Didier Revel, Eric Bonnefoy, Michel Ovize, Pierre Croisille. (2011) Comparison of visual scoring and quantitative planimetry methods for estimation of global infarct size on delayed enhanced cardiac MRI and validation with myocardial enzymes. European Journal of Radiology 78:1, 87-92
CrossRef65
W. Desmet, J. Bogaert, C. Dubois, P. Sinnaeve, T. Adriaenssens, C. Pappas, J. Ganame, S. Dymarkowski, S. Janssens, A. Belmans, F. Van de Werf. (2011) High-dose intracoronary adenosine for myocardial salvage in patients with acute ST-segment elevation myocardial infarction. European Heart Journal 32:7, 867-877
CrossRef66
Vivian C. Tuei, Ji-Sook Ha, Chung-Eun Ha. (2011) Effects of human serum albumin complexed with free fatty acids on cell viability and insulin secretion in the hamster pancreatic β-cell line HIT-T15. Life Sciences 88:17-18, 810-818
CrossRef67
Nassir Rostambeigi, Ian R. Lanza, Petras P. Dzeja, Michael C. Deeds, Brian A. Irving, Honey V. Reddi, Pranathi Madde, Song Zhang, Yan W. Asmann, Jarett M. Anderson, Jill M. Schimke, K. Sreekumaran Nair, Norman L. Eberhardt, Yogish C. Kudva. (2011) Unique Cellular and Mitochondrial Defects Mediate FK506-Induced Islet β-Cell Dysfunction. Transplantation 91:6, 615-623
CrossRef68
Derek J. Hausenloy, Sandrine Lecour, Derek M. Yellon. (2011) Reperfusion Injury Salvage Kinase and Survivor Activating Factor Enhancement Prosurvival Signaling Pathways in Ischemic Postconditioning: Two Sides of the Same Coin. Antioxidants & Redox Signaling 14:5, 893-907
CrossRef69
Javier Inserte, Marisol Ruiz-Meana, Antonio Rodríguez-Sinovas, Ignasi Barba, David Garcia-Dorado. (2011) Contribution of Delayed Intracellular pH Recovery to Ischemic Postconditioning Protection. Antioxidants & Redox Signaling 14:5, 923-939
CrossRef70
Michael V. Cohen, James M. Downey. (2011) Ischemic Postconditioning: From Receptor to End-Effector. Antioxidants & Redox Signaling 14:5, 821-831
CrossRef71
Fabio Di Lisa, Marcella Canton, Andrea Carpi, Nina Kaludercic, Roberta Menabò, Sara Menazza, Martina Semenzato. (2011) Mitochondrial Injury and Protection in Ischemic Pre- and Postconditioning. Antioxidants & Redox Signaling 14:5, 881-891
CrossRef72
Christopher P. Baines. (2011) The Mitochondrial Permeability Transition Pore and the Cardiac Necrotic Program. Pediatric Cardiology 32:3, 258-262
CrossRef73
Kerstin Boengler, Gerd Heusch, Rainer Schulz. (2011) Mitochondria in Postconditioning. Antioxidants & Redox Signaling 14:5, 863-880
CrossRef74
Fabrice Ivanes, Gilles Rioufol, Christophe Piot, Michel Ovize. (2011) Postconditioning in Acute Myocardial Infarction Patients. Antioxidants & Redox Signaling 14:5, 811-820
CrossRef75
Olivér Rosero, Péter Ónody, Rita Stangl, Viktor Hegedűs, Gábor Lotz, Anna Blázovics, Péter Kupcsulik, Attila Szijártó. (2011) Posztkondicionálás kísérletes vizsgálata vékonybél ischaemiás-reperfusiós modelljében. Magyar Sebészet (Hungarian Journal of Surgery) 64:1, 28-36
CrossRef76
Santiago Garcia, Timothy D. Henry, Yale L. Wang, Ivan J. Chavez, Wesley R. Pedersen, John R. Lesser, Gautam R. Shroff, Luke Moore, Jay H. Traverse. (2011) Long-term Follow-up of Patients Undergoing Postconditioning During ST-Elevation Myocardial Infarction. Journal of Cardiovascular Translational Research 4:1, 92-98
CrossRef77
Jiunn-Jye Sheu, Sarah Chua, Cheuk-Kwan Sun, Li-Teh Chang, Chia-Hung Yen, Chiung-Jen Wu, Morgan Fu, Hon-Kan Yip. (2011) Intra-coronary administration of cyclosporine limits infarct size, attenuates remodeling and preserves left ventricular function in porcine acute anterior infarction. International Journal of Cardiology 147:1, 79-87
CrossRef78
M. Cour, J. Loufouat, M. Paillard, L. Augeul, J. Goudable, M. Ovize, L. Argaud. (2011) Inhibition of mitochondrial permeability transition to prevent the post-cardiac arrest syndrome: a pre-clinical study. European Heart Journal 32:2, 226-235
CrossRef79
Valentina O. Puntmann, Peter C. Taylor, Manuel Mayr. (2011) Coupling Vascular and Myocardial Inflammatory Injury into a Common Phenotype of Cardiovascular Dysfunction: Systemic Inflammation and Aging – A Mini-Review. Gerontology 57:4, 295-303
CrossRef80
H. Lanclas, S. Ricômes, J. Fichet, A. Cariou. (2011) L’arrêt cardiaque — Protection cérébrale post-arrêt cardiaque. Réanimation 20:S2, 621-629
CrossRef81
Sabzali Javadov, J. Craig Hunter, Giselle Barreto-Torres, Rebecca Parodi-Rullan. (2011) Targeting the Mitochondrial Permeability Transition: Cardiac Ischemia-Reperfusion <i>Versus</i> Carcinogenesis. Cellular Physiology and Biochemistry 27:3-4, 179-190
CrossRef82
Chun-Man Yuen, Cheuk-Kwan Sun, Yu-Chun Lin, Li-Teh Chang, Ying-Hsien Kao, Chia-Hung Yen, Yung-Lung Chen, Tzu-Hsien Tsai, Sarah Chua, Pei-Lin Shao, Steve Leu, Hon-Kan Yip. (2011) Combination of cyclosporine and erythropoietin improves brain infarct size and neurological function in rats after ischemic stroke. Journal of Translational Medicine 9:1, 141
CrossRef83
Laurice Fretwell, John M. Dickenson. (2011) Role of large-conductance Ca 2+ -activated K + channels in adenosine A 1 receptor-mediated pharmacological postconditioning in H9c2 cells. Canadian Journal of Physiology and Pharmacology 89:1, 24-30
CrossRef84
D. Coquerel, F. Tamion. (2011) Ischémie-reperfusion myocardique — Aspects physiopathologiques. Réanimation 20:S2, 267-273
CrossRef85
L. Argaud, M. Cour. (2011) Ischémie-reperfusion myocardique — Postconditionnement: protéger de l’ischémie à la reperfusion. Réanimation 20:S2, 280-288
CrossRef86
G. Ganesha Babu, J. Malcolm Walker, D. M. Yellon, D. J. Hausenloy. (2011) Peri-procedural myocardial injury during percutaneous coronary intervention: an important target for cardioprotection. European Heart Journal 32:1, 23-31
CrossRef87
Magnus J. Hansson, Saori Morota, Li Chen, Nagahisa Matsuyama, Yoshiaki Suzuki, Satoshi Nakajima, Tadashi Tanoue, Akibumi Omi, Futoshi Shibasaki, Motohide Shimazu, Yukio Ikeda, Hiroyuki Uchino, Eskil Elmér. (2011) Cyclophilin D-Sensitive Mitochondrial Permeability Transition in Adult Human Brain and Liver Mitochondria. Journal of Neurotrauma 28:1, 143-153
CrossRef88
Magalie Viallon, Nathan Mewton, Franck Thuny, Jens Guehring, Thomas O'Donnell, Alto Stemmer, Xiaoming Bi, Stanislas Rapacchi, Sven Zuehlsdorff, Didier Revel, Pierre Croisille. (2011) T2-weighted cardiac MR assessment of the myocardial area-at-risk and salvage area in acute reperfused myocardial infarction: Comparison of state-of-the-art dark blood and bright blood T2-weighted sequences. Journal of Magnetic Resonance Imagingn/a-n/a
CrossRef89
R. Tissier, M. Chenoune, B. Ghaleh, M. V. Cohen, J. M. Downey, A. Berdeaux. (2010) The small chill: mild hypothermia for cardioprotection?. Cardiovascular Research 88:3, 406-414
CrossRef90
Robert F. Zimmerman. (2010) Remote Ischemic Preconditioning: Is the Groove in the Heart?. American Journal of Kidney Diseases 56:6, 1019-1022
CrossRef91
Mohammad Ali Husainy, John M. Dickenson, Manuel Galiñanes. (2010) The MPTP Status During Early Reoxygenation is Critical for Cardioprotection. Journal of Surgical Research
CrossRef92
Erica Dall'Armellina, Theodoros D. Karamitsos, Stefan Neubauer, Robin P. Choudhury. (2010) CMR for characterization of the myocardium in acute coronary syndromes. Nature Reviews Cardiology 7:11, 624-636
CrossRef93
Kerstin Boengler, Denise Hilfiker-Kleiner, Gerd Heusch, Rainer Schulz. (2010) Inhibition of permeability transition pore opening by mitochondrial STAT3 and its role in myocardial ischemia/reperfusion. Basic Research in Cardiology 105:6, 771-785
CrossRef94
Roya Naderi, Alireza Imani, Mahdieh Faghihi, Maryam Moghimian. (2010) Phenylephrine Induces Early and Late Cardioprotection Through Mitochondrial Permeability Transition Pore in the Isolated Rat Heart. Journal of Surgical Research 164:1, e37-e42
CrossRef95
J.-P. Monassier, J. Shayne, J.-M. Sommier, R. Schultz, O. Ider. (2010) Le postconditionnement au cours de l’infarctus myocardique aigu : l’angioplastie primaire revisitée ?. Annales de Cardiologie et d'Angéiologie 59:5, 294-305
CrossRef96
Lionel H. Opie, Sandrine Lecour, Harshawardhan Mardikar, Gaurang P. Deshpande. (2010) Cardiac survival strategies: an evolutionary hypothesis with rationale for metabolic therapy of acute heart failure. Transactions of the Royal Society of South Africa 65:3, 185-189
CrossRef97
Giancarlo Marenzi, Marco Giorgio, Mirella Trinei, Marco Moltrasio, Paolo Ravagnani, Daniela Cardinale, Fabio Ciceri, Annalisa Cavallero, Fabrizio Veglia, Cesare Fiorentini, Carlo M. Cipolla, Antonio L. Bartorelli, Piergiuseppe Pelicci. (2010) Circulating Cytochrome c as Potential Biomarker of Impaired Reperfusion in ST-Segment Elevation Acute Myocardial Infarction. The American Journal of Cardiology 106:10, 1443-1449
CrossRef98
D. A. Brown, B. O'Rourke. (2010) Cardiac mitochondria and arrhythmias. Cardiovascular Research 88:2, 241-249
CrossRef99
Derek J. Hausenloy, Gary Baxter, Robert Bell, Hans Erik Bøtker, Sean M. Davidson, James Downey, Gerd Heusch, Masafumi Kitakaze, Sandrine Lecour, Robert Mentzer, Mihaela M. Mocanu, Michel Ovize, Rainer Schulz, Richard Shannon, Malcolm Walker, Gail Walkinshaw, Derek M. Yellon. (2010) Translating novel strategies for cardioprotection: the Hatter Workshop Recommendations. Basic Research in Cardiology 105:6, 677-686
CrossRef100
G. Niccoli, R. K. Kharbanda, F. Crea, A. P. Banning. (2010) No-reflow: again prevention is better than treatment. European Heart Journal 31:20, 2449-2455
CrossRef101
Gordon T.C. Wong, Zhiyong Huang, Shangyi Ji, Michael G. Irwin. (2010) Remifentanil Reduces the Release of Biochemical Markers of Myocardial Damage After Coronary Artery Bypass Surgery: A Randomized Trial. Journal of Cardiothoracic and Vascular Anesthesia 24:5, 790-796
CrossRef102
Maaike Kockx, Wendy Jessup, Leonard Kritharides. (2010) Cyclosporin A and atherosclerosis — Cellular pathways in atherogenesis. Pharmacology & Therapeutics 128:1, 106-118
CrossRef103
S.-B. Ong, D. J. Hausenloy. (2010) Mitochondrial morphology and cardiovascular disease. Cardiovascular Research 88:1, 16-29
CrossRef104
M. Ruiz-Meana, C. Fernandez-Sanz, D. Garcia-Dorado. (2010) The SR-mitochondria interaction: a new player in cardiac pathophysiology. Cardiovascular Research 88:1, 30-39
CrossRef105
Peter Riis Hansen, Helene Thibault, Jawdat Abdulla. (2010) Postconditioning during primary percutaneous coronary intervention: A review and meta-analysis. International Journal of Cardiology 144:1, 22-25
CrossRef106
M. S. Haas, E. M. Alicot, F. Schuerpf, I. Chiu, J. Li, F. D. Moore, M. C. Carroll. (2010) Blockade of self-reactive IgM significantly reduces injury in a murine model of acute myocardial infarction. Cardiovascular Research 87:4, 618-627
CrossRef107
Carolyn M. Porteous, Angela Logan, Cameron Evans, Elizabeth C. Ledgerwood, David K. Menon, Franklin Aigbirhio, Robin A.J. Smith, Michael P. Murphy. (2010) Rapid uptake of lipophilic triphenylphosphonium cations by mitochondria in vivo following intravenous injection: Implications for mitochondria-specific therapies and probes. Biochimica et Biophysica Acta (BBA) - General Subjects 1800:9, 1009-1017
CrossRef108
Giampaolo Niccoli, Marcello Marino, Cristina Spaziani, Filippo Crea. (2010) Prevention and treatment of no-reflow. Acute Cardiac Care 12:3, 81-91
CrossRef109
R. H. LIE, N. STOETTRUP, E. SLOTH, J. M. HASENKAM, R. KROYER, T. T. NIELSEN. (2010) Post-conditioning with cyclosporine A fails to reduce the infarct size in an in vivo porcine model. Acta Anaesthesiologica Scandinavica 54:7, 804-813
CrossRef110
M. Ovize, G. F. Baxter, F. Di Lisa, P. Ferdinandy, D. Garcia-Dorado, D. J. Hausenloy, G. Heusch, J. Vinten-Johansen, D. M. Yellon, R. Schulz. (2010) Postconditioning and protection from reperfusion injury: where do we stand? * Position Paper from the Working Group of Cellular Biology of the Heart of the European Society of Cardiology. Cardiovascular Research 87:3, 406-423
CrossRef111
Jacob Lønborg, Marek Treiman, Thomas Engstrøm. (2010) Ischemic postconditioning: a clinical perspective. Interventional Cardiology 2:4, 579-589
CrossRef112
Aslan T. Turer, Joseph A. Hill. (2010) Pathogenesis of Myocardial Ischemia-Reperfusion Injury and Rationale for Therapy. The American Journal of Cardiology 106:3, 360-368
CrossRef113
K. Schmidt, R. Tissier, B. Ghaleh, T. Drogies, S. B. Felix, T. Krieg. (2010) Cardioprotective effects of mineralocorticoid receptor antagonists at reperfusion. European Heart Journal 31:13, 1655-1662
CrossRef114
Ronen Jaffe, Alexander Dick, Bradley H. Strauss. (2010) Prevention and Treatment of Microvascular Obstruction-Related Myocardial Injury and Coronary No-Reflow Following Percutaneous Coronary Intervention. JACC: Cardiovascular Interventions 3:7, 695-704
CrossRef115
Christian Weber. (2010) Far from the Heart: Receptor cross-talk in remote conditioning. Nature Medicine 16:7, 760-762
CrossRef116
Xiulan Yang, Michael V. Cohen, James M. Downey. (2010) Mechanism of Cardioprotection by Early Ischemic Preconditioning. Cardiovascular Drugs and Therapy 24:3, 225-234
CrossRef117
Masafumi Kitakaze. (2010) How to Mediate Cardioprotection in Ischemic Hearts—Accumulated Evidence of Basic Research Should Translate to Clinical Medicine. Cardiovascular Drugs and Therapy 24:3, 217-223
CrossRef118
Zhi-Qing Zhao. (2010) Postconditioning in Reperfusion Injury: A Status Report. Cardiovascular Drugs and Therapy 24:3, 265-279
CrossRef119
L Galiuto, L Paraggio, G Liuzzo, AR de Caterina, F Crea. (2010) Predicting the no-reflow phenomenon following successful percutaneous coronary intervention. Biomarkers in Medicine 4:3, 403-420
CrossRef120
Claudia Wagner, Diana Tillack, Gregor Simonis, Ruth H. Strasser, Christof Weinbrenner. (2010) Ischemic post-conditioning reduces infarct size of the in vivo rat heart: role of PI3-K, mTOR, GSK-3β, and apoptosis. Molecular and Cellular Biochemistry 339:1-2, 135-147
CrossRef121
Valentina Giorgio, Maria Eugenia Soriano, Emy Basso, Elena Bisetto, Giovanna Lippe, Michael A. Forte, Paolo Bernardi. (2010) Cyclophilin D in mitochondrial pathophysiology. Biochimica et Biophysica Acta (BBA) - Bioenergetics 1797:6-7, 1113-1118
CrossRef122
Peter W. Henderson, Andrew L. Weinstein, Josephine Sung, Sunil P. Singh, Vijay Nagineni, Jason A. Spector. (2010) Hydrogen Sulfide Attenuates Ischemia-Reperfusion Injury in In Vitro and In Vivo Models of Intestine Free Tissue Transfer. Plastic and Reconstructive Surgery 125:6, 1670-1678
CrossRef123
Fabrice Ivanes, Nathan Mewton, Gilles Rioufol, Christophe Piot, Meyer Elbaz, Didier Revel, Pierre Croisille, Michel Ovize. (2010) Cardioprotection in the Clinical Setting. Cardiovascular Drugs and Therapy 24:3, 281-287
CrossRef124
M. Trendelenburg, P. Theroux, A. Stebbins, C. Granger, P. Armstrong, M. Pfisterer. (2010) Influence of functional deficiency of complement mannose-binding lectin on outcome of patients with acute ST-elevation myocardial infarction undergoing primary percutaneous coronary intervention. European Heart Journal 31:10, 1181-1187
CrossRef125
Eloisa Arbustini, Jagat Narula. (2010) Cyclosporin A in Reperfusion Injury: Not Opening to Cell Death Knocking at the Door?. The Annals of Thoracic Surgery 89:5, 1349-1351
CrossRef126
Muneaki Matsubara, Mahsa Ranji, Bradley G. Leshnower, Mio Noma, Sarah J. Ratcliffe, Britton Chance, Robert C. Gorman, Joseph H. Gorman. (2010) In Vivo Fluorometric Assessment of Cyclosporine on Mitochondrial Function During Myocardial Ischemia and Reperfusion. The Annals of Thoracic Surgery 89:5, 1532-1537
CrossRef127
Jonas Hallén, Peter Petzelbauer, Jürg Schwitter, Bernard Geudelin, Peter Buser, Dan Atar. (2010) Impact of time to therapy and presence of collaterals on the efficacy of FX06 in acute ST elevation myocardial infarction: a substudy of the F.I.R.E., the Efficacy of FX06 in the prevention of myocardial reperfusion injury trial. EuroIntervention 5:8, 946-952
CrossRef128
G. Heusch, R. Schulz. (2010) Kardioprotektive Konditionierung. Der Kardiologe 4:2, 157-162
CrossRef129
Russell S. Whelan, Vladimir Kaplinskiy, Richard N. Kitsis. (2010) Cell Death in the Pathogenesis of Heart Disease: Mechanisms and Significance. Annual Review of Physiology 72:1, 19-44
CrossRef130
Martina A. McAteer, Asim M. Akhtar, Constantin von zur Muhlen, Robin P. Choudhury. (2010) An approach to molecular imaging of atherosclerosis, thrombosis, and vascular inflammation using microparticles of iron oxide. Atherosclerosis 209:1, 18-27
CrossRef131
Gerd Heusch, Kerstin Boengler, Rainer Schulz. (2010) Inhibition of mitochondrial permeability transition pore opening: the holy grail of cardioprotection. Basic Research in Cardiology 105:2, 151-154
CrossRef132
Nathaniel Reichek, Kambiz Parcham-Azad. (2010) Reperfusion Injury. Journal of the American College of Cardiology 55:12, 1206-1208
CrossRef133
Antje Hönisch, Norman Theuring, Bernd Ebner, Claudia Wagner, Ruth H. Strasser, Christof Weinbrenner. (2010) Postconditioning with levosimendan reduces the infarct size involving the PI3K pathway and KATP-channel activation but is independent of PDE-III inhibition. Basic Research in Cardiology 105:2, 155-167
CrossRef134
Nathan Mewton, Pierre Croisille, Gerald Gahide, Gilles Rioufol, Eric Bonnefoy, Ingrid Sanchez, Thien Tri Cung, Catherine Sportouch, Denis Angoulvant, Gérard Finet, Xavier André-Fouët, Geneviève Derumeaux, Christophe Piot, Hélène Vernhet, Didier Revel, Michel Ovize. (2010) Effect of Cyclosporine on Left Ventricular Remodeling After Reperfused Myocardial Infarction. Journal of the American College of Cardiology 55:12, 1200-1205
CrossRef135
Paul S. Pagel. (2010) Cardioprotection by Noble Gases. Journal of Cardiothoracic and Vascular Anesthesia 24:1, 143-163
CrossRef136
Andreas Skyschally, Rainer Schulz, Gerd Heusch. (2010) Cyclosporine A at Reperfusion Reduces Infarct Size in Pigs. Cardiovascular Drugs and Therapy 24:1, 85-87
CrossRef137
Michel Ovize, Eric Bonnefoy. (2010) Giving the ischaemic heart a shot in the arm. The Lancet 375:9716, 699-700
CrossRef138
Hans Erik Bøtker, Rajesh Kharbanda, Michael R Schmidt, Morten Bøttcher, Anne K Kaltoft, Christian J Terkelsen, Kim Munk, Niels H Andersen, Troels M Hansen, Sven Trautner, Jens Flensted Lassen, Evald Høj Christiansen, Lars R Krusell, Steen D Kristensen, Leif Thuesen, Søren S Nielsen, Michael Rehling, Henrik Toft Sørensen, Andrew N Redington, Torsten T Nielsen. (2010) Remote ischaemic conditioning before hospital admission, as a complement to angioplasty, and effect on myocardial salvage in patients with acute myocardial infarction: a randomised trial. The Lancet 375:9716, 727-734
CrossRef139
Alan R. Morrison, Albert J. Sinusas. (2010) Advances in radionuclide molecular imaging in myocardial biology. Journal of Nuclear Cardiology 17:1, 116-134
CrossRef140
W.H. Wilson Tang, Gary S. Francis. (2010) The Year in Heart Failure. Journal of the American College of Cardiology 55:7, 688-696
CrossRef141
Sylvanie Malouitre, Henry Dube, David Selwood, Martin Crompton. (2010) Mitochondrial targeting of cyclosporin A enables selective inhibition of cyclophilin-D and enhanced cytoprotection after glucose and oxygen deprivation. Biochemical Journal 425:1, 137-148
CrossRef142
Xi-Ming Yang, Yanping Liu, Yongge Liu, Narendra Tandon, Junichi Kambayashi, James M. Downey, Michael V. Cohen. (2010) Attenuation of infarction in cynomolgus monkeys: preconditioning and postconditioning. Basic Research in Cardiology 105:1, 119-128
CrossRef143
Gjin Ndrepepa, Dritan Keta, Stefanie Schulz, Robert A. Byrne, Julinda Mehilli, Jürgen Pache, Melchior Seyfarth, Albert Schömig, Adnan Kastrati. (2010) Prognostic value of minimal blood flow restoration in patients with acute myocardial infarction after reperfusion therapy. Clinical Research in Cardiology 99:1, 13-19
CrossRef144
Ilias Rentoukas, Georgios Giannopoulos, Andreas Kaoukis, Charalampos Kossyvakis, Konstantinos Raisakis, Metaxia Driva, Vasiliki Panagopoulou, Konstantinos Tsarouchas, Sofia Vavetsi, Vlasios Pyrgakis, Spyridon Deftereos. (2010) Cardioprotective Role of Remote Ischemic Periconditioning in Primary Percutaneous Coronary Intervention. JACC: Cardiovascular Interventions 3:1, 49-55
CrossRef145
Louis Maximilian Buja, Priya Weerasinghe. (2010) Unresolved issues in myocardial reperfusion injury. Cardiovascular Pathology 19:1, 29-35
CrossRef146
Anna Teresa Mazzeo, Gretchen M. Brophy, Charlotte B. Gilman, Óscar Luís Alves, Jaime R. Robles, Ronald L. Hayes, John T. Povlishock, M. Ross Bullock. (2009) Safety and Tolerability of Cyclosporin A in Severe Traumatic Brain Injury Patients: Results from a Prospective Randomized Trial. Journal of Neurotrauma 26:12, 2195-2206
CrossRef147
Stefan G De Hert, Benedikt Preckel, Markus W Hollmann, Wolfgang S Schlack. (2009) Drugs mediating myocardial protection. European Journal of Anaesthesiology 26:12, 985-995
CrossRef148
Han W. Kim, Afshin Farzaneh-Far, Raymond J. Kim. (2009) Cardiovascular Magnetic Resonance in Patients With Myocardial Infarction. Journal of the American College of Cardiology 55:1, 1-16
CrossRef149
G. Heusch. (2009) No RISK, no ... cardioprotection? A critical perspective. Cardiovascular Research 84:2, 173-175
CrossRef150
L. Lacerda, S. Somers, L. H. Opie, S. Lecour. (2009) Ischaemic postconditioning protects against reperfusion injury via the SAFE pathway. Cardiovascular Research 84:2, 201-208
CrossRef151
Antonio Rodríguez-Sinovas, Alberto Cabestrero, Bruno García del Blanco, Javier Inserte, Angeles García, David García-Dorado. (2009) Intracoronary acid infusion as an alternative to ischemic postconditioning in pigs. Basic Research in Cardiology 104:6, 761-771
CrossRef152
Hotchkiss, Richard S., Strasser, Andreas, McDunn, Jonathan E., Swanson, Paul E., . (2009) Cell Death. New England Journal of Medicine 361:16, 1570-1583
Full Text153
G. Heusch. (2009) A BEAUTIFUL lesson--ivabradine protects from ischaemia, but not from heart failure: through heart rate reduction or more?. European Heart Journal 30:19, 2300-2301
CrossRef154
Andreas Skyschally, Patrick Caster, Efstathios K. Iliodromitis, Rainer Schulz, Dimitrios T. Kremastinos, Gerd Heusch. (2009) Ischemic postconditioning: experimental models and protocol algorithms. Basic Research in Cardiology 104:5, 469-483
CrossRef155
Anna Teresa Mazzeo, Alessandri Beat, Amanpreet Singh, M. Ross Bullock. (2009) The role of mitochondrial transition pore, and its modulation, in traumatic brain injury and delayed neurodegeneration after TBI. Experimental Neurology 218:2, 363-370
CrossRef156
Saori Morota, Roland Månsson, Magnus J. Hansson, Kazuhiko Kasuya, Motohide Shimazu, Erika Hasegawa, Shigeru Yanagi, Akibumi Omi, Hiroyuki Uchino, Eskil Elmér. (2009) Evaluation of putative inhibitors of mitochondrial permeability transition for brain disorders — Specificity vs. toxicity. Experimental Neurology 218:2, 353-362
CrossRef157
K. R. Sipido, A. Tedgui, S. D. Kristensen, G. Pasterkamp, H. Schunkert, M. Wehling, P. G. Steg, W. Eisert, F. Rademakers, B. Casadei, V. Fuster, E. Cerbai, G. Hasenfuss, F. Fernandez-Aviles, D. Garcia-Dorado, M. Vidal, M. Hallen, V. Dambrauskaite. (2009) Identifying needs and opportunities for advancing translational research in cardiovascular disease. Cardiovascular Research 83:3, 425-435
CrossRef158
D. Garcia-Dorado, M. Ruiz-Meana, H. M. Piper. (2009) Lethal reperfusion injury in acute myocardial infarction: facts and unresolved issues. Cardiovascular Research 83:2, 165-168
CrossRef159
L. Gomez, B. Li, N. Mewton, I. Sanchez, C. Piot, M. Elbaz, M. Ovize. (2009) Inhibition of mitochondrial permeability transition pore opening: translation to patients. Cardiovascular Research 83:2, 226-233
CrossRef160
J. Inserte, J. A. Barrabes, V. Hernando, D. Garcia-Dorado. (2009) Orphan targets for reperfusion injury. Cardiovascular Research 83:2, 169-178
CrossRef161
K. Boengler, R. Schulz, G. Heusch. (2009) Loss of cardioprotection with ageing. Cardiovascular Research 83:2, 247-261
CrossRef162
D. B. Zorov, M. Juhaszova, Y. Yaniv, H. B. Nuss, S. Wang, S. J. Sollott. (2009) Regulation and pharmacology of the mitochondrial permeability transition pore. Cardiovascular Research 83:2, 213-225
CrossRef163
A. Granfeldt, D. J. Lefer, J. Vinten-Johansen. (2009) Protective ischaemia in patients: preconditioning and postconditioning. Cardiovascular Research 83:2, 234-246
CrossRef164
M. Kato, M. Akao, M. Matsumoto-Ida, T. Makiyama, M. Iguchi, T. Takeda, S. Shimizu, T. Kita. (2009) The targeting of cyclophilin D by RNAi as a novel cardioprotective therapy: evidence from two-photon imaging. Cardiovascular Research 83:2, 335-344
CrossRef165
Giampaolo Niccoli, Francesco Burzotta, Leonarda Galiuto, Filippo Crea. (2009) Myocardial No-Reflow in Humans. Journal of the American College of Cardiology 54:4, 281-292
CrossRef166
Sandrine Lecour. (2009) Activation of the protective Survivor Activating Factor Enhancement (SAFE) pathway against reperfusion injury: Does it go beyond the RISK pathway?. Journal of Molecular and Cellular Cardiology 47:1, 32-40
CrossRef167
Vinod Venugopal, Andrew Ludman, Derek M. Yellon, Derek J. Hausenloy. (2009) ‘Conditioning’ the heart during surgery. European Journal of Cardio-Thoracic Surgery 35:6, 977-987
CrossRef168
Stephan Achenbach, Vasken Dilsizian, Christopher M. Kramer, William A. Zoghbi. (2009) The Year in Coronary Artery Disease. JACC: Cardiovascular Imaging 2:6, 774-786
CrossRef169
Fabio Di Lisa, Paolo Bernardi. (2009) A CaPful of mechanisms regulating the mitochondrial permeability transition. Journal of Molecular and Cellular Cardiology 46:6, 775-780
CrossRef170
G. Gritsopoulos, E. K. Iliodromitis, A. Zoga, D. Farmakis, E. Demerouti, A. Papalois, I. A. Paraskevaidis, D. T. Kremastinos. (2009) Remote Postconditioning is More Potent than Classic Postconditioning in Reducing the Infarct Size in Anesthetized Rabbits. Cardiovascular Drugs and Therapy 23:3, 193-198
CrossRef171
Simon R. Dixon, Cindy L. Grines, William W. O'Neill. (2009) The Year in Interventional Cardiology. Journal of the American College of Cardiology 53:22, 2080-2097
CrossRef172
Andrew P. Halestrap. (2009) What is the mitochondrial permeability transition pore?. Journal of Molecular and Cellular Cardiology 46:6, 821-831
CrossRef173
Melanie Paillard, Ludovic Gomez, Lionel Augeul, Joseph Loufouat, Edward J. Lesnefsky, Michel Ovize. (2009) Postconditioning inhibits mPTP opening independent of oxidative phosphorylation and membrane potential. Journal of Molecular and Cellular Cardiology 46:6, 902-909
CrossRef174
Derek J. Hausenloy, Derek M. Yellon. (2009) Preconditioning and postconditioning: Underlying mechanisms and clinical application. Atherosclerosis 204:2, 334-341
CrossRef175
Christopher P. Baines. (2009) The molecular composition of the mitochondrial permeability transition pore. Journal of Molecular and Cellular Cardiology 46:6, 850-857
CrossRef176
Mirja Neizel, Marcus Katoh, Elisabeth Schade, Tienush Rassaf, Gabriele A. Krombach, Malte Kelm, Harald P. Kühl. (2009) Rapid and accurate determination of relative infarct size in humans using contrast-enhanced magnetic resonance imaging. Clinical Research in Cardiology 98:5, 319-324
CrossRef177
Sandrine Lecour. (2009) Multiple protective pathways against reperfusion injury: A SAFE path without Aktion?. Journal of Molecular and Cellular Cardiology 46:5, 607-609
CrossRef178
Karin Nowikovsky, Rudolf J. Schweyen, Paolo Bernardi. (2009) Pathophysiology of mitochondrial volume homeostasis: Potassium transport and permeability transition. Biochimica et Biophysica Acta (BBA) - Bioenergetics 1787:5, 345-350
CrossRef179
Richard Souktani, Sandrine Pons, Christelle Guegan, Omar Bouhidel, Patrick Bruneval, Roland Zini, Chantal Mandet, Brigitte Onteniente, Alain Berdeaux, Bijan Ghaleh. (2009) Cardioprotection against myocardial infarction with PTD-BIR3/RING, a XIAP mimicking protein. Journal of Molecular and Cellular Cardiology 46:5, 713-718
CrossRef180
Dwaine S Burley, Gary F Baxter. (2009) Pharmacological targets revealed by myocardial postconditioning. Current Opinion in Pharmacology 9:2, 177-188
CrossRef181
Andrew P. Halestrap. (2009) Mitochondria and reperfusion injury of the heart—A holey death but not beyond salvation. Journal of Bioenergetics and Biomembranes 41:2, 113-121
CrossRef182
Derek J. Hausenloy, Sang-Bing Ong, Derek M. Yellon. (2009) The mitochondrial permeability transition pore as a target for preconditioning and postconditioning. Basic Research in Cardiology 104:2, 189-202
CrossRef183
Christopher P. Baines. (2009) The mitochondrial permeability transition pore and ischemia-reperfusion injury. Basic Research in Cardiology 104:2, 181-188
CrossRef184
Dan Atar, Peter Petzelbauer, Jürg Schwitter, Kurt Huber, Benno Rensing, Jaroslaw D. Kasprzak, Christian Butter, Lars Grip, Peter R. Hansen, Tim Süselbeck, Peter M. Clemmensen, Marcos Marin-Galiano, Bernard Geudelin, Peter T. Buser. (2009) Effect of Intravenous FX06 as an Adjunct to Primary Percutaneous Coronary Intervention for Acute ST-Segment Elevation Myocardial Infarction. Journal of the American College of Cardiology 53:8, 720-729
CrossRef185
Marisol Ruiz-Meana, David García-Dorado. (2009) Fisiopatología del daño miocárdico por isquemia-reperfusión: nuevas oportunidades terapéuticas en el infarto agudo de miocardio. Revista Española de Cardiología 62:2, 199-209
CrossRef186
John G.T. Augoustides. (2009) The Year in Cardiothoracic and Vascular Anesthesia: Selected Highlights From 2008. Journal of Cardiothoracic and Vascular Anesthesia 23:1, 1-7
CrossRef187
José A. Barrabés, Juan Sanchís, Pedro L. Sánchez, Alfredo Bardají. (2009) Actualización en cardiopatía isquémica. Revista Española de Cardiología 62, 80-91
CrossRef188
Jong Wha Lee, Yon Hee Shim. (2009) Mitochondrial Permeability Transition Pore and Cardioprotection Against Ischemia-reperfusion Injury. Journal of the Korean Medical Association 52:10, 1007
CrossRef189
Derek J Hausenloy, Derek M Yellon. (2009) Myocardial protection: is primary PCI enough?. Nature Clinical Practice Cardiovascular Medicine 6:1, 12-13
CrossRef190
P. G. Steg, G. Ducrocq. (2008) Devices to protect against embolization during primary angioplasty for ST-segment elevation myocardial infarction: the good, the bad and the ugly. European Heart Journal 29:24, 2953-2954
CrossRef191
(2008) Limiting myocardial infarct size: a new role for cyclosporine. Nature Clinical Practice Cardiovascular Medicine 5:12, 750-751
CrossRef192
(2008) Cyclosporine in Acute Myocardial Infarction. New England Journal of Medicine 359:21, 2286-2289
Full Text193
Shey-Shing Sheu, Wang Wang, Heping Cheng, Robert T Dirksen. (2008) Superoxide flashes: illuminating new insights into cardiac ischemia and reperfusion injury. Future Cardiology 4:6, 551-554
CrossRef194
Jacyntha A. Sterling. (2008) Hospital Pharmacy Pulse - Recent Publications on Medications and Pharmacy. Hospital Pharmacy 43:10, 846-852
CrossRef195
Hausenloy, Derek J., Yellon, Derek M., . (2008) Time to Take Myocardial Reperfusion Injury Seriously. New England Journal of Medicine 359:5, 518-520
Full Text
- Letters
