Coronary Artery Reperfusion

Maroko, Peter R.; Libby, Peter; Ginks, W. R.; Bloor, Colin M.; Shell, William E.; Sobel, Burton E.; Ross, John

doi:10.1172/jci107090

Cited by 309 publications

(23 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Although today it is unequivocally clear that timely reperfusion of an occluded coronary artery is the only way to rescue myocardium from impending infarction, this notion is a little more than 40 years old and goes back to the study by Ross and collaborators 39,40 who first reported that reperfusion after 180-minute coronary occlusion reduced infarct size in dogs. These findings were quickly translated to humans with acute myocardial infarction who were reperfused by thrombolysis or percutaneous coronary interventions (PCIs).…”

Section: Coronary Circulation As a Determinant Of Reperfusion And Repmentioning

confidence: 99%

The Coronary Circulation as a Target of Cardioprotection

Heusch

2016

Circulation Research

206

160

View full text Add to dashboard Cite

Abstract:The atherosclerotic coronary vasculature is not only the culprit but also a victim of myocardial ischemia/ reperfusion injury. Manifestations of such injury are increased vascular permeability and edema, endothelial dysfunction and impaired vasomotion, microembolization of atherothrombotic debris, stasis with intravascular cell aggregates, and finally, in its most severe form, capillary destruction with hemorrhage. In animal experiments, local and remote ischemic pre-and postconditioning not only reduce infarct size but also these manifestations of coronary vascular injury, as do drugs which recruit signal transduction steps of conditioning. Clinically, no-reflow is frequently seen after interventional reperfusion, and it carries an adverse prognosis. The translation of cardioprotective interventions to clinical practice has been difficult to date. Only 4 drugs (brain natriuretic peptide, exenatide, metoprolol, and esmolol) stand unchallenged to date in reducing infarct size in patients with reperfused acute myocardial infarction; unfortunately, for these drugs, no information on their impact on the ischemic/reperfused coronary circulation is available. (Circ Res.

show abstract

Section: Coronary Circulation As a Determinant Of Reperfusion And Repmentioning

confidence: 99%

The Coronary Circulation as a Target of Cardioprotection

Heusch

2016

Circulation Research

206

160

View full text Add to dashboard Cite

show abstract

“…The crucial importance of early reperfusion in the limitation of contractile dysfunction and irreversible ischemic damage has been clearly demonstrated [21]. Dogs submitted to reperfusion even up to 6 hours after coronary occlusion showed smaller infarct size than dogs submitted to chronic coronary occlusion [2].…”

Section: Reversible Ischemia: Patterns Of Cardiac Survivalmentioning

confidence: 99%

Pre-Emptive Conditioning of the Ischemic Heart

Vitale

Qiu²,

Depré³

2008

CHAMC

View full text Add to dashboard Cite

Ischemic heart disease remains one of the most frequent causes of morbidity and mortality worldwide. Although the prognosis of myocardial ischemia has been dramatically improved by the techniques of early reperfusion, the prevention of irreversible ischemic damage remains a critical aspect of the treatment. An appealing novel therapeutic avenue for the prevention of myocardial ischemia relates to the possibility of a pre-emptive conditioning of the heart, in which an activation of survival pathways could be achieved in patients with ischemic heart disease who are at risk for a subsequent lethal ischemia. These patients would include those with unstable angina, or with severe and repetitive ischemic episodes, and patients scheduled for surgical revascularization. In these situations, the pre-emptive activation of survival signaling mechanisms would confer a prophylactic cardioprotection during the following ischemic stress. During the last twenty years, it became clear that the heart can trigger survival mechanisms when submitted to stress, in such conditions as myocardial stunning, hibernation and preconditioning. The goal of the pre-emptive conditioning is to activate such survival pathways as a prophylactic measure to prevent myocardial cell death when the heart is threatened by potentially lethal ischemia. Based on the experimental data collected at the bench side, we review how this approach could be applied in the clinical setting.

show abstract

“…1 However, reperfusion itself can paradoxically cause additional injury; a phenomenon termed 'reperfusion injury'. 2 Reperfusion injury may cause myocardial Microvascular obstruction (MVO), which prevents sufficient myocardial tissue perfusion despite complete coronary artery revascularisation.…”

Section: Introductionmentioning

confidence: 99%

Dimethyl Sulfoxide Reduces Microvascular Obstruction and Intramyocardial Hemorrhagein a Porcine Ischemia-Reperfusion Model

Pedersen¹,

Grøndal²,

Andersen³

et al. 2015

Heart Res Open J

View full text Add to dashboard Cite

The pathophysiology of reperfusion injury is characterized by release of reactive oxygen species and inflammation. We investigated whether post-ischemic reperfusion with Dimethyl sulfoxide (DMSO), an organic solvent with therapeutic anti-inflammatory and antioxidant capabilities, could diminish or even abrogate the development of MVO and IMH in a porcine myocardial ischemia/reperfusion model. Methods and Results: Myocardial ischemia was induced in 20 pigs by balloon occlusion of the Left anterior descending artery (LAD) for 65 minutes. The pigs were allocated to one-hour reperfusion with DMSO or placebo. Eight days post-injury, IMH, MVO, left ventricular function, and myocardial salvage were assessed by Cardiovascular Magnetic Resonance (CMR) imaging; and IMH and myocardial salvage were also assessed by gross pathology. All pigs in the placebo group (100%) but only 10% of the pigs in the DMSO group had IMH. CMR imaging showed presence of MVO in all placebo-treated pigs (100%) and 88% of the DMSO-treated pig and the MVO size was 45% (p=0.03) smaller in DSMO treated pigs. No difference in myocardial salvage between the placebo and the DMSO group was found by CMR, and pathological investigation and global left ventricular function examination showed no difference between the two study groups. Conclusion: Reperfusion with a DMSO-containing solvent applied during ischemic reperfusion protected against IMH and MVO in a porcine myocardial ischemic/reperfusion model.

show abstract

Coronary Artery Reperfusion

Abstract: A B S T R A C T The effects

Cited by 309 publications

References 22 publications

The Coronary Circulation as a Target of Cardioprotection

The Coronary Circulation as a Target of Cardioprotection

Pre-Emptive Conditioning of the Ischemic Heart

Dimethyl Sulfoxide Reduces Microvascular Obstruction and Intramyocardial Hemorrhagein a Porcine Ischemia-Reperfusion Model

Contact Info

Product

Resources

About