Acceleration of cell necrosis following reperfusion after ischemia in the pig heart without collateral circulation

Fujiwara, Hisayoshi; Onodera, Tomoya; Tanaka, Masaru; Miyazaki, Shunichi; Wu, Dongshuang; Matsuda, Mitsuo; Kawamura, Atsushi; Ishida, Moriharu; Takemura, Genzou; Fujiwara, Yasunori; Fujiwara, Takako; Kawai, Chuichi

doi:10.1016/0002-9149(89)90224-5

Cited by 30 publications

(15 citation statements)

References 11 publications

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“…In turn, this pattern differed from that observed after reperfusion, which produced a short-term arrhythmogenic peak (reperfusion arrhythmias), but also expedited arrhythmogenic quiescence (almost concurrent with that observed after coagulation necrosis). This finding is indicative of the accelerated evolution of myocardial necrosis after reperfusion and confirms previous conclusions in the porcine heart [37].…”

Section: Insights On the Pathophysiology Of Ischemia-related Arrhythmiassupporting

confidence: 91%

Arrhythmogenesis after acute myocardial necrosis with and without preceding ischemia in rats

Kolettis¹,

Kontonika²,

Valenti³

et al. 2013

Journal of Basic and Clinical Physiology and Pharmacology

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Section: Insights On the Pathophysiology Of Ischemia-related Arrhythmiassupporting

confidence: 91%

Arrhythmogenesis after acute myocardial necrosis with and without preceding ischemia in rats

Kolettis¹,

Kontonika²,

Valenti³

et al. 2013

Journal of Basic and Clinical Physiology and Pharmacology

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“…It can be explained as a result of strong and inhomogeneous mechanical forces. In the heart in situ exposed to transient coronary occlusion the area of necrosis is composed almost exclusively of contraction band necrosis [2,3]. The extent of contraction band necrosis correlates well with the magnitude of macroscopic myocardial shrinkage during the first minutes of reperfusion, and with the magnitude of enzyme release occurring during the initial minutes of reflow [4].…”

Section: Introductionmentioning

confidence: 99%

The first minutes of reperfusion: a window of opportunity for cardioprotection

Piper

Abdallah

Schäfer

2004

Cardiovascular Research

302

219

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During the past decade, the understanding has grown that control of the conditions of reperfusion is critical for salvaging ischemic-reperfused myocardium. The first few minutes of reperfusion constitute a critical phase, as here lethal tissue injury in addition to that already developed during ischemia may be initiated. The identification of the mechanisms of reperfusion-induced cell death opens a new window of opportunity for cardioprotection in the clinic. Development of cardiomyocyte hypercontracture is a predominant feature of reperfusion injury. We and others have shown that control of hypercontracture in reperfusion reduces the extent of tissue injury. On the cellular level, it was shown that reperfusion-induced hypercontracture might either originate from a rigor-type mechanism, when energy recovery proceeds very slowly, or from Ca2+ overload, when energy recovery is rapid but cytosolic Ca2+ load is high. These two mechanisms can be influenced by various interventions that either connect with cytosolic Ca2+ control or myofibrillar Ca2+ sensitivity or with mitochondrial energy production. These experimental approaches will hopefully lead to novel strategies for clinical cardioprotection during the early phase of reperfusion.

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“…Reperfusion normally reduces the concentration of extracellular potassium by wash-out, leading to a reduction of ST-segment elevation. However, in some patients reperfusion accelerates cell necrosis of irreversibly injured myocardial cells [28]. This phenomenon is called reperfusion injury.…”

Section: Discussionmentioning

confidence: 99%

Additional ST-segment elevation during thrombolytic therapy in patients with acute ST-elevation myocardial infarction: Impact on myocardial salvage and final infarct size

Schreiber

Kittler

Herkner

et al. 2003

Wien Klin Wochenschr

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The aim of the study was to investigate the clinical significance of additional ST-segment elevation that occurs during thrombolytic therapy. Therefore, we classified 153 patients with a first acute myocardial infarction (MI) into two groups: Group A, 55 patients with additional ST-segment elevation > or = 1 mm above the initial ST elevation during thrombolytic therapy and Group B, 98 patients without this electrocardiographic pattern. Among the patients with anterior MI, Group A (n = 33) had no reduction from ST-predicted to final QRS-estimated infarct size (+12% versus -27%; p = 0.0005) and a larger final infarct size (QRS-score: 18% versus 12%; p = 0.0002) than Group B (n = 41). Among the patients with inferior MI, Group A (n = 22) had a smaller reduction from ST-predicted to final QRS-estimated infarct size (-30% versus -53%; p = 0.03) and a larger final infarct size (QRS-score: 15% versus 9%; p = 0.03) than Group B (n = 57). The area under the curve (AUC) of CK and CK-MB was higher in patients from Group A compared with those from Group B (anterior MI: AUC-CK: 22,048 versus 19,490 U.h.l-1; p = 0.07; AUC-MB: 2227 versus 2016 U.h.l-1; p = 0.11; inferior MI: AUC-CK: 17,206 versus 11,004 U.h.l-1; p = 0.01; AUC-MB: 2193 versus 1046 U.h.l-1; p = 0.007). Both global left ventricular function and ST-segment elevation resolution were significantly better in Group B. Two and three vessel disease was observed more frequently in Group A. Additional ST-segment elevation during thrombolytic therapy suggests reduced myocardial salvage by thrombolytic therapy and thus may result in larger final infarct size.

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Acceleration of cell necrosis following reperfusion after ischemia in the pig heart without collateral circulation

Cited by 30 publications

References 11 publications

Arrhythmogenesis after acute myocardial necrosis with and without preceding ischemia in rats

Arrhythmogenesis after acute myocardial necrosis with and without preceding ischemia in rats

The first minutes of reperfusion: a window of opportunity for cardioprotection

Additional ST-segment elevation during thrombolytic therapy in patients with acute ST-elevation myocardial infarction: Impact on myocardial salvage and final infarct size

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