関: myocardial hibernation、stunned myocardium

WordNet

strikingly beautiful or attractive; "quite stunning with large dark eyes and a beautiful high-bosomed figure"; "stunning photographs of Canadas wilderness areas"
causing great astonishment and consternation; "the strike came as a stunning protest against management"; "a stunning defeat"
causing or capable of causing bewilderment or shock or insensibility; "laid the poor fellow senseless with one stunning blow"; "a stunning detonation with volumes of black smoke"
of or relating to the myocardium

PrepTutorEJDIC

気絶させるような / すごくすてきな,すばらしく美しい

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2013/05/02 15:00:16」(JST)

wiki en

In cardiology, stunned myocardium is a state when some section of the myocardium (corresponding to area of a major coronary occlusion) shows a form of contractile abnormality. This is a segmental dysfunction which persists for a variable period of time, about two weeks, even after ischemia has been relieved (by for instance angioplasty or coronary artery bypass surgery). In this situation, while myocardial blood flow (MBF) returns to normal, function is still depressed for a variable period of time.

Myocardial stunning is the reversible reduction of function of heart contraction^[1] after reperfusion not accounted for by tissue damage or reduced blood flow.^[2]

After total ischemia occurs, the myocardium switches immediately form aerobic glycolysis to anaerobic glycolysis resulting in the reduced ability to produce high energy phosphates such as ATP and Creatinine Phosphate. At this point, the lack of the energy and lactate accumulation results in cessation of contraction within 60 seconds of ischemia (i.e. Vessel Occlusion). Subsequent to this is a period of "myocardial stunning," in which reversible ischemic damage is taking place. At approximately 30 minutes after the onset of total ischemia the damage becomes irreversible, thereby ending the phase of myocardial stunning.

Clinical situations of stunned myocardium are:

acute myocardial infarction (AMI)
after percutaneous transluminal coronary angioplasty (PTCA)
after cardiac surgery
'neurogenic' stunned myocardium following an acute cerebrovascular event such as a subarachnoid hemorrhage

References

^ Myocardial Stunning at the US National Library of Medicine Medical Subject Headings (MeSH)
^ Grund F (February 2001). "[Three cardiac mysteries--stunning, hibernation and ischemic preconditioning]". Tidsskr. Nor. Laegeforen. (in Norwegian) 121 (4): 440–4. PMID 11255859.

External links

"Myocardial “stunning” in man"
Baker C, Rimoldi O, Camici P, Barnes E, Chacon M, Huehns T, Haskard D, Polak J, Hall R (1999). "Repetitive myocardial stunning in pigs is associated with the increased expression of inducible and constitutive nitric oxide synthases.". Cardiovasc Res 43 (3): 685–97. doi:10.1016/S0008-6363(99)00149-2. PMID 10690340.
Wittstein IS, Thiemann DR, Lima JA et al. (February 2005). "Neurohumoral features of myocardial stunning due to sudden emotional stress". N. Engl. J. Med. 352 (6): 539–48. doi:10.1056/NEJMoa043046. PMID 15703419.

This article about a disease, disorder, or medical condition is a stub. You can help Wikipedia by expanding it.

UpToDate Contents

全文を閲覧するには購読必要です。 To read the full text you will need to subscribe.

1. 気絶心筋または冬眠心筋の臨床的症候群 clinical syndromes of stunned or hibernating myocardium
2. 気絶心筋または冬眠心筋の病態生理 pathophysiology of stunned or hibernating myocardium
3. 心臓の虚血性再潅流障害 ischemic reperfusion injury of the heart
4. 冬眠心筋の評価 evaluation of hibernating myocardium
5. ストレス誘発性（たこつぼ型）心筋症 stress induced takotsubo cardiomyopathy

English Journal

Ischaemic memory imaging using metabolic radiopharmaceuticals: overview of clinical settings and ongoing investigations.

Yoshinaga K, Naya M, Shiga T, Suzuki E, Tamaki N.Author information Department of Molecular Imaging, Hokkaido University Graduate School of Medicine, Sapporo, Japan.Abstract"Ischaemic memory" is defined as a prolonged functional and/or biochemical alteration remaining after a particular episode of severe myocardial ischaemia. The biochemical alteration has been reported as metabolic stunning. Metabolic imaging has been used to detect the footprint left by previous ischaemic episodes evident due to delayed recovery of myocardial metabolism (persistent dominant glucose utilization with suppression of fatty acid oxidation). β-Methyl-p-[(123)I]iodophenylpentadecanoic acid (BMIPP) is a single-photon emission computed tomography (SPECT) radiotracer widely used for metabolic imaging in clinical settings in Japan. In patients with suspected coronary artery disease but no previous myocardial infarction, BMIPP has shown acceptable diagnostic accuracy. In particular, BMIPP plays an important role in the identification of prior ischaemic insult in patients arriving at emergency departments with acute chest pain syndrome. Recent data also show the usefulness of (123)I-BMIPP SPECT for predicting cardiovascular events in patients undergoing haemodialysis. Similarly, SPECT or PET imaging with (18)F-FDG injected during peak exercise or after exercise under fasting conditions shows an increase in FDG uptake in postischaemic areas. This article will overview the roles of ischaemic memory imaging both under established indications and in ongoing investigations.
European journal of nuclear medicine and molecular imaging.Eur J Nucl Med Mol Imaging.2014 Feb;41(2):384-93. doi: 10.1007/s00259-013-2615-4. Epub 2013 Nov 12.
"Ischaemic memory" is defined as a prolonged functional and/or biochemical alteration remaining after a particular episode of severe myocardial ischaemia. The biochemical alteration has been reported as metabolic stunning. Metabolic imaging has been used to detect the footprint left by previous isch
PMID 24218099

Exercise-induced improvements in myocardial antioxidant capacity: the antioxidant players and cardioprotection.

Powers SK, Sollanek KJ, Wiggs MP, Demirel HA, Smuder AJ.Author information Department of Applied Physiology and Kinesiology, University of Florida , Gainesville, FL , USA.AbstractAbstract Endurance exercise training is known to promote beneficial adaptations to numerous tissues including the heart. Indeed, endurance exercise training results in a cardioprotective phenotype that resists injury during an ischemia-reperfusion (IR) insult. Because IR-induced cardiac injury is due, in part, to increased production of radicals and other reactive oxygen species, many studies have explored the impact of exercise training on myocardial antioxidant capacity. Unfortunately, the literature describing the effects of exercise on the cardiac antioxidant capacity is widely inconsistent. Nonetheless, a growing body of evidence indicates that regular bouts of endurance exercise promote an increase in the expression of both superoxide dismutase 1 and 2 in cardiac mitochondria. Moreover, emerging evidence suggests that exercise also increases accessory antioxidant enzymes in the heart. Importantly, robust evidence indicates that as few as five consecutive days of endurance exercise training results in a cardiac phenotype that resists IR-induced arrhythmias, myocardial stunning, and infarction. Further, mechanistic studies indicate that exercise-induced increases in mitochondrial superoxide dismutase 2 play a key role in this adaptation. Future studies are required to provide a complete picture regarding the cellular adaptations that are responsible for exercise-induced cardioprotection.
Free radical research.Free Radic Res.2014 Jan;48(1):43-51. doi: 10.3109/10715762.2013.825371. Epub 2013 Oct 7.
Abstract Endurance exercise training is known to promote beneficial adaptations to numerous tissues including the heart. Indeed, endurance exercise training results in a cardioprotective phenotype that resists injury during an ischemia-reperfusion (IR) insult. Because IR-induced cardiac injury is du
PMID 23915097

Upregulation of genes involved in cardiac metabolism enhances myocardial resistance to ischemia/reperfusion in the rat heart.

Ravingerová T, Carnická S, Ledvényiová V, Barlaka E, Galatou E, Chytilová A, Mandíková P, Nemčeková M, Adameová A, Kolář F, Lazou A.Author information Institute for Heart Research, Slovak Academy of Sciences, Bratislava, Slovak Republic. usrdravi@savba.sk.AbstractGenes encoding enzymes involved in fatty acids (FA) and glucose oxidation are transcriptionally regulated by peroxisome proliferator-activated receptors (PPAR), members of the nuclear receptor superfamily. Under conditions associated with O(2) deficiency, PPAR-alpha modulates substrate switch (between FA and glucose) aimed at the adequate energy production to maintain basic cardiac function. Both, positive and negative effects of PPAR-alpha activation on myocardial ischemia/reperfusion (I/R) injury have been reported. Moreover, the role of PPAR-mediated metabolic shifts in cardioprotective mechanisms of preconditioning (PC) is relatively less investigated. We explored the effects of PPAR-alpha upregulation mimicking a delayed "second window" of PC on I/R injury in the rat heart and potential downstream mechanisms involved. Pretreatment of rats with PPAR-alpha agonist WY-14643 (WY, 1 mg/kg, i.p.) 24 h prior to I/R reduced post-ischemic stunning, arrhythmias and the extent of lethal injury (infarct size) and apoptosis (caspase-3 expression) in isolated hearts exposed to 30-min global ischemia and 2-h reperfusion. Protection was associated with remarkably increased expression of PPAR-alpha target genes promoting FA utilization (medium-chain acyl-CoA dehydrogenase, pyruvate dehydrogenase kinase-4 and carnitine palmitoyltransferase I) and reduced expression of glucose transporter GLUT-4 responsible for glucose transport and metabolism. In addition, enhanced Akt phosphorylation and protein levels of eNOS, in conjunction with blunting of cardioprotection by NOS inhibitor L-NAME, were observed in the WY-treated hearts. Conclusions: upregulation of PPAR-alpha target metabolic genes involved in FA oxidation may underlie a delayed phase PC-like protection in the rat heart. Potential non-genomic effects of PPAR-alpha-mediated cardioprotection may involve activation of prosurvival PI3K/Akt pathway and its downstream targets such as eNOS and subsequently reduced apoptosis.
Physiological research / Academia Scientiarum Bohemoslovaca.Physiol Res.2013 Dec 12;62 Suppl 1:S151-63.
Genes encoding enzymes involved in fatty acids (FA) and glucose oxidation are transcriptionally regulated by peroxisome proliferator-activated receptors (PPAR), members of the nuclear receptor superfamily. Under conditions associated with O(2) deficiency, PPAR-alpha modulates substrate switch (betwe
PMID 24329695

Japanese Journal

Comparative Effects of Azelnidipine and Amlodipine on Myocardial Function and Mortality After Ischemia/Reperfusion in Dogs

Kano Seiichiro,Ichihara Kazuo,Komatsu Ken-ichi,Satoh Kumi
Journal of Pharmacological Sciences 116(2), 181-187, 2011
… In conclusion, improvement in myocardial stunning after pretreatment with azelnidipine is associated with an increase in CF after reperfusion. …
NAID 130000835862

Postischemic infusion of sivelestat sodium hydrate, a selective neutrophil elastase inhibitor, protects against myocardial stunning in swine.

AKIYAMA Daiji,HARA Tetsuya,YOSHITOMI Osamu,MAEKAWA Takuji,CHO Sungsam,SUMIKAWA Koji
Journal of anesthesia 24(4), 575-581, 2010-08-20
… PURPOSE: It seems controversial whether or not neutrophil elastase inhibitors are effective in attenuating myocardial ischemia/reperfusion injury. … We thus investigated possible protective effects of sivelestat, a neutrophil elastase inhibitor, against myocardial stunning i.e., prolonged myocardial dysfunction following a brief episode of ischemia. …
NAID 10026632664