Evidence for stunned myocardium in humans: a 2001 update

Kloner, Robert A.; Arimie, Raluca; Kay, Gregory L.; Cannom, David S.; Matthews, Ray V.; Bhandari, Anil K.; Shook, Thomas; Pollick, Charles; Burstein, Steven

doi:10.1097/00019501-200108000-00003

Cited by 48 publications

(43 citation statements)

References 67 publications

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“…Stunning is an important causative factor in the development of ischemic cardiomyopathy, where repeated episodes of myocardial ischemia and reperfusion might lead to the development of heart failure. 14,15) Reperfusion of the ischemic heart might result in ROS generation 2) and could be associated with myocardial "stunning" after reversible I/R injury. 16,17) Mitochondrial DNA damage is induced by ROS, which leads to the generation of more ROS, 18) and perhaps a burst of ROS production.…”

Section: Discussionmentioning

confidence: 99%

Determination of Oxidative Stress and Cardiac Dysfunction after Ischemia/Reperfusion Injury in Isolated Rat Hearts

Ichikawa

Kuniyoshi

Yamashiro

et al. 2013

Ann Thorac Cardiovasc Surg

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Background: Oxidative stress due to reactive oxygen species (ROS) is thought to play a considerable role in ischemia/reperfusion (I/R) injury that impairs cardiac function. The present study examined oxidative damage in I/R injury and investigated the correlation between oxidative stress and impaired cardiac function after I/R injury of the isolated rat heart. Methods: Hearts isolated from male Sprague-Dawley rats were mounted on a Langendorff apparatus. Hearts arrested using St. Thomas cardioplegic solution and then they were reperfused. The hearts were divided into three groups depending on the frequency (0-2) of I/R. After I/R, left ventricular developed pressure (LVDP), left ventricular end-diastolic pressure (LVEDP), positive maximum left ventricular developing pressure (max LV dP/dt) and coronary flow (CF) were measured. Creatine kinase (CK) was measured in the coronary effluent and 8-hydroxy-2'deoxyguanosine (8OHdG), a marker of oxidative DNA damage, was measured. Adenosine triphosphate (ATP) was measured from frozen myocardial tissue after experiment. Results: We immunohistochemically demonstrated and quantified levels of 8-OHdG after I/ R injury of the heart. The frequency of I/R injury and cardiac dysfunction significantly and negatively correlated. The ATP products were similar among the three groups. The incidence of ventricular arrhythmias was not by affected oxidative stress. Conclusion: The frequency of I/R injury had more of an effect on 8-OHdG products and on impaired cardiac function with less myocyte damage than ischemic duration within 30 minutes of ischemia.Keywords: oxidative stress, ischemia/reperfusion injury, 8-hydroxy-2'deoxyguanosine (8OHdG), cardiac dysfunction tion might cause negative effects and a worse prognosis, with myocardial dysfunction (stunning) and coronary noreflow phenomenon. 1) Reactive oxygen species (ROS), which can be produced from reperfusion of the ischemic myocardium 2) and Ca 2 + overload in myocytes, contribute to cardiac ischemia/reperfusion (I/R) injury. 3)Reactive oxygen species cause the oxidation of DNAs, membranous phospholipids and proteins, and these are implicated in the pathogenesis of I/R injury, degenerative disease, carcinogenesis and aging. In particular, ROS have the potential to injure cardiac myocytes, endothelial cells and initiate chemical reactions in myocardial I/R injury.

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Section: Discussionmentioning

confidence: 99%

Determination of Oxidative Stress and Cardiac Dysfunction after Ischemia/Reperfusion Injury in Isolated Rat Hearts

Ichikawa

Kuniyoshi

Yamashiro

et al. 2013

Ann Thorac Cardiovasc Surg

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“…Thus, one can argue that the myocardial stunning (caused by an ischemic episode) and TS may be the same disease entity. Before the era of TS, almost all left ventricular dysfunction induced by noncardiac physical stressors, which currently are classified under TS, were described as myocardial stunning [10,20,21]. Interestingly, Dote et al [21] who labeled the moniker ‘Takotsubo’ in the beginning of the 1990s, also described their first 5 patients with TS as myocardial stunning due to multivessel coronary spasm.…”

Section: Discussionmentioning

confidence: 99%

Bromocriptine-Induced Coronary Spasm Caused Acute Coronary Syndrome, Which Triggered Its Own Clinical Twin – Takotsubo Syndrome

Y‐Hassan

Jernberg²

2011

Cardiology

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Bromocriptine-induced coronary spasm (BICS) causing myocardial infarction has been reported. Association between BICS and Takotsubo syndrome (TS) has not been described. We report on a 37-year-old woman presenting with a clinical picture of acute coronary syndrome 1 day after initiation of treatment with bromocriptine for ablactation 3 weeks after a full-term spontaneous vaginal delivery. Coronary angiography showed diffuse narrowing of a large diagonal branch. Left ventriculography showed widespread hypokinesia extending beyond the diagonal branch supply region. There was a slight elevation of myocardial infarction biomarkers that was disproportional to the degree of left ventricular dysfunction. Follow-up coronary angiography, intravascular ultrasound and left ventriculography showed normal coronary arteries including the diagonal branch and complete normalization of the left ventricular function. Cardiac magnetic resonance examination showed no signs of late myocardial gadolinium enhancement. The clinical picture and course of the disease was consistent with TS. Consequently, we describe for the first time a case of TS triggered by myocardial ischemia caused by BICS. Furthermore, our case and sufficient supporting data from the literature demonstrate that acute coronary syndrome is an important and frequent but up till now missed trigger factor for TS.

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“…29 Miyokardiyal sersemleme, İ/R'ye bağlı geri dönüşümsüz zedelenme olmamasına ve reperfüzyonun tüm veya tüme yakın bir biçimde sürmesine karşın, kalpte oluşan uzamış mekanik işlev bozukluğudur ve genellikle global iskemik ataklardan sonra gözlenir. 30 Ancak, kısa sü-reli iskemiyi izleyen dönemlerde bile miyokardiyal sersemleme beklenmedik derecede uzun sürebilir. Örneğin; köpek kalbinde oluşturulan 15 dakikalık iskeminin, 24 saatlik miyokardiyal sersemlemeye yol açtığı gözlenmiştir.…”

Section: Mi̇yokardi̇yal İskemi̇/reperfüzyon Zedelenmesi̇unclassified

Myocardial and Renal Ischemia/Reperfusion Injury and Experimental Models: Review

Şenol¹,

Tunçtan²

2016

Turkiye Klinikleri J Pharm Sci

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Ö ÖZ ZE ET T Doku iskemisi, miyokard infarktüsü ve inme gibi klinik durumlarda ya da damar cerrahisi ve organ transplantasyonunda komplikasyon olarak ortaya çıkabilen bir durumdur. Reperfüzyon, iskemiye maruz kalan dokunun yeniden kanlanarak oksijenlenmesidir. İskemi/reperfüzyon (İ/R) zedelenmesi, kan akışının yeniden düzenlenmesiyle gelişen inflamatuar tepkilerin bir sonucudur. Erken evrede glikoliz yoluyla laktat üretimi sonucu hücre içi pH değeri düşer. Hücreleri nekroza karşı koruyan bu düşüş, reperfüzyon sıra-sında normal pH değerine yükseldiğinde iskemik hücrelerin ölümünü hızlandırır. Orta evre ise oksidatif stres ile belirgindir. Oksidatif stres belli bir eşiği aşarsa hücresel işlev bozukluğu, geri döndürülemez zedelenme ve hücre ölümü gerçekleşir. Geç evrede, inflamatuar hücreler ve adezyon molekülleri baskındır. Birçok inflamatuar molekül tarafından uyarılan nötrofil etkinliği İ/R süreci boyunca görülür. Miyokardiyal İ/R zedelenmesi miyokardiyal sersemleme (stunning), reperfüzyon aritmileri, miyositlerde nekroz ile koroner endotelyal ve mikrovasküler işlev bozukluğu gibi istenmeyen durumların ortaya çıkmasına yol açabilir. Deneysel olarak çalışılan konular miyokardiyal sersemleme, hibernasyon, reperfüzyon aritmileri ve ön koşul-lamadır. Akut renal yetmezlik (ARY) insanlarda yüksek mortalite ile ilişkili majör bir böbrek hastalığıdır. Kalp debisinin azalması, renal vasküler oklüzyon veya obstrüksiyon ile renal transplantasyon gibi durumların neden olduğu iskemi, ARY gelişmesine neden olabilir. Deneysel olarak çift taraflı (bilateral) ve tek taraflı (unilateral) renal İ/R zedelenmesi oluşturulabilmektedir. Çift taraflı iskemik ARY modeli insandaki patolojik duruma çok daha uygun olmasından dolayı yaygın olarak kullanılmaktadır. Bu çalışmada, ilaçla-rın miyokardiyal veya renal İ/R zedelenmesine bağlı olarak gelişen fizyopatolojik değişiklikler üzerindeki etkilerinin araştırılması amacıyla kullanılan deneysel modeller üzerinde durulmuştur.A An na ah h t ta ar r K Ke e l li i m me e l le er r: : İskemi; reperfüzyon hasarı; oksidatif stres; inflamasyon; miyokardiyal reperfüzyon hasarı; akut böbrek hasarı A AB BS S T TR RA AC CT T Tissue ischemia is a condition that can occur with clinical conditions like myocardial infarction and stroke or as a complication of vascular surgery and organ transplantation. Reperfusion is reoxygenation of tissue exposed to ischemia by restoration of blood flow. Ischemia/reperfusion (I/R) injury is a consequence of inflammatory reaction induced by modulating blood flow. Intracellular pH falls as a result of lactate production through glycolysis at early stage. The decrease protecting cells against necrosis accelerates ischemic cell death at normal pH value during reperfusion. Intermediate phase is characterized by oxidative stress. If oxidative stress exceeds a certain threshold, cellular dysfunction, irreversible injury, and cell death occurs. At the late stage, inflammatory cells and adhesion molecules are dominant. Neutrophil activity stimulated by many inflammatory molecules ...

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Evidence for stunned myocardium in humans: a 2001 update

Cited by 48 publications

References 67 publications

Determination of Oxidative Stress and Cardiac Dysfunction after Ischemia/Reperfusion Injury in Isolated Rat Hearts

Determination of Oxidative Stress and Cardiac Dysfunction after Ischemia/Reperfusion Injury in Isolated Rat Hearts

Bromocriptine-Induced Coronary Spasm Caused Acute Coronary Syndrome, Which Triggered Its Own Clinical Twin – Takotsubo Syndrome

Myocardial and Renal Ischemia/Reperfusion Injury and Experimental Models: Review

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