Infarct size reduction in acute myocardial infarction

McAlindon, Elisa; Bucciarelli-Ducci, Chiara; Suleiman, M‐Saadeh; Baumbach, Andreas

doi:10.1136/heartjnl-2013-304289

Cited by 26 publications

(21 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…All enrolled subjects were also treated with PCI using distal protection device. Medications, such as GIIb/IIIa inhibitor, adenosine, and nitric oxide donors, were also demonstrated as determinants of myocardial infarction size 32 ) . There were no impacts of medication on myocardial infarction size in the present study, partly because all participants received ACE inhibitors, β -blockers, statins, and nicorandil after PCI.…”

Section: Discussionmentioning

confidence: 99%

Significant Association of Serum Adiponectin and Creatine Kinase-MB Levels in ST-Segment Elevation Myocardial Infarction

Natsukawa

Maeda

Fukuda

et al. 2017

J Atheroscler Thromb

View full text Add to dashboard Cite

Aims: Adiponectin, an adipocyte-specific secretory protein, abundantly exists in the blood stream while its concentration paradoxically decreases in obesity. Hypoadiponectinemia is one of risks of cardiovascular diseases. However, impact of serum adiponectin concentration on acute ischemic myocardial damages has not been fully clarified. The present study investigated the association of serum adiponectin and creatine kinase (CK)-MB levels in subjects with ST-segment elevation myocardial infarction (STEMI).Methods: This study is a physician-initiated observational study and is also registered with the University Hospital Medical Information Network (Number: UMIN 000014418). Patients were admitted to Senri Critical Care Medical Center, given a diagnosis of STEMI, and treated by primary percutaneous coronary intervention (PCI). Finally, 49 patients were enrolled and the association of serum adiponectin, CK-MB, and clinical features were mainly analyzed.Results: Serum adiponectin levels decreased rapidly and reached the bottom at 24 hours after recanalization. Such reduction of serum adiponectin was inversely correlated with the area under the curve (AUC) of serum CK-MB (p = 0.013). Serum adiponectin concentrations were inversely correlated with AUC of serum CK-MB. In multivariate analysis, serum adiponectin concentration on admission (p = 0.002) and collateral (p = 0.037) were significantly and independently correlated with serum AUC of CK-MB.Conclusion: Serum AUC of CK-MB in STEMI subjects was significantly associated with serum adiponectin concentration on admission and reduction of serum adiponectin levels from baseline to bottom. The present study may provide a possibility that serum adiponectin levels at acute phase are useful in the prediction for prognosis after PCI-treated STEMI subjects.

show abstract

Section: Discussionmentioning

confidence: 99%

Significant Association of Serum Adiponectin and Creatine Kinase-MB Levels in ST-Segment Elevation Myocardial Infarction

Natsukawa

Maeda

Fukuda

et al. 2017

J Atheroscler Thromb

View full text Add to dashboard Cite

show abstract

“…While current therapies improve survival from the initial myocardial infarction (Simoons et al, 1986;Hollenbeck et al, 2014), many patients ultimately develop heart failure (Liang & Delehanty, 2009), which poses great financial burden on the healthcare system (Braunwald, 2013) and significantly diminishes quality of life. It is believed that the extent of cardiac tissue damage is correlated with the development of heart failure (Foo et al, 2005;McAlindon et al, 2015); however, no clinically available therapy directly targets cardiomyocytes in order to reduce damage after ischemia/reperfusion (I/R) injury. Therefore, the development of novel therapies targeting cardiomyocyte death is essential.…”

Section: Introductionmentioning

confidence: 99%

Reduction in mitochondrial iron alleviates cardiac damage during injury

et al. 2016

View full text Add to dashboard Cite

Excess cellular iron increases reactive oxygen species (ROS) production and causes cellular damage. Mitochondria are the major site of iron metabolism and ROS production; however, few studies have investigated the role of mitochondrial iron in the development of cardiac disorders, such as ischemic heart disease or cardiomyopathy (CM). We observe increased mitochondrial iron in mice after ischemia/reperfusion (I/R) and in human hearts with ischemic CM, and hypothesize that decreasing mitochondrial iron protects against I/R damage and the development of CM. Reducing mitochondrial iron genetically through cardiac-specific overexpression of a mitochondrial iron export protein or pharmacologically using a mitochondria-permeable iron chelator protects mice against I/R injury. Furthermore, decreasing mitochondrial iron protects the murine hearts in a model of spontaneous CM with mitochondrial iron accumulation. Reduced mitochondrial ROS that is independent of alterations in the electron transport chain's ROS producing capacity contributes to the protective effects. Overall, our findings suggest that mitochondrial iron contributes to cardiac ischemic damage, and may be a novel therapeutic target against ischemic heart disease.

show abstract

“…Irreversible myocardial damage after AMI is divided into ischemic and reperfusion injury, but they share some mechanisms and sometimes hard to clearly separate two components. 29 Of course, longer duration of coronary artery occlusion (CAO) leads to larger infarct size, and therefore, early reperfusion improves prognosis by reducing infarct size and morality. 30 31 32 Current guidelines strongly recommends within 90 minutes coronary angioplasty as timely reperfusion for ST elevation AMI.…”

Section: Rationale For Mild Hypothermiamentioning

confidence: 99%

Therapeutic Hypothermia for Cardioprotection in Acute Myocardial Infarction

2016

View full text Add to dashboard Cite

Mild therapeutic hypothermia of 32–35℃ improved neurologic outcomes in outside hospital cardiac arrest survivor. Furthermore, in experimental studies on infarcted model and pilot studies on conscious patients with acute myocardial infarction, therapeutic hypothermia successfully reduced infarct size and microvascular resistance. Therefore, mild therapeutic hypothermia has received an attention as a promising solution for reduction of infarction size after acute myocardial infarction which are not completely solved despite of optimal reperfusion therapy. Nevertheless, the results from randomized clinical trials failed to prove the cardioprotective effects of therapeutic hypothermia or showed beneficial effects only in limited subgroups. In this article, we reviewed rationale for therapeutic hypothermia and possible mechanisms from previous studies, effective methods for clinical application to the patients with acute myocardial infarction, lessons from current clinical trials and future directions.

show abstract

Infarct size reduction in acute myocardial infarction

Cited by 26 publications

References 20 publications

Significant Association of Serum Adiponectin and Creatine Kinase-MB Levels in ST-Segment Elevation Myocardial Infarction

Significant Association of Serum Adiponectin and Creatine Kinase-MB Levels in ST-Segment Elevation Myocardial Infarction

Reduction in mitochondrial iron alleviates cardiac damage during injury

Therapeutic Hypothermia for Cardioprotection in Acute Myocardial Infarction

Contact Info

Product

Resources

About