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Myocardial Infarction Stabilization

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161. Rescue pulmonary vein isolation for hemodynamically unstable atrial fibrillation storm in a patient with an acute extensive myocardial infarction. (PubMed)

Rescue pulmonary vein isolation for hemodynamically unstable atrial fibrillation storm in a patient with an acute extensive myocardial infarction. New-onset atrial fibrillation in patients hospitalized for an acute myocardial infarction often leads to hemodynamic deterioration and has serious adverse prognostic implications; mortality is particularly high in patients with congestive heart failure and/or a reduced left ventricular ejection fraction. The mechanism of atrial fibrillation (...) in the context of an acute myocardial infarction has not been well characterized and an effective treatment other than optimal medical therapy and mechanical hemodynamic support are expected.A 71 year-old male with an acute myocardial infarction due to an occlusion of the left main coronary artery was treated with percutaneous coronary intervention. He had developed severe congestive heart failure with a left ventricular ejection fraction of 34%. The systemic circulation was maintained with an intraaortic

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2012 BMC Cardiovascular Disorders

162. Left ventricular diastolic dysfunction during acute myocardial infarction: Effect of mild hypothermia. (PubMed)

) an acute loss of end-diastolic LV compliance is a major component of acute cardiac pump failure during experimental myocardial infarction, and that (ii) MH does not potentiate this diastolic LV failure, but stabilizes haemodynamics and improves systemic oxygen supply/demand imbalance by reducing demand.Copyright © 2012 Elsevier Ireland Ltd. All rights reserved. (...) Left ventricular diastolic dysfunction during acute myocardial infarction: Effect of mild hypothermia. Mild hypothermia (MH) decreases infarct size and mortality in experimental reperfused myocardial infarction, but may potentiate ischaemia-induced left ventricular (LV) diastolic dysfunction.In anaesthetized pigs (70 ± 2 kg), polystyrol microspheres (45 μm) were infused repeatedly into the left circumflex artery until cardiac power output decreased >40%. Then, pigs were assigned to normothermia

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2012 Resuscitation

163. Safety and feasibility of hospital discharge 2 days following primary percutaneous intervention for ST-segment elevation myocardial infarction. (PubMed)

Safety and feasibility of hospital discharge 2 days following primary percutaneous intervention for ST-segment elevation myocardial infarction. Primary percutaneous coronary intervention (PPCI) produces more effective coronary reperfusion and allows immediate risk stratification compared with fibrinolysis. We investigated the safety and feasibility of very early discharge at 2 days following PPCI in selected low-risk cases.This was a prospective observational cohort study of 2779 patients who (...) ) out to a median of 2.8 years (IQR range: 1.3-4.4 years).1309 (49.3%) PPCI patients met very early discharge criteria, of whom 1117 (85.3%) were actually discharged at 2 days. 620 (23.4%) were discharged at 3 days, and 916 (34.5%) >3 days after admission (median 5, IQR: 4-8) days). Patients discharged at 2 days were younger, and had lower rates of diabetes, renal dysfunction, multivessel coronary artery disease, previous myocardial infarction, and previous coronary artery bypass surgery, compared

2012 Heart

164. Usefulness of Fractional Flow Reserve to Improve Diagnostic Efficiency in Patients With Non-ST Elevation Myocardial Infarction. (PubMed)

Usefulness of Fractional Flow Reserve to Improve Diagnostic Efficiency in Patients With Non-ST Elevation Myocardial Infarction. Myocardial fractional flow reserve (FFR) has emerging clinical utility and prognostic value in medically stabilized patients with non-ST-segment elevation myocardial infarction (NSTEMI). The aim of this study was to investigate whether measurement of FFR compared to coronary angiography alone improves diagnostic efficiency in patients with NSTEMIs. One hundred

2012 American Journal of Cardiology

165. Bio-tea prevents membrane destabilization during Isoproterenol-induced myocardial injury (PubMed)

Bio-tea prevents membrane destabilization during Isoproterenol-induced myocardial injury The present study was undertaken to determine the membrane-stabilizing effect of Bio-tea in the prevention of myocardial injury caused by isoproterenol in rats. The efficiency of Bio-tea pretreatment was compared against black tea pretreatment and the positive control (rats with isoproterenol-induced myocardial infarction) and negative control (normal control rats). For this purpose, biochemical analysis (...) of the in vivo antioxidants (superoxide dismutase, catalase, and reduced glutathione), glycoprotein components (hexose, hexosamine, sialic acid, and fucose), lipids (total, ester and free cholesterol, triglycerides, free fatty acids, and phospholipids), and transmembrane protein activities (Na+/K+ ATPase, Ca2+ ATPase, and Mg2+ ATPase) was carried out along with the histological and ultrastructural study of the myocardial tissue. Induction of myocardial infarction using isoproterenol resulted in a significant

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2016 Journal of Microscopy and Ultrastructure

166. Stress and Rest Myocardial Tomoscintigraphies Using Mono- or Double-isotope Protocol With a Semiconductor Camera

Stress and Rest Myocardial Tomoscintigraphies Using Mono- or Double-isotope Protocol With a Semiconductor Camera Stress and Rest Myocardial Tomoscintigraphies Using Mono- or Double-isotope Protocol With a Semiconductor Camera - Full Text View - ClinicalTrials.gov Hide glossary Glossary Study record managers: refer to the if submitting registration or results information. Search for terms x × Study Record Detail Saved Studies Save this study Warning You have reached the maximum number of saved (...) studies (100). Please remove one or more studies before adding more. Stress and Rest Myocardial Tomoscintigraphies Using Mono- or Double-isotope Protocol With a Semiconductor Camera (D-SPECT BIS) The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our for details. ClinicalTrials.gov Identifier: NCT02869126 Recruitment Status : Completed First Posted

2016 Clinical Trials

167. Overexpression of A kinase interacting protein 1 attenuates myocardial ischemia / reperfusion injury, but does not influence heart failure development. (PubMed)

ventricular fibrosis were also similar in AKIP1-TG mice and WT littermates. When subjected to 45 min of ischaemia followed by 24 h of reperfusion, AKIP1-TG mice displayed a significant two-fold reduction in myocardial infarct size and reductions in cardiac apoptosis. In contrast to previous reports, AKIP1 did not co-immunoprecipitate with or regulate the activity of the signalling molecules NF-κB, protein kinase A, or AKT. AKIP1 was, however, enriched in cardiac mitochondria and co-immunoprecipitated (...) with a key component of the mitochondrial permeability transition (MPT) pore, ATP synthase. Finally, mitochondria isolated from AKIP1-TG hearts displayed markedly reduced calcium-induced swelling, indicative of reduced MPT pore formation.In contrast to in vitro studies, AKIP1 overexpression does not influence cardiac remodelling in response to chronic cardiac stress. AKIP1 does, however, reduce myocardial I/R injury through stabilization of the MPT pore. These findings suggest that AKIP1 deserves further

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2016 Cardiovascular Research

168. Seabuckthorn Pulp Oil Protects against Myocardial Ischemia–Reperfusion Injury in Rats through Activation of Akt/eNOS (PubMed)

model of myocardial infarction in rats and underlying mechanism mediating activation of Akt/eNOS signaling pathway. Male albino Wistar rats were orally administered SBT pulp oil (5, 10, and 20 ml/kg/day) or saline for 30 days. On the day 31, ischemia was induced by one-stage ligation of left anterior descending coronary artery for 45 min followed by reperfusion for 60 min. SBT pulp oil pretreatment at the dose of 20 ml/kg observed to stabilize cardiac function and myocardial antioxidants (...) Seabuckthorn Pulp Oil Protects against Myocardial Ischemia–Reperfusion Injury in Rats through Activation of Akt/eNOS Seabuckthorn (SBT) pulp oil obtained from the fruits of seabuckthorn [Hippophae rhamnoides L. (Elaeagnaceae)] has been used traditionally for its medicinal and nutritional properties. However, its role in ischemia-reperfusion (IR) injury of myocardium in rats has not been elucidated so far. The present study reports the cardioprotective effect of SBT pulp oil in IR-induced

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2016 Frontiers in pharmacology

169. Importance of Suitable Reference Gene Selection for Quantitative Real-Time PCR: Special Reference to Mouse Myocardial Infarction Studies (PubMed)

Importance of Suitable Reference Gene Selection for Quantitative Real-Time PCR: Special Reference to Mouse Myocardial Infarction Studies Quantitative real-time PCR (qPCR) is a widely used technique for gene expression analysis. Its reliability is highly dependent upon selection of the appropriate reference genes for accurate gene expression normalization. In this study, we investigated the expression stability of 10 commonly used reference genes in a mouse myocardial infarction model.The (...) expression stability of the 10 reference genes (Actb, B2m, Eef1a1, Gapdh, Hprt, Polr2a, Ppia, Rpl13a, Tbp, Tpt1) was analyzed using the geNorm software. Overall, the combination of Hprt, Rpl13a and Tpt1 was the most stable reference gene set in our experiments. Gapdh, Polr2a and Actb consistently showed the highest gene expression variability and the expression levels of Gapdh, Polr2a, Actb, B2m and Eef1a1 were found to be selectively up- or downregulated after myocardial infarction. We normalized

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2011 PloS one

170. Assessment of adiponectin and the risk of recurrent cardiovascular events in patients presenting with an acute coronary syndrome: observations from the Pravastatin Or atorVastatin Evaluation and Infection Trial-Thrombolysis in Myocardial Infarction 22 (PR (PubMed)

Assessment of adiponectin and the risk of recurrent cardiovascular events in patients presenting with an acute coronary syndrome: observations from the Pravastatin Or atorVastatin Evaluation and Infection Trial-Thrombolysis in Myocardial Infarction 22 (PR Adiponectin, an adipocytokine, is secreted by fatty cells and exerts a regulatory role in atherogenesis, modulating foam cell formation and cellular adhesion. In stable atherosclerosis, plasma adiponectin has been reported to be associated (...) regression, we adjusted for age, sex, race, ACS type, diabetes, smoking status, triglycerides, blood pressure, body mass index, estimated glomerular filtration rate, treatment group (atorvastatin), B-type natriuretic peptide, and C-reactive protein.Adiponectin correlated negatively with age, diabetes, body mass index, and triglycerides (each, P < .001) but showed a positive relationship with the risk of death (P = .01), myocardial infarction (P = .01), and heart failure (P < .001). After adjusting

2011 American heart journal

171. Rapid complete reversal of systemic hypoperfusion after intra-aortic balloon pump counterpulsation and survival in cardiogenic shock complicating an acute myocardial infarction. (PubMed)

Rapid complete reversal of systemic hypoperfusion after intra-aortic balloon pump counterpulsation and survival in cardiogenic shock complicating an acute myocardial infarction. In patients with cardiogenic shock (CS) complicating an acute myocardial infarction, a strategy of early revascularization (ERV) versus initial medical stabilization (IMS) improves survival. Intra-aortic balloon counterpulsation (IABC) provides hemodynamic support and facilitates coronary angiography

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2011 American heart journal

172. Frequency and Healing of Nonculprit Coronary Artery Plaque Disruptions in Patients With Acute Myocardial Infarction. (PubMed)

Frequency and Healing of Nonculprit Coronary Artery Plaque Disruptions in Patients With Acute Myocardial Infarction. The pathophysiology of plaque disruption and healing in nonculprit segments has not been clarified. Therefore, we investigated the frequency of plaque disruptions in nonculprit segments and whether those plaques are stabilized during follow-ups in patients with acute myocardial infarction (AMI) by serial angioscopic observations. Analyzed were 13 consecutive patients with AMI (...) in whom infarct-related arteries were serially observed by angioscopy immediately after reperfusion and at 1- and 6-month follow-ups. Color of plaques was graded as 0 (white), 1 (slight yellow), 2 (yellow), or 3 (intensive yellow). Plaques with thrombus were defined as disrupted. Although number of nonculprit yellow plaques did not change from immediately after reperfusion to 6 months, the maximum color grade of those plaques and incidence of disrupted plaques in nonculprit segments (immediate vs 1

2011 American Journal of Cardiology

173. Ezetimibe In Addition To Atorvastatin Therapy On The Plaque Composition In Patients With Acute Myocardial Infarction.

Ezetimibe In Addition To Atorvastatin Therapy On The Plaque Composition In Patients With Acute Myocardial Infarction. Ezetimibe In Addition To Atorvastatin Therapy On The Plaque Composition In Patients With Acute Myocardial Infarction. - Full Text View - ClinicalTrials.gov Hide glossary Glossary Study record managers: refer to the if submitting registration or results information. Search for terms x × Study Record Detail Saved Studies Save this study Warning You have reached the maximum number (...) of saved studies (100). Please remove one or more studies before adding more. Ezetimibe In Addition To Atorvastatin Therapy On The Plaque Composition In Patients With Acute Myocardial Infarction. (OCTIVUS) The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our for details. ClinicalTrials.gov Identifier: NCT01385631 Recruitment Status : Completed First

2011 Clinical Trials

174. Intracoronary Human Wharton's Jelly- Derived Mesenchymal Stem Cells (WJ-MSCs) Transfer in Patients With Acute Myocardial Infarction (AMI)

Intracoronary Human Wharton's Jelly- Derived Mesenchymal Stem Cells (WJ-MSCs) Transfer in Patients With Acute Myocardial Infarction (AMI) Intracoronary Human Wharton's Jelly- Derived Mesenchymal Stem Cells (WJ-MSCs) Transfer in Patients With Acute Myocardial Infarction (AMI) - Full Text View - ClinicalTrials.gov Hide glossary Glossary Study record managers: refer to the if submitting registration or results information. Search for terms x × Study Record Detail Saved Studies Save this study (...) Warning You have reached the maximum number of saved studies (100). Please remove one or more studies before adding more. Intracoronary Human Wharton's Jelly- Derived Mesenchymal Stem Cells (WJ-MSCs) Transfer in Patients With Acute Myocardial Infarction (AMI) (WJ-MSC-AMI) The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our for details

2011 Clinical Trials

175. Effect of the Interleukin-6 Receptor Antagonist Tocilizumab in Non-ST Elevation Myocardial Infarction

. The investigators hypothesize that a single administration of the anti-Interleukin 6 receptor antagonist Tocilizumab, in patients with NSTEMI, may interrupt the self-perpetuating inflammatory loops which could improve plaque stability, with potential secondary beneficial effects on myocardial damage. This will be investigated in a randomized, double blind, placebo-controlled study, including a total of 120 patients. Condition or disease Intervention/treatment Phase Non-ST Elevation Myocardial Infarction Drug (...) Effect of the Interleukin-6 Receptor Antagonist Tocilizumab in Non-ST Elevation Myocardial Infarction Effect of the Interleukin-6 Receptor Antagonist Tocilizumab in Non-ST Elevation Myocardial Infarction - Full Text View - ClinicalTrials.gov Hide glossary Glossary Study record managers: refer to the if submitting registration or results information. Search for terms x × Study Record Detail Saved Studies Save this study Warning You have reached the maximum number of saved studies (100). Please

2011 Clinical Trials

176. Noninvasive Ventilation in Acute Myocardial Infarction

Inclusion Criteria: acute myocardial infarction with Killip I classification, hemodynamic stability, between 24 and 72 hours post event; agreement to participate in the study, according written informed consent; 45 to 80 years old age. Exclusion Criteria: unstable angina; systolic blood pressure < 80 mmHg; patients who presented ST elevation > 2 mm or with second-degree atrioventricular block; presence of pacemaker. Contacts and Locations Go to Information from the National Library of Medicine To learn (...) Noninvasive Ventilation in Acute Myocardial Infarction Noninvasive Ventilation in Acute Myocardial Infarction - Full Text View - ClinicalTrials.gov Hide glossary Glossary Study record managers: refer to the if submitting registration or results information. Search for terms x × Study Record Detail Saved Studies Save this study Warning You have reached the maximum number of saved studies (100). Please remove one or more studies before adding more. Noninvasive Ventilation in Acute Myocardial

2011 Clinical Trials

177. Biomaterial strategies for alleviation of myocardial infarction (PubMed)

Biomaterial strategies for alleviation of myocardial infarction World Health Organization estimated that heart failure initiated by coronary artery disease and myocardial infarction (MI) leads to 29 per cent of deaths worldwide. Heart failure is one of the leading causes of death in industrialized countries and is expected to become a global epidemic within the twenty-first century. MI, the main cause of heart failure, leads to a loss of cardiac tissue impairment of left ventricular function (...) . The damaged left ventricle undergoes progressive 'remodelling' and chamber dilation, with myocyte slippage and fibroblast proliferation. Repair of diseased myocardium with in vitro-engineered cardiac muscle patch/injectable biopolymers with cells may become a viable option for heart failure patients. These events reflect an apparent lack of effective intrinsic mechanism for myocardial repair and regeneration. Motivated by the desire to develop minimally invasive procedures, the last 10 years observed

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2011 Journal of the Royal Society Interface

178. Cardiac myosin binding protein-C is a potential diagnostic biomarker for myocardial infarction (PubMed)

Cardiac myosin binding protein-C is a potential diagnostic biomarker for myocardial infarction Cardiac myosin binding protein-C (cMyBP-C) is a thick filament assembly protein that stabilizes sarcomeric structure and regulates cardiac function; however, the profile of cMyBP-C degradation after myocardial infarction (MI) is unknown. We hypothesized that cMyBP-C is sensitive to proteolysis and is specifically increased in the bloodstream post-MI in rats and humans. Under these circumstances (...) the proteolytic pattern of cMyBP-C post-MI, the left anterior descending coronary artery was ligated in adult male rats. Degradation of cMyBP-C was confirmed by a reduction in total cMyBP-C and the presence of degradation products in the infarct tissue. Phosphorylation levels of cMyBP-C were greatly reduced in ischemic areas of the MI heart compared to non-ischemic regions and sham control hearts. Post-MI plasma samples from these rats, as well as humans, were assayed for cMyBP-C and its fragments by sandwich

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2011 Journal of Molecular and Cellular Cardiology

179. Aortic dissection with concomitant acute myocardial infarction: From diagnosis to management (PubMed)

Aortic dissection with concomitant acute myocardial infarction: From diagnosis to management Acute aortic dissection an extremely severe condition having a high risk of mortality. The classic symptom may mimic other conditions such as myocardial ischemia, leading to misdiagnosis. Coronary malperfusion associated with aortic dissection is relatively rare, but when it occurs, it may have a fatal result for the patient. The diagnosis of acute coronary syndrome may lead to the inappropriate (...) administration of thrombolytic or anticoagulant treatment resulting in catastrophic consequences. Emergency imaging techniques help to guide the correct diagnosis. Transthoracic echocardiography is useful as a first imaging test, and may be followed by transesophageal echocardiography, or other imaging techniques. Surgery represents the treatment for these patients. However, with the aim to stabilize the patient and to reduce myocardial damage, initial preoperative endovascular coronary intervention has been

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2011 Journal of Emergencies, Trauma and Shock

180. Reduction of early ventricular arrhythmia by acebutolol in patients with acute myocardial infarction. (PubMed)

of ventricular extrasystoles, acebutolol effected a prompt reduction in frequencies of ventricular extrasystoles and repetitive arrhythmias, whereas values were not significantly changed in controls during the corresponding intervals. Accordingly, acebutolol may be a useful antiarrhythmic agent in selected patients with acute myocardial infarction with adversely altering haemodynamic stability or enzymatically estimated infarct size. (...) Reduction of early ventricular arrhythmia by acebutolol in patients with acute myocardial infarction. To assess the effects of intravenously administered acebutolol (1-20 mg every 4 hours for 24 hours) on cardiac rhythm and performance, we studied 72 patients with evolving myocardial infarction. Twenty-five patients were treated with acebutolol beginning 6 hours after the first increase in the level of plasma creatine kinase. Enzymatically estimated infarct size was compared with that of 25

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1979 British Heart Journal

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