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Myocardial Infarction Stabilization

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61. Changes of coronary plaque composition correlate with C-reactive protein levels in patients with ST-elevation myocardial infarction following high-intensity statin therapy. (PubMed)

Changes of coronary plaque composition correlate with C-reactive protein levels in patients with ST-elevation myocardial infarction following high-intensity statin therapy. Levels of inflammatory biomarkers associate with changes of coronary atheroma burden in statin-treated patients with stable coronary artery disease. This study sought to determine changes of plaque composition in vivo in relation to high-sensitivity C-reactive protein (hs-CRP) levels in patients with ST-elevation myocardial (...) infarction (STEMI) receiving high-intensity statin therapy.The IBIS-4 study performed serial (baseline and 13-month), 2-vessel intravascular ultrasound (IVUS) and radiofrequency-IVUS of the non-infarct-related arteries in patients with STEMI treated with high-intensity statin therapy. The present analysis included 44 patients (80 arteries) with serial measurements of hs-CRP.At follow-up, median low-density lipoprotein cholesterol (LDL-C) levels decreased from 126 to 77 mg/dl, HDL-C increased from 44

2016 Atherosclerosis

62. Intraprocedural left ventricular free wall rupture diagnosed by left ventriculogram in a patient with infero-posterior myocardial infarction and severe aortic stenosis. (PubMed)

Intraprocedural left ventricular free wall rupture diagnosed by left ventriculogram in a patient with infero-posterior myocardial infarction and severe aortic stenosis. Left ventricular wall rupture remains a major lethal complication of acute myocardial infarction and hypertension is a well-known predisposing factor of cardiac rupture after myocardial infarction.An 87-year-old man was admitted to our hospital, diagnosed as acute myocardial infarction (AMI). The echocardiogram showed 0.67-cm(2 (...) AS, the administration of catecholamine to stabilize the blood pressure probably increased the intraventricular pressures considerably despite apparently normal measurements of the central aortic pressure. IABP, temporary pacemaker, or both are recommended instead of intravenous catecholamines for patients with AMI complicated with significant AS to stabilize hemodynamic function during angioplasty.

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2016 BMC Cardiovascular Disorders

63. Ventricular septal rupture complicating acute myocardial infarction in the modern era with mechanical circulatory support: a single center observational study (PubMed)

Ventricular septal rupture complicating acute myocardial infarction in the modern era with mechanical circulatory support: a single center observational study Ventricular septal rupture (VSR) is a rare but devastating complication after acute myocardial infarction (AMI). While the incidence has decreased, the mortality rate from VSR has remained extremely high. The use of mechanical circulatory support with intra-aortic balloon pump (IABP) and extracorporal membrane oxygenation (ECMO) may (...) be useful in providing hemodynamic stability and time for myocardial scarring. However, the optimal timing for surgical repair remains an enigma. Retrospective analysis of 14 consecutive patients diagnosed with VSR after AMI at Montefiore Medical Center between January 2009 and June 2015. A chart review was performed with analysis of baseline characteristics, hemodynamics, imaging, percutaneous interventions, surgical timing, and outcomes. The survival group had a higher systolic BP (145 vs 98, p<0.01

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2016 American journal of cardiovascular disease

64. Paraganglioma masquerading as acute myocardial infarction and cardiogenic shock (PubMed)

Paraganglioma masquerading as acute myocardial infarction and cardiogenic shock Paragangliomas, extra-adrenal pheochromocytomas, are rare catecholamine-secreting tumor. A 34-year-old lady admitted with diagnosis of ST elevation acute myocardial infarction with cardiogenic shock. Left ventricular function, severely depressed, returned to normal after initial stabilization. Coronary angiogram was normal. A para-aortic paraganglioma was diagnosed during the patient's work-up with biochemical (...) studies, computed tomography of abdomen and functional radioisotopes imaging and was eventually surgically resected. This case shows that acute myocardial infarction may be the initial manifestation of these neuroendocrine tumors. Hypertensive emergency, much less elevated blood pressure may not be present at time of presentation.Copyright © 2015 Cardiological Society of India. Published by Elsevier B.V. All rights reserved.

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2016 Indian heart journal

65. Exome Sequencing in a Family Identifies RECQL5 Mutation Resulting in Early Myocardial Infarction. (PubMed)

Exome Sequencing in a Family Identifies RECQL5 Mutation Resulting in Early Myocardial Infarction. Coronary artery disease (CAD) including myocardial infarction (MI) is the leading cause of death worldwide and is commonly caused by the interaction between genetic factors and environmental risks. Despite intensive efforts using linkage and candidate gene approaches, the genetic etiology for the majority of families with a multigenerational early CAD /MI predisposition is unknown.In this study, we (...) used whole-exome sequencing of 10 individuals from 1 early MI family, in which 4 siblings were diagnosed with MI before the age of 55, to identify potential predisposing genes.We identified a mutation in the RECQL5 gene, 1 of the 5 members of the RECQ family which are involved in the maintenance of genomic stability. This novel mutation, which is a TG insert at position 73,626,918 on the 13 chromosome and occurs before the last nucleotide of the introns 11 acceptor splice site affecting splicing

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2016 Medicine

66. Semaphorin 3A attenuates cardiac autonomic disorders and reduces inducible ventricular arrhythmias in rats with experimental myocardial infarction. (PubMed)

Semaphorin 3A attenuates cardiac autonomic disorders and reduces inducible ventricular arrhythmias in rats with experimental myocardial infarction. To investigate the effects of semaphorin 3A (sema 3A) on cardiac autonomic regulation and subsequent ventricular arrhythmias (VAs) in post-infarcted hearts.In order to explore the functions of sema 3A in post-infarcted hearts, lentivirus-Sema 3A-shRNA and negative control vectors were delivered to the peri-infarcted myocardium rats respectively (...) . Meanwhile, recombinant sema 3A and control (0.9% NaCl solution) were injected intravenously into infarcted rats to test the therapeutic potential of sema 3A. Results indicated that levels of sema 3A were higher in post-infarcted hearts compared with sham rats. However, sema 3A silencing leaded to sympathetic hyperinnervation, increased myocardial norepinephrine (NE) content and inducible VAs. Conversely, the intravenous administration of sema 3A to infarcted rats reduced sympathetic nerve sprouting

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2016 BMC Cardiovascular Disorders

67. A novel model for evaluating thrombolytic therapy in dogs with ST-elevation myocardial infarction. (PubMed)

hours of therapy, compared to zero dogs without rt-PA treatment. The size of myocardial infarction in rt-PA group reduced significantly compared with white embolus group using TTC staining method.The white embolism model was more convenient experimentally and had a higher uniformity, stability and success rate. The major innovation of our study is that we applied fibrin-rich white thrombi to establish beagle model possessing features of clinically observed coronary thrombi in time window (...) A novel model for evaluating thrombolytic therapy in dogs with ST-elevation myocardial infarction. There is still no standard large animal model for evaluating the effectiveness of potential thrombolytic therapies. Here, we aimed to develop a new beagle model with ST-elevation myocardial infarction (STEMI) by injecting autologous emboli with similar components of coronary thrombus.18 male beagles were included and divided into three groups: red embolus group (n = 6), white embolus group (n = 6

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2016 BMC Cardiovascular Disorders

68. ESC/EACTS Guidelines on Myocardial Revascularization

Coronary artery bypass grafting 111 6.3.3 Percutaneous coronary intervention vs. coronary artery bypass grafting 111 6.4 Gaps in the evidence 112 7 Revascularization in ST-segment elevation myocardial infarction 112 7.1 Time delays 112 7.2 Selection of reperfusion strategy 112 7.3 Primary percutaneous coronary intervention 113 7.4 Percutaneous coronary intervention after thrombolysis and in patients with late diagnosis 114 7.5 Gaps in the evidence 114 8 Myocardial revascularization in patients (...) Choice of treatment and pre-treatment 138 17.1.2 Peri-interventional treatment 138 17.1.3 Post-interventional and maintenance treatment 139 17.2 Non-ST-segment elevation acute coronary syndrome 141 17.2.1 Choice of treatment and pre-treatment 141 17.2.2 Peri-interventional treatment 141 17.2.3 Post-interventional and maintenance treatment 141 17.3 ST-segment elevation myocardial infarction 144 17.3.1 Choice of treatment and pre-treatment 144 17.3.2 Peri-interventional treatment 144 17.3.3 Post

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2018 European Society of Cardiology

69. Delayed Cardiac Rupture Induced by Traumatic Myocardial Infarction: Consequence of a 45-Magnum Blast Injury; A Comprehensive Case Review (PubMed)

Delayed Cardiac Rupture Induced by Traumatic Myocardial Infarction: Consequence of a 45-Magnum Blast Injury; A Comprehensive Case Review A penetrating chest trauma, a myocardial contusion or a myocardial infarction can lead to a cardiac rupture, which is linked to an extreme high death rate. Only few cases with delayed perforation of the myocardium have been reported in literature. We report about a penetrating gunshot injury, which led to a myocardial contusion with secondary delayed rupture (...) of the left ventricle and the left inferior lobe of the lung. The leakage of the lesion in the left ventricle could be sealed sufficiently with fibrin-coated collagen fleeces after adapting stitches with Prolene 2-0. For additional stabilization of the vulnerable myocardium area, a bovine patch has been placed on the damaged ventricle. Fibrin fleeces are used successfully in cardiac surgery, as in our case, to seal the leakage of the lesion in the left ventricle. The implantation of a bovine patch

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2018 Bulletin of emergency & trauma

70. Rivaroxaban in Patients Stabilized after a ST-Elevation Myocardial Infarction: Results from the ATLAS ACS 2-TIMI 51 Trial. (PubMed)

Rivaroxaban in Patients Stabilized after a ST-Elevation Myocardial Infarction: Results from the ATLAS ACS 2-TIMI 51 Trial. The present analysis reports on the pre-specified subgroup of ST-elevation myocardial infarction (STEMI) patients, in whom anticoagulant therapy has been of particular interest.In ATLAS ACS-2-TIMI-51 (Anti-Xa Therapy to Lower Cardiovascular Events in Addition to Standard Therapy in Subjects with Acute Coronary Syndrome-Thrombolysis In Myocardial Infarction-51), rivaroxaban (...) of cardiovascular death, myocardial infarction, or stroke, compared with placebo (ITT: 8.4% vs. 10.6%, hazards ratio [HR]: 0.81, 95% confidence interval [CI]: 0.67 to 0.97, p = 0.019; mITT: 8.3% vs. 9.7%, HR: 0.85, 95% CI: 0.70 to 1.03, p = 0.09). This reduction emerged by 30 days (ITT and mITT: 1.7% vs. 2.3%, p = 0.042) and was evident in analyses that included events while patients received background dual antiplatelet therapies (ITT: 7.9% vs. 11.9%, p = 0.010; mITT: 7.7% vs. 10.1%, p = 0.061). In terms

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2013 Journal of the American College of Cardiology

71. The Influence of Different Training Regimens on Electrical Stability Following Myocardial Infarction

The Influence of Different Training Regimens on Electrical Stability Following Myocardial Infarction The Influence of Different Training Regimens on Electrical Stability Following 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. The Influence of Different Training Regimens on Electrical Stability Following Myocardial Infarction 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: NCT01912690 Recruitment Status : Completed First Posted : July 31, 2013 Last Update Posted : September 22

2013 Clinical Trials

72. Comparison of glucose-insulin-potassium and insulin-glucose as adjunctive therapy in acute myocardial infarction: a contemporary meta-analysis of randomised controlled trials

Comparison of glucose-insulin-potassium and insulin-glucose as adjunctive therapy in acute myocardial infarction: a contemporary meta-analysis of randomised controlled trials Comparison of glucose-insulin-potassium and insulin-glucose as adjunctive therapy in acute myocardial infarction: a contemporary meta-analysis of randomised controlled trials Comparison of glucose-insulin-potassium and insulin-glucose as adjunctive therapy in acute myocardial infarction: a contemporary meta-analysis (...) of randomised controlled trials Zhao YT, Weng CL, Chen ML, Li KB, Ge YG, Lin XM, Zhao WS, Chen J, Zhang L, Yin JX, Yang XC CRD summary The review found that glucose-insulin-potassium did not reduce mortality in patients with acute myocardial infarction. Limitations in the evidence on insulin infusion for glycaemic control meant that an effect on mortality could not be ruled out. The authors' conclusions reflected the limited evidence base, but should be considered tentative due to further limitations

2010 DARE.

73. Apelin modulates pathological remodeling of lymphatic endothelium after myocardial infarction (PubMed)

Apelin modulates pathological remodeling of lymphatic endothelium after myocardial infarction Lymphatic endothelium serves as a barrier to control fluid balance and immune cell trafficking to maintain tissue homeostasis. Long-term alteration of lymphatic vasculature promotes edema and fibrosis, which is an aggravating factor in the onset of cardiovascular diseases such as myocardial infarction. Apelin is a bioactive peptide that plays a central role in angiogenesis and cardiac contractility (...) . Despite an established role of apelin in lymphangiogenesis, little is known about its function in the cardiac lymphatic endothelium. Here, we show that apelin and its receptor APJ were exclusively expressed on newly formed lymphatic vasculature in a pathological model of myocardial infarction. Using an apelin-knockout mouse model, we identified morphological and functional defects in lymphatic vasculature associated with a proinflammatory status. Surprisingly, apelin deficiency increased

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2017 JCI insight

74. Parasympathetic dysfunction and antiarrhythmic effect of vagal nerve stimulation following myocardial infarction (PubMed)

Parasympathetic dysfunction and antiarrhythmic effect of vagal nerve stimulation following myocardial infarction Myocardial infarction causes sympathetic activation and parasympathetic dysfunction, which increase risk of sudden death due to ventricular arrhythmias. Mechanisms underlying parasympathetic dysfunction are unclear. The aim of this study was to delineate consequences of myocardial infarction on parasympathetic myocardial neurotransmitter levels and the function of parasympathetic (...) firing frequency, while neurons that were suppressed by left vagal nerve stimulation had abnormally high basal activity. Myocardial infarction increased sympathetic inputs to parasympathetic convergent neurons. However, the underlying parasympathetic cardiac neuronal network remained intact. Augmenting parasympathetic drive with vagal nerve stimulation reduced ventricular arrhythmia inducibility by decreasing ventricular excitability and heterogeneity of repolarization of infarct border zones

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2017 JCI insight

75. Sex Differences in Clinical Characteristics, Psychosocial Factors, and Outcomes Among Patients With Stable Coronary Heart Disease: Insights from the STABILITY (Stabilization of Atherosclerotic Plaque by Initiation of Darapladib Therapy) Trial (PubMed)

factors, treatments, and outcomes of men versus women with stable coronary heart disease and explored the association of sex with psychosocial characteristics and cardiovascular risk. Cox proportional hazards models were used to assess the relationship between sex and outcomes. Interactions among sex, psychosocial factors, and the composite of cardiovascular death, nonfatal myocardial infarction, and nonfatal stroke were tested. Of 15 828 patients, 2967 (19%) were women. Among women, 21.2% felt often (...) Sex Differences in Clinical Characteristics, Psychosocial Factors, and Outcomes Among Patients With Stable Coronary Heart Disease: Insights from the STABILITY (Stabilization of Atherosclerotic Plaque by Initiation of Darapladib Therapy) Trial Greater understanding of differences between men and women with coronary heart disease is needed.In this post hoc analysis of the STABILITY (Stabilization of Atherosclerotic Plaque by Initiation of Darapladib Therapy) trial, we described psychosocial

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2017 Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

76. Inflammatory Biomarkers Interleukin‐6 and C‐Reactive Protein and Outcomes in Stable Coronary Heart Disease: Experiences From the STABILITY (Stabilization of Atherosclerotic Plaque by Initiation of Darapladib Therapy) Trial (PubMed)

death (HR, 2.15; 95% CI, 1.53-3.04; P<0.0001); myocardial infarction (HR, 1.53; 95% CI, 1.14-2.04; P<0.05); all-cause mortality (HR, 2.11; 95% CI, 1.62-2.76; P<0.0001); and risk of hospitalization for heart failure (HR, 2.28; 95% CI, 1.34-3.89; P<0.001). Cancer death was doubled in the highest IL-6 quartile group (HR, 2.34; 95% CI, 1.20-4.53; P<0.05). High-sensitivity C-reactive protein was associated with both cardiovascular and non-cardiovascular events in the unadjusted model, but these did (...) not remain after multivariable adjustments.IL-6, an upstream inflammatory marker, was independently associated with the risk of major adverse cardiovascular events, cardiovascular and all-cause mortality, myocardial infarction, heart failure, and cancer mortality in patients with stable coronary heart disease. IL-6 might reflect a pathophysiological process involved in the development of these events.URL: http://www.clinicaltrials.gov. Unique identifier: NCT00799903.© 2017 The Authors and GlaxoSmithKline

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2017 Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease

77. Myocardial Infarction Stabilization

Myocardial Infarction Stabilization Myocardial Infarction Stabilization Toggle navigation Brain Head & Neck Chest Endocrine Abdomen Musculoskeletal Skin Infectious Disease Hematology & Oncology Cohorts Diagnostics Emergency Findings Procedures Prevention & Management Pharmacy Resuscitation Trauma Emergency Procedures Ultrasound Cardiovascular Emergencies Lung Emergencies Infectious Disease Pediatrics Neurologic Emergencies Skin Exposure Miscellaneous Abuse Cancer Administration 4 Myocardial (...) Infarction Stabilization Myocardial Infarction Stabilization Aka: Myocardial Infarction Stabilization From Related Chapters II. Course: Hospital See Angiography, and stenting has modified the inpatient ACS protocol dramatically Prior protocols with prolonged hospital stays, ICU admits and prolonged have been replaced Evaluation prior to discharge prior to discharge Consider sub-maximal stress test prior to discharge See III. Disposition: Discharge Planning See See See IV. Complications (common) V

2015 FP Notebook

78. Study design and rationale for the Stabilization of pLaques usIng Darapladib-Thrombolysis in Myocardial Infarction (SOLID-TIMI 52) trial in patients after an acute coronary syndrome. (PubMed)

Study design and rationale for the Stabilization of pLaques usIng Darapladib-Thrombolysis in Myocardial Infarction (SOLID-TIMI 52) trial in patients after an acute coronary syndrome. Higher levels of lipoprotein-associated phospholipase A(2) (Lp-PLA(2)) are associated with a higher risk of cardiovascular events and may play a causal role in atherogenesis. Darapladib inhibits Lp-PLA(2) activity in plasma and in arterial plaques and may confer clinical benefit in preventing cardiovascular (...) events.The SOLID-TIMI 52 trial is a randomized, double-blind, placebo-controlled, multicenter, event-driven trial. Approximately 13,000 subjects are being randomized to darapladib (160 mg enteric-coated tablet daily) or matching placebo within 30 days of hospitalization with an acute coronary syndrome. The primary end point is the composite of cardiovascular death, nonfatal myocardial infarction, or nonfatal stroke. Secondary end points include major and total coronary events, individual components

2011 American heart journal

79. Uncoupling of increased cellular oxidative stress and myocardial ischemia reperfusion injury by directed sarcolemma stabilization. (PubMed)

Uncoupling of increased cellular oxidative stress and myocardial ischemia reperfusion injury by directed sarcolemma stabilization. Myocardial ischemia/reperfusion (I/R) injury is a major clinical problem leading to cardiac dysfunction and myocyte death. It is widely held that I/R causes damage to membrane phospholipids, and is a significant mechanism of cardiac I/R injury. Molecular dissection of sarcolemmal damage in I/R, however, has been difficult to address experimentally. We studied here (...) stabilization of adult cardiac myocytes did not affect the status of myocyte-generated oxidants or lipid peroxidation in two independent assays. We also investigated the loss of sarcolemmal integrity using two independent genetic mouse models, dystrophin-deficient mdx or dysferlin knockout (Dysf KO) mice. Both models of sarcolemmal loss-of-function were severely affected by I/R injury ex vivo, and this was lessened by CSS. In vivo studies also showed that infarct size was significantly reduced in CSS

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2014 Journal of Molecular and Cellular Cardiology

80. Does intra-aortic balloon support for myocardial infarction with cardiogenic shock improve outcome? (PubMed)

Does intra-aortic balloon support for myocardial infarction with cardiogenic shock improve outcome? Thiele H, Zeymer U, Neumann FJ, Ferenc M, Olbrich HG, Hausleiter J, Richardt G, Hennersdorf M, Empen K, Fuernau G, Desch S, Eitel I, Hambrecht R, Fuhrmann J, Böhm M, Ebelt H, Schneider S, Schuler G, Werdan K; IABP-SHOCK II Trial Investigators: Intraaortic balloon support for myocardial infarction with cardiogenic shock. N Engl J Med 2012, 367:1287-1296.In the current international guidelines (...) , intra-aortic balloon pump (IABP) counterpulsation is considered a class I treatment for acute myocardial infarction complicated by cardiogenic shock. However, evidence is based mainly on registry data, and there is a paucity of randomized clinical trials.To test the hypothesis that IABP counterpulsation, as compared with the best available medical therapy alone, results in a reduction in mortality among patients with acute myocardial infarction complicated by cardiogenic shock for whom early

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2015 Critical care (London, England)

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