Academic literature on the topic 'Myocardial reperfusion Complications Prevention'
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Journal articles on the topic "Myocardial reperfusion Complications Prevention"
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Kozlov, I. A. "PREVENTION OF COMPLICATIONS CAUSED BY MYOCARDIAL ISCHEMIA-REPERFUSION IN NONCARDIAC SURGICAL PROCEDURES." Bulletin of Siberian Medicine 15, no. 3 (July 1, 2016): 102–19. http://dx.doi.org/10.20538/1682-0363-2016-3-102-119.
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Shved, M. I., and I. O. Yastremska. "PREVENTION OF COMPLICATIONS IN PATIENTS WITH MYOCARDIAL INFARCTION AND CONCOMITANT METABOLIC SYNDROME." Актуальні проблеми сучасної медицини: Вісник Української медичної стоматологічної академії 20, no. 4 (December 30, 2020): 101–7. http://dx.doi.org/10.31718/2077-1096.20.4.101.
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In Ukraine, coronary heart disease is still occupying the first place in the structure of the causes of death and primary disability (22.8%), and the incidence of myocardial infarction among people of working age is 48.9 per 100 thousand. The aim of this study was to increase the effectiveness of the treatment and prevention of complications in patients with acute coronary syndrome (myocardial infarction) and concomitant metabolic syndrome by including L-carnitine and L-arginine to the integrated therapy. The study involved 71 patients with acute coronary syndrome (ACS) with ST-segment elevation and concomitant metabolic syndrome. Among the 37 individuals who were prescribed a course of cytoprotective therapy additional to the standard drug therapy according to the protocol of the Ministry of Health, formed a test group. The control group consisted of 34 patients who only received standard protocol treatment with corticosteroids (MI). The diagnosis of acute myocardial infarction was verified according to the ESC recommendations (2017). Diagnosis of metabolic syndrome (MS) was established based on the recommendations of the International Diabetes Federation (IDF, 2016). It was found that due to the integrated therapy including L-arginine and L-carnitine, the patients with ACS (MI) and concomitant MS achieved a significant improvement in central cardiohemodynamics and the restoration of vascular endothelial function that was often accompanied by the following complications of corticosteroids (MI) as reperfusion arrhythmias and blockades and acute heart (left ventricular) failure. The patients with acute myocardial infarction and concomitant MS demonstrated pronounced deterioration of morpho-functional parameters of the heart, and namely the development of its post infarction remodelling with subsequent impairments of systolic and diastolic heart function and the development of heart failure and endothelial vascular dysfunction. A mixture of L-arginine and L-carnitine added to the standard therapy significantly reduces the incidence and severity of complications of acute MI such as reperfusion arrhythmias and acute left ventricular failure.
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Hashemi, Baran, Majid Maleki, Amir Darbandi Azar, Morteza Zare, Seyed Mohammad Mazloomi, and Nasim Naderi. "Prevention of kidney injury after myocardial ischemia reperfusion is achievable with short-term protein restriction." Journal of Renal Injury Prevention 8, no. 4 (September 15, 2019): 301–5. http://dx.doi.org/10.15171/jrip.2019.55.
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Introduction: Kidney injury is a serious complication after cardiovascular surgery. Left ventricular dysfunction, pre-operative kidney dysfunction and inflammation can predict kidney injury after myocardial reperfusion. Objectives: We aimed to study whether short-term protein restriction (PR) would influence blood urea nitrogen (BUN) levels after myocardial reperfusion injury. Materials and Methods: Male Wistar rats fed with either AIN-93M or AIN-93M protein restricted diet one week before myocardial reperfusion injury. After surgery, feeding continued with AIN-93M for 1 week. Results: BUN levels increased significantly compared to the pre-operative level in the control group (P=0.03) and decreased significantly in the protein-restricted group (P=0.01). Multivariate analysis showed that PR through its effect on blood glucose (β=1.2, 95% CI=0.1- 2.34), IL-6 (β=-2.22, 95% CI=-3.9–-0.54) and left ventricular ejection fraction (LVEF) (β=-1.21, 95% CI=-2.34- 0.09) was able to protect the kidney from myocardial reperfusion. Conclusion: Short-term PR through modulating pre-operative IL-6, post-operative blood glucose levels and LVEF could prevent kidney injury after myocardial reperfusion injury.
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Iskhakov, M. M., D. R. Tagirova, N. V. Gazizov, L. A. Nugaybekova, and R. G. Sayfutdinov. "«No-reflow» phenomenon: clinical aspects of reperfusion failure." Kazan medical journal 96, no. 3 (June 15, 2015): 391–96. http://dx.doi.org/10.17750/kmj2015-391.
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«No-reflow» phenomenon is the most striking example of myocardial reperfusion clinical failure. It is caused by a lack of adequate blood flow in tissues after successful recanalization of infarct-related artery and is of multifactorial nature. The main reason for «no-reflow» is microvascular damage, of both structural and functional nature. Microvascular microemboli formation is also of particular importance in developing this phenomenon. In patients with acute coronary syndrome undergoing thrombolysis, percutaneous coronary intervention or coronary artery bypass surgery, the risk for «no-reflow» is about 30% or more. In case of planned endovascular interventions, «no-reflow» prevalence ranges from 0.3 to 2%. Patients with «no-reflow» have highly increased risk of complications such as reduced systolic function, heart muscle remodeling, dilatation, cardiac chambers hypertrophy/hyperplasia, left ventricular aneurysm etc. In addition, «no-reflow» increases the risk of death. Predisposition for «no-reflow» might be associated with a number of local and systemic factors. For diagnosing this phenomenon, angiographic grading of coronary blood flow restoration (Thrombolysis in Myocardial Infarction - TIMI) and myocardial perfusion (Myocardial Blush Grade - MBG) is recommended. For the most accurate «no-reflow» diagnosis, different methods for myocardium visualization might be used. The most studied treatments of ongoing «no-reflow» are: vasodilators administered intracoronary (verapamil, adenosine, sodium nitroprusside) at percutaneous coronary intervention or coronary artery bypass surgery; systemic antiplatelet agents; mechanical protection from distal embolization. Given the multifactorial nature of the «no-reflow», further search for the novel methods for prevention and treatment of this phenomenon is needed.
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Liu, Yuezhu, Hua Zeng, and Junmei Xu. "Recent Advance on Drug Therapy Related to Myocardial Ischemia Reperfusion Injury." Journal of Biomaterials and Tissue Engineering 12, no. 2 (February 1, 2022): 299–305. http://dx.doi.org/10.1166/jbt.2022.2899.
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Myocardial ischemia reperfusion injury (MIRI) means complete or partial artery obstruction of coronary artery, and ischemic myocardium will be recirculating in a period of time. Although the ischemic myocardium can be restored to normal perfusion, its tissue damage will instead be progressive. An aggravated pathological process. MIRI is a complex entity where many inflammatory mediators play different roles, both to enhance myocardial infarction-derived damage and to heal injury. Therefore, the research and development of drugs for the prevention and treatment of this period has also become the focus. This article first studied pathophysiology of MIRI, and reviewed the research progress of MIRI-related drugs. Research results show that: MIRI is inevitable for myocardial ischemia, with the possible to double damage via the ischemic condition. Therefore, it is a serious complication and one of the most popular diseases in the world. It has always been difficult to find an effective treatment for this disease, because it is difficult to explore the inflammation behind its pathophysiology.
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Radovanovic, Nebojsa, Mina Radosavljevic-Radovanovic, Milan Dobric, Nebojsa Antonijevic, and Predrag Mitrovic. "Acute myocardial infarction – timely management (chain of care)." Acta chirurgica Iugoslavica 63, no. 2 (2016): 9–13. http://dx.doi.org/10.2298/aci1602009r.
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The mortality rate from ST elevation myocardial infarction (STEMI) varies in European countries, from 6 to 14%. Timely established diagnosis and urgent reperfusion therapy, primarily by primary percutanous intervention with stent implantation (pPCI) in an infarct related artery is essential for mortality reduction and prevention of complications. European Society of Cardiology has made recommendations for preferred and acceptable time frames for diagnosis and therapy of STEMI. The preferred time for diagnosis of STEMI from the first medical contact (FMC) is = 10 min. From the FMC to balloon inflation in the infarct related artery (reperfusion) maximal accepted time is 120 min. If that time frame cannot be reached, fibinolysis is indicated. In order to ameliorate the treatment of these patients, STEMI network has been established in the European countries, including Serbia. Serbia has 12 primary PCI hospitals and, in spite of numerous obstacles, more than 4000 pPCI procedures have been performed during 2015.
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Gilyarov, M. Yu, I. I. Ivanov, E. V. Konstantinova, N. I. Raschetnova, and N. A. Shostak. "No-reflow phenomenon and reperfusion injury. Mechanisms and treatment." Clinician 15, no. 1-4 (March 5, 2022): 10–19. http://dx.doi.org/10.17650/1818-8338-2021-15-1-4-k645.
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Currently, one of the key methods of treating a patient with ST-elevation myocardial infarction is to restore blood flow to the infarct-related artery as quickly, completely and steadily as possible. However, in some cases, it is not possible to achieve adequate myocardial reperfusion, despite the restoration of coronary blood flow. This phenomenon was named no-reflow. Due to the lack of a unified approach to the diagnosis of no-reflow, its occurrence varies widely – from 2 to 44 %. Failure to achieve adequate myocardial perfusion leads to a higher mortality rate – from 7.4 to 30.3 %, as well as to more aggressive remodeling of the myocardium. For a long time, distal embolization in percutaneous coronary intervention was considered one of the leading mechanisms. However, the routine use of protective devices did not show a pronounced effect on the outcome and prognosis, although it is justified in certain clinical situations. Ischemic injury directly plays a significant role due to overload of cardiomyocytes with calcium, cellular edema, necrosis and apoptosis, which is significantly aggravated by myocardial reperfusion and forms obstruction at the level of the microcirculatory bed. More data is being accumulated about immune-mediated injury through activation of cellular immunity, intense inflammation and thrombosis in situ. Despite the success in the animal experiment, the clinical use of certain groups of drugs showed an ambiguous results. According to the latest recommendations European Society of Cardiology / European Association for Cardio-Thoracic Surgery (ESC / EACTS) 2018, GPIIb / IIIa platelet receptor inhibitors are recommended in the case of no-reflow. Besides this, according to the literature nicorandil and sodium nitroprusside, as well as IL-1β antagonists, seem to be promising. As a non-drug therapy, selective intracoronary hypothermia also has shown its effectiveness and safety in a pilot study. To date, it is clear that the no-reflow phenomenon is a manifestation of a complex cascade of reactions, including ischemic, reperfusion and immune-related injury, as well as distal embolization. Considering its significant contribution to the frequency of adverse outcomes and late complications, it seems necessary to introduce unified approaches to the diagnosis, prevention and treatment of no-reflow, which requires high-quality clinical studies.
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Mayasi, Yunis, and Romergryko G. Geocadin. "Updates on the Management of Neurologic Complications of Post–Cardiac Arrest Resuscitation." Seminars in Neurology 41, no. 04 (August 2021): 388–97. http://dx.doi.org/10.1055/s-0041-1731310.
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AbstractSudden cardiac arrest (SCA) is one of the leading causes of mortality and morbidity in the United States, and survivors are frequently left with severe disability. Of the 10% successfully resuscitated from SCA, only around 10% of these live with a favorable neurologic outcome. Survivors of SCA commonly develop post–cardiac arrest syndrome (PCAS). PCAS is composed of neurologic, myocardial, and systemic injury related to inadequate perfusion and ischemia–reperfusion injury with free radical formation and an inflammatory cascade. While targeted temperature management is the cornerstone of therapy, other intensive care unit–based management strategies include monitoring and treatment of seizures, cerebral edema, and increased intracranial pressure, as well as prevention of further neurologic injury. In this review, we discuss the scientific evidence, recent updates, future prospects, and knowledge gaps in the treatment of post–cardiac arrest patients.
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Heinen, André, Vera Welke, Friederike Behmenburg, Martin Stroethoff, Volker Stoldt, Till Hoffmann, Markus W. Hollmann, and Ragnar Huhn. "Haemotherapy with Fibrinogen for Perioperative Bleeding Prevention—A view on Arterial Thrombogenesis and Myocardial Infarction in the Rat In Vivo." Journal of Clinical Medicine 8, no. 6 (June 19, 2019): 880. http://dx.doi.org/10.3390/jcm8060880.
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Major blood loss during cardiac surgery is associated with increased morbidity and mortality. Clinical pilot studies indicated that preoperative fibrinogen supplementation reduces postoperative blood loss without increasing thrombotic complications. However, an increase in fibrinogen concentration might rather aggravate pre-existing thrombosis than increase the incidence of thrombotic events. Therefore, we investigated, in the present study, whether fibrinogen supplementation influences (1) arterial thrombus formation, (2) the extent of myocardial infarction and (3) the cardioprotective effect of ischaemic preconditioning. Arterial thrombogenesis of the femoral artery was induced by topic FeCl3 treatment in anaesthetised Wistar rats after pretreatment with 60 mg/kg (Fiblow), 120 mg/kg (Fibhigh) or vehicle (Con). Vessel blood flow was monitored, and time to vessel occlusion was analysed as a marker for arterial thrombogenesis. In addition, regional myocardial I/R injury was induced by temporary left coronary artery occlusion in rats pretreated with or without fibrinogen supplementation. In additional groups, ischaemic preconditioning (IPC) was induced by 3 cycles of 5 min of ischaemia/reperfusion. In all groups, myocardial infarct size was determined by triphenyltetrazoliumchlorid staining. Arterial thrombogenesis was not affected by fibrinogen pretreatment. No differences in time until vessel occlusion between Con, Fiblow and Fibhigh groups were observed. In addition, fibrinogen supplementation in low and high concentrations had no effect on infarct size after regional myocardial ischaemia and reperfusion (Fiblow: 66 ± 10%, Fibhigh: 62 ± 9%; each ns vs. Con). IPC reduced infarct size from 62 ± 14% to 34 ± 12% (p < 0.05 vs. Con). Furthermore, both fibrinogen concentrations did not affect cardioprotection by ischaemic preconditioning (Fiblow + IPC: 34 ± 11%, Fibhigh + IPC: 31 ± 13%; each ns vs. IPC). Haemotherapy with fibrinogen did not affect arterial thrombogenesis, myocardial infarction and the cardioprotective effect of ischaemic preconditioning.
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Zykov, M. V., V. V. Butsev, and R. R. Suleymanov. "Myocardial Infarction Complicated by Ischemic Stroke: Risk Factors, Prognosis, Unresolved Problems and Possible Methods of Prevention." Rational Pharmacotherapy in Cardiology 17, no. 1 (March 3, 2021): 73–82. http://dx.doi.org/10.20996/1819-6446-2021-02-09.
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The present work is devoted to the analysis of modern publications on various aspects of the development and course of ischemic stroke in the presence of acute myocardial infarction. A literature search was conducted on the websites of cardiological and neurological societies, as well as on the PubMed, EMBASE, eLibrary databases using the keywords: myocardial infarction, acute coronary syndrome, stroke, acute cerebrovascular accident, myocardial infarction, acute coronary syndrome, stroke. The authors of this review found that although stroke is a relatively rare complication of myocardial infarction, its prevention is an extremely significant task, since it is associated with high mortality, disability and a significant increase in the cost of treatment. So, it is extremely important to detect thrombosis of the left ventricular cavity in a timely manner, to register preexisting atrial fibrillation that occurs earlier or for the first time, followed by the appointment of anticoagulant therapy. Timely reperfusion treatment, the use of statins and modern dual antithrombotic therapy can reduce the risk of developing cerebrovascular accident in patients with myocardial infarction. It is likely that a decrease in the activity of subclinical inflammation after myocardial infarction will also reduce the risk of stroke, as was recently shown in the COLCOT study. Currently, it remains relevant to search for new knowledge about the risk factors for stroke, which complicated the course of myocardial infarction, which will allow developing more effective and personalized preventive measures in a patient with acute coronary syndrome.
Dissertations / Theses on the topic "Myocardial reperfusion Complications Prevention"
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Van, Vuuren Derick. "The role of Protein Phosphatase 2A (PP2A) in myocardial ischaemia/reperfusion injury." Thesis, Stellenbosch : Stellenbosch University, 2014. http://hdl.handle.net/10019.1/86397.
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Thesis (PhD)--Stellenbosch University, 2014.ENGLISH ABSTRACT: Ischaemic heart disease is a major contributor to global morbidity and mortality rates. Manoeuvres such as ischaemic preconditioning confer cardioprotection against ischaemia/reperfusion (I/R) injury by activating several intracellular signalling pathways. These pathways have been defined solely in terms of the kinases involved, despite the realization in recent years that protein phosphatase activity also contributes significantly to the attributes of the propagated signal. Protein phosphatase 2A (PP2A) is a heteromultimeric enzyme involved in an array of phosphatase reactions. We hypothesized that PP2A is an important participant in the myocardial response to I/R by regulating intracellular signalling. This project aimed to (i) characterize PP2A during myocardial I/R; (ii) determine the importance of its contribution to the cellular response to I/R; and (iii) investigate its role in the signalling pathways mediated by PKB/Akt, GSK-3β, ERK p42/p44 and p38 MAPK. Two models were used to characterize PP2A during I/R: (i) H9c2 cells exposed to simulated ischaemia (SI) buffer in conjunction with hypoxia (0.5% O2) for a maximum of 2 hours, followed by reoxygenation in standard growth medium for up to 30 minutes; and (ii) isolated working rat hearts exposed to a maximum of 20 minutes global ischaemia and 10 minutes reperfusion. In both models samples were collected at several time points during I/R for Western blotting analysis. PP2A-C (the catalytic subunit) accumulated in the nucleus during early ischaemia, but later redistributed to the cytosol. At the end of ischaemia there was an elevation of PP2A-C relative to PP2A-A in the unfractionated whole cell preparation concomitant with an increase in the inhibitory phosphorylation of PP2A-C. The impact of PP2A activity was evaluated by either inhibiting PP2A using okadaic acid (OA, 10 nM) or activating it by administering FTY720 (1 μM) in an isolated working rat heart model exposed to either 35 minutes of regional ischaemia (RI) with infarct size (IFS) as primary end-point, or 20 minutes global ischaemia (GI) with functional recovery as end-point. The results showed that the pre-ischaemic administration of OA or FTY720 reduced or exacerbated IFS respectively, indicating that PP2A activation during I/R favours cell death. OA and FTY720 were also employed to assess the contribution of PP2A to intracellular signalling in an isolated working rat heart exposed to I/R. Samples were collected at several timepoints and analyzed using Western Blotting. Pre-ischaemic administration of OA enhanced the phosphorylation of PKB/Akt, ERK p42/p44 and GSK-3β at the onset of reperfusion, while FTY720 given before ischaemia reduced the phosphorylation of GSK-3β, p38 MAPK and PKB/Akt at the end of ischaemia and onset of reperfusion. In summary, PP2A is part of an early nuclear-based response to ischaemia, while long-term ischaemia induces an increase in PP2A-C. A portion of this PP2A-C is stored in an inactive form, while an active portion acts as a regulator of the pro-survival signalling components PKB/Akt, GSK- 3β and ERK p42/p44 at the end of ischaemia and the onset of reperfusion. PP2A is therefore an important component of the myocardial response to I/R by regulating pro-survival signalling.
AFRIKAANSE OPSOMMING: Iskemiese hartsiekte is een van die belangrikste komponente wat bydra tot globale morbiditeit en mortaliteit. Ingrepe soos iskemiese prekondisionering aktiveer veelvoudige intrasellulêre seintransduksiepaaie om kardiobeskerming teen iskemie/herperfusie (I/H)-besering te ontlok. Die kinases betrokke in hierdie seintransduksiepaaie is reeds deeglik nagevors, terwyl die potensiële belang van die proteïenfosfatases in seintransduksie tot onlangs misken is. Ons hipotese was dat Proteïenfosfatase 2A (PP2A), wat in ‘n wye verskeidenheid fosfatase reaksies betrokke is, ‘n belangrike rolspeler in die miokardiale reaksie op I/H-besering is, deur deelname aan die regulering van intrasellulêre seintransduksie. Hierdie projek het ten doel gehad om (i) PP2A te karakteriseer tydens miokardiale I/H; (ii) die belang van PP2A in die sellulêre reaksie op I/H-besering te bepaal; en (iii) PP2A se rol in die seintransduksiepaaie, gemedieer deur PKB/Akt, GSK-3β, ERK p42/p44 en p38 MAPK, te evalueer. Twee modelle is aangewend om PP2A tydens I/H te karakteriseer: (i) H9c2-selle blootgestel aan ‘n simuleerde iskemiebuffer tesame met hipoksie (0.5% O2) vir ‘n maksimum van 2 uur gevolg deur heroksiginasie in standaardgroeimedium vir verskillende tydsperiodes tot ‘n maksimum van 30 minute; en (ii) geïsoleerde, werkende rotharte blootgestel aan ‘n maksimum van 20 minute globale iskemie en 10 minute herperfusie. In beide modelle is monsters op verskillende tye versamel vir Western-kladanalise. Tydens vroeë iskemie het PP2A-C in die kern toegeneem, waarna dit met verloop van tyd na die sitosol herversprei het. Teen die einde van iskemie was daar ‘n toename in die vlakke van PP2A-C relatief tot PP2A-A in ongefraksioneerde weefselhomogenate, tesame met ‘n toename in die inhibitoriese fosforilering van PP2A-C. Die belang van PP2A-aktiwiteit is ondersoek deur die effek te bepaal van die inhibisie of aktivering daarvan op infarktgrootte (IFS) en funksionele herstel in ‘n geïsoleerde werkende rothartmodel, blootgestel aan onderskeidelik 35 minute streeksiskemie (RI) of 20 minute globale iskemie. Preiskemiese toediening van die PP2A-inhibitor okadaïensuur (OA, 10 nM), of aktiveerder FTY720 (1 μm) het infarktgrootte respektiewelik beperk of vergroot. PP2A-aktivering tydens I/H is dus nadelig. OA en FTY720 is ook aangewend om die bydrae van PP2A tot I/H-verwante, intrasellulêre seintransduksie in die geïsoleerde, werkende rothart te bepaal. Monsters is op verskeie tydintervalle versamel en ontleed deur gebruik te maak van die Western-kladtegniek. Preiskemiese toediening van OA het die fosforilering van PKB/Akt, ERK p42/p44 en GSK-3β by die aanvang van herperfusie bevoordeel, terwyl pre-iskemiese toediening van FTY720, die fosforilering van GSK-3β, p38 MAPK en PKB/Akt aan die einde van iskemie en die begin van herperfusie verminder het. Ter opsomming: PP2A is deel van ‘n vroeë gelokaliseerde kerngebaseerde reaksie op iskemie, terwyl langdurige iskemie ‘n toename in PP2A-C relatief tot PP2A-A induseer. ‘n Deel van hierdie PP2A-C is onaktief, terwyl die res funksioneer in die regulering van die seintransduksiekomponente PKB/Akt, GSK-3β en ERK p42/p44 wat oorlewing fasiliteer met die aanvang van herperfusie. PP2A is dus ‘n belangrike komponent in die miokardiale reaksie op I/H deurdat dit tot die beheer van seintransduksiepaaie bydra.
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Esterhuyse, Adriaan Johannes. "Dietary red palm oil-supplementation offers cardioprotection against Ischaemia/Reperfusion injury : possible cellular mechanisms involved." Thesis, Stellenbosch : University of Stellenbosch, 2005. http://hdl.handle.net/10019.1/16514.
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Dissertation (PhD)--University of Stellenbosch, 2005.ENGLISH ABSTRACT: Activation of the NO-cGMP pathway is associated with myocardial protection against ischaemia/reperfusion injury. However, high-cholesterol diets alter function of this pathway and these alterations have been implicated in both ischaemic/reperfusion injury and the development of ischaemic heart disease. Little is known about the effects of supplements such as Red Palm Oil (RPO) on the myocardial NO-cGMP-signalling pathway. RPO consists of saturated, mono-unsaturated and poly-unsaturated fatty acids and is rich in antioxidants such as β-carotene and Vitamin E (tocopherols and tocotrienols). The aims of this study were: 1) to determine whether dietary RPO-supplemention protects against ischaemia/reperfusion injury in rats fed a standard rat chow (control) and cholesterol-enriched diets and 2) if so, to investigate possible mechanisms for this protection. Male Long-Evans rats were fed a standard rat chow or a standard rat chow plus cholesterol and/or RPO-supplementation for 6 weeks. Myocardial functional recovery was measured and hearts were freeze-clamped for determination of myocardial phospholipid, cAMP/cGMP concentrations, total myocardial nitric oxide concentrations, lipid hydroperoxide production and superoxide dismutase- and nitric oxide synthase activity in isolated rat hearts subjected to 25 minutes of normothermic total global ischaemia. In addition, the degree of phosphorylation of extracellular signal-regulated kinase (ERK), p38, c-Jun N-terminal protein kinase (JNK) and protein kinase B (PKB/Akt) was investigated. Furthermore, the effect of RPO-supplementation on caspase-3 activation and poly (ADP-ribose) polymerase (PARP)-cleavage in hearts subjected to ischaemia and reperfusion was also investigated. Our data show that dietary RPO-supplementation protects the hearts of rats on a standard rat chow (control) and hypercholesterolaemic diet against ischaemia/reperfusion injury as reflected by improved aortic output recovery. Increased intracellular cardiomyocyte NO concentrations as observed in control hearts supplemented with RPO after 120 minutes hypoxia may contribute to the elevated cGMP concentration and may confer some of the cardioprotection to the ischaemic/reperfused heart. Although improved functional recovery with RPO-supplementation of a high-cholesterol diet was also associated with an increase in intracellular cardiomyocyte NO production after hypoxia compared to the non-hypoxic conditions, it could not be linked to increased NO-cGMP signalling. These data are in agreement with other studies, which showed that high-cholesterol diet impairs NO-cGMP signalling and confirms our hypothesis that elevated cGMP concentrations may not be the only mechanism of protection. We have also shown that RPOsupplementation caused increased phosphorylation of p38 and PKB, reduced phosphorylation of JNK and attenuation of PARP cleavage, which may contribute to the protection of the cell against apoptosis. Based on our results we propose that the myocardial protection offered by RPO-supplementation of rats on a normal and hypercholesterolaemic diet may be associated with either its antioxidant characteristics and/or changes in the fatty acid composition of the myocardium during ischaemia/reperfusion. Furthermore, we demonstrated for the first time that RPO-supplementation protects the isolated perfused working rat heart during reperfusion from ischaemia/reperfusion-induced injury through a MAPK-dependent pathway.
AFRIKAANSE OPSOMMING: Aktivering van die NO-cGMP sein transduksie pad word geassosieer met miokardiale beskerming teen isgemie/herperfusie skade. Hoë cholesterol diëte verander egter die funksie van die pad en hierdie veranderings speel ‘n rol in beide isgemie/herperfusie besering en die ontwikkeling van isgemiese hartsiekte. Daar is egter min inligting beskikbaar oor die uitwerking van aanvullings soos rooi palm olie (RPO) op die miokardiale NO-cGMP sein transduksie pad. RPO bevat versadigde, mono-onversadigde en poli-onversadigde vetsure en is ryk aan anti-oksidante nl. β-karotene en vitamien E (tokoferole en tokotriënole). Die doelwitte van hierdie studie was: 1) om vas te stel of ‘n RPO-aanvulling beskerming bied teen isgemie/herperfusie besering in rotte wat gevoed is met ‘n standaard rotmengsel (kontrole) en cholesterol-verrykte dieet en 2) indien wel, om moontlike meganismes van beskerming te ondersoek. Long-Evans manlike rotte is vir 6 weke gevoer met ‘n standaard rotmengsel of ‘n standaard rotmengsel plus cholesterol en/of RPO-aanvulling. Miokardiale funksionele herstel is gemeet en harte is gevriesklamp vir die bepaling van miokardiale fosfolipied, cAMP/cGMP, totale stikstofoksied, lipied hidroperoksied, superoksied dismutase en stikstofoksied sintase in geïsoleerde rotharte wat vir 25 minute onderwerp was aan normotermiese totale globale isgemie. Hiermee saam is die graad van fosforilering van ekstrasellulêre sein gereguleerde kinase (ERK), p38 mitogeen-geaktiveerde proteïen kinase (p38 MAPK), c-Jun-N-terminale proteïenkinase (JNK) en proteïen kinase B (PKB/Akt) ondersoek, asook kaspase-3 aktivering en poli (ADP-ribose) polimerase (PARP) kliewing in harte blootgestel aan isgemie en herperfusie. Ons resultate toon dat RPO-aanvulling van rotte op ‘n normale en hipercholesterolemiese dieet die hart beskerm soos getoon deur verbeterde herstel van aortiese uitset. Verhoogde intrasellulêre miokardiale NO vlakke in kontrole harte met ‘n RPO-aanvulling wat blootgestel was aan 120 minute hipoksie, mag bygedra het tot die verhoogde cGMP vlakke en beskerming van die hart tydens isgemie en herperfusie. Alhoewel verbeterde funksionele herstel met RPO-aanvulling van ‘n hoë cholesterol dieet ook geassosieer is met ‘n toename in intrasellulêre miokardiale NO produksie ná hipoksiese toestande, kon dit nie verbind word met verhoogde aktivering van die NOcGMP sein transduksie pad nie. Hierdie resultate stem ooreen met ander studies wat aangetoon het dat hoë-cholesterol diëte die NO-cGMP seinpad onderdruk. Hierdie bevinding bevestig ons hipotese dat verhoogde cGMP vlakke moontlik nie die enigste beskermingsmeganisme is nie. Ons resultate het ook gewys dat RPO-aanvulling fosforilering van p38 en PKB/Akt verhoog, fosforilering van JNK verminder en PARP kliewing onderdruk. Dit dui op beskerming van die sel teen apoptose. Ons resultate dui aan dat die miokardiale beskerming wat RPO-dieet aanvulling bied moontlik geassosieer kan word met sy anti-oksidant eienskap en/of veranderinge in die vetsuur samestelling van die miokardium tydens isgemie/herperfusie. Ons het ook vir die eerste keer bewys dat RPO-aanvulling die geïsoleerde geperfuseerde werkende rothart gedurende herperfusie beskerm teen isgemie/herperfusie besering deur die aktivering en/of deaktivering van die MAPK afhanklike pad.
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Yamazaki, Kazuhiro. "Prevention of myocardial reperfusion injury by poly(ADP-ribose) synthetase inhibitor, 3-aminobenzamide, in cardioplegic solution : in vitro study of isolated rat heart model." Kyoto University, 2007. http://hdl.handle.net/2433/135743.
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Maarman, Gerald Jerome. "The effect of CPT-1 inhibition on myocardial function and resistance to ischemia/reperfusion injury in a rodent model of the metabolic syndrome." Thesis, Stellenbosch : University of Stellenbosch, 2010. http://hdl.handle.net/10019.1/5354.
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Thesis (MScMedSc (Dept. of Biomedical Sciences. Medical Physiology))University of Stellenbosch, 2010.ENGLISH ABSTRACT: Background: Obesity is associated with dyslipidemia, insulin resistance and glucose intolerance and together these components characterise the metabolic syndrome (Dandona et al. 2005). In the state of obesity, there are high levels of circulating free fatty acids and increased rates of fatty oxidation which inhibit glucose oxidation. This: (i) reduce the heart‘s contractile ability, (ii) exacerbates ischemic/reperfusion injury and (iii) decreases cardiac mechanical function during reperfusion (Kantor et al. 2000; Liu et al. 2002; Taegtmeyer, 2000). Aim: The aim of our study was to investigate the effect of inhibiting fatty acid oxidation, with oxfenicine (4-Hydroxy-L-phenylglycine), on (i) cardiac mechanical function, (ii) mitochondrial respiration, (iii) myocardial tolerance to ischemia/reperfusion injury, (iv) CPT-I expression, MCAD expression, IRS-1 activation, total GLUT- 4 expression and (v) the RISK pathway (ERK42/44 and PKB/Akt). Methods: Male Wistar rats were fed a control rat chow diet or a high calorie diet (HCD) for 16 weeks. The HCD caused diet induced obesity (DIO). The animals were randomly divided into 4 groups [Control, DIO, Control + oxfen and DIO + oxfen]. The drug was administered for the last 8 weeks of feeding (200mg/kg/day). Animals were sacrificed and the hearts were perfused on the Langendorff perfusion system. After being subjected to regional ischemia and two hours of reperfusion, infarct size was determined. A separate series of animals were fed and/or treated and hearts were collected after 25 minutes global ischemia followed by 30 min reperfusion for determination of GLUT- 4, CPT-1, IRS -1, MCAD, ERK (42/44) and PKB/Akt expression/phosphorylation using Western blot analysis. A third series of hearts were excised and used for the isolation of mitochondria. Results: In the DIO rats, chronic oxfenicine treatment improved cardiac mechanical function by improving mitochondrial respiration. Oxfenicine inhibited CPT-1 expression but had no effect on MCAD or GLUT- 4 expression. Oxfenicine decreased IRS-1 iv expression, but not IRS-1 activation. Oxfenicine also improved myocardial tolerance to ischemia/reperfusion without activation of the RISK pathway (ERK & PKB). In the control rats, chronic oxfenicine treatment worsened cardiac mechanical function by adversely affecting mitochondrial respiration. Oxfenicine also worsened myocardial tolerance to ischemia/reperfusion in the control rats without changes in the RISK pathway (ERK & PKB). Oxfenicine had no effect on CPT-1, MCAD or GLUT- 4 expression. Oxfenicine increased IRS-1 expression, but not IRS-1 activity. Conclusion: Chronic oxfenicine treatment improved cardiac mechanical function and myocardial resistance to ischemia/reperfusion injury in obese animals, but worsened it in control animals. The improved cardiac mechanical function and tolerance to ischemia/reperfusion injury may be due to improvement in mitochondrial respiration.
AFRIKAANSE OPSOMMING: Agtergrond: Vetsug word geassosieer met dislipidemie, insulien weerstandigheid en glukose intoleransie, wat saam die metaboliese sindroom karakteriseer (Dandona et al. 2005). Met vetsug is daar ‗n hoë sirkulasie van vetsure, sowel as verhoogde vertsuur oksidasie wat gevolglik glukose oksidasie onderdruk. Dit: (i) verlaag die hart se vermoë om saam te trek, (ii) vererger isgemiese/herperfusie skade en (iv) verlaag kardiale effektiwiteit gedurende herperfusie (Kantor et al. 2000; Liu et al. 2002; Taegtmeyer, 2000). Doel: Die doel van die studie was om die effekte van vetsuur onderdrukking m.b.v. oksfenisien (4-Hidroksie-L-fenielglisien) op (i) meganiese hart funksie, (ii) mitokondriale respirasie, (iii) miokardiale toleransie teen isgemiese/herperfusie skade, (iv) CPT-I uitdrukking, MCAD uitdrukking, IRS-1 aktiwiteit, totale GLUT-4 uitdrukking en (v) die RISK pad (ERK42/44 en PKB/Akt) te ondersoek. Metodes: Manlike Wistar rotte was gevoer met ‗n kontrole rot dieet of ‗n hoë kalorie dieet (HKD) vir 16 weke. Die HKD lei tot dieet-geïnduseerde vetsug (DGV). Die diere was lukraak verdeel in 4 groepe [kontrole, DGV, kontrole + oksfen en DGV + oksfen]. Die behandeling met die middel was toegedien vir die laaste 8 weke van die voeding protokol (200mg/kg/dag). Die diere was geslag en die harte was geperfuseer op die Langendorff perfusie sisteem. Na blootstelling aan streeks- of globale isgemie en 2 ure herperfusie was infark groottes bepaal. ‗n Aparte reeks diere was gevoer en/of behandel en die harte was versamel na 25 minute globale isgemie gevolg deur 30 minute herperfusie vir die bepaling van GLUT-4, CPT 1, IRS -1, MCAD, ERK (42/44) en PKB/Akt uitdrukking/aktivering d.m.v. Western blot analise. ‗n Derde reeks diere was gebruik vir die isolasie van mitokondria. Resultate: In die DGV diere, het kroniese oksfenisien behandeling meganiese hart funksie verbeter d.m.v. die verbetering van mitokondriale respirasie. Oksfenisien het CPT-1 uitdrukking verlaag terwyl GLUT- 4 en MCAD uitdrukking nie geaffekteer was vi nie. Oksfenisien het IRS-1 uitdrukking verlaag, maar nie IRS-1 aktiwiteit nie. Oksfenisien het ook miokardiale weerstand teen isgemiese/herperfusie verbeter met sonder aktivering van die RISK pad (ERK & PKB). In die kontrole diere, het kroniese oksfenisien behandeling die meganiese hart funksie versleg d.m.v. negatiewe effekte op mitokondriale respirasie. Oksfenisien het die miokardiale weerstand teen isgemiese/herperfusie van die kontrole rotte versleg sonder veranderinge in die RISK pad (ERK & PKB). Oksfenisien het geen effek gehad op CPT-1, MCAD en GLUT-4 uitdrukking nie. Oksfenisien het IRS-1 uitdrukking verhoog, maar nie IRS-1 aktiwiteit nie. Samevatting: Kroniese oksfenisien behandeling het die meganiese hart funksie en miokardiale weerstand teen isgemiese/herperfusie skade in die vet diere verbeter, maar versleg in die kontrole diere. Hierdie verbetering van meganiese hart funksie en weerstand teen isgemiese/herperfusie skade kon dalk wees a.g.v. ‗n verbetering in mitokondriale respirasie.
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Cavalcante, Leonardo Pessoa. "Efeito da administração aguda de 17beta-estradiol ou de progesterona em modelo de isquemia-reperfusão medular em ratos." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/5/5156/tde-06022017-103854/.
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INTRODUÇÃO: A lesão medular isquêmica continua sendo uma complicação devastadora das intervenções cirúrgicas na aorta torácica descendente e aorta toracoabdominal. Relatos das diferenças de desfechos clínicos neurológicos entre os gêneros após lesões cerebrais isquêmicas e traumáticas têm levantado o interesse nas influências hormonais, bem como gerado outros estudos buscando a comprovação dos efeitos neuroprotetores do estradiol e da progesterona. Nossa hipótese foi a de que a administração aguda de 17beta-estradiol ou de progesterona seria capaz de prevenir ou atenuar a lesão medular isquêmica causada pela oclusão transitória da aorta torácica descendente proximal. OBJETIVO: Analisar os efeitos na medula espinhal da administração aguda de 17?-estradiol ou de progesterona em modelo experimental de isquemia-reperfusão medular por oclusão transitória da aorta torácica descente proximal de ratos machos. MÉTODOS: Ratos machos, da linhagem wistar, foram divididos aleatoriamente em 3 grupos para a administração de 280ug/Kg de 17beta-estradiol (n=12) ou de 4mg/Kg de progesterona (n=8) ou do veículo de infusão (grupo controle) (n=12), 30 minutos antes da oclusão transitória da aorta torácica descendente por 12 minutos. A confirmação da oclusão efetiva aórtica deu-se por meio da monitorização contínua da pressão arterial média distal com o uso de cateter colocado na artéria caudal dos animais (mantida em 10mmHg). A oclusão da aorta torácica descendente deu-se por meio do posicionamento de um cateter de Fogarty no. 2, passado no sentido caudal, via dissecção da artéria carótida comum esquerda do animal. A função locomotora dos animais foi avaliada no 1o, 3o, 5o, 7o, e 14o dia pós-operatório. No 14o dia pós-operatório, os animais, após anestesia profunda, foram sacrificados e tiveram suas medulas espinhais retiradas para análise histológica e imunohistoquímica. RESULTADOS: Houve comprometimento significativo da função locomotora inicialmente nos 3 grupos de estudo, com recuperação parcial da mesma ao longo do período de observação, não havendo diferença entre os grupos durante o período de observação. A análise histológica da substância cinzenta evidenciou escassos neurônios viáveis e importante vacuolização celular nos 3 grupos de estudo no 14o dia. A análise imunohistoquímica da substância cinzenta medular com anticorpos anti-Bcl2 e anti-anexina V foi similar nos 3 grupos. Houve marcação positiva de necrose celular com o iodeto de propídio, sendo a mesma semelhante nos 3 grupos estudados. CONCLUSÃO: A administração aguda de estradiol ou de progesterona, 30 minutos antes da oclusão transitória da aorta descendente proximal de ratos machos não foi capaz de prevenir ou atenuar a lesão medular isquêmica, até o 14o dia de observação, do ponto vista funcional ou histológicoBACKGROUND: Spinal cord ischemic injury remains a dreadful complication following thoracic and thoracoabdominal aortic interventions. Reports on gender-related neurological outcomes after ischemic and traumatic brain injuries have raised interest in hormonal influences, and have generated studies into neuroprotective effects of estrogen and progesterone. We hypothesized that the acute pre-operative administration of estradiol or of progesterone would prevent or attenuate spinal cord ischemic injury induced by transitory occlusion of the proximal descending thoracic aorta. OBJECTIVE: Evaluate the spinal cord effects of the acute administration of 17beta-estradiol or of progesterone in a spinal cord ischemia-reperfusion model. METHODS: Male rats were divided to receive 280ug/Kg of 17beta-estradiol (n=12) or 4mg/Kg of progesterone (n=8) or vehicle (control group) (n=12) 30 minutes before transitory occlusion of the proximal descending thoracic aorta, mean distal arterial blood pressure was maintained at 10mmHg during 12 minutes. Hind limb motor function was assessed at 1, 3, 5, 7 and 14 days after reperfusion. At the 14th day, a segment of the thoracolumbar spinal cord was harvested and prepared to histological and imunohistochemical analyses. RESULTS: There was an important hind limb motor function impairment initially in the 3 study groups, with partial improvement along time, but no difference was detected between groups during de observational period. Gray matter analysis showed scarce viable neurons and a marked cellular vacuolation in all three groups, but the number of viable neurons per section areas was not different between study groups at day 14th. Immunostaining of the spinal cord gray matter with antibodies anti-Bcl2 and anti-annexin V was similar among the 3 study groups. There was positive staining for the necrotic marker propidium iodide, with all groups presenting a similar staining pattern. CONCLUSION: We found that a single-dose administration of estradiol or of progesterone, 30 minutes before transitory occlusion of the proximal descending thoracic aorta of male rats, was not able to prevent spinal cord ischemic injury through analysis of functional and histological outcomes at 14 days of observation
Books on the topic "Myocardial reperfusion Complications Prevention"
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A, Salerno Tomas, and Ricci Marco, eds. Myocardial protection. Elmsford, N.Y: Blackwell Pub., 2004.
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S, Dhalla Naranjan, ed. Myocardial ischemia and preconditioning. Boston: Kluwer Academic, 2003.
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H, Opie Lionel, ed. Stunning, hibernation, and calcium in myocardial ischemia and reperfusion. Boston: Kluwer Academic, 1992.
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Seibu, Mochizuki, ed. The ischemic heart. Boston: Kluwer Academic Publishers, 1998.
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Ostadal, Bohuslav. Cardiac ischemia: From injury to protection. Boston: Kluwer Academic Publishers, 1999.
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František, Kolář, ed. Cardiac ischemia: From injury to protection. Boston: Kluwer Academic Publishers, 1999.
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M, Mentzer Robert, ed. Adenosine, cardioprotection, and its clinical application. Boston: Kluwer Academic Publishers, 1997.
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L, Hess Michael, ed. Free radicals, cardiovascular dysfunction, and protection strategies. Austin: R.G. Landes Co., 1994.
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Antoine, Lafont, and Topol Eric J. 1954-, eds. Arterial remodeling: A critical factor in restenosis. Boston: Kluwer Academic Publishers, 1997.
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Scientific basis of healthcare: AIDS and pregnancy. Boca Raton, FL: CRC Press/Taylor & Francis Group, 2011.
Find full textBook chapters on the topic "Myocardial reperfusion Complications Prevention"
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Kuijt, Wichert J., Judson Williams, Christopher B. Granger, Mitchell W. Krucoff, and Matthew T. Roe. "Current Approaches to Prevention and Management of Reperfusion Injury." In Management of Myocardial Reperfusion Injury, 215–38. London: Springer London, 2012. http://dx.doi.org/10.1007/978-1-84996-019-9_10.
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Hugenholtz, P. G., M. L. Simoons, P. W. Serruys, P. J. De Feyter, M. Van Den Brand, and P. Fioretti. "Late Results of Reperfusion with Intracoronary Streptokinase." In Secondary Prevention in Coronary Artery Disease and Myocardial Infarction, 315–26. Dordrecht: Springer Netherlands, 1985. http://dx.doi.org/10.1007/978-94-009-5024-5_33.
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Ramrakha, Punit S., Kevin P. Moore, and Amir H. Sam. "Cardiac emergencies." In Oxford Handbook of Acute Medicine, 1–170. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198797425.003.0001.
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This chapter describes cardiac emergencies, including adult life support (basic and advanced), universal treatment algorithm, acute coronary syndrome (ACS), ST-elevation myocardial infarction (STEMI; diagnosis, general measures, reperfusion therapy, thrombolysis, reperfusion by primary percutaneous coronary intervention (PCI), surgery, predischarge risk stratification, complications), ventricular septal defect post-myocardial infarction (MI), atrial tachyarrhythmia post-MI, bradyarrhythmias and indications for pacing, hypotension and shock post-MI, cardiogenic shock, non-ST-elevation MI (NSTEMI; diagnosis, risk stratification, medical management, invasive and non-invasive strategies, discharge, and secondary prevention), arrhythmias, tachyarrhythmias, tachycardia (broad complex, monomorphic, polymorphic, ventricular, narrow complex), atrial fibrillation (AF), atrial flutter, multifocal atrial tachycardia (MAT), accessory pathway tachycardia, atriventricular nodal re-entry tachycardia (AVNRT), bradyarrhythmias, sinus bradycardia, intraventricular conduction disturbances, pulmonary oedema, endocarditis (infective, culture-negative, right-sided, prosthetic valve, prophylaxis), acute aortic regurgitation (AR), acute mitral regurgitation (MR), deep vein thrombosis (DVT), pulmonary embolism (PE), fat embolism, hypertensive emergencies, hypertensive encephalopathy, aortic dissection, acute pericarditis, bacterial pericarditis, cardiac tamponade, and congenital heart disease in adults.
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Rabai, Ferenc, Michol A. Cooper, and Derek B. Covington. "Postoperative Management of Vascular Surgery Patients and Complications." In Vascular Anesthesia Procedures, 241–58. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780197506073.003.0017.
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Vascular surgery carries an increased risk of a variety of complications in the immediate and extended postoperative periods. Major vascular operations, such as thoracoabdominal aortic aneurysm repairs and limb revascularizations, are commonly associated with prolonged operative time, ischemic reperfusion injuries, large blood losses, and systemic inflammatory response syndrome. Additionally, vascular patients usually present with a high burden of comorbidities. These factors increase the risk of multiple organ systems failing postoperatively. Myocardial injury, postoperative pulmonary complications, acute kidney injury, and neurovascular complications are relatively common and have been shown to increase morbidity and mortality. Close monitoring and an appropriate level of care ensure a safe transition into the postoperative phase. Recent data suggest that risk stratification with modern diagnostic tools and laboratory tests using sensitive biomarkers play pivotal roles in the early detection of deteriorating organ function and initiation of timely intervention. Evidence-based postoperative management guidelines and care bundles (e.g., prehabilitation, enhanced screening for myocardial injury, lung-protective ventilator management, kidney protection strategies, and enhanced recovery protocols) show promise in preventing, mitigating, and effectively treating complications with an overarching goal of optimizing postoperative outcomes and ensuring that patients recover successfully.
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Hollenberg, Steven M. "Management of Complications." In Reperfusion Therapy for Acute Myocardial Infarction, 280–99. Informa Healthcare, 2008. http://dx.doi.org/10.3109/9781420019179.017.
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Mariani, Serena, Francesco Formica, and Giovanni Paolini. "Mechanical Complications of Myocardial Infarction." In Coronary Artery Disease - Assessment, Surgery, Prevention. InTech, 2015. http://dx.doi.org/10.5772/61373.
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Vasa-Nicotera, Mariuca, and Tony Gershlick. "Stent thrombosis." In Oxford Textbook of Interventional Cardiology, 503–24. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780199569083.003.029.
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Over the past three decades, new strategies have rapidly evolved to achieve coronary reperfusion of ischaemic myocardium in patients with coronary artery disease (CAD). Studies comparing percutaneous coronary intervention (PCI) with coronary artery bypass grafting (CABG) have shown that the long-term rates of death and/or myocardial infarction (MI) are substantially the same, justifying the increasing and widespread use of PCI. PCI is the dominant reperfusion therapy for such patients with the ratio of numbers of PCIs undertaken to CABG performed being 4:1 in the United Kingdom and up to 8:1 in other parts of Europe. A recurrent issue during the evolution of PCI has been the difference between PCI and CABG in the percentage of patients requiring a repeat procedure (reintervention). To date, the need of reintervention has been less with CABG and this is due to the development of in-stent restenosis that occurs after PCI. Restenosis is the re-narrowing of the vessel, which requires a repeat procedure. The rate of restenosis with early balloon angioplasty has been high. The implantation of bare metal stents (BMS) and then drug-eluting stents (DES) has reduced significantly the incidence of restenosis. While such improved overall clinical outcomes with DES has supported the use of these in preference to BMS, another long-term complication has somewhat tempered the enthusiasm for their use: the possibility that implantation of DES would result in an excess of occlusive stent thrombosis (ST). This chapter will analyse the data on the incidence, causes, and clinical consequences of ST, and will outline the ongoing and future preventive and therapeutic initiatives. Finally, the risk/benefit of DES will be addressed.
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Puerto, Elena, and Héctor Bueno. "Mechanical complications of myocardial infarction." In The ESC Textbook of Intensive and Acute Cardiovascular Care, edited by Marco Tubaro, Pascal Vranckx, Eric Bonnefoy-Cudraz, Susanna Price, and Christiaan Vrints, 513–30. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198849346.003.0041.
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Mechanical complications of acute myocardial infarction are those caused by ruptures or geometrical distortions of cardiac structures. Cardiac ruptures are currently rare complications, less than 1% in the era of reperfusion therapy, but often with catastrophic consequences, and include free wall rupture, the most frequent, interventricular septal rupture, and papillary muscle rupture. The clinical presentation may vary from unusually milder presentations to sudden presentation with severe hypotension, cardiogenic shock or electro-mechanical dissociation. Therefore, immediate diagnosis is key, generally by echocardiography, followed by resuscitation and/or hemodynamic support, pharmacological or mechanical. In the majority of cases, these complications require urgent surgical repair. In some cases percutaneous therapies may be a valid alternative. Mechanical complications due to geometrical distortion include functional ischemic mitral regurgitation, ventricular aneurysms and intraventricular thrombosis. These complications are more frequent than ruptures and, in general, less severe, ranging from accidental findings by imaging techniques in asymptomatic patients to advanced heart failure. Most often these complications can be treated medically and occasionally may need surgical therapy.
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Pizarro, Gonzalo, Rodrigo Fernández-Jiménez, and Borja Ibanez. "Prevention of Microvascular Obstruction by Addressing Ischemia Reperfusion Injury—Part B." In Coronary Microvascular Obstruction in Acute Myocardial Infarction, 277–93. Elsevier, 2018. http://dx.doi.org/10.1016/b978-0-12-812528-1.00016-6.
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Stiermaier, Thomas, Ingo Eitel, Domenico D’Amario, and Giampaolo Niccoli. "Prevention of Coronary Microvascular Obstruction by Addressing Ischemia Reperfusion Injury—Part A." In Coronary Microvascular Obstruction in Acute Myocardial Infarction, 255–76. Elsevier, 2018. http://dx.doi.org/10.1016/b978-0-12-812528-1.00015-4.
Full textConference papers on the topic "Myocardial reperfusion Complications Prevention"
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Egbring, R., C. Bethge, A. Behling, and R. A. Seitz. "ANTITHROMBIN III (AT III) REPLACEMENT FOR THE PREVENTION OF REOCCLUSION AFTER INTRACORONARY THROMBOLYSIS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643677.
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Within 4 hours of acute myocardial infarction thrombolysis of an intracoronary thrombus leads to reperfusion in 40-707. of all cases, when streptokinase (SK), urokinase (UK) andtissue plasminogen activato(TPA) areused as thrombolytic agent.Although reperfusion could be demonstrated after thrombolysis, reocclusion occurred to different extents. There are several reasons for reocclusion: 1. Reocclusion occurs at the site of theprevious thrombus, as the vessel wall is deprived of endothelium and thethrombogenic surface is exposed; 2. The post-thrombolytic anticoagulant treatment (ACT) is not sufficient oris not performed correctly. When ACT was carried out with high doses of heparin, bleeding complications could be observed. Therefore we have tried in an open pilot study to increase the anticoagulant effect by additional replacement of AT III concentrates for 5 days as follows. The first group of patients (30) was given 1000 U AT III concentrate daily with an average dose of 24000 U heparin daily for 5 days. The second group (9)received more than 30000 U heparin daily. In the first group of 30 patients neither hemorrhage nor reocclusion of the infarction vessel was observed, the AT III levels rose gradually. In 3 of 9 patients of the secondgroup, hemorrhage occurred, necessitating reduction of the heparin dose.Subsequent reocclusion of the infarction arteries occurred in all 3 cases. The mean AT III level decreased in these patients to the lower limit.Conclusion: After reperfusion of coronary arteries following thrombolytic therapy reocclusion may occur for several reasons. The present studies show that reocclusion is rare ifanticoagulant treatment is performedwith AT III concentrate replacement in combination with ACT with heparin.Although the initial AT III levelsare not decreased beneath the critical level of 707o, the substitution leading to a further gradual increase seems to prevent reocclusive thrombosis. According to Reeve (1982) the amount of circulating thrombin is dependent on the equation 1:(AT III)2.
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Milazzotto, F., M. Carelli, C. Citone, G. Di Macro Tullio, G. C. Gambelli, P. Giampaolo, U. Malinconico, C. Polizzi, and U. Cornelli. "EFFECTIVENESS OF DEFIBROTIDE IN THE TREATMENT OF ACUTE MYOCARDIAL INFARCTION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643146.
Full textAbstract:
Defibrotide (D) is an extractive polydesoxyribonucleotide. In preclinical studies the product was shown to be active as a pro -fibrinolytic, antithrombotic and thrombolytic agent while comply tely devoid of anticoagulant activity. In animal models, D was found to afford striking protection from the effects of acute lethal and non lethal myocardial ischemia as well as from myo -cardial injury following reperfusion. In this open single - blim trial, D was administered to patients with acute myocardial infaj ction (AMI) for the prevention of complicating arrhythmias; throy bus formation, pericarditis, etc.Sixty patients with AMI were divided randomly into two groups of 30 patients each. One group was treated with D by 6-hour drip infusion for 3 consecutive days (2.8 g on the first day, then 2.4 g daily). The other group was treated with equal volumes of physiological salt solution. All patients received conventional trea_t ment for AMI. The two trial groups were sufficiently homogeneous in terms of AMI type, age and sex distribution, PCT, Forrester index, Holter, and Peel index. D treatment proved effective in reducing the incidence of severe arrhythmia (p < 0.05), thrombus formation (p < 0.05), and pericarditis (p < 0.01). CPK, TT and PTT readings were not modified by the treatment; the incidence of post-AMI angina and the number of deaths (4 in each group) were similar in the two groups. The results of this pilot study are encouraging; further clinical trials are currently in progress to assess D activity in larger groups of patients treated with the product at higher dosages.
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Anderson, J., R. Rothbard, R. Hackworthy, S. Sorensen, P. Fitzpatrick, and V. Harder. "COMPARISON OF INTRAVENOUS ANISOYLATED PLASMINOGEN STREPTOKINASE ACTIVATOR COMPLEX (APSAC) AND INTRACORONARY STREPTOKINASE IN ACUTE MYOCARDIAL INFARCTION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643621.
Full textAbstract:
To compare the reperfusion potential of intravenous anisoy-lated plasminogen streptokinase activator complex (APSAC) a new thrombolytic, and standard therapy with intracoronary streptokinase in acute myocardial infarction (AMI), a randomized multicenter reperfusion trial was performed. Consenting patients with clinical signs of AMI and documented coronary occlusion (flow grade 0 or 1) were randomized to treatment within 6 hours of symptoms (mean, 3.4h) with intravenous APSAC (30 U in 2-4 min) or intracoronary streptokinase (bolus, then 2,000 U/min x 60 min). Reperfusion success was defined as grade 2 or 3 flow at 60 min for intracoronary and 90 min for intravenous therapy. A total of 189 patients (pt) were randomized and 179 pt were evaluable for efficacy. Reperfusion was similar for the two treatments: 52% (49/94) for APSAC and 61% (52/85) for streptokinase (p≤0.2). Success was dependent on initial occlusion grade (p≤0.001): 49% (65/133) for grade 0 (APSAC= 45%, streptokinase=54%), but 78% for grade 1 (APSAC=80%, strepto-kinase=77%). The success of intravenous (APSAC) therapy was also dependent on time to treatment: 59% for ≤4h, versus 36% after 4h (p<0.04). APSAC was well tolerated, the change in mean blood pressure after bolus injection being modest (−11 mmHg). Systemic fibrinolysis was somewhat greater after APSAC than low dose streptokinase: fibrinogen levels averaged 39 ± 4% (SE) of control at 90 minutes after APSAC, versus 64 ± 5% after streptokinase (p<0.01) in the subgroup tested. The rate of bleeding complications was acceptable for both regimens, and other adverse reactions were comparable. Rates of early occlusion were low in both treatment groups, and evolution of ECG and enzymatic indicators were similar. Thus, APSAC provides approximately similar reperfusion results as intracoronary streptokinase, especially when given within 4h, but is easier to administer and is well tolerated.
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Schmitz-Huebner, U., H. Ostermann, D. G. Mathey, J. Schofer, Ch Diefenbach, and R. Erbel. "INFLUENCE OF RECOMBINANT PRO-UROKINASE ON THE HEMOSTATIC SYSTEM IN PATIENTS WITH ACUTE MYOCARDIAL INFARCTION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643572.
Full textAbstract:
Recombinant unglycosylated pro-urokinase (recombinant single chain urokinase-type plasminogen activator, CG4509) was given to twelve patients (pts.) with acute myocardial infarction as a 20 mg bolus followed by a 60 mg intravenous infusion (iv.inf.) over 1 hour and to twelve pts. as a 10 mg bolus followed by a 30 mg iv.inf. over 1 hour. Reperfusion was angiographically confirmed in 9/12 pts. with the higher dose and in 6/12 pts. who obtained the lower dose. Different parameters of hemostasis were determined before administration, 30 min after the beginning of inf.,at the end of inf., 60 min thereafter and 6-12 hours afterwards .The most significant systemic changes were observed 60 min after the end of inf. when the following mean values ± SEM were determined (pre-inf. values in brackets):Fibrinolytic activity in plasma determined on fibrin plates was highest in both groups 30 min after the beginning of inf. and hardly measurable 60 min after the end of inf. No bleeding complications were observed. Based on these results,a randomized double-blind multicenter trial was started to study the effects of 80 mg CG 4509 versus 1.5 million U streptokinase iv.
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Loerakker, Sandra, Anke Stekelenburg, Gustav J. Strijkers, Klaas Nicolay, Dan L. Bader, Frank P. T. Baaijens, and Cees W. J. Oomens. "Effect of Continuous and Intermittent Mechanical Loading on the Development of Skeletal Muscle Damage - A Combined Experimental/Numerical Approach." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206354.
Full textAbstract:
Prolonged mechanical loading of soft tissues, as present when individuals are bedridden or wheelchair-bound, can lead to degeneration of skeletal muscle tissue. This can result in a condition termed pressure-related deep tissue injury (DTI), a severe kind of pressure ulcer that initiates in deep tissue layers, e.g. skeletal muscle, near bony prominences and progresses towards the skin. Complications associated with DTI include sepsis, renal failure, and myocardial infarction. Damage pathways leading to DTI involve ischemia, ischemia-reperfusion injury, impaired lymphatic drainage, and sustained tissue deformation. Recently, the role of tissue deformation in the onset of skeletal muscle damage was established by combining animal experiments with finite element (FE) modeling [1]. After 2 hours of continuous loading, a clear correlation between maximum shear strain and damage was found.
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Liebert, Ann. "Translational research in the prevention of myocardial reperfusion injury by PBM: a review of molecular mechanisms and current research results (Conference Presentation)." In Mechanisms of Photobiomodulation Therapy XIII, edited by Michael R. Hamblin, James D. Carroll, and Praveen Arany. SPIE, 2018. http://dx.doi.org/10.1117/12.2292128.
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Poniewierski, M., M. Barthels, and H. Poliwoda. "THE SAFETY AND EFFICACY OF A LOW MOLECULAR WEIGHT HEPARIN (FRAGMIN) IN THE PREVENTION OF DEEP VEIN THROMBOSIS IN MEDICAL PATIENTS: A RANDOMIZED DOUBLE-BLIND TRIAL." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643224.
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The safety and efficacy of 2500 anti-Factor Xa U of a low molecular weight heparin (Kabi 2165, Fragmin) subcutaneously once a day, and 5000 IU of standard unfractionated Heparin (KabiVitrum, Stockholm) subcutaneously twice daily as thromboprophylaxis was compared in 200 medical patients in a randomized double blind trial. According to the risk of DVT the patients were stratified before randomization in a high and low risk group. The high risk group consisted of 100 patients mainly with malignant diseases and/or previous history of thromboembolism, the low risk group of 100 patients with mainly myocardial infarction and/or coronary heart disease. The prophylaxis was given for seven to ten days. In 192 consecutive patients the clinical status and thermographic screening for DVT (leg temperature profiles, DeVeTherm) were daily evaluated. In two cases of suspected DVT and one case of suspected PE, the following phlebography or pulmonary scintigraphy were found to be negative. In the high risk group, one patient treated with Fragmin having a central venous catheter developed on day 10 symptoms of an arm vein thrombosis. There were no bleeding complications observed in either of the two treatment groups. Two patients with trombocytopenia (25.000 and 22.000/pl) due to chemotherapy and underlying malignant disease were successfully treated with Fragmin without developing any bleeding complications. In eight patients during Fragmin prophylaxis invasive diagnostic methods as heart catheterization, gastroscopy, bronchoscopy or spinal puncture were performed without noticing any bleeding events. 2500 anti-Factor Xa U of Fragmin gave plasma levels by anti-Factor Xa assay (S-2222, Kabi) of mean 0,1 U/ml when blood was sampled three to four hours after the subcutaneus application. There was no accumulation during the treatment periode observed.This study suggests that 2500 anti-Factor Xa U of Fragmin once daily is as safe and effective as 5000 IU of standard heparin twice daily in these medical patients. Especially in patients who need prophylaxis for a long time eg. with malignant disease, the once daily injection is welcomed.