Journal articles: '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.

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Dugbartey, George J., and Andrew N. Redington. "Prevention of contrast-induced nephropathy by limb ischemic preconditioning: underlying mechanisms and clinical effects." American Journal of Physiology-Renal Physiology 314, no. 3 (March 1, 2018): F319—F328. http://dx.doi.org/10.1152/ajprenal.00130.2017.

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Contrast-induced nephropathy (CIN) is an important complication following diagnostic radiographic imaging and interventional therapy. It results from administration of intravascular iodinated contrast media (CM) and is currently the third most common cause of hospital-acquired acute kidney injury. CIN is associated with increased morbidity, prolonged hospitalization, and higher mortality. Although the importance of CIN is widely appreciated, and its occurrence can be mitigated by the use of pre- and posthydration protocols and low osmolar instead of high osmolar iodine-containing CM, specific prophylactic therapy is lacking. Remote ischemic preconditioning (RIPC), induced through short cycles of ischemia-reperfusion applied to the limb, is an intriguing new strategy that has been shown to reduce myocardial infarction size in patients undergoing emergency percutaneous coronary intervention. Furthermore, multiple proof-of-principle clinical studies have suggested benefit in several other ischemia-reperfusion syndromes, including stroke. Perhaps somewhat surprisingly, RIPC also is emerging as a promising strategy for CIN prevention. In this review, we discuss current clinical and experimental developments regarding the biology of CIN, concentrating on the pathophysiology of CIN, and cellular and molecular mechanisms by which limb ischemic preconditioning may confer renal protection in clinical and experimental models of CIN.

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Menzorov, Maksim V., Alexander M. Shutov, Vladimir S. Sakharov, and Vera N. Kabanova. "Acute kidney injury in acute coronary syndrome." Kazan medical journal 103, no. 5 (October 3, 2022): 797–806. http://dx.doi.org/10.17816/kmj2022-797.

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Acute kidney injury is a common complication of acute coronary syndrome that aggravates its prognosis. The article presents the current criteria and stratification of the acute kidney injury severity, its place in the structure of cardiorenal syndromes, renal and cardiorenal continuums. The data on the frequency, severity and clinical variants of complications in acute coronary syndrome, myocardial infarction, unstable angina pectoris are presented. The risk factors for the development of acute kidney injury and its contrast-induced variant are described. The data on the significance of acute renal dysfunction in changing the trajectory of cardiovascular disease, worsening the immediate and long-term prognosis, the development and progression of chronic kidney disease, ischemic complications are presented. The effect of mechanical and pharmacological reperfusion on the incidence of acute kidney injury is described. Promising approaches to the diagnostics of acute kidney injury, including the significance of biomarkers and the problems associated with their use, are outlined. The article presents data on the role of radiopaque agents in the development of acute kidney injury, describes the difference between contrast-induced nephropathy, its contrast-associated, post-contrast and contrast-induced variants. The current approaches to the prevention and treatment of acute kidney injury from the point of view of various professional communities are outlined. Approaches to risk stratification and the possibility of using risk scales are described. The main measures for the prevention and treatment of acute kidney injury, depending on its severity, the place of renal replacement therapy are presented. The paper presents the current hydration regimens and describes the principles of their modification depending on the clinical characteristics of patients, proposed by experts from the Scientific Society of Nephrology of Russia and the consensus of the American College of Radiology, the US National Kidney Foundation.

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Wang, Wen-Hwa, Guang-Yuan Mar, Kai-Che Wei, Chin-Chang Cheng, and Wei-Chun Huang. "Risk Factors and Outcomes of Heart Failure Following First-Episode of Acute Myocardial Infarction—A Case Series Study of 161,384 Cases." Healthcare 9, no. 10 (October 16, 2021): 1382. http://dx.doi.org/10.3390/healthcare9101382.

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Background: Heart failure (HF) is one of the important complications of acute myocardial infarction (AMI), but the epidemiology, associated risks and outcomes have not been well investigated in the era of broad use of fluoroscopy-guided angiographic intervention. Methods: We analysed 161,384 subjects who had experienced the first episode of AMI during 1 January 2000 and 31 December 2012 using the Taiwan National Health Insurance Research Database. Results: During the index AMI hospitalization, 23.6% of cases developed HF. Female, ≥65 years-old, non-ST-segment elevation type of MI, diabetes mellitus (DM), peripheral vascular occlusion disease (PAOD), chronic obstructive pulmonary disease (COPD), atrial fibrillation, and ventricular tachycardia/fibrillation (VT/VF) were associated with higher risks of developing HF. HF cases had inferior survival outcomes compared to non-HF cases in both the short and long term. Among those HF patients, ≥65 years, DM, PAOD, and VT/VF were associated with worse outcomes. On the contrary, coronary reperfusion intervention and treat-to-target pharmacologic treatment were associated with favourable survival outcomes. Conclusions: HF remains common in the modern age and poses negative impacts in survival of AMI patients. It highlights that prudent prevention and early treatment of HF during AMI hospitalization is an important medical issue.

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Caccioppo, Andrea, Luca Franchin, Alberto Grosso, Filippo Angelini, Fabrizio D’Ascenzo, and Maria Felice Brizzi. "Ischemia Reperfusion Injury: Mechanisms of Damage/Protection and Novel Strategies for Cardiac Recovery/Regeneration." International Journal of Molecular Sciences 20, no. 20 (October 11, 2019): 5024. http://dx.doi.org/10.3390/ijms20205024.

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Ischemic diseases in an aging population pose a heavy social encumbrance. Moreover, current therapeutic approaches, which aimed to prevent or minimize ischemia-induced damage, are associated with relevant costs for healthcare systems. Early reperfusion by primary percutaneous coronary intervention (PPCI) has undoubtedly improved patient’s outcomes; however, the prevention of long-term complications is still an unmet need. To face these hurdles and improve patient’s outcomes, novel pharmacological and interventional approaches, alone or in combination, reducing myocardium oxygen consumption or supplying blood flow via collateral vessels have been proposed. A number of clinical trials are ongoing to validate their efficacy on patient’s outcomes. Alternative options, including stem cell-based therapies, have been evaluated to improve cardiac regeneration and prevent scar formation. However, due to the lack of long-term engraftment, more recently, great attention has been devoted to their paracrine mediators, including exosomes (Exo) and microvesicles (MV). Indeed, Exo and MV are both currently considered to be one of the most promising therapeutic strategies in regenerative medicine. As a matter of fact, MV and Exo that are released from stem cells of different origin have been evaluated for their healing properties in ischemia reperfusion (I/R) settings. Therefore, this review will first summarize mechanisms of cardiac damage and protection after I/R damage to track the paths through which more appropriate interventional and/or molecular-based targeted therapies should be addressed. Moreover, it will provide insights on novel non-invasive/invasive interventional strategies and on Exo-based therapies as a challenge for improving patient’s long-term complications. Finally, approaches for improving Exo healing properties, and topics still unsolved to move towards Exo clinical application will be discussed.

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Chabanovych, N. B., M. Yu Mamonova, S. V. Konotopchyk, D. V. Shchehlov, and M. B. Vyval. "Analysis of the experience of anesthetic management during endovascular mechanical thrombectomy in ischemic cerebral stroke." Endovascular Neuroradiology 34, no. 4 (December 31, 2020): 70–81. http://dx.doi.org/10.26683/2304-9359-2020-4(34)-70-81.

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Objective ‒ to analyze our own experience of anesthetic management during mechanical thrombectomy (MTE) in patients with acute ischemic stroke (AIS) caused by large cerebral vessels occlusion. Materials and methods. Treatment of patients with AIS caused by large cerebral vessels occlusion was carried out in accordance with the recommendations of the European Stroke Organization (ESO). MTE was performed in 63 patients (23 women and 40 men aged 36 to 82 years, mean age ‒ 62.00 ± 16.31 years). The severity of neurological symptoms in the acute period of ischemic stroke was assessed over time using the National Institutes of Health Stroke Scale (NIHSS). The degree of disability due to stroke was assessed using a modified Rankine scale (mSR) before discharge and after 90 days. The results by mRS after 90 days were the most indicative. Early ischemic changes in the brain on computed tomograms were assessed using the Alberta Stroke Program Early CT score (ASPECTS). To reduce the time «onset-to groin time» (puncture of the femoral artery), all patients were immediately sent to the operating room upon hospitalization after neuroimaging. For MTE in 50 (79 %) cases conscious sedation with local anesthesia (sibazon, fentanyl) was used, in 13 (21%) cases ‒ general anesthesia (propofol, fentanyl, atracurium besylate). Regardless of the anesthesia method, vital signs were monitored and postoperative complications were assessed. The assessment of other important indicators related to the expiration of anesthesia was carried out: the time «onset-the the groin time» the time «from groin – to recanalization», the level of saturation, the stability of mean arterial pressure, the use of vasopressors or labetolol, the number of postoperative complications (pneumonia, dislocation with decompression craniotomy, nausea, myocardial infarction). Results. The algorithm for anesthetic management of the perioperative period included the anesthesia during MTE, postoperative anesthetic monitoring and correction of deviations over the next 72 hours. Mandatory components of anesthetic support of MTE were to maintain blood pressure of at least 140/90 mm Hg. before reperfusion and FiO2 0.45‒0.5%. Anesthetic management also included infusion therapy, prevention of vomiting and regurgitation, and symptomatic therapy. Special attention was paid to the control of hemodynamics in the postoperative period. The results of treatment according to mRS after 90 days showed that more than half of the patients ‒ 32 (50.8%) after MTE were independent of outside help (0‒2 points), 24 (38.1 %) ‒ 3‒5 points, 6 points (mortality) ‒ 7 (11.1 %). After general anesthesia during MTE, 2 (15.4 %) deaths were registered, after MTE with conscious sedation using ‒ 5 (10.0%). There more patients with the vasopressors or labetalol using and the number of postoperative pneumonia were identified in the group with general anesthesia. For other indicators, there was no statistically significant difference in the results depending on the type of anesthesia. There was no statistically significant difference in the results in depending on anesthesia method. Conclusions. The choice of the anesthesia method during MTE for large cerebral vessels should be individual. There was no statistically significant difference in the results in treatment of patients with AIS using MTE (in particular, in mortality), depending on the type of anesthetic management. It is also wasn’t found in the time «onset – to groin time» and the time «groin – to recanalization» with various methods of anesthesia. Indications of vital functions, saturation, mean arterial pressure in patients did not have a significant difference. Differences were revealed in terms of the vasopressors or labetolol using and the number of postoperative pneumonia, depending on the anesthesia type. The anesthesia team should be involved in patient management from the moment of hospitalization, regardless of the method of anesthesia. The results of AIS treatment depend on the initial NIHSS and ASPECTS scores, comorbidity, collateral development, perioperative complications, and the degree of reperfusion after surgery. Special attention should be paid to hemodynamics before and after reperfusion recovery after vessel recanalization, taking into account the degree of reperfusion. The influence of the type of anesthesia on the results of the treatment of AIS with the MTE using remains under the further discussion.

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Serhiyenko, V. A., and A. A. Serhiyenko. "Diabetes mellitus and acute coronary syndromes." INTERNATIONAL JOURNAL OF ENDOCRINOLOGY (Ukraine) 17, no. 4 (August 17, 2021): 346–60. http://dx.doi.org/10.22141/2224-0721.17.4.2021.237351.

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This review article summarizes the existing literature on the current state of the problem of diabetes mellitus and acute coronary syndromes. In particular, the issues are analyzed related to the etiology, epidemiology, main pathophysiological features, classification of acute coronary syndromes, acute coronary syndromes without persistent ST-segment elevation on the electrocardiogram, acute coronary syndromes with ST-segment elevation, non-atherosclerotic causes of acute coronary syndrome, laboratory and instrumental diagnostic tests. Issues were analyzed related to the main approaches to the treatment of acute coronary syndromes, management of patients with diabetes mellitus and acute coronary syndromes, recommendations for secondary prevention. Initial treatment with corticosteroids includes acetylsalicylic acid, bolus heparin and intravenous heparin infusion (in the absence of contraindications). Antiplatelet therapy with ticagrelor or clopidogrel is also recommended. Pain is controlled using morphine/fentanyl and oxygen in case of hypoxia. Nitroglycerin can also be used sublingually or by infusion to relieve pain. Continuous monitoring of myocardial activity for arrhythmia is required. The choice of reperfusion strategy in patients with diabetes mellitus should be based on many factors, including assessment of clinical status (hemodynamic/electrical instability, prolonged ischemia), complications of chronic coronary syndrome, ischemic load, echocardiography, assessment of left ventricular function and any other comorbidities. In addition, various methods for assessing coronary artery disease and predicting mortality due to surgery are needed to make a final decision. Advances in the sensitivity of cardiac biomarkers and the use of risk assessment tools now enable rapid diagnosis within a few hours of symptom onset. Advances in the invasive management and drug therapy have resulted in improved clinical outcomes with resultant decline in mortality associated with acute coronary syndrome.

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Qin, Chengxue, Suwan Yap, and Owen L. Woodman. "Antioxidants in the prevention of myocardial ischemia/reperfusion injury." Expert Review of Clinical Pharmacology 2, no. 6 (November 2009): 673–95. http://dx.doi.org/10.1586/ecp.09.41.

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Quintana, Miguel, Thomas Kahan, and Paul Hjemdahl. "Pharmacological Prevention of Reperfusion Injury in Acute Myocardial Infarction." American Journal of Cardiovascular Drugs 4, no. 3 (2004): 159–67. http://dx.doi.org/10.2165/00129784-200404030-00003.

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Garcia-Dorado, David, and Marisol Ruiz-Meana. "Propagation of Cell Death During Myocardial Reperfusion." Physiology 15, no. 6 (December 2000): 326–30. http://dx.doi.org/10.1152/physiologyonline.2000.15.6.326.

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During myocardial reperfusion, increased cytosolic Ca2+ concentration may cause hypercontracture and cell death. Hypercontracture can propagate to adjacent cells by a gap junction-dependent mechanism. This propagation explains infarct geometry and increases the final extent of necrosis. Its prevention may represent a new therapeutic strategy for treating patients with myocardial infarction.

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Bellis, Alessandro, Ciro Mauro, Emanuele Barbato, Giuseppe Di Gioia, Daniela Sorriento, Bruno Trimarco, and Carmine Morisco. "The Rationale of Neprilysin Inhibition in Prevention of Myocardial Ischemia-Reperfusion Injury during ST-Elevation Myocardial Infarction." Cells 9, no. 9 (September 21, 2020): 2134. http://dx.doi.org/10.3390/cells9092134.

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During the last three decades, timely myocardial reperfusion using either thrombolytic therapy or primary percutaneous intervention (pPCI) has allowed amazing improvements in outcomes with a more than halving in 1-year ST-elevation myocardial infarction (STEMI) mortality. However, mortality and left ventricle (LV) remodeling remain substantial in these patients. As such, novel therapeutic interventions are required to reduce myocardial infarction size, preserve LV systolic function, and improve survival in reperfused-STEMI patients. Myocardial ischemia-reperfusion injury (MIRI) prevention represents the main goal to reach in order to reduce STEMI mortality. There is currently no effective therapy for MIRI prevention in STEMI patients. A significant reason for the weak and inconsistent results obtained in this field may be the presence of multiple, partially redundant, mechanisms of cell death during ischemia-reperfusion, whose relative importance may depend on the conditions. Therefore, it is always more recognized that it is important to consider a “multi-targeted cardioprotective therapy”, defined as an additive or synergistic cardioprotective agents or interventions directed to distinct targets with different timing of application (before, during, or after pPCI). Given that some neprilysin (NEP) substrates (natriuretic peptides, angiotensin II, bradykinin, apelins, substance P, and adrenomedullin) exert a cardioprotective effect against ischemia-reperfusion injury, it is conceivable that antagonism of proteolytic activity by this enzyme may be considered in a multi-targeted strategy for MIRI prevention. In this review, by starting from main pathophysiological mechanisms promoting MIRI, we discuss cardioprotective effects of NEP substrates and the potential benefit of NEP pharmacological inhibition in MIRI prevention.

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Cohen, Alexander T. "Prevention of perioperative myocardial ischaemia and its complications." Lancet 351, no. 9100 (February 1998): 385–86. http://dx.doi.org/10.1016/s0140-6736(05)78348-3.

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Merx, Marc W., and Malte Kelm. "Myocardial reperfusion injury and the challenging quest for its prevention*." Critical Care Medicine 35, no. 7 (July 2007): 1793–94. http://dx.doi.org/10.1097/01.ccm.0000269355.63009.c1.

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23

Stewart, James R., Stephen L. Crute, Victor Loughlin, Michael L. Hess, and Lazar J. Greenfield. "Prevention of free radical-induced myocardial reperfusion injury with allopurinol." Journal of Thoracic and Cardiovascular Surgery 90, no. 1 (July 1985): 68–72. http://dx.doi.org/10.1016/s0022-5223(19)38664-7.

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CHEN, C. "Experimental study of prevention of myocardial reperfusion injury with anisodamin." Journal of Molecular and Cellular Cardiology 22 (July 1990): 3. http://dx.doi.org/10.1016/0022-2828(90)90134-n.

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25

Asaf, Roy, Shany Blum, Rachel Miller-Lotan, and Andrew Levy. "BXT-51072 and the Prevention of Myocardial Ischemia-Reperfusion Injury." Letters in Drug Design & Discovery 4, no. 2 (March 1, 2007): 160–62. http://dx.doi.org/10.2174/157018007779422479.

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Khubulava, G. G., A. N. Shishkevich, S. S. Mikhailov, and E. Yu Bessonov. "Myocardial reperfusion syndrome. Pathogenesis, clinic, diagnosis." Bulletin of the Russian Military Medical Academy 22, no. 1 (December 15, 2020): 196–200. http://dx.doi.org/10.17816/brmma25992.

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The basics of pathogenesis, clinic and diagnosis of myocardial reperfusion syndrome are considered. Myocardial reperfusion syndrome is defined. Its relevance as one of the most poorly studied and formidable complications of cardiac reperfusion in myocardial infarction with elevation of the S-T segment has been explained. A brief review of the historical review of this problem and such types of manifestations of myocardial reperfusion syndrome as: diastolic myocardial dysfunction, post-reperfusion disturbances of the heart rhythm, the phenomenon of no-reflow and irreversible damage to the myocardium are briefly reviewed. The modern views on the pathological physiology of diastolic myocardial dysfunction, post-reperfusion damage to the myocardium, and the no-reflow phenomenon are analyzed. A review of current views on the pathological physiology of the development of post-reperfusion disturbances in heart rhythm is carried out. The clinical picture and the effect on the hemodynamics of such a manifestation of myocardial reperfusion syndrome as diastolic myocardial dysfunction are described. A brief description of the clinical picture of irreversible post-reperfusion damage to the myocardium is given. The clinical picture and types of post-reperfusion rhythm disturbances are described. The diagnostics of the no-reflow phenomenon has been analyzed in detail, the coronary angiographic scales for assessing thrombolysis in myocardial infarction and for assessing myocardial perfusion are graphically shown. A description of the basics of diagnosing post-reperfusion disturbances in heart rhythm, diastolic myocardial dysfunction, and post-reperfusion irreversible damage to the myocardium is given. A brief description of the known in the world literature predictors of the development of myocardial reperfusion syndrome is presented.

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Shybekа, N., L. Gelis, and T. Rusak. "DIAGNOSTIC SIGNS OF MYOCARDIAL REPERFUSION INJURY AFTER CORONARY ARTERY BYPASS GRAFTING." Emergency Cardiology and Cardiovascular Risks 5, no. 1 (2021): 1167–72. http://dx.doi.org/10.51922/2616-633x.2021.5.2.1167.

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One of the main causes for operative mortality and perioperative complications after coronary artery bypass grafting is myocardial reperfusion injury following the restoration of the coronary circulation in the ischemic zone of the myocardium and characterized by myocardial, electrophysiological and vascular dysfunction. In order to identify the diagnostic signs of myocardial reperfusion injury after coronary artery bypass grafting, a prospective study was conducted, which included 89 patients with ischemic heart disease and forthcoming coronary artery bypass grafting either on-pump or off-pump. Postischemic myocardial dysfunction was assessed using transesophageal echocardiography, morphological and functional signs of myocardial reperfusion injury were detected using cardiac magnetic resonance imaging, moreover, the level of highly sensitive troponin, myoglobin, creatine phosphokinase-MB, metalloproteinase-2, and highly sensitive C-reactive protein was measured to assess the contribution of biomarkers to the development of reperfusion injuries. The obtained data allowed us to assess the morphological and functional characteristics of postischemic myocardial dysfunction and identify diagnostic signs of irreversible reperfusion injuries.

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Vytrykhovskyi, Andriy I., and Muhaylo V. Fedorchenko. "REPERFUSION INJURY IN ACUTE PERIOD OF MYOCARDIAL INFARCTION – WAYS OF PREVENTION AND CORRECTION." Wiadomości Lekarskie 75, no. 10 (2022): 2514–18. http://dx.doi.org/10.36740/wlek202210137.

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The aim: To identify pathophysiological peculiarities of myocardial reperfusion injury and ways of its reduction based on the literature data analysis. Materials and methots: This literature review was made by searching the PubMed database using key words . Additional data were sought in the Google search engine by entering key words: “ risk factors, ischemic heart disease, arrhythmia, sudden cardiac death, heart rhythm, heart failure.” in the Polish, English, Russian and Ukrainian language versions Conclusions: Considering conducted data analysis, provided data indicate the prospects of phosphocreatine usage in treatment scheme of heart rhythm disorders and heart failure on the background of myocardial ischemia and elimination of reperfusion injury and myocardial remodeling consequences.

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Boyarinov, G. A., A. A. Usanova, I. S. Kotlov, A. S. Saushev, and A. P. Komkov. "Drug Prevention of Reperfusion Lesions during Thrombolytic Therapy for Myocardial Infarction." General Reanimatology 6, no. 1 (February 20, 2010): 64. http://dx.doi.org/10.15360/1813-9779-2010-1-64.

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Vrints, Christiaan JM. "Improving diagnosis, reperfusion therapy and secondary prevention in acute myocardial infarction." European Heart Journal: Acute Cardiovascular Care 7, no. 6 (September 2018): 495–96. http://dx.doi.org/10.1177/2048872618804940.

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Vatazin, A. V., D. V. Artemov, and A. B. Zulkarnaev. "PREVENTION AND TREATMENT OF ISCHEMIA-REPERFUSION SYNDROME." Nephrology (Saint-Petersburg) 23, no. 2 (February 21, 2019): 41–48. http://dx.doi.org/10.24884/1561-6274-2019-23-2-41-48.

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The main negative consequences of ischemia-reperfusion of the kidneys are the early developing severe chronic dysfunction of the graft, and in the most severe cases the function of the transplanted kidney is not restored (primary non-functioning graft). As a result of loss of transplant function, the patient usually returns to dialysis. These complications are more common in kidney transplants from “donors with extended criteria,” since these organs are most sensitive to damage resulting from ischemia-reperfusion syndrome (IR syndrome). At the same time, the share of such (suboptimal) donors is gradually increasing in Russia. Cold preservation of the organ in special solutions remains the gold standard for kidney transplantation, however, it is not able to fully protect the organ. The article presents the main promising methods that reduce the severity of ischemic and reperfusion injury: donor conditioning, ischemic preconditioning, various variants of kidney preservation, effects on inflammatory mediators, application of biological target drugs. Nevertheless, the pathogenesis of ischemia-reperfusion syndrome has been studied much better than the methods of its correction. Currently, there are only indirect or experimental evidence that the severity of the syndrome of IR can be reduced due to the pharmacoprotection of the ogran before donation, during preservation, as well as in the early postoperative period. Further research is needed to find ways to reduce the severity of ischemic and reperfusion injury of the graft.

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Marinescu, Mihnea-Cosmin, Andrada-Luciana Lazar, Monica Mihaela Marta, Angela Cozma, and Cristina-Sorina Catana. "Non-Coding RNAs: Prevention, Diagnosis, and Treatment in Myocardial Ischemia–Reperfusion Injury." International Journal of Molecular Sciences 23, no. 5 (March 1, 2022): 2728. http://dx.doi.org/10.3390/ijms23052728.

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Recent knowledge concerning the role of non-coding RNAs (ncRNAs) in myocardial ischemia/reperfusion (I/R) injury provides new insight into their possible roles as specific biomarkers for early diagnosis, prognosis, and treatment. MicroRNAs (miRNAs) have fewer than 200 nucleotides, while long ncRNAs (lncRNAs) have more than 200 nucleotides. The three types of ncRNAs (miRNAs, lncRNAs, and circRNAs) act as signaling molecules strongly involved in cardiovascular disorders (CVD). I/R injury of the heart is the main CVD correlated with acute myocardial infarction (AMI), cardiac surgery, and transplantation. The expression levels of many ncRNAs and miRNAs are highly modified in the plasma of MI patients, and thus they have the potential to diagnose and treat MI. Cardiomyocyte and endothelial cell death is the major trigger for myocardial ischemia–reperfusion syndrome (MIRS). The cardioprotective effect of inflammasome activation in MIRS and the therapeutics targeting the reparative response could prevent progressive post-infarction heart failure. Moreover, the pharmacological and genetic modulation of these ncRNAs has the therapeutic potential to improve clinical outcomes in AMI patients.

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Woodman, Owen L. "Approaches to the Prevention of Coronary Vascular Dysfunction Caused by Myocardial Ischaemia and Reperfusion." Current Pharmaceutical Design 5, no. 12 (December 1999): 1077–87. http://dx.doi.org/10.2174/1381612805666230112214526.

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The endothelium is an important regulator of coronary vascular tone due to its ability to release potent vasoactive substances such as the vasodilators nitric oxide (NO), endothelium-derived hyperpolarizing factor (EDHF), prostacyclin (PGl2) and the potent vasoconstrictor endothelin. Endothelial dysfunction has been associated with a number of pathological states such as atherosclerosis, hypertension, diabetes and congestive heart failure. A disturbance of endothelial function may also contribute to the adverse effects that ischaemia and reperfusion exerts on the coronary vasculature. After ischaemia and reperfusion there is usually a selective impairment of endothelium-dependent relaxation in isolated coronary arteries. However, in the intact coronary circulation, there is a general loss of vasodilator reserve as responses to both endothelium-dependent and endothelium-independent agonists are attenuated. The release of vasoconstrictor(s) and plugging of capillaries with leukocytes may contribute to that impairment of the capacity of the coronary circulation to dilate together with the reduction in basal blood flow (no-reflow phenomenon). Ischaemic preconditioning is able to prevent ischaemic damage to the myocardium but the vasculature is less well protected as reperfusion is enhanced but the vasodilator reserve continues to be limited. Pharmacological preservation of vascular function has proved more successful with inhibitors of leukocyte adhesion, calcium channel blockers, endothelin receptor antagonists and inhibitors of oxygen radical generation all offering protection. Further refinement of protocols to preserve endothelial and vascular function after ischaemia will aid reperfusion, enhance vasodilator reserve and maximise recovery of myocardial function.

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Fuentes, Eduardo, Rodrigo Moore-Carrasco, Antonio Marcus de Andrade Paes, and Andres Trostchansky. "Role of Platelet Activation and Oxidative Stress in the Evolution of Myocardial Infarction." Journal of Cardiovascular Pharmacology and Therapeutics 24, no. 6 (July 7, 2019): 509–20. http://dx.doi.org/10.1177/1074248419861437.

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Myocardial infarction, commonly known as heart attack, evolves from the rupture of unstable atherosclerotic plaques to coronary thrombosis and myocardial ischemia–reperfusion injury. A body of evidence supports a close relationship between the alterations following an ischemia–reperfusion injury-induced oxidative stress and platelet activity. Through their critical role in thrombogenesis and inflammatory responses, platelets are fully (totally) implicated from atherothrombotic plaque formation to myocardial infarction onset and expansion. However, mere platelet aggregation prevention does not offer full protection, suggesting that other antiplatelet therapy mechanisms may also be involved. Thus, the present review discusses the integrative role of platelets, oxidative stress, and antiplatelet therapy in triggering myocardial infarction pathophysiology.

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Zalewski, Jaroslaw, Karol Nowak, Patrycja Furczynska, and Magdalena Zalewska. "Complicating Acute Myocardial Infarction. Current Status and Unresolved Targets for Subsequent Research." Journal of Clinical Medicine 10, no. 24 (December 16, 2021): 5904. http://dx.doi.org/10.3390/jcm10245904.

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Mechanical reperfusion with primary angioplasty, as the treatment of choice in acute myocardial infarction (MI), is associated not only with a high percentage of full epicardial and tissue reperfusion but also with a very good immediate and long-term clinical outcome. However, the Achilles heel of MI treatment is its ensemble of complications, such as cardiogenic shock due to severe systolic and/or diastolic dysfunction or MI mechanical complications, including perforation of the left ventricular free wall, papillary muscle rupture with acute mitral regurgitation and ventricular septal rupture. They are associated with an increased or, sometimes, with an extremely high mortality rate, determining the overall mortality in an MI patient population. In this review we summarize the mechanisms of MI complications, current therapeutic management and alternative directions for overcoming their devastating consequences. Moreover, we have sought to indicate gaps in the evidence on current treatments as the potential targets for further clinical research. From the perspective of mortality trends that are not improving, the forthcoming therapeutic management of complicated MI will require an individualized and novel approach based on their thorough pathobiology.

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Zhao, Wei-kun, Yao Zhou, Tong-tong Xu, and Qi Wu. "Ferroptosis: Opportunities and Challenges in Myocardial Ischemia-Reperfusion Injury." Oxidative Medicine and Cellular Longevity 2021 (October 23, 2021): 1–12. http://dx.doi.org/10.1155/2021/9929687.

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Ferroptosis is a newly discovered form of regulated cell death dependent on iron and reactive oxygen species (ROS). It directly or indirectly affects the activity of glutathione peroxidases (GPXs) under the induction of small molecules, causing membrane lipid peroxidation due to redox imbalances and excessive ROS accumulation, damaging the integrity of cell membranes. Ferroptosis is mainly characterized by mitochondrial shrinkage, increased density of bilayer membranes, and the accumulation of lipid peroxidation. Myocardial ischemia-reperfusion injury (MIRI) is an unavoidable risk event for acute myocardial infarction. Ferroptosis is closely associated with MIRI, and this relationship is discussed in detail here. This review systematically summarizes the process of ferroptosis and the latest research progress on the role of ferroptosis in MIRI to provide new ideas for the prevention and treatment of MIRI.

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Stamenkovic, Aleksandra, Kimberley A. O’Hara, David C. Nelson, Thane G. Maddaford, Andrea L. Edel, Graham Maddaford, Elena Dibrov, et al. "Oxidized phosphatidylcholines trigger ferroptosis in cardiomyocytes during ischemia-reperfusion injury." American Journal of Physiology-Heart and Circulatory Physiology 320, no. 3 (March 1, 2021): H1170—H1184. http://dx.doi.org/10.1152/ajpheart.00237.2020.

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Oxidized phosphatidylcholines (OxPC) generated during reperfusion injury are potent inducers of cardiomyocyte death. Our studies have shown that OxPCs exert this effect through a ferroptotic process that can be attenuated. A better understanding of the OxPC cell death pathway can prove a novel strategy for prevention of cell death during myocardial reperfusion injury.

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Yang, Yongjian, Yi Yang, Xiong Wang, Jin Du, Juanni Hou, Juan Feng, Yue Tian, Lei He, Xiuchuan Li, and Haifeng Pei. "Does growth differentiation factor 11 protect against myocardial ischaemia/reperfusion injury? A hypothesis." Journal of International Medical Research 45, no. 6 (August 25, 2016): 1629–35. http://dx.doi.org/10.1177/0300060516658984.

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The pathogenesis of myocardial ischaemia/reperfusion injury is multifactorial. Understanding the mechanisms of myocardial ischaemia/reperfusion will benefit patients with ischaemic heart disease. Growth differentiation factor 11 (GDF11), a member of the secreted transforming growth factor-β superfamily, has been found to reverse age-related hypertrophy, revealing the important role of GDF11 in cardiovascular disease. However, the functions of GDF11 in myocardial ischaemia/reperfusion have not been elucidated yet. A number of signalling molecules are known to occur downstream of GDF11, including mothers against decapentaplegic homolog 3 (SMAD3) and forkhead box O3a (FOXO3a). A hypothesis is presented that GDF11 has protective effects in acute myocardial ischaemia/reperfusion injury through suppression of oxidative stress, prevention of calcium ion overload and promotion of the elimination of abnormal mitochondria via both canonical (SMAD3) and non-canonical (FOXO3a) pathways. Since circulating GDF11 may mainly derive from the spleen, the lack of a spleen may make the myocardium susceptible to damaging insults. Administration of GDF11 may be an efficacious therapy to protect against cardiovascular diseases in splenectomized patients.

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Alekseeva, Ya V., E. V. Vyshlov, V. Yu Ussov, and V. A. Markov. "MICROVASCULAR INJURY PHENOMENA IN MYOCARDIAL INFARCTION." Siberian Medical Journal 33, no. 4 (February 13, 2019): 19–26. http://dx.doi.org/10.29001/2073-8552-2018-33-4-19-26.

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At a time of a wide use of coronary reperfusion for treatment of acute myocardial infarction, the microvascular phenomena significantly affecting the postinfarction state of the myocardium have been discovered. These phenomena include microvascular obstruction with a clinical presentation in the form of the no-reflow phenomenon and intramyocardial hemorrhage that strongly aggravate cardiac damage. The aim of this review was to analyze accumulated data on the prevalence, pathophysiology, diagnostic modalities, and approaches for prevention and treatment of microvascular injury.

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Bril, Antoine, and Luc Rochette. "Prevention of reperfusion-induced ventricular arrhythmias in isolated rat heart with magnesium." Canadian Journal of Physiology and Pharmacology 68, no. 6 (June 1, 1990): 694–99. http://dx.doi.org/10.1139/y90-105.

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The effects of magnesium (from 1.2 to 7.2 mM) were investigated in isolated perfused rat heart subjected to coronary artery ligation and reperfusion. Increasing magnesium concentrations, of the medium containing 3.00 mM of calcium, induced a significant bradycardia and a protective effect towards reperfusion arrhythmias. A significant correlation was found between the heart rate and the antiarrhythmic activity of increasing magnesium concentrations. The effects of high magnesium concentration (4.8 mM) were also investigated after labelling of internal stores of noradrenaline with [3H]noradrenaline. Without any marked change in the pattern of release of radioactivity, a significant reduction of the sudden release of radioactivity was observed during the reperfusion. However, magnesium did not change the uptake of noradrenaline by the heart. Our results suggest that the antiarrhythmic effect of magnesium might be of importance in the clinical treatment of myocardial ischemia.Key words: magnesium, isolated rat heart, reperfusion, arrhythmias, noradrenaline.

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Sharma, H. S., and D. K. Das. "Role of cytokines in myocardial ischemia and reperfusion." Mediators of Inflammation 6, no. 3 (1997): 175–83. http://dx.doi.org/10.1080/09629359791668.

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Mediators of myocardial inflammation, predominantly cytokines, have for many years been implicated in the healing processes after infarction. In recent years, however, more attention has been paid to the possibility that the inflammation may result in deleterious complications for myocardial infarction. The proinflammatory cytokines may mediate myocardial dysfunction associated with myocardial infarction, severe congestive heart failure, and sepsis. A growing body of literature suggests that inflammatory mediators could play a crucial role in ischemia–reperfusion injury. Furthermore, ischemia–reperfusion not only results in the local transcriptional and translational upregulation of cytokines but also leads to tissue infiltration by inflammatory cells. These inflammatory cells are a ready source of a variety of cytokines which could be lethal for the cardiomyocytes. At the cellular level it has been shown that hypoxia causes a series of well documented changes in cardiomyocytes that includes loss of contractility, changes in lipid metabolism and subsequent irreversible cell membrane damage leading to cell death. For instance, hypoxic cardiomyocytes produce interleukin-6 (IL-6) which could contribute to the myocardial dysfunction observed in ischemia reperfusion injury. Ischemia followed by reperfusion induces a number of other multi-potent cytokines, such as IL-1, IL-8, tumor necrosis factor-α (TNF-α), transforming growth factor-β1 (TGF-β1) as well as an angiogenic cytokine/ growth factor, vascular endothelial growth factor (VEGF), in the heart. Intrestingly, these multipotent cytokines (e.g. TNF-α) may induce an adaptive cytoprotective response in the reperfused myocardium. In this review, we have included a number of cytokines that may contribute to ventricular dysfunction and/or to the cytoprotective and adaptive changes in the reperfused heart.

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Tripathi, Byomesh, Vikas Aggarwal, Jinnette Dawn Abbott, Dharam J. Kumbhani, Jay Giri, Ankur Kalra, Partha Sardar, and Saurav Chatterjee. "Mechanical Complications in ST-Elevation Myocardial Infarction (STEMI) Based on Different Reperfusion Strategies." American Journal of Cardiology 156 (October 2021): 79–84. http://dx.doi.org/10.1016/j.amjcard.2021.06.012.

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Wang, Jianying, Jinchang Leng, Xiaowei Sun, Kun Peng, Xaojuan Ma, Shiqin Huang, and Fang Wang. "Protective Role of Amiodarone on Reperfusion Arrhythmia in Patients of Acute Myocardial Infarction with Percutaneous Coronary Intervention Treatment." Evidence-Based Complementary and Alternative Medicine 2022 (August 26, 2022): 1–5. http://dx.doi.org/10.1155/2022/2597173.

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With the development and popularity of percutaneous coronary intervention (PCI), ischemia-reperfusion injury (IRI) has attracted more and more clinical attention. Reperfusion arrhythmia (RA), one of the common manifestations during and after PCI, can affect the postoperative cardiac function of patients with acute myocardial infarction (AMI). Therefore, effective intervention on RA has important clinical significance. This study observed the effect of amiodarone on reperfusion arrhythmia (RA) after percutaneous coronary intervention (PCI) in patients with acute myocardial infarction (AMI) and explored its possible mechanism. The results showed that amiodarone had good clinical efficacy in the prevention of RA in patients with AMI after PCI, and it could reduce the levels of serum IL-6, hs-CRP, CK-MB, and cTnI in patients and reduce the damage caused by reperfusion, thereby reducing the occurrence of RA.

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Gurevich, Konstantin G., Aleksandr L. Urakov, Eugeniy L. Fisher, Timer A. Abzalilov, Kseniya A. Khairzamanova, Timur A. Yagudin, and Aleksandr V. Samorodov. "Possibilities of pharmacological correction of reperfusion injury of ischemic myocardium (review)." Reviews on Clinical Pharmacology and Drug Therapy 19, no. 3 (October 8, 2021): 259–67. http://dx.doi.org/10.17816/rcf193259-267.

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Timely and effective reperfusion in ischemia and reoxygenation in hypoxia of the heart muscle prevent myocardial infarction. Delayed reperfusion and reoxygenation in myocardial ischemia and hypoxia can cause reversible damage in it, which, with a favorable outcome, disappear without a trace. Excessively late reperfusion and reoxygenation inevitably ends with irreversible damage to the myocardium, which is widely known as a myocardial infarction, and which, together with other complications of cardiac ischemia, can cause disability and death of the patient. In recent years, reperfusion injury of the ischemic heart muscle has been recognized as an independent link in the pathogenesis of myocardial infarction. The mechanisms of this link of pathogenesis have been partially studied in experimental conditions. The phenomena of preconditioning and post-conditioning have been discovered, the effects of which are currently determined fairly reliably. After determining the mechanisms of reperfusion injury of the ischemic myocardium, the search and development of pharmacological agents capable of inducing such a phenomenon as cardioprotection began. In parallel, studies of specific microRNAs that claim to be diagnostic markers are being conducted, as well as the search for drugs that affect the level of their expression is being conducted. The information about the achieved successes in this direction is given.

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Neimark, M. I., S. V. Zayashnikov, O. A. Kalugina, and L. N. Berestennikova. "Non-invasive mechanical ventilation for reperfusion myocardial injury prevention after endovascular surgeries in patients with ST-elevation myocardial infarction (STEMI)." Kazan medical journal 94, no. 1 (February 15, 2013): 50–54. http://dx.doi.org/10.17816/kmj1769.

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Aim. To determine the need for pressure controlled non-invasive mechanical ventilation for reperfusion myocardial injury prevention in patients with ST-elevation myocardial infarction (STEMI). Methods. The study enrolled 61 patients admitted to the intensive care unit within 6 hours from the debut of chest pain, ST-segment elevation on electrocardiogram and oxygen saturation less than 90%. A percutaneous coronary intervention on an affected coronary artery was performed in all patients 30-90 minutes from admission. Non-invasive mechanical ventilation using the «MAQUET Servo-s» machine was started in patients of the first group (31 patients, mean age 66.3±10.7 years, males - 19, females - 12) with positive end expiratory pressure of 2-6 cm H2O, pressure support of 6-10 cm H2O, 40-60% O2 gas mix. Patients of the second group (comparison group, 30 patients, mean age 63.5±9.8 years, males - 16, females - 14) were offered a conventional treatment of ST-elevation myocardial infarction, including inhalations of humidified oxygen (6-8 liters per minute) using a nasal cannula. Results. Systolic, diastolic blood pressure and heart rate were 123.0±9.4 mm Hg, 81.2±11.3 mm Hg, 70.1±6.1 beats per minute in patients of the first group in 6 hours after admission. In patients of the comparison group the following parameters were measured as 157±12.4 mm Hg, 90.2±10.1 mm Hg, 92.6±10.2 beats per minute. The absolute risk increase of arrhythmias related to reperfusion myocardial injury was 17.8% (р 0.05) for the patients from the second group. Ejection fraction on a transthoracic echocardiogram (Teichholz method) was measured as 47.0±4.0 and 60.5±7.4% in patients from the first and the second groups respectively (р 0.05). Conclusion. Non-invasive mechanical ventilation decreases the risk for arrhythmias related to reperfusion myocardial injury, and increases the ejection fraction compared to conventional treatment and can be applied in patients with STEMI.

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Hou Di, Wei-yong Liu, Fo-zhen Fang, Mo Jian, Su-fen Sun, Wei-ran Shi, Jin-ming Ye, Yan-fang Guan, and Liu Jian. "The experimental study of prevention of myocardial reperfusion injury with free radical scavengers." Perfusion 3, no. 3 (July 1988): 205–12. http://dx.doi.org/10.1177/026765918800300306.

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Lavie, Carl J., James H. O'Keefe, James H. Chesebro, Ian P. Clements, and Raymond J. Gibbons. "Prevention of late ventricular dilatation after acute myocardial infarction by successful thrombolytic reperfusion." American Journal of Cardiology 66, no. 1 (July 1990): 31–36. http://dx.doi.org/10.1016/0002-9149(90)90731-f.

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He, Ji-Fang, Yi-Xing Yang, Jiang-Yuan Li, Lu Liang, Li Xu, Yu Liu, Zong-Sheng Guo, et al. "A Novel Reperfusion Strategy for Primary Percutaneous Coronary Intervention in Patients with Acute ST-Segment Elevation Myocardial Infarction: A Prospective Case Series." Journal of Clinical Medicine 12, no. 2 (January 5, 2023): 433. http://dx.doi.org/10.3390/jcm12020433.

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Background: Ischemia reperfusion injury (IRI) remains a major problem in patients with acute ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI). We have developed a novel reperfusion strategy for PCI and named it “volume-controlled reperfusion (VCR)”. The aim of the current study was to assess the safety and feasibility of VCR in patients with STEMI. Methods: Consecutive patients admitted to Beijing Chaoyang Hospital with STEMI were prospectively enrolled. The feasibility endpoint was procedural success. The safety endpoints included death from all causes, major vascular complications, and major adverse cardiac event (MACE), i.e., a composite of cardiac death, myocardial reinfarction, target vessel revascularization (TVR), and heart failure. Results: A total of 30 patients were finally included. Procedural success was achieved in 28 (93.3%) patients. No patients died during the study and no major vascular complications or MACE occurred during hospitalization. With the exception of one patient (3.3%) who underwent TVR three months after discharge, no patient encountered death (0.0%), major vascular complications (0.0%), or and other MACEs (0.0%) during the median follow-up of 16 months. Conclusion: The findings of the pilot study suggest that VCR has favorable feasibility and safety in patients with STEMI. Further larger randomized trials are required to evaluate the effectiveness of VCR in STEMI patients.

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Kandula, Nirupama, Saurabh Kumar, Venkata Kiran Kumar Mandlem, Aneela Siddabathuni, Sanjay Singh, and Ramoji Kosuru. "Role of AMPK in Myocardial Ischemia-Reperfusion Injury-Induced Cell Death in the Presence and Absence of Diabetes." Oxidative Medicine and Cellular Longevity 2022 (October 11, 2022): 1–18. http://dx.doi.org/10.1155/2022/7346699.

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Recent studies indicate cell death is the hallmark of cardiac pathology in myocardial infarction and diabetes. The AMP-activated protein kinase (AMPK) signalling pathway is considered a putative salvaging phenomenon, plays a decisive role in almost all cellular, metabolic, and survival functions, and therefore entails precise regulation of its activity. AMPK regulates various programmed cell death depending on the stimuli and context, including autophagy, apoptosis, necroptosis, and ferroptosis. There is substantial evidence suggesting that AMPK is down-regulated in cardiac tissues of animals and humans with type 2 diabetes or metabolic syndrome compared to non-diabetic control and that stimulation of AMPK (physiological or pharmacological) can ameliorate diabetes-associated cardiovascular complications, such as myocardial ischemia-reperfusion injury. Furthermore, AMPK is an exciting therapeutic target for developing novel drug candidates to treat cell death in diabetes-associated myocardial ischemia-reperfusion injury. Therefore, in this review, we summarized how AMPK regulates autophagic, apoptotic, necroptotic, and ferroptosis pathways in the context of myocardial ischemia-reperfusion injury in the presence and absence of diabetes.

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Topaz, On, Allyne Topaz, and Pritam R. Polkampally. "Thrombectomy in Acute Myocardial Infarction." Interventional Cardiology Review 4, no. 1 (2009): 86. http://dx.doi.org/10.15420/icr.2009.4.1.86.

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Percutaneous coronary intervention (PCI) is the preferred management strategy for ST-segment-elevation myocardial infarction (STEMI) patients. However, a significant number of revascularisations result insuboptimal restoration of epicardial antegrade flow and inadequate myocardial tissue perfusion. This is mainly attributed to the underlying thrombus burden within the infarct-related vessel. Interventions for thrombotic lesions are clearly associated with an increased risk of acute and long-term complications. Thrombus remains a predictor of ischaemic complications, immediate and late stent thrombosis, increased in-hospital complications, death at six months and recurrent MI. Two types of thrombus removal device are available for utilisation in the setting of acute MI (AMI): aspiration-based catheters and mechanical thrombectomy. Administration of either systemic or selective adjunct pharmacotherapy can be useful in conjunction with application of all thrombus removal devices. Recent studies have demonstrated that thrombus aspiration is applicable and safe in a large majority of patients with STEMI, resulting in better reperfusion and clinical outcomes than standard PCI. However, it is unclear whether these findings are a direct result of a reduction in thrombus burden, facilitation of direct stenting or a combination of the two. The heavier the underlying thrombus burden, the higher the yield of mechanical thrombectomy over aspiration catheter. The role of thrombectomy as a useful adjunct therapy aimed specifically at direct contact and clearance of AMI-related thrombus continues to evolve.

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Journal articles on the topic 'Myocardial reperfusion Complications Prevention'

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