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Books on the topic 'Myocardial reperfusion Complications Prevention'

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Published: 10 December 2022
Last updated: 29 January 2023

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1

A, Salerno Tomas, and Ricci Marco, eds. Myocardial protection. Elmsford, N.Y: Blackwell Pub., 2004.

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2

S, Dhalla Naranjan, ed. Myocardial ischemia and preconditioning. Boston: Kluwer Academic, 2003.

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3

H, Opie Lionel, ed. Stunning, hibernation, and calcium in myocardial ischemia and reperfusion. Boston: Kluwer Academic, 1992.

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4

Seibu, Mochizuki, ed. The ischemic heart. Boston: Kluwer Academic Publishers, 1998.

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5

Ostadal, Bohuslav. Cardiac ischemia: From injury to protection. Boston: Kluwer Academic Publishers, 1999.

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6

František, Kolář, ed. Cardiac ischemia: From injury to protection. Boston: Kluwer Academic Publishers, 1999.

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7

M, Mentzer Robert, ed. Adenosine, cardioprotection, and its clinical application. Boston: Kluwer Academic Publishers, 1997.

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8

L, Hess Michael, ed. Free radicals, cardiovascular dysfunction, and protection strategies. Austin: R.G. Landes Co., 1994.

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9

Antoine, Lafont, and Topol Eric J. 1954-, eds. Arterial remodeling: A critical factor in restenosis. Boston: Kluwer Academic Publishers, 1997.

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10

Scientific basis of healthcare: AIDS and pregnancy. Boca Raton, FL: CRC Press/Taylor & Francis Group, 2011.

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11

Levin, Rhoda F. Vivre avec un cardiaque: Les voies de la serenite et de l'espoir. [Montreal]: Editions de l'Homme, 1992.

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12

Ricci, Marco. Myocardial Protection. Blackwell Publishing Limited, 2003.

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13

Salerno, Tomas A., and Marco Ricci. Myocardial Protection. Wiley & Sons, Incorporated, John, 2008.

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14

Salerno, Tomas A., and Marco Ricci. Myocardial Protection. Wiley & Sons, Incorporated, John, 2008.

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15

Salerno, Tomas A., and Marco Ricci. Myocardial Protection. Wiley & Sons, Limited, John, 2007.

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16

Takeda, Nobuakira, Naranjan S. Dhalla, Manjeet Singh, and Anton Lukas. Myocardial Ischemia and Preconditioning. Springer, 2012.

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17

(Editor), Naranjan S. Dhalla, Nobuakira Takeda (Editor), Manjeet Singh (Editor), and Anton Lukas (Editor), eds. Myocardial Ischemia and Preconditioning (Progress in Experimental Cardiology). Springer, 2002.

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18

Erlinge, David, and Göran Olivecrona. Diagnosis and management of ST-elevation of myocardial infarction. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0147.

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ST-elevation myocardial infarction (STEMI) is generally caused by a ruptured plaque that triggers local thrombus formation, which occludes the coronary artery. STEMI should be diagnosed rapidly, based on the combination of ST-segment elevation and symptoms of acute myocardial infarction. The main treatment objective is myocardial tissue reperfusion as quickly as possible. The preferred method of reperfusion is primary percutaneous coronary interventionif transport time is below 2 hours, and thrombolysis if longer STEMI patients with acute onset cardiogenic shock should be evaluated by echocardiography to exclude mechanical complications, such as flail mitral insufficiency, ventricular septal defect or tamponade. Secondary prevention includes aspirin, adenosine diphosphate receptor antagonists, statins, beta-blockers, angiotensin-converting enzymeinhibitors, and lifestyle changes.
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19

López-Sendón, José, and Esteban López de Sá. Mechanical complications of myocardial infarction. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0045.

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Mechanical complications after an acute infarction include different forms of heart rupture, including free wall rupture, interventricular septal rupture, and papillary muscle rupture. Its incidence decreased dramatically with the widespread use of reperfusion therapies but may occur in 2–3% of ST-elevation myocardial infarction patients, and mortality is very high if not properly diagnosed, as surgery is the only effective treatment. Echocardiography is the most important tool for diagnosis that should be suspected in patients with hypotension, heart failure, or recurrent chest pain. Awareness and well-established protocols are crucial for an early diagnosis. Modern imaging techniques permit a more reliable and direct identification of left ventricular free wall rupture, which is almost impossible to identify with conventional echocardiography. Mitral regurgitation, secondary to papillary muscle ischaemia or necrosis or left ventricular dilatation and remodelling, without papillary muscle rupture, is frequent after myocardial infarction and is considered as an independent risk factor for outcomes. Revascularization to control ischaemia and surgical repair should be considered in all patients with severe or symptomatic mitral regurgitation in the absence of severe left ventricular dysfunction. Other mechanical complications include true aneurysms and thrombus formation in the left ventricle. Again, these complications have decreased with the use of early reperfusion therapies and, for thrombus formation, with aggressive antithrombotic treatment. In a single large randomized trial (STICH), surgical remodelling of the left ventricle failed to demonstrate a significant improvement in outcomes, although it still may be an option in selected patients.
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20

López-Sendón, José, and Esteban López de Sá. Mechanical complications of myocardial infarction. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0045_update_001.

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Mechanical complications after an acute infarction include different forms of heart rupture, including free wall rupture, interventricular septal rupture, and papillary muscle rupture. Its incidence decreased dramatically with the widespread use of reperfusion therapies but may occur in 2–3% of ST-elevation myocardial infarction patients, and mortality is very high if not properly diagnosed, as surgery is the only effective treatment. Echocardiography is the most important tool for diagnosis that should be suspected in patients with hypotension, heart failure, or recurrent chest pain. Awareness and well-established protocols are crucial for an early diagnosis. Modern imaging techniques permit a more reliable and direct identification of left ventricular free wall rupture, which is almost impossible to identify with conventional echocardiography. Mitral regurgitation, secondary to papillary muscle ischaemia or necrosis or left ventricular dilatation and remodelling, without papillary muscle rupture, is frequent after myocardial infarction and is considered as an independent risk factor for outcomes. Revascularization to control ischaemia and surgical repair should be considered in all patients with severe or symptomatic mitral regurgitation in the absence of severe left ventricular dysfunction. Other mechanical complications include true aneurysms and thrombus formation in the left ventricle. Again, these complications have decreased with the use of early reperfusion therapies and, for thrombus formation, with aggressive antithrombotic treatment. In a single large randomized trial (STICH), surgical remodelling of the left ventricle failed to demonstrate a significant improvement in outcomes, although it still may be an option in selected patients.
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21

López-Sendón, José, and Esteban López de Sá. Mechanical complications of myocardial infarction. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0045_update_002.

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Mechanical complications after an acute infarction include different forms of heart rupture, including free wall rupture, interventricular septal rupture, and papillary muscle rupture. Its incidence decreased dramatically with the widespread use of reperfusion therapies but may occur in 2–3% of ST-elevation myocardial infarction patients, and mortality is very high if not properly diagnosed, as surgery is the only effective treatment. Echocardiography is the most important tool for diagnosis that should be suspected in patients with hypotension, heart failure, or recurrent chest pain. Awareness and well-established protocols are crucial for an early diagnosis. Modern imaging techniques permit a more reliable and direct identification of left ventricular free wall rupture, which is almost impossible to identify with conventional echocardiography. Mitral regurgitation, secondary to papillary muscle ischaemia or necrosis or left ventricular dilatation and remodelling, without papillary muscle rupture, is frequent after myocardial infarction and is considered as an independent risk factor for outcomes. Revascularization to control ischaemia and surgical repair should be considered in all patients with severe or symptomatic mitral regurgitation in the absence of severe left ventricular dysfunction. Other mechanical complications include true aneurysms and thrombus formation in the left ventricle. Again, these complications have decreased with the use of early reperfusion therapies and, for thrombus formation, with aggressive antithrombotic treatment. In a single large randomized trial (STICH), surgical remodelling of the left ventricle failed to demonstrate a significant improvement in outcomes, although it still may be an option in selected patients.
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22

López-Sendón, José, and Esteban López de Sá. Mechanical complications of myocardial infarction. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0045_update_003.

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Abstract:
Mechanical complications after an acute infarction involve different forms of heart rupture, including free wall rupture, interventricular septal rupture, and papillary muscle rupture. Its incidence decreased dramatically with the widespread use of reperfusion therapies occurring in <1% of ST-elevation myocardial infarction patients, and mortality is very high if not properly diagnosed, as surgery is the only effective treatment (Ibanez et al, 2017). Echocardiography is the most important tool for diagnosis that should be suspected in patients with hypotension, heart failure, or recurrent chest pain. Awareness and well-established protocols are crucial for an early diagnosis. Modern imaging techniques permit a more reliable and direct identification of left ventricular free wall rupture, which is almost impossible to identify with conventional echocardiography. Mitral regurgitation, secondary to papillary muscle ischaemia or necrosis or left ventricular dilatation and remodelling, without papillary muscle rupture, is frequent after myocardial infarction and is considered as an independent risk factor for outcomes. Revascularization to control ischaemia and surgical repair should be considered in all patients with severe or symptomatic mitral regurgitation in the absence of severe left ventricular dysfunction. Other mechanical complications include true aneurysms and thrombus formation in the left ventricle. Again, these complications have decreased with the use of early reperfusion therapies and, for thrombus formation, with aggressive antithrombotic treatment. In a single large randomized trial (STICH), surgical remodelling of the left ventricle failed to demonstrate a significant improvement in outcomes, although it still may be an option in selected patients.
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23

Michel, Piper Hans, and Preusse C. J, eds. Ischemia-reperfusion in cardiac surgery. Dordrecht: Kluwer Academic Publishers, 1993.

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24

H, Opie Lionel. Stunning, Hibernation, and Calcium in Myocardial Ischemia and Reperfusion. Springer London, Limited, 2012.

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25

Friedhelm, Beyersdorf, ed. Ischemia-reperfusion injury in cardiac surgery. Georgetown, Tx: Landes Bioscience, 2000.

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26

Beyersdorf, Friedhelm. Ischemia-Reperfusion Injury in Cardiac Surgery. Taylor & Francis Group, 2000.

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27

Nagano, Makoto, Nobuakira Takeda, Naranjan S. Dhalla, and Seibu Mochizuki. Ischemic Heart. Springer London, Limited, 2007.

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28

A, Kloner Robert, and Przyklenk Karin 1956-, eds. Stunned myocardium: Properties, mechanisms, and clinical manifestations. New York: Dekker, 1993.

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29

(Editor), Bohuslav Ost'ádal, and Frantisek Kolár (Editor), eds. Cardiac Ischemia: - From Injury to Protection (Basic Science for the Cardiologist). Springer, 1999.

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30

Kitakaze, Masafumi, James M. Downey, Masatsugu Hori, and Robert M. Mentzer Jr. Adenosine, Cardioprotection and Its Clinical Application. Springer London, Limited, 2012.

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31

Pharm, Boucher Michel B., and Canadian Coordinating Office for Health Technology Assessment., eds. The role of clopidogrel in the secondary prevention of recurrent ischemic vascular events after acute myocardial ischemia: A critical appraisal of the CURE Trial. Ottawa, Ont: Canadian Coordinating Office for Health Technology Assessment, 2002.

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32

Hausenloy, Derek, and Derek Yellon, eds. An Introduction to Cardioprotection. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199544769.003.0001.

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• In its broadest sense, the term ‘cardioprotection’ encompasses ‘all mechanisms and means that contribute to the preservation of the heart by reducing or even preventing myocardial damage’• However, for the purposes of this book, the term ‘cardioprotection’ will refer to the endogenous mechanisms and therapeutic strategies that reduce or prevent myocardial damage induced by acute ischaemia-reperfusion injury• In this context, cardioprotection begins with the primary prevention of coronary heart disease and includes the reduction of myocardial injury sustained during coronary artery bypass graft surgery, and an acute myocardial infarction, conditions with considerable morbidity and mortality• An understanding of the pathophysiology of acute myocardial ischaemia-reperfusion injury is essential when designing new cardioprotective strategies• Several methods exist for both quantifying myocardial damage induced by acute ischaemia-reperfusion injury and for assessing myocardial salvage following the application of cardioprotective strategies• Importantly, novel cardioprotective strategies must be capable of preventing and reducing myocardial damage over and above that provided by current optimal therapy.
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33

Arterial Remodeling: A Critical Factor in Restenosis (Developments in Cardiovascular Medicine). Springer, 1997.

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34

Greenberg, Barry. Cardiac Remodeling: Mechanisms and Treatment (Fundamental and Clinical Cardiology). Informa Healthcare, 2005.

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35

Greenberg, Barry. Cardiac Remodeling: Mechanisms and Treatment. Taylor & Francis Group, 2005.

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36

Greenberg, Barry. Cardiac Remodeling: Mechanisms and Treatment. Taylor & Francis Group, 2005.

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37

Greenberg, Barry. Cardiac Remodeling: Mechanisms and Treatment. Taylor & Francis Group, 2005.

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38

Greenberg, Barry. Cardiac Remodeling: Mechanisms and Treatment. Taylor & Francis Group, 2005.

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39

van Lier, Felix, and Robert Jan Stolker. Preoperative assessment and optimization. Edited by Jonathan G. Hardman. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0040.

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Perioperative cardiovascular complications (including myocardial ischaemia and myocardial infarction) are the predominant cause of morbidity and mortality in patients undergoing non-cardiac surgery. The pathophysiology of perioperative myocardial infarction is complex. Prolonged myocardial ischaemia due to the stress of surgery in the presence of a haemodynamically significant coronary lesion, leading to subendocardial ischaemia, and acute coronary artery occlusion after plaque rupture and thrombus formation contribute equally to these devastating events. Perioperative management aims at optimizing the patient’s condition by identification and modification of underlying cardiac risk factors and diseases. The first part of this chapter covers current knowledge on preoperative risk assessment. Current risk indices, the value of additional testing, and new preoperative cardiac risk makers are investigated. During recent decades there has been a shift from the assessment and treatment of the underlying culprit coronary lesion towards a systemic medical therapy aiming at prevention of myocardial oxygen supply–demand mismatch and coronary plaque stabilization. In the second part of this chapter, risk-reduction strategies are discussed, including β‎-blocker therapy, statins, and aspirins. A central theme in this chapter will focus on long-term cardiovascular risk reduction. Patients who undergo non-cardiac (vascular) surgery are particularly prone to long-term adverse cardiac outcomes. The goal of perioperative cardiovascular risk identification and modification should not be limited to the perioperative period, but should extend well into the postoperative period.
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40

Rao, Chethan P. Venkatasubba, and Jose Ignacio Suarez. Management of non-traumatic subarachnoid haemorrhage in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0239.

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Non-traumatic subarachnoid haemorrhage (ntSAH) is a complex disease affecting multiple systems and the hospital course of affected patients can be variable. ntSAH is associated with high morbidity and mortality, with the causes of early deaths being either rebleeding or hydrocephalus. The risk of rebleeding is reduced by immediate control of arterial blood pressure and early securing of ruptured aneurysms by either endovascular coiling or surgical clipping. Ongoing management focuses on prevention, detection, and management of delayed neurological deficits. Current recommendations include prophylactic use of nimodipine, maintenance of hypertension and euvolaemia or hypervolaemia, and endovascular treatment of vasospasm that fails to respond to medical therapy. Systemic complications following ntSAH include myocardial injury, acute lung injury, venous and pulmonary thromboembolism, fluid and electrolyte abnormalities, and severe sepsis. Each of these complications should be treated on its merits. Due to the complexity of management patients with ntSAH should be treated in a critical care environment by a collaborative team of neurosurgeons, neuroradiologists, neurologists and intensivists.
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41

Mannucci, Pier Mannuccio. Bleeding and haemostasis disorders. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0070.

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The main cause of haemostasis defects and related bleeding complications in patients with acute coronary syndromes admitted to the intensive cardiac care unit is the use of multiple antithrombotic drugs, alone or concomitantly with invasive procedures such as percutaneous coronary intervention with stent deployment and coronary artery bypass surgery. These drugs, that act upon several components of haemostasis (platelet function, coagulation, fibrinolysis), are associated with bleeding complications, particularly in elderly patients (more so in women than in men), those who are underweight, and those with comorbid conditions such as renal and liver insufficiency and diabetes. The identification of patients at higher risk of bleeding is the most important preventive strategy. Red cell and platelet transfusions, which may become necessary in patients with severe bleeding, should be used with caution, because transfused patients with acute coronary syndrome have a high rate of adverse outcomes (death, myocardial infarction, and stroke). To reduce the need of transfusion, haemostatic agents that decrease blood loss and transfusion requirements (antifibrinolytic amino acids, plasmatic prothrombin complex concentrates, recombinant factor VIIa) may be considered. However, the efficacy of these agents in the control of bleeding complications in acute coronary syndrome is not unequivocally established, and there is concern for an increased risk of re-thrombosis. A low platelet count is another cause of bleeding in the intensive cardiac care unit. The main aetiologies are drugs (unfractionated heparin and glycoprotein IIb/IIIa inhibitors), thrombotic microangiopathies, such as thrombotic thrombocytopenic purpura, and disseminated intravascular coagulation, that are often paradoxically associated with thrombotic manifestations. In conclusion, evidence-based recommendations for the management of bleeding in patients admitted to the intensive cardiac care unit are lacking. Accurate assessments of the risk of bleeding in the individual and prevention measures are the most valid strategies.
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42

Mannucci, Pier Mannuccio. Bleeding and haemostasis disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0070_update_001.

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The main cause of haemostasis defects and related bleeding complications in patients with acute coronary syndromes admitted to the intensive cardiac care unit is the use of multiple antithrombotic drugs, alone or concomitantly with invasive procedures such as percutaneous coronary intervention with stent deployment and coronary artery bypass surgery. These drugs, that act upon several components of haemostasis (platelet function, coagulation, fibrinolysis), are associated with bleeding complications, particularly in elderly patients (more so in women than in men), those who are underweight, and those with comorbid conditions such as renal and liver insufficiency and diabetes. The identification of patients at higher risk of bleeding is the most important preventive strategy. Red cell and platelet transfusions, which may become necessary in patients with severe bleeding, should be used with caution, because transfused patients with acute coronary syndrome have a high rate of adverse outcomes (death, myocardial infarction, and stroke). To reduce the need of transfusion, haemostatic agents that decrease blood loss and transfusion requirements (antifibrinolytic amino acids, plasmatic prothrombin complex concentrates, recombinant factor VIIa) may be considered. However, the efficacy of these agents in the control of bleeding complications in acute coronary syndrome is not unequivocally established, and there is concern for an increased risk of re-thrombosis. A low platelet count is another cause of bleeding in the intensive cardiac care unit. The main aetiologies are drugs (unfractionated heparin and glycoprotein IIb/IIIa inhibitors), thrombotic microangiopathies, such as thrombotic thrombocytopenic purpura, and disseminated intravascular coagulation, that are often paradoxically associated with thrombotic manifestations. In conclusion, evidence-based recommendations for the management of bleeding in patients admitted to the intensive cardiac care unit are lacking. Accurate assessments of the risk of bleeding in the individual and prevention measures are the most valid strategies.
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43

Mannucci, Pier Mannuccio. Bleeding and haemostasis disorders. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0070_update_002.

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The main cause of haemostasis defects and related bleeding complications in patients with acute coronary syndromes admitted to the intensive cardiac care unit is the use of multiple antithrombotic drugs, alone or concomitantly with invasive procedures such as percutaneous coronary intervention with stent deployment and coronary artery bypass surgery. These drugs, that act upon several components of haemostasis (platelet function, coagulation, fibrinolysis), are associated with bleeding complications, particularly in elderly patients (more so in women than in men), those who are underweight, and those with comorbid conditions such as renal and liver insufficiency and diabetes. The identification of patients at higher risk of bleeding is the most important preventive strategy. Red cell and platelet transfusions, which may become necessary in patients with severe bleeding, should be used with caution, because transfused patients with acute coronary syndrome have a high rate of adverse outcomes (death, myocardial infarction, and stroke). To reduce the need of transfusion, haemostatic agents that decrease blood loss and transfusion requirements (antifibrinolytic amino acids, plasmatic prothrombin complex concentrates, recombinant factor VIIa) may be considered. However, the efficacy of these agents in the control of bleeding complications in acute coronary syndrome is not unequivocally established, and there is concern for an increased risk of re-thrombosis. A low platelet count is another cause of bleeding in the intensive cardiac care unit. The main aetiologies are drug usage (unfractionated heparin and glycoprotein IIb/IIIa inhibitors), such thrombotic microangiopathies as thrombotic thrombocytopenic purpura and disseminated intravascular coagulation, that are often paradoxically associated with thrombotic manifestations. In conclusion, evidence-based recommendations for the management of bleeding in patients admitted to the intensive cardiac care unit are lacking. Accurate assessments of the risk of bleeding in the individual and prevention measures are the most valid strategies.
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