Books on the topic 'Atrial fibrillation; myocardial infarction'
To see the other types of publications on this topic, follow the link: Atrial fibrillation; myocardial infarction.
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 17 books for your research on the topic 'Atrial fibrillation; myocardial infarction.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse books on a wide variety of disciplines and organise your bibliography correctly.
1
Meyer, Mark Louis. Silent cerebral infarction in patients with nonrheumatic atrial fibrillation. [New Haven, Conn: s.n.], 1994.
Find full text
2
Johannes, Janse Michiel, ed. The ventricular arrhythmias of ischemia and infarction: Electrophysiological mechanisms. Mount Kisco, NY: Futura Pub. Co., 1993.
Find full text
3
Braidwood Commission on Conducted Energy Weapon Use (B.C.). Restoring public confidence: Restricting the use of conducted energy weapons. Victoria, B.C: Braidwood Commission on Conducted Energy Weapon Use, 2009.
Find full text
4
Bowker, Lesley K., James D. Price, Ku Shah, and Sarah C. Smith. Cardiovascular. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198738381.003.0010.
Full textAbstract:
This chapter provides information on the ageing cardiovascular system, chest pain, stable angina, acute coronary syndromes, myocardial infarction, hypertension, treatment of hypertension, presentation of arrhythmias, management of arrhythmias, atrial fibrillation, rate/rhythm control in atrial fibrillation, stroke prevention in atrial fibrillation, bradycardia and conduction disorders, common arrhythmias and conduction abnormalities, heart failure assessment, acute heart failure, chronic heart failure, dilemmas in heart failure, heart failure with preserved left ventricular function, valvular heart disease, peripheral oedema, preventing venous thromboembolism in an older person, peripheral vascular disease, gangrene in peripheral vascular disease, and vascular secondary prevention.
5
Brady, Peter A. Specific Arrhythmias and Syncope. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0044.
Full textAbstract:
Bradycardia is defined as a heart rate less than 60 beats per minute at rest or a decreased heart rate response to exercise. Causes of bradycardia include high vagal tone (most cases occur in asymptomatic and often fit and healthy persons), sinus node dysfunction, drug therapy, heart block, and myocardial infarction. A conduction system disorder is present when there is a delay in impulses from the sinus node reaching the ventricles or when some impulses do not reach the ventricles because of block within the AV node or distal conduction system (His-Purkinje system). Conduction system disorders can be divided into first-degree, second-degree, and third-degree (complete) heart block. The tachycardias (atrial fibrillation and atrial flutter) and syncope (as a transient loss of consciousness with spontaneous recovery) are also reviewed.
6
Turc, Guillaume, David Calvet, and Jean-Louis Mas. Cardiac aetiology. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198722366.003.0005.
Full textAbstract:
Cardiac aetiology accounts for approximately 20% of strokes in young adults. Although atrial fibrillation is a leading cause of stroke in the general population, it is uncommon in young adults. In such patients, more diverse causes of ischaemic stroke are observed, including valvular heart diseases, infective endocarditis, Libman–Sacks endocarditis, dilated cardiomyopathies, congenital heart diseases, myocardial infarction, and intracardiac tumours. Patent foramen ovale is commonly observed in young adults with ischaemic stroke, but this association may be incidental in a sizeable proportion of patients. Young adults who are the most likely to have a stroke-related patent foramen ovale are also those with the lowest recurrence risk.
7
Banerjee, Ashis, and Clara Oliver. Cardiac emergencies. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198786870.003.0009.
Full textAbstract:
Chest pain is a common presenting complaint for patients in the emergency department. This chapter focuses on the management and recent changes to non-ST-segment elevation myocardial infarction (NSTEMI) and STEMI pathways, in keeping with national guidance. Arrhythmia management including atrial fibrillation as well as the use of scoring systems as the CHADVASC score also commonly appears in the short-answer question (SAQ) paper, which is covered in this chapter in line with current NICE guidance. In addition, there is also a section on the diagnosis and differentiation on managing a patient with a transient loss of consciousness and the associated risk factors of sudden cardiac death. This chapter also includes sections on hypertensive emergencies and the management of heart failure.
8
Kelley, Roger E. Cardiac Disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0188.
Full textAbstract:
Heart disease is a major contributor to stroke and other neurologic disorders in adults. Cardioembolic stroke accounts for roughly 15% of all stroke, and the most common mechanism is cardiac arrhythmia, with atrial fibrillation the leading contributor. Anticoagulation such as using aspirin or warfarin is chosen based on the presence of associated risk factors including congestive heart failure, hypertension, age, and diabetes mellitus. Heart failure ranks second in the incidence of stroke from cardioembolism, with other risk factors being endocarditis, severe cardiomyopathy, acute myocardial infarction, and patent foramen ovale. Recent clinical trials indicate that induction of total body hyopthermia after cardiac arrest to a target temperature of 32°C to 34°C, for 24 hours, had a more favorable neurological outcome compared with a normothermia group.
9
Sinnaeve, Peter, and Frans Van de Werf. Fibrinolytic, antithrombotic, and antiplatelet drugs in acute coronary syndromes. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0044.
Full textAbstract:
Antithrombotic therapy is a major cornerstone in the treatment for acute coronary syndromes, as thrombus formation upon a plaque rupture or an erosion plays a pivotal role in non-ST-segment elevation as well as ST-segment elevation acute coronary syndromes. Both acute and long-term oral antiplatelet therapies, targeting specific platelet activation pathways, have demonstrated significant short- and long-term benefits. The use of anticoagulants is currently largely confined to the acute setting, except in patients with a clear indication for long-term treatment, including atrial fibrillation or the presence of intraventricular thrombi. Despite the benefit of primary percutaneous coronary intervention in ST-segment elevation myocardial infarction, fibrinolysis continues to play an important role throughout the world as well. In this chapter, the fibrinolytic, antiplatelet, and anticoagulant agents used in the management of acute coronary syndrome patients are discussed.
10
Sinnaeve, Peter, and Frans Van de Werf. Fibrinolytic, antithrombotic, and antiplatelet drugs in acute coronary syndromes. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0044_update_001.
Full textAbstract:
Antithrombotic therapy is a major cornerstone in the treatment for acute coronary syndromes, as thrombus formation upon a plaque rupture or an erosion plays a pivotal role in non-ST-segment elevation as well as ST-segment elevation acute coronary syndromes. Both acute and long-term oral antiplatelet therapies, targeting specific platelet activation pathways, have demonstrated significant short- and long-term benefits. The use of anticoagulants is currently largely confined to the acute setting, except in patients with a clear indication for long-term treatment, including atrial fibrillation or the presence of intraventricular thrombi. Despite the benefit of primary percutaneous coronary intervention in ST-segment elevation myocardial infarction, fibrinolysis continues to play an important role throughout the world as well. In this chapter, the fibrinolytic, antiplatelet, and anticoagulant agents used in the management of acute coronary syndrome patients are discussed.
11
Cheong, Adrian, Gabriel Steg, and Stefan K. James. ST-segment elevation myocardial infarction. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0043.
Full textAbstract:
Acute myocardial infarction with ST-segment elevation is a common and dramatic manifestation of coronary artery disease. It is caused by the rupture of an atherosclerotic plaque in a coronary artery, leading to its total thrombotic occlusion and resultant ischaemia and necrosis of downstream myocardium. The diagnosis of ST-segment elevation myocardial infarction is based on a syndrome of ischaemic chest pain symptoms, associated with typical ST-segment elevation on the electrocardiogram and an eventual rise in biomarkers of myocardial necrosis. The treatment of ST-segment elevation myocardial infarction is focused on re-establishing blood flow in the coronary artery involved, preferably by percutaneous coronary intervention, or by pharmacological thrombolysis in the case of expected lengthy time delays or lack of availability of facilities. Early mortality from ST-segment elevation myocardial infarction can be attributed to the sequelae or complications of myocardial ischaemia, or complications related to therapy. The former include arrhythmias (such as ventricular tachycardia or fibrillation), mechanical complications (such as ventricular free wall, septal, and mitral chordal rupture), and pump failure leading to cardiogenic shock. The latter includes haemorrhagic complications and coronary stent thrombosis. Given that myocardial necrosis is a critically time-dependent process, the organization of an ST-segment elevation myocardial infarction care system and adherence to the latest clinical trial evidence and guidelines are crucial to ensure that patients are treated in an optimal manner.
12
Cheong, Adrian P., Gabriel Steg, and Stefan K. James. ST-segment elevation MI. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0043_update_001.
Full textAbstract:
Acute myocardial infarction with ST-segment elevation is a common and dramatic manifestation of coronary artery disease. It is caused by the rupture of an atherosclerotic plaque in a coronary artery, leading to its total thrombotic occlusion and resultant ischaemia and necrosis of downstream myocardium. The diagnosis of ST-segment elevation myocardial infarction is based on a syndrome of ischaemic chest pain symptoms, associated with typical ST-segment elevation on the electrocardiogram and an eventual rise in biomarkers of myocardial necrosis. The treatment of ST-segment elevation myocardial infarction is focused on re-establishing blood flow in the coronary artery involved, preferably by percutaneous coronary intervention, or by pharmacological thrombolysis in the case of expected lengthy time delays or lack of availability of facilities. Early mortality from ST-segment elevation myocardial infarction can be attributed to the sequelae or complications of myocardial ischaemia, or complications related to therapy. The former include arrhythmias (such as ventricular tachycardia or fibrillation), mechanical complications (such as ventricular free wall, septal, and mitral chordal rupture), and pump failure leading to cardiogenic shock. The latter includes haemorrhagic complications and coronary stent thrombosis. Given that myocardial necrosis is a critically time-dependent process, the organization of an ST-segment elevation myocardial infarction care system and adherence to the latest clinical trial evidence and guidelines are crucial to ensure that patients are treated in an optimal manner.
13
Jumean, Marwan F., and Mark S. Link. Post-cardiac arrest arrhythmias. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0065.
Full textAbstract:
Our understanding of arrhythmias following resuscitated cardiac arrest has evolved over the past two decades to entail complex pathophysiological processes including, in part, ischaemia and ischaemia-reperfusion injury. Electrical instability after the return of spontaneous circulation (ROSC) is common, ranging from atrial fibrillation to recurrent ventricular tachycardia and fibrillation. Electrical instability following out-of-hospital cardiac arrest is most commonly due to myocardial ischaemia and post-arrest myocardial dysfunction. However, electrolyte disturbances, elevated catecholamine levels, the frequent use of vasopressors and inotropes, and underlying structural heart disease or channelopathies also contribute in the acute setting. Limited data exists that specifically address the management of arrhythmias in the immediate post-arrest period. In addition to treating any potential reversible cause, the management in the haemodynamically-stable patient includes beta-blockers, class I (lignocaine and procainamide) and III anti-arrhythmic agents (amiodarone). Defibrillation is often needed for recurrent ventricular arrhythmias.
14
Reffelmann, Thorsten, and Robert Kloner. Adjunctive Reperfusion Therapy Post-AMI. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199544769.003.0009.
Full textAbstract:
• Reperfusion of the occluded coronary artery in an ST-segment-elevation myocardial infarction is the most effective approach for reducing infarct size, preserving left ventricular ejection fraction, lowering the incidence and severity of congestive heart failure and improving prognosis• Hence, several pharmacologic agents intended to improve target vessel patency as an adjunct to thrombolysis or primary percutaneous coronary intervention have been shown to be beneficial in patients with reperfusion therapy for acute myocardial infarction, namely antiplatelet and anticoagulation agents• Animal investigations have suggested that coronary reperfusion may also result in undesirable cardiac alterations, termed ‘reperfusion injury’, such as reversible contractile dysfunction (‘stunning’), microvascular obstruction (‘no-reflow’), and in several studies the progression of myocardial necrosis (‘lethal reperfusion injury’)• Clinical investigations of various pharmacologic interventions as an adjunctive therapy to reperfusion to reduce final infarct size, the amount of contractile dysfunction and to improve prognosis have been mostly inconsistent; only a few interventions, e.g. adenosine and atrial natriuretic peptide seem to show promise at least in certain subgroups.
15
Cardim, Nuno, Denis Pellerin, and Filipa Xavier Valente. Hypertrophic cardiomyopathy. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0042.
Full textAbstract:
Hypertrophic cardiomyopathy is a common inherited heart disease caused by genetic mutations in cardiac sarcomeric proteins. Although most patients are asymptomatic and many remain undiagnosed, the clinical presentation and natural history include sudden cardiac death, heart failure, and atrial fibrillation. Echocardiography plays an essential role in the diagnosis, serial monitoring, prognostic stratification, and family screening. Advances in Doppler myocardial imaging and deformation analysis have improved preclinical diagnosis as well as the differential diagnosis of left ventricular hypertrophy. Finally, echocardiography is closely involved in patient selection and in intraoperative guidance and monitoring of septal reduction procedures. This chapter describes the pathophysiology, clinical presentation, role of echocardiography, morphological features, differential diagnosis, diagnostic criteria in first-degree relatives, echo guidance for the treatment of symptomatic left ventricular outflow tract obstruction, and follow-up and monitoring of patients with hypertrophic cardiomyopathy.
16
Freye, Enno. Management of poisoning by amphetamine or ecstasy. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0322.
Full textAbstract:
While amphetamine and especially methamphetamine (speed) is being misused by all social classes in order to increase stamina, intellectual expansion, endurance, and euphoria, the drug 3,4-methylenedioxy-N-methylamphetamine (MDMA) (ecstasy) is preferentially abused by the younger generation for the feeling of empathy, the touching within, and enhancement of the senses. Acute intoxication differs in regard to their effects on the person. The predominant sympathetic overstimulation after methamphetamine results in cardiovascular and CNS hyperactivity accompanied by agitation and seizures, while tachycardia is a prodrome of fibrillation. The excess hypertonia often leads into myocardial infarction and may even induce cerebral haemorrhage. MDMA intoxication often seen in the emergency department is predominantly characterized by hyperthermia, the most important condition to treat, followed by rhabdomyolysis and acute renal failure. Since there is no specific antidote available, in both cases therapy consists of treatment until the acute effects are gone.
17
Farmakis, Dimitrios, John Parissis, and Gerasimos Filippatos. Acute heart failure: epidemiology, classification, and pathophysiology. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0051.
Full textAbstract:
Acute heart failure is defined as the rapid development or change of symptoms and signs of heart failure that requires urgent medical attention and usually hospitalization. Acute heart failure is the first reason for hospital admission in individuals aged 65 or more and accounts for nearly 70% of the total health care expenditure for heart failure. It is characterized by an adverse prognosis, with an in-hospital mortality rate of 4-7%, a 2-3-month post-discharge mortality of 7-11%, and a 2-3-month readmission rate of 25-30%. The majority of patients have a previous history of heart failure and present with normal or increased blood pressure, while about half of them have a preserved left ventricular ejection fraction. A high prevalence of cardiovascular or non-cardiovascular comordid conditions is further observed, including coronary artery disease, arterial hypertension, atrial fibrillation, diabetes mellitus, renal dysfunction, chronic lung disease, and anaemia. Different classification systems have been proposed for acute heart failure, reflecting the clinical heterogeneity of the syndrome; the categorization to acutely decompensated chronic heart failure vs de novo acute heart failure and to hypertensive, normotensive, and hypotensive acute heart failure are among the most widely used and clinically relevant classifications. The pathophysiology of acute heart failure involves several pathogenetic mechanisms, including volume overload, pressure overload, myocardial loss, and restrictive filling, while several cardiovascular and non-cardiovascular causes or precipitating factors lead to acute heart failure through a single of these mechanisms or a combination of them. Regardless of the underlying mechanism, peripheral and/or pulmonary congestion is the hallmark of acute heart failure, resulting from fluid retention and/or fluid redistribution. Myocardial injury and renal dysfunction are also involved in the precipitation and progression of the syndrome.