Antithrombotic Agents in Coronary Artery Disease

Cairns, John A.; Théroux, Pierre; Lewis, H. Daniel; Ezekowitz, Michael D.; Meade, T. W.

doi:10.1378/chest.119.1_suppl.228s

Cited by 107 publications

(44 citation statements)

References 131 publications

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“…Approximately half of cardioembolic strokes occur within the first week, although stroke risk remains high for as many as 3 months post-MI before decreasing gradually [78][79][80][81][82][83][84]. Myocardial infarction that involves the anterior myocardial wall carries a higher stroke risk than inferior wall myocardial infarction (25% vs 5%) [84].…”

Section: MImentioning

confidence: 99%

“…Myocardial infarction that involves the anterior myocardial wall carries a higher stroke risk than inferior wall myocardial infarction (25% vs 5%) [84]. Patients who have experienced MI from coronary artery disease are often treated with heparin, which also reduces the risk of ventricular wall thrombus formation [79][80][81]84]. Patients with anterior wall MI with ventricular wall thrombus should be treated with warfarin, with the goal of attaining an INR of 2.0 to 3.0 for as many as 6 months [84].…”

Section: MImentioning

confidence: 99%

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Prevention of Cardioembolic Stroke

Freeman

Aguilar

2011

Neurotherapeutics

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Cardiac causes of ischemic stroke lead to severe neurological deficits from large intracranial artery occlusion compared to small vessel ischemic stroke. The most common cause of cardioembolic stroke is atrial fibrillation (AF), which has an increasing incidence with age. AF stroke trials demonstrate that anti-coagulation is superior to anti-platelet therapy in terms of ischemic stroke prevention. Recently, warfarin was compared with dabigatran, an oral, direct thrombin inhibitor, and was found to be at least equally effective in reducing ischemic stroke with less intracranial bleeding risk. Future research is investigating other direct thrombin inhibitors as potential alternatives to warfarin, which has a narrow therapeutic index, requires frequent blood monitoring, has multiple drug interactions, and a higher rate of intracranial bleeding. Other causes of cardioembolic stroke include myocardial infarction, left ventricular thrombus, reduced ejection fraction, valvular abnormalities, and endocarditis. Patent foramen ovale is a common finding on echocardiograms in patients with and without stroke (up to 20% of the population), and it is a controversial source of cryptogenic stroke. The best way to prevent cardioembolic stroke remains early detection and treatment of AF, and treating the underlying stroke mechanism. Cardiac magnetic resonance imaging is an emerging technology and reveals some sources of cardiac embolism missed by echocardiography, and might provide an additional diagnostic tool in investigating cardioembolic stroke.

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Section: MImentioning

confidence: 99%

Section: MImentioning

confidence: 99%

Prevention of Cardioembolic Stroke

Freeman

Aguilar

2011

Neurotherapeutics

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“…A eficácia dos anticoagulantes orais em pacientes com IAM foi analisada inicialmente em três estudos clínicos randomizados. Em dois desses estudos observou-se redução significativa do risco de AVC, sem impacto na mortalidade; entretanto, no estudo restante, houve redução da mortalidade [208][209][210] (The Combination Hemotherapy and Mortality Prevention) não encontrou nenhum benefício do uso do warfarin (RNI de 1,5-2,5) associado a 81 mg por dia de AAS versus 162 mg por dia de AAS quanto à mortalidade total, mortalidade cardiovascular, AVC, e IAM não fatal (média de seguimento de 2,7 anos pós-IAM).…”

Section: -Anticoagulantes Oraisunclassified

Diretrizes

2009

Arq. Bras. Cardiol.

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-Atendimento pré-hospitalarO interesse no atendimento pré-hospitalar do infarto agudo do miocárdio (IAM) teve início na década de 1960, devido ao grande número de óbitos que ocorriam antes que os paciente chegassem ao hospital.A maioria das mortes por IAM ocorre nas primeiras horas de manifestação da doença, sendo 40%-65% dos casos na primeira hora e, aproximadamente, 80% nas primeiras 24 horas [1][2][3] . Assim, a maior parte das mortes por IAM acontece fora do ambiente hospitalar, geralmente desassistidas pelos médicos 4 . A modalidade mais frequente de parada cardiorrespiratória nas primeiras horas do IAM é a fibrilação ventricular 3 . -Período pré-hospitalar.O período pré-hospitalar compreende dois momentos: a) do início dos sintomas (geralmente dor torácica aguda) até a decisão de procurar atendimento; b) da decisão de procurar atendimento até a chegada ao hospital.No infarto agudo do miocárdio com elevação do segmento ST (IAMCST), o tempo desde o início dos sintomas (oclusão da artéria coronária) até a instituição do tratamento (reperfusão química ou mecânica) é diretamente proporcional à ocorrência de eventos clinicamente relevantes. Esse tempo é fator fundamental para o benefício do tratamento, tanto imediato quanto tardio 5 .No entanto, sabe-se que a fase pré-hospitalar (em ambos os momentos descritos) é caracterizada por ser demorada, especialmente em pacientes idosos, do sexo feminino e com baixa condição socioeconômica 4 . Alguns fatores estão relacionados ao aumento desse tempo tão precioso (Quadro 1.1.1.1) 6 . O componente pré-hospitalar no atraso do atendimento ao paciente com dor torácica é de tal magnitude que, na prática clínica, apenas cerca de 20% destes pacientes chegam ao setor de emergência com até duas horas após o início dos sintomas 7 . -Medidas na fase pré-hospitalarApesar da significativa redução da mortalidade hospitalar do IAM nas últimas décadas 8,9 , houve pouco avanço no conhecimento sobre a epidemiologia e o tratamento na fase pré-hospitalar. É notória a necessidade de mudanças nesse cenário, embora poucas sejam as evidências geradas para este fim.A abordagem do paciente com suspeita de síndrome coronária aguda em ambiente extra-hospitalar deve, idealmente, ser feita por profissional de saúde, com realização de uma história clínica direcionada, investigando as características dos sintomas atuais (momento do início, tempo de duração, qualidade, intensidade, relação com o esforço e repouso) e a presença de doença coronária estabelecida (angina prévia). Algumas características são reconhecidamente determinantes para a manifestação atípica de um evento coronariano e devem ser lembradas quando um indivíduo for abordado na fase pré-hospitalar, por mascararem o quadro de IAM (Tabela 1.1.2.1) [10][11][12] .O eletrocardiograma executado no local de atendimento e interpretado por um médico habilitado (na ambulância ou em local remoto) mostrou ser um método que reduz em 34% o tempo porta-agulha e em 18% o tempo porta-balão, além de proporcionar maiores taxas de tempo porta-balão ideal (men...

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“…46 Despite treatment with thrombolytic agents, left ventricular thrombus may occur in 28% of patients who have an acute anterior myocardial infarction, with even higher rates in the presence of apical hypokinesis. 47,48 The high risk of subsequent embolic events (OR 5.45, 95% CI 3.02-9.83) may be significantly reduced with anticoagulation (OR 0.14, 95% CI 0.04-0.52) 49 and has been suggested for 1-3 months after anterior myocardial infarction 50 especially when complicated by severe left ventricle dysfunction or previous emboli.…”

Section: Atrial Fibrillationmentioning

confidence: 99%

Current and future concepts in stroke prevention

O’Rourke

Dean

Akhtar

et al. 2004

Canadian Medical Association Journal

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STROKE IS A MAJOR CAUSE OF MORBIDITY and mortality in an aging population. The current understanding of the pathophysiology of atherosclerotic diseases, the most common cause of stroke, and the evidence for existing therapeutic interventions for the prevention of stroke are presented. Specifically, we review the evidence for antiplatelet agents, anticoagulants, antihypertensive medications, lipidlowering agents and carotid endarterectomy for stroke prevention. primary preventive measure, antiplatelet agents do not reduce the risk of ischemic stroke among patients without vascular disease. They are associated with an increased risk of intracranial hemorrhage (odds ratio [OR] 1.35, 95% confidence interval [CI] 0.88-2.10) 23 and major noncerebral hemorrhage (OR 1.73, 95% CI 1.14-2.63 ). 24 The benefits of ASA in the secondary prevention of stroke have been well documented in the period immediately after a stroke 25 (Table 1). Long-term antiplatelet treatment after stroke shows an even more impressive reduction of 25 nonfatal strokes and 36 serious vascular events per 1000 treated over a 29-month follow-up period. 25 There appears to be no difference in efficacy between low (50 mg) and higher doses (up to 1500 mg) of ASA. 29,30 The combination of dipyridamole and ASA has been shown to reduce the relative risk of recurrent stroke compared with ASA alone 26 (Table 1). Dipyridamole inhibits platelet aggregation by increasing levels of cyclic adenosine monophosphate and cyclic guanosine monophosphate. The limiting factor in the use of the ASAdipyridamole combination is the latter's potential effects on coronary perfusion. Dipyridamole can cause coronary vasodilation, which results in increased blood flow to nonstenosed coronary arteries. The result is that myocardial ischemia may be provoked during exercise. As such, the current American College of Cardiology/American Heart Association guidelines recommend that dipyridamole not be used in patients with chronic stable angina. 31 However, this recommendation was based on shortacting dipyridamole, which also reduced myocardial ischemia in a similar number of patients in the study quoted by these guidelines. 32 With the use of sustained-release dipyridamole, no increase in cardiac events was observed in subjects with prior coronary artery disease. 33 Thienopyridines block adenosine-diphosphate-mediated platelet aggregation. Ticlopidine was the first of this class of drug to be studied for stroke prevention. One clinical trial demonstrated that patients treated with ticlopidine had similar rates of stroke as those treated with ASA 28 (Table 1). However, serious granulocytopenia associated with ticlo- Leukocytes localize in the earliest atherosclerotic lesions, binding to vascular cell adhesion molecules (VCAM-1) on the vascular endothelium and migrating into the intima. This initiates and perpetuates a local inflammatory response. Monocytes mature into lipid-scavenging macrophages and subsequently foam cells. T-lymphocytes express inflammatory cytokines, which cont...

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Antithrombotic Agents in Coronary Artery Disease

Cited by 107 publications

References 131 publications

Prevention of Cardioembolic Stroke

Prevention of Cardioembolic Stroke

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Current and future concepts in stroke prevention

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