Role of Clopidogrel in Unstable Angina and Non–ST-Segment Elevation Myocardial Infarction: From Literature and Guidelines to Practice

2004 ◽  
Vol 24 (8) ◽  
pp. 1037-1049 ◽  
Author(s):  
Jessica L. Kerr ◽  
Thomas F. Oppelt ◽  
Randall C. Rowen
Keyword(s):  
Myocardial Infarction ◽  
Unstable Angina ◽  
St Segment Elevation ◽  
Segment Elevation Myocardial Infarction ◽  
St Segment

Unstable Angina and Other Acute Coronary Syndromes

2013 ◽  
Author(s):  
R Scott Wright ◽  
Joseph G Murphy
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery ◽  
Risk Stratification ◽  
Unstable Angina ◽  
The United States ◽  
Cardiac Biomarkers ◽  
St Segment Elevation ◽  
Coronary Syndrome ◽  
Segment Elevation Myocardial Infarction ◽  
St Segment

Patients with coronary artery disease (CAD) present clinically when their disease enters an unstable phase known as an acute coronary syndrome (ACS), in which the cap of a previously stable atheromatous coronary plaque ruptures or erodes, which in turn activates a thrombotic cascade that may lead to coronary artery occlusion, myocardial infarction (MI), cardiogenic shock, and patient death. There are nearly 2 million episodes of ACS in the United States annually; it is the most common reason for hospitalization with CAD and is the leading cause of death in the developed world. ACS patients include those with unstable angina (UA), non–ST segment elevation myocardial infarction (non-STEMI), and ST segment elevation myocardial infarction (STEMI) and patients who die suddenly of an arrhythmia precipitated by coronary occlusion. The distinction among various ACS subgroups reflects varying characteristics of clinical presentation (presence or absence of elevated cardiac biomarkers) and the type of electrocardiographic (ECG) changes manifested on the initial ECG at the time of hospitalization. This chapter focuses on UA and non-STEMI. A graph outlines mortality risks faced by patients with varying degrees of renal insufficiency. An algorithm describes the suggested management of patients admitted with UA or non-STEMI. Tables describe the risk stratification of the patient with chest pain, categories of Killip class, examination findings of a patient with high-risk ACS, diagnosis of MI, causes of troponin elevation other than ischemic heart disease, initial risk stratification of ACS patients, and long-term medical therapies and goals in ACS patients. This review contains 2 highly rendered figures, 11 tables, and 76 references.

scholarly journals Gene mutations of platelet glycoproteins and response to tirofiban in acute coronary syndrome

2016 ◽  
Vol 134 (3) ◽  
pp. 199-204
Author(s):  
Antonio de Padua Mansur ◽  
Alessandra Roggerio ◽  
Júlio Yoshio Takada ◽  
Pérola Michelle Vasconcelos Caribé ◽  
Solange Desirée Avakian ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Platelet Aggregation ◽  
Unstable Angina ◽  
Gene Mutations ◽  
Coronary Intervention ◽  
St Segment Elevation ◽  
Segment Elevation Myocardial Infarction ◽  
St Segment ◽  
Percutaneous Coronary ◽  
Glycoprotein Iiia

CONTEXT AND OBJECTIVES: Glycoprotein inhibitors (abciximab, eptifibatide and tirofiban) are used in patients with unstable angina and non-ST-segment elevation myocardial infarction before percutaneous coronary intervention. Of these, tirofiban is the least effective. We hypothesized that the response to tirofiban might be associated with glycoprotein gene mutations. DESIGN AND SETTING: Prospective study at Emergency Unit, Heart Institute (InCor), University of São Paulo. METHOD: Intrahospital evolution and platelet aggregation in response to tirofiban were analyzed in relation to four glycoprotein mutations in 50 patients indicated for percutaneous coronary intervention: 17 (34%) with unstable angina and 33 (66%) with non-ST-segment elevation myocardial infarction. Platelet aggregation was analyzed using the Born method. Blood samples were obtained before and one hour after tirofiban infusion. Glycoproteins Ia (807C/T ), Ib (Thr/Met) , IIb (Ile/Ser ) and IIIa (PIA ) were the mutations selected. RESULTS: Hypertension, dyslipidemia, diabetes, smoking, previous coronary artery disease and stroke were similar between the groups. Mutant glycoprotein IIIa genotypes had lower platelet aggregation before tirofiban administration than that of the wild genotype (41.0% ± 22.1% versus 55.9% ± 20.8%; P = 0.035). Mutant glycoprotein IIIa genotypes correlated moderately with lower platelet inhibition (r = -0.31; P = 0.030). After tirofiban administration, platelet glycoprotein Ia, Ib, IIb and IIIa mutations did not influence the degree of inhibition of platelet aggregation or intrahospital mortality. CONCLUSIONS: Mutations of glycoproteins Ia, Ib, IIb and IIIa did not influence platelet aggregation in response to tirofiban in patients with unstable angina and non-ST-segment elevation myocardial infarction.

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