Acute coronary syndromes infarction

Fondaparinux, the factor Xa-binding pentasaccharide (Arixtra, MW 1,728 Da), is prepared synthetically, unlike UFH, LMWH and danaparoid, which are obtained from animal sources. Despite only inactivating free factor Xa, clinical trials indicate that fondaparinux is an effective antithrombotic agent, both for venous thromboembolism prophylaxis and treatment, as well as for acute coronary syndrome and ST elevation myocardial infarction [4]. 

GPIIb/IIIa antagonists have to be administered parenterally. They are currently used prophylactically during intracoronary interventions such as percutaneous transluminal revascularization with balloon angioplasty or intracoronary stenting, as well as to treat acute coronary syndromes like unstable angina and acute myocardial infarction. The main complications... 

Acute coronary syndromes most often result from a physical disruption of the fibrous cap, either frank cap fracture or superficial endothelial erosion, allowing the blood to make contact with the thrombogenic material in the lipid core or the subendothelial region of the intima. This contact initiates the formation of a thrombus, which can lead to a sudden and dramatic blockade of blood flow through the affected artery. If the thrombus is nonocclusive or transient, it may either be clinically silent or manifest as symptoms characteristic of unstable angina. Importantly, if collateral vessels have previously formed, for example, due to chronic ischemia produced by multi vessel disease, even total occlusion of one coronary artery may not lead to an acute myocardial infarction. 

O Ischemic heart disease results from an imbalance between myocardial oxygen demand and oxygen supply that is most often due to coronary atherosclerosis. Common clinical manifestations of ischemic heart disease include chronic stable angina and the acute coronary syndromes of unstable angina, non-ST-segment elevation myocardial infarction, and ST-segment elevation myocardial infarction. 

List key electrocardiographic and clinical features identifying a patient with non-ST-segment elevation acute coronary syndrome who is at high risk of myocardial infarction or death. 

Acute coronary syndromes Ischemic chest discomfort at rest, most often accompanied by ST-segment elevation, ST-segment depression, or T-wave inversion on the 12-lead electrocardiogram. Furthermore, it is caused by plaque rupture and partial or complete occlusion of the coronary artery by thrombus. Acute coronary syndromes include myocardial infarction and unstable angina. Former terms used to describe types of acute coronary syndromes include Q-wave myocardial infarction, non-Q-wave myocardial infarction, and unstable angina. 

A specific immunoassay for measuring two-chain factor VIIa levels in plasma has been developed to identify activation of factor VII in patients with acute coronary syndromes suchs as myocardial infarction and unstable angina (12). Because regulation of factor VIIa is believed to be mediated by tissue factor pathway inhibitor (TFPI), its measurement is also useful in assessing thombotic and cardio-vasular disorders. Because TFPI is released by heparin, its measurement is also useful in assessing the efficacy of heparin and endothelial cell function (93). 

FIGURE 5-2. Biochemical markers in suspected acute coronary syndrome. (AMI, acute myocardial infarction CK-MB, creatine kinase myocardial band Ml, myocardial infarction.)... 

Fig. 5.3 Results of TACTICS TIMI 18. Primary end point of death, non-fatal myocardial infarction, and rehospitalization for acute coronary syndrome at 6 months based on baseline patient characteristics ( 2001 Massachusetts Medical Society)...

Drug therapy of acute coronary syndromes including unstable angina and non-Q-wave myocardial infarction includes use of aspirin, heparin and anti-ischaemic drugs and is similar in older patients to other age groups. Activation of platelet thromboxane production in the coronary circulation has been demonstrated in unstable angina. The risk of myocardial infarction or death is reduced by approximately 50% by early aspirin therapy in recommended doses of 160-325 mg per day and continued... 

Cohen M, Adams PC, Parry G, Xiong J, Chamberlain D, Wieczorek 1 et al. Combination antithrombotic therapy in unstable rest angina and non-Q-wave infarction in nonprior aspirin users. Primary end points analysis from the ATACS trial. Antithrombotic Therapy in Acute Coronary Syndromes Research Group. Circulation 1994 89(l) 81-8. 

E. Therapeutic response In human studies, eptifibatide inhibited ex vivo platelet aggregation induced by adenosine diphosphate (ADP) and other agonists in a dose- and concentration-dependent manner. The effect of eptifibatide was observed immediately after administration of a 180pg/kg intravenous bolus. In a placebo-controlled study of patients with acute coronary syndrome, Integrilin reduced the occurrence of death from any cause or new myocardial infarction. Similar benefits were observed in patients undergoing coronary angioplasty. 

Randomized comparison of direct thrombin inhibition versus heparin in conjunction with fibrinolytic therapy for acute myocardial infarction results from the GUSTO-lib Trial. Global Use of Strategies to Open Occluded Coronary Arteries in Acute Coronary Syndromes (GUSTO-lib) Investigators. J Am Coll Cardiol, 1998.31(7) 1493-8. 

Patients with acute coronary syndromes such as acute myocardial infarction and unstable angina remain at risk for recurrent myocardial ischemia despite therapy with antiplatelet agents and heparin. Although first clinical trials indicate a possible use of oral direct TIs for the prevention of cardiovascular events in patients after acute myocardial infarction, the presently available data are still limited and it has not... 

To understand the evolution of therapy of the acute coronary syndrome (ACS), which includes unstable angina, acute myocardial infarction, and interventional therapy— percutaneous coronary intervention (PCI), it is most useful to trace the historical events that provided a rationale for the use of anticoagulant and antiplatelet drugs, The focus of this chapter is upon the explosion in knowledge of the physiology of the hemostatic mechanism and will trace the rational development of therapy based upon the pathophysiology of the ACS over the past 40 years. 

Abbreviations ACS. acute coronary syndrome AECG. ambulatory electrocardiogram FLORIDA, fluvastatin on risk diminishment after acute myocardial infarction Ml. myocardial infarction MIRACL, myocardial ischemia reduction with aggressive cholesterol lowering nfMI. nonfatal myocardial infarction PACT, pravastatin in acute coronary treatment PROVE-IT TIMI 22. pravastatin or atoivastatin evaluation and infection therapy—thrombolysis in myocardial infarction 22 UAP, unstable anginapectoris. 

---