Unstable Angina

Abstract

During the past 15 years, we have learned an enormous amount about the pathogenesis and treatment of unstable angina. In most cases of unstable rest angina, the pathogenesis is a mural thrombus formation on a ruptured or eroded atherosclerotic plaque. However, any process that acutely changes the supply-demand ratio (decreased supply or increased demand in the presence of a decrease in supply) can precipitate the clinical presentation of unstable angina. Standard acute antithrombotic drug therapy is effective in decreasing progression to infarction. Newer agents (low-molecular-weight heparin and platelet glycoprotein IIb/IIIa inhibitors) are more effective, and their use is evolving. Percutaneous intervention and bypass surgery can reduce symptoms and multiple hospitalizations, in most cases without a decrease in the long-term mortality rate. Because the cost of hospitalization is extremely high and the clinical presentation and outcome are heterogeneous, better triage methods are required.

Myocardial infarction with unusual presentation of otalgia: a case report

“…Chest pain is a typical symptom of acute coronary syndrome (ACS), of which there are three common types: unstable angina (UA), ST segment elevation (STEMI) of myocardial infarction (MI), and non-ST-segment elevation of MI (NSTEMI) [1, 2]. The underlying pathology is atherothrombosis.…”

Effect of oligodeoxynucleotide thrombin aptamer on thrombin inhibition by heparin cofactor II and antithrombin

“…The goals of anticoagulant therapy in cardiovascular disease are to inhibit fibrin deposition and platelet aggregation, which prevent ongoing ischemic events and to prolong the patients life [36–39]. There are many established antithrombotic agents like aspirin, coumarin and unfractionated heparin.…”

“…There are many established antithrombotic agents like aspirin, coumarin and unfractionated heparin. While these agents have well‐established biological actions there are some limitations to their effectiveness; thus, a search for new and novel antithrombotics has been underway for the past 15 years [36–39]. The thrombin aptamer described by Bock and co‐workers [16–18] is a potent antithrombotic, both in vitro and in vivo, and it possesses some potential for clinical application [24].…”

Platelet Glycoprotein IIb/IIIa Blockade in Acute Ischemic Stroke

“…Our knowledge of the pathophysiology of acute arterial ischemic syndromes has been greatly improved by the studies of symptomatic coronary artery disease during the last 10–15 years [21]. These studies have shown that the majority of acute coronary syndromes occur as a result of intravascular thrombosis at the site of rupture or superficial erosion of an unstable atherosclerotic plaque [22].…”