Acute coronary syndrome pathophysiology

Badimon JJ, Zaman A, Helft G, Fayad Z, Fuster V (1999) Acute coronary syndromes pathophysiology and preventive priorities. Thromb Haemost 82 997-1004... 

Differentiate between the pathophysiology of chronic stable angina and acute coronary syndromes. 

Reprinted from Spinier SA, de Denus S. Acute Coronary Syndromes. In DiPiro JT, Talbert RL, Yee GC, et al, (eds.) Pharmacotherapy A Pathophysiologic Approach. 6th ed. New York McGraw-Hill 2005 299-302, with permission.)... 

Massberg S, Schulz C, Gawaz M. Role of platelets in the pathophysiology of acute coronary syndrome. Semin Vase Med. 2003 3 147-162. 

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. 

The early clinical benefits observed in statin trials of acute coronary syndrome patients (MIRACL and PROVE-IT TIM 1-22) where coronary vascular inflammation, thrombosis, and unstable plaque are critical pathophysiologic elements that may be positively modified by statins compared to the more delayed benefits observed in statin trials of patients with stable coronary artery disease. 

This review summarizes the available morphological evidence for coronary microembolization in patients who died from coronary artery disease, most notably from sudden death. Then the experimental pathophysiology of coronary microembolization in animal models of acute coronary syndromes is detailed. Finally, the review presents the available clinical evidence for coronary microembolization in patients, highlights its key features - arrhythmias, contractile dysfunction, microinfarcts and reduced coronary reserve -, compares these features to those of the experimental model and addresses its prevention by mechanical protection devices and glycoprotein Ilb/IIIa antagonism. 

Peripheral arterial occlusion can be the initial manifestation of cardiac or systemic disease. At times, patients with chronic stable claudication may experience abrupt shortening of the distance at which claudication occurs, and this may be the only symptomatic evidence of an acute arterial occlusion either by embolization of by thrombus formation on a pre-existing arterial stenosis. The situation is not chronic and stable any more, but acute and unstable. As ischemia becomes more severe, the patient with chronic peripheral arterial disease develops ischemic pain at rest. The pathophysiologic mechanisms and the clinical presentation parallel the evolution of chronic stable angina pectoris to unstable angina and acute coronary syndromes. 

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