![]() ![]() Seven variables at presentation were independently predictive of outcome (Fig. ![]() The TIMI (Thrombolysis in Myocardial Infarction) risk score, which predicts the risk of 14-day all-cause mortality and new or recurrent MI, is a validated risk-prediction model based on data from the TIMI IIB and ESSENCE trials and is the most commonly used. 17-1).Īlthough the risks of individual patients presenting with NSTE-ACS vary widely, several risk scores have been devised to risk-stratify patients and help identify those who may benefit from an early invasive strategy. This can be achieved by a combination of anti-ischemic, antiplatelet, and antithrombotic therapy with or without PCI ( Fig. The optimal management of unstable angina or NSTEMI, therefore, is twofold: immediate relief of ischemia and the prevention of progression to acute MI or cardiac death. 7 NSTE-ACS patients and STE-ACS patients have similar prognoses, likely due to a high prevalence of multivessel disease as well as a higher incidence of recurrent ischemia (35% vs. Patients with NSTE-ACS have long-term outcomes similar to those of patients with STE-ACS and worse than those of patients with unstable angina. 5 Thus in evaluating individual patients with ACS, it is important to consider the most likely etiology, especially if an invasive strategy is being considered, given that PCI is not necessarily an appropriate therapy for all causes of ACS. Although plaque rupture or erosion with associated thrombosis is the most common cause of ACS, it may also be caused by dynamic obstruction (i.e., Prinzmetal’s angina or vasospasm secondary to drug abuse), spontaneous coronary artery dissection (most commonly occurring in peripartum women), severe coronary narrowing without thrombus or spasm (i.e., advanced progressive atherosclerosis or severe restenosis from prior PCI), or a precipitating condition extrinsic to the coronary circulation (i.e., fever, sepsis, tachycardia, hypotension, anemia, hypoxemia, etc.). It is important to note that within the first few months after an initial episode of coronary instability, there is a strong tendency for repeat instability caused by progression in the severity of the culprit stenosis or that of remote lesions. All clinical manifestations of ACS share a common pathophysiological pathway (plaque rupture/erosion and some degree of thrombosis and vasoconstriction), but the duration (transient or permanent) and severity (subtotal or total coronary occlusion) are different and associated either with myocardial necrosis (STEMI and NSTEMI) or no evidence of myocardial necrosis (UA) as manifest by negative cardiac biomarkers. Thus ACS may have different clinical presentations: UA, NSTEMI, STEMI, and sudden death. Although the initial stenosis may evolve silently, healing of a ruptured or eroded plaque may lead to more rapid progression of the stenosis this may remain clinically silent or cause angina pectoris. Rupture or erosion of this high-risk plaque triggers the formation of intracoronary thrombosis, which can lead to a critical stenosis or occlusion of the coronary artery as well as associated vasospasm. 5 This chapter discusses PCI for patients with NSTE-ACS, focusing on the pathophysiology, risk stratification, adjunctive treatment during PCI, invasive versus conservative strategy, and the most recent AHA/ACC guidelines for the management of patients with NSTE-ACS.īackground and Rationale for Percutaneous Coronary Intervention in Patients with Non-St-Segment Elevation Acute Coronary SyndromeĬoronary atherosclerosis is a chronic disease in which atheromatous material generally evolves silently over time it may eventually result in the development of a high-risk (i.e., vulnerable) plaque 6 ( Fig. NSTE-ACS includes patients with unstable angina (UA) or non-ST-segment elevation myocardial infarction (NSTEMI) STE-ACS includes patients with ST-segment elevation myocardial infarction (STEMI) 4 Various strategies have been proposed for the management of NSTE-ACS, with more recent guidelines and clinical trials increasingly supporting an invasive strategy for high-risk ACS and a less invasive/more conservative strategy for patients deemed to be at lower risk. 1 – 3 ACS comprises the spectrum of clinical signs and symptoms that occur as a result of acute myocardial ischemia and is classified as a non-ST-segment elevation ACS (NSTE-ACS) or as an ST-segment elevation ACS (STE-ACS). Over the past 31 years percutaneous coronary intervention (PCI) has evolved from a somewhat tenuous and experimental procedure to a durable and mainstream therapy as a result, the clinical indications for PCI have broadened to include patients with both stable angina pectoris and acute coronary syndrome (ACS). ![]()
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