ABSTRACT
Introduction The management of acute coronary syndromes without persistent ST segment elevation continues to be a challenge. As our understanding of the pathophysiology and natural history of this group of conditions changes, there is a corresponding expansion in our therapeutic targeting. Unstable angina and non-Q-wave myocardial infarction (NQWMI), which now account for the majority of admissions to coronary care units, are characterized by myocardial ischemia and share the same underlying pathophysiology of thrombus formation superimposed on a fissured or eroded atherosclerotic plaque. The high proportion of macrophages observed within ruptured plaques highlights an inflammatory process, which is also reflected in a number of markers such as C-reactive protein (CRP) measured systemically. Intraluminal thrombi, which limit blood flow but do not occlude the vessel, are common. The cardiac isoforms of troponin T and I are exclusively expressed in cardiac myocytes and when elevated reflect myocardial cellular necrosis. Current recommendations are that troponin T or I should be measured on admission in patients with suspected acute ischemic heart disease, and repeated 6 to 12 hours later.1 Ele-
strongly related to long-term risk of death from cardiac causes in patients with acute coronary syndromes.2 The principal difference between unstable angina and NQWMI is the longer duration of arterial obstruction which results in myocardial necrosis in the latter group of patients.3 There are prognostic differences also. In the TIMI IIIB trial,4 NQWMI patients had a 70% greater risk of death or myocardial infarction (MI) at 6 weeks (8.6% NQWMI vs 5.0% unstable angina, p = 0.05). Table 8.1 outlines how also, despite antithrombotic therapy, patients with NQWMI have a significantly higher rate of reinfarction and death at 12 weeks.5 While, long-term, 1-year unstable angina mortality can be as high as 12% (most of this occurring after the first months of hospital discharge),6 it can be up to 15% in NQWMI.7 Although the in-hospital mortality in NQWMI is lower, the long-term and cumulative prognosis in terms of morbid and fatal events is at least equal and possibly greater than in Q-wave MI. This reflects the higher recurrent angina and reinfarction rates attributable to residual jeopardized myocardium in NQWMI patients.8 It has been estimated that if treatment guidelines9 were adhered to then 1-year mortality could be reduced by a relative 22%.6
