3
Figure 1 Notes
The top half of the figure illustrates the progression of plaque formation
and onset and complications of NSTE-ACS, with management at each
stage. The numbered section of an artery depicts the process of
atherogenesis from 1) normal artery to 2) extracellular lipid in the
subintima to 3) fibrofatty stage to 4) procoagulant expression and
weakening of the fibrous cap. ACS develops with 5) disruption of the
fibrous cap, which is the stimulus for thrombogenesis. 6) Thrombus
resorption may be followed by collagen accumulation and smooth muscle
cell growth. Thrombus formation and possible coronary vasospasm
reduce blood flow in the affected coronary artery and cause ischemic
chest pain.
The bottom half of the figure illustrates the clinical, pathological,
electrocardiographic, and biomarker correlates in ACS and the general
approach to management. Flow reduction may be related to a completely
occlusive thrombus (bottom half, right side) or subtotally occlusive
thrombus (bottom half, left side). Most patients with ST elevation (thick
white arrow in bottom panel) develop QwMI, and a few (thin white arrow)
develop NQMI. Those without ST elevation have either UA or NSTEMI
(thick red arrows), a distinction based on cardiac biomarkers. Most
patients presenting with NSTEMI develop NQMI; a few may develop
QwMI. The spectrum of clinical presentations including UA, NSTEMI,
and STEMI is referred to as ACS. This NSTE-ACS CPG includes sections
on initial management before NSTE-ACS, at the onset of NSTE-ACS, and
during the hospital phase. Secondary prevention and plans for long-
term management begin early during the hospital phase. Patients with
noncardiac etiologies make up the largest group presenting to the ED
with chest pain (dashed arrow).
