NON ST-SEGMENT ELEVATION ACUTE CORONARY SYNDROME (NSTE-ACS)

Patients with acute coronary syndrome (ACS) commonly are classified into two groups to facilitate
evaluation and management, namely patients with acute myocardial infarction with ST-segment
elevation (STEMI) on their presenting electrocardiogram (ECG) and those with non ST-segment
elevation acute coronary syndrome (NSTE-ACS) with evidence of myocyte necrosis. NSTE-ACS is
caused by an imbalance between myocardial oxygen supply and demand resulting from processes
that lead to thrombus formation. (Harrison’s Principles of Internal Medicine 20 th ed. P. 1866).
Harrison’s
 Thrombus formation
Principles of
 While plaque rupture remains the most common
Etiology Internal
etiology of coronary thrombosis, erosion of an
Medicine 20th
intracoronary plaque is increasing in frequency.
ed. P. 1866
 Relative incidence of NSTEMI is rising due to the
increasing burden of diabetes and chronic kidney
disease in an aging population, while STEMI is
declining due to greater use of aspirin, statins, and Harrison’s
less smoking. Principles of
Epidemiology  Among patients with NSTE-ACS, the proportion Internal
with NSTEMI is rising while that with Unstable Medicine 20th
Angina is falling because of the wider use of ed. P. 1866
troponin assays with higher sensitivity to detect
myocyte necrosis, thereby reclassifying UA as
NSTEMI.
 Age ≥65 years old
 3 or more of the traditional risk factors for
coronary heart disease Harrison’s
Non-modifiable risk  Known history of coronary artery disease or Principles of
factors OR predisposing coronary stenosis of at least 50% Internal
factors  More than one anginal episode in the past 24 h Medicine 20th
 ST segment deviation of at least 0.5 mm ed. P. 1866
 Elevated cardiac specific biomarker above the
upper limit of normal
 Daily aspirin use in the prior week Harrison’s
 Diabetes mellitus Principles of
Modifiable risk factors
 Left ventricular dysfunction Internal
OR precipitating factors
 Renal dysfunction Medicine 20th
 Elevated levels of B-type natriuretic peptides. ed. P. 1866
Pathophysiology  NSTE-ACS is caused by an imbalance between Harrison’s
myocardial oxygen supply and demand resulting Principles of
from one or more of the following four processes Internal
that lead to thrombus formation: Medicine 20th
- Disruption of an unstable coronary plaque ed. P. 1866
due to plaque rupture, erosion, or a calcified
protruding nodule that leads to intracoronary
thrombus formation and an inflammatory
response;
- Coronary arterial vasoconstriction;
 - Gradual intraluminal narrowing;
 Increased myocardial oxygen demand produced by
conditions such as fever, tachycardia, and
thyrotoxicosis in the presence of fixed epicardial
coronary obstruction.
 Typically, chest discomfort is severe & has at least
one of three:
- Occurrence at rest (or minimal exertion),
lasting >10 min;
- Relatively recent onset (i.e., within the prior
2 weeks);
- Crescendo pattern, i.e., distinctly more Harrison’s
severe, prolonged, or frequent than previous Principles of
History (Subjective
episodes. Internal
complaints)
 Chest discomfort is located in the substernal Medicine 20th
region and radiates to the left arm, left shoulder, ed. P. 1868
and/or superiorly to the neck and jaw.
 Anginal equivalents such as dyspnea, epigastric
discomfort, nausea, or weakness may occur
instead of chest discomfort. They appear to be
more frequent in women, the elderly, and
patients with diabetes mellitus.
 If the patient has a large area of myocardial Harrison’s
ischemia or a large NSTEMI, the physical findings Principles of
PE Findings can include diaphoresis; pale, cool skin; sinus Internal
tachycardia; a third and/or fourth heart sound; Medicine 20th
basilar rales; and, sometimes, hypotension. ed. P. 1868
 Electrocardiogram: new ST-segment depression
may occur. It may be transient but may persist for
several days following NSTEMI. T-wave changes are
more common but are less specific signs.
 Cardiac Biomarkers: elevated biomarkers of
Harrison’s
necrosis, such as cardiac troponin (cTn) I or T,
Diagnostic tests to Principles of
which are specific, sensitive, and the preferred
request and its expected Internal
markers of myocardial necrosis. There is a
findings or results Medicine 20th
characteristic temporal rise and fall peaking 12–24
ed. P. 1868
h post onset of symptoms of the plasma
concentration of these markers and a direct
relationship between the degree of elevation and
mortality.
 Stress testing
Medical treatment  Nitroglycerin:  direct relaxant effect on vascular Harrison’s
(include the drug smooth muscles, and the dilation of coronary Principles of
classification, mechanism vessels improves oxygen supply to the Internal
of action, dosage, route, myocardium. The dilation of peripheral veins, and Medicine 20th
and frequency) in higher doses peripheral arteries, reduces preload ed. P. 1868,
and afterload, and thereby lowers myocardial 1869
 oxygen consumption. First be given sublingually or
by buccal spray (0.3–0.6 mg) if the patient is
experiencing ischemic discomfort. If symptoms
persists after three doses given 5 min apart,
intravenous nitroglycerin (5–10 μg/min using
nonabsorbing tubing) is recommended.
 Verapamil: inhibits entry of Ca ions into the slow
channels or select voltage-sensitive areas of
vascular smooth muscle and myocardium during
depolarisation. It relaxes coronary vascular smooth
muscle and coronary vasodilation, increases
myocardial oxygen delivery, and slows automaticity MIMS PH
and AV node conduction. 120 mg tid or 80 mg tid in
patients w/ angina of effort. As modified-release:
Up to 480 mg daily.
 Aspirin: It is a selective and irreversible inhibitor of
cyclooxygenase-1 (COX-1) enzyme resulting in
direct inhibition of the biosynthesis of
prostaglandins and thromboxanes from arachidonic
acid. Additionally, it also inhibits platelet
aggregation. For primary prevention: Loading: 150-
300 mg.  Long term: 75-150 mg once daily. Short
term: 150-300 mg daily.
Harrison’s
Principles of
 Coronary arteriography followed by coronary Internal
Surgical treatment
revascularization (PCI or CABG) Medicine 20th
ed. P. 1868,
1869
 Patients should be placed at bed rest with
Harrison’s
continuous ECG monitoring for ST-segment
Principles of
deviation and cardiac arrhythmias.
Nonpharmacological Internal
 Ambulation is permitted if the patient shows no
treatment Medicine 20th
recurrence of ischemia (symptoms or ECG changes)
ed. P. 1868,
and does not develop an elevation of a biomarker
1869
of necrosis for 12–24 h.
 Thrombotic (coronary ischemia, mural thrombosis) Harrison’s
 Inflammatory (pericarditis, post MI syndrome) Principles of
 Mechanical dysfunction (heart failure, rupture Internal
Complications
aneurysm) Medicine 20th
 Electrical dysfunction (conduction disturbance, ed. P. 1868,
arrhythmias) 1869
Harrison’s
 Lifestyle modification Principles of
Prevention  Therapeutic disease prevention to progression Internal
 Management of future plaque rupture/erosion. Medicine 20th
ed. P. 1868
  Patients with documented NSTE-ACS exhibit a wide
spectrum of early (30 days) risk of death, ranging
from 1 to 10%, and a recurrent ACS rate of 5–15% Harrison’s
during the first year Principles of
Prognosis or outcome  An early invasive strategy conferred a 40% Internal
reduction in recurrent cardiac events in patients Medicine 20th
with an elevated cardiac troponin level, whereas ed. P. 1868
no benefit was observed in those without
detectable troponin.