Diagnosis of NSTEMI

In diagnosing patient with Non-ST Elevation Myocardial Infarction(NSTEMI), one should

know how to differentiate between unstable angina, NSTEMI and ST Elevation Myocardial
Infarction(STEMI). Those three which actually often arise from pathophysiology has its own
characteristic respectively.

The figure above shows different presentation of thrombus which lead to different diagnosis.
To sum up, small thrombus mostly gives no clinical presentation and will self-healed
eventually, partial occlusive thrombus may lead to transient ischemia which causing changes
in ECG and serum biomarkers(unstable angina pectoris(UAP) and NSTEMI) and total
occlusion may lead to prolong ischemia can cause ST elevation in ECG and positive in serum
biomarkers(STEMI). Systematically, the diagnosis should be made based on three modalities:
clinical manifestation, ECG and serum biomarkers.
Clinical manifestation
Patient usually came with complain of angina. The angina can be typical angina or atypical
angina. In typical angina pectoris, mostly patient will come with complain of pressure on the
retrosternal area with radiation to the left side of the chest, arm, jaw, back, shoulder and
epigastric area. The angina may present with duration of more than 20 minutes or
intermittent. The angina also usually comes with other symptoms such as diaphoresis, nausea,
dyspneu, and syncope. The atypical may have similar presentation but with different
characteristic of the pain. To sum up, table below has list of clinical features across various
aetiology of angina.
ECG
ECG abnormalities, which reflect abnormal electrical currents during ACS, are usually
manifest in characteristic ways. In UAP or NSTEMI, ST segment depression and/or T wave
inversions are most common. These abnormalities may be transient, occurring just during
chest pain episodes in UA, or they may persist in patients with NSTEMI. STEMI presents
with a temporal sequence of abnormalities: initial ST segment elevation, followed over the
course of several hours by inversion of the T wave and Q wave development.
Serum Biomarkers(Laboratory Examination)
In ACS, necrosis of myocardial is a sign of myocardial infarction is happening. Some
molecules will be come out due to the breakdown of myocardial cells. Detection of such
molecules in the serum, particularly cardiac-specific troponins and creatine kinase MB
isoenzyme, serves important diagnostic and prognostic roles. In patients with STEMI or
NSTEMI, these markers rise above a threshold level in a defined temporal sequence.

Management
Indonesian Heart Assosciation(IHA/Perki) has released guideline of managing ACS which
standardize step-by-step management from diagnosis to inward care. The management is
actually based on each diagnosis. They also release guideline of what to do in suspect ACS
which the diagnosis may have not established.
Treatment
In STEMI, revascularisation is important during golden period(the first 12 hr). In dealing
with UAP and NSTEMI, risk assessment should be conducted to choose the appropriate
treatment. The risk assessment score is called TIMI. Low risk is 0-2,medium risk is 3-4 and
high risk is 5-7.
Drugs of choice
1. Beta-blocker
It decrease sympathetic drive to the myocardium, thus reducing oxygen demand, and
contribute to electrical stability. This group of drugs reduces the likelihood of
progression from UA to MI and lowers mortality rates in patients who present with
infarction. In the absence of contraindications (e.g., marked bradycardia,
bronchospasm, decompensated heart failure, or hypotension), a B-blocker is usually
initiated in the first 24 hours to achieve a target heart rate of approximately 60
beats/min. Such therapy is usually continued indefinitely after hospitalization because
of proven longterm mortality benefits following an MI.
2. Nitrate
It help bring about anginal relief through venodilation, which lowers myocardial
oxygen demand by diminishing venous return to the heart (reduced preload and
therefore less wall stress). Nitrates may also improve coronary flow and prevent
vasospasm through coronary vasodilation. In UA or NSTEMI, nitroglycerin is often
initially administered by the sublingual route, followed by a continuous intravenous
infusion. In addition to providing symptomatic relief of angina, intravenous
nitroglycerin is useful as a vasodilator in patients with ACS accompanied by heart
failure or severe hypertension.
3. Aspirin
Aspirin inhibits platelet synthesis of thromboxane A2, a potent mediator of platelet
activation, and is one of the most important interventions to reduce mortality in
patients with all forms of ACS. It should be administered immediately on presentation
and continued indefinitely in patients without contraindications to its use (e.g., allergy
or underlying bleeding disorder). Clopidogrel can also be added to boost the effect of
anti-platelet
4. Anti-coagulant
Intravenous unfractionated heparin (UFH) has long been standard anticoagulant
therapy for UA and NSTEMI. It binds to antithrombin, which greatly increases the
potency of that plasma protein in the inactivation of clotforming thrombin. UFH
additionally inhibits coagulation factor Xa, slowing thrombin formation and thereby
further impeding clot development. In patients with UA or NSTEMI, UFH improves
cardiovascular outcomes and reduces the likelihood of progression from UA to MI. It
is administered as a weight-based bolus, followed by continuous intravenous infusion.
Because of a high degree of pharmacodynamic variability, its anticoagulant effect
must be monitored, and its dose adjusted, through serial measurements of the serum
activated partial thromboplastin time (aPTT).