A case study about

Acute coronary
syndrome - NSTEMI
 Patient‘s demographics
● Name: M.A
● MRN: 29814
● Ward:4 / room: 30
● Age: 50 years old / Gender: female
● Nationality: Emirati
● Occupation: Does not work
● Marital status: Unmarried
● Blood group: O positive
● Date of admission: 5-2-2023
 1
Chief complaint
Chest pain
History of presenting illness

M.A, a 50 years old female, a known case of essential thrombocytosis, presented to the
emergency department yesterday complaining of a sudden onset chest pain at rest. It was
described as squeezing pain, as a pressure sensation over the chest; heaviness in the centre
of the chest. She reported a radiation of pain to the left jaw, neck and shoulder. Walking
or minimal physical exertion exacerbates the pain, but nothing relieves it, not even rest.
Since the pain started it has gotten worse over time with an increase in its frequency. She
rated the pain as 7 out of 10. She also has on and off palpitations. She has been sweating
heavily since the past few days, and no other abnormality was noted in her skin.
Cont..

She also stated having episodes of shortness of breath which lasts for maximum 1 minute and
happen 3 times a day. She was having difficulty in talking because of the heaviness sensation
she had over her chest. Since yesterday she had 3 episodes of loose motion, she described the
stool as semi solid and didn’t report any blood or mucus in the stool. She also reported having a
mild abdominal pain; epigastric pain, with a feeling of fullness almost all the time.
She stated that when she wakes up in the morning she experiences a moment of lightheadedness,
without syncope. She has a feeling of malaise and fatigue as well. She had anxiety as well as she is the
one taking care of the whole family since her parents died and she worries about them all. She stated
that she is an overthinking person and she can’t stop being so.
Cont..

The patient had experienced multiple episodes of intermittent chest pain 2 weeks before she
presented to the emergency department. She went to a clinic near her house and she was given
omeprazole because the doctor was suspecting a reflux, but no improvement was noticed in her
symptoms. An ECG was not performed at that time.
The patient ignored the pain as she thought it is because she was being anxious about her brother
who had an accident days ago, but on the day of her arrival she was severely unable to breath and had
a feeling of heaviness over her chest associated with severe pain on rest that gets worse with minimal
physical exertion. That’s why she decided to show up to the emergency department this time.
 Main complaints

A B
Chest pain Shortness of breath
Squeezing & Heaviness At rest and exacerbates by
Radiates to the left physical exertion
shoulder, jaw and neck
 Associated Symptoms
Diaphoresis
Dizziness
Lightheadedness Especially in the morning

Fatigue and Malaise

Difficulty while
Palpitations talking
Because of the breathing
At rest and exacerbates by
difficulty
physical exertion

3 episodes of loose motion

Mild epigastric pain
Semisolid, no mucus or blood
Feeling of fullness and
indigestion
 Past Medical History

Essentials Hypothyroidism GERD

thrombocytosis Since 2013 Long history of it
Since 2014 - JAK2
positive

No past surgical history

 Medications

Hydroxyurea Euthyroxine Nexium

To manage her essential To manage her To manage her GERD
thrombocytosis - But she hypothyroidism symptoms
stated she is not
compliant

No allergies toward food or medications

Family history
Her family history is significant of hypertension, and her mother has diabetes.
But none of her family has a similar condition as hers or presented with the same
symptoms before. No history of cardiac issues.

Social history
She is a non-smoker, does not consume alcohol.
Her diet is mainly home-cooked traditional food, she sometimes eat junk.
She does not exercise and has no recent travel history.
 Vitals At Admission

1 2 3
Temperature Pulse Respiration rate
36.8 ̊C 82 bpm 18 br/min

4 5 6
Blood pressure SpO2 Measurements
164/90 mmHg 98% Weight: 80 kg
Height: 162 cm
Body mass index: 30.483 kg/m2
 Physical Examination (Full CVS)

Temperature Hands - Arms Face

it was normal and same on No clubbing, tar stains, peripheral cyanosis. No No mitral facies, but has a puffy face.No
both hands tendon xanthomata or splinter haemorrhage. No pallor, corneal arcus or icterus. No central
osler’s nodes or janeway lesions. No bruising cyanosis or high arched palate
were noted

Pulse Blood pressure Neck

rate was 70 beats per minute, the rhythm was
irregular, the volume was average and the character
was normal. I assessed the character by doing a
water hammer pulse and pulses alternans and both
were of normal character.
was slightly high, it was
122/66 mmHg
JVP was not elevated, it was average and the waveform
was normal, the height was less than 3 cm, so the
pressure is normal. Hepatojugular reflex was also
normal, as it created a transient rise in pressure. The
carotid artery character and volume is normal
 The chest
Upon inspection
It appears normal, no scars, no skeletal
abnormalities, no visible pulsation or pacemaker.

Upon palpation
I palpated the apex beat, I felt it was not in its normal
position, but i am not sure. There was no parasternal
impulse and no thrills.

Upon auscultation
No murmurs were heard. I repeated the auscultation
as S3 or S4 can sometimes be heard in MI.

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 Differential Diagnosis

1 2 3 4

Acute Coronary Stable Angina Acute Aortic

Syndrome Pericarditis dissection
 Investigations
Cardiac Profile
● Troponin: 2402.96 (HIGH)
● Creatine kinase-MB: 11.91 ug/L (HIGH)
● BNP: 130 (HIGH)
cardiac biomarkers are high, going more toward NSTEMI or STEMI. We need to do
ECG to confirm the diagnosis of NSTEMI

Electrolyte panel: to evaluate for renal dysfunction and electrolyte abnormalities

CO2: 24.6 umol/L
Sodium: 135 mmol/L
Potassium: 4.44 mmol/L
Chloride: 104.0 mmol/L
Lipid profile: we do this test because hypercholesterolemia may unfavourably influence the course of the
acute myocardial infarction
Cholesterol: 4.5 umol/L (high)
HDL: 0.94 mmol/L (low)
Everything else were within normal limits
Stool analysis was also done and showed: A soft stool, no pus cells or red cells were found, no blood, no
mucous and no fat globules
●
 Investigations

CBC
Platelets: 1284 (very high) the patient is a known case of essential HbA1c: 5.6 U/L I suppose we do this test because
thrombocytosis - and she admitted that she is not adherent to her hyperglycemia can occur when normal hormonal control of
medications and she is not on a regular follow up with the doctor blood glucose concentration is disturbed by the stress associated
regarding her condition. Probably that’s why her platelets count with acute myocardial infarction
spiked and lead to her MI. APTT: 45.6 seconds (high) blood is clotted faster than normal,
RBC: 5.78 (high) related to her history
MCV: 74 (low) Liver profile: All the liver function tests were within normal
MCHC: 36.7 (high) range
Haemoglobin: 14.7 microcytic hypochromic we should evaluate for Urea: 3.1 mmol/L (low) to check for acute kidney injury or
anaemia because it can exacerbates myocardial ischemia chronic kidney disease because sometime they could predispose
HCT: 42.9% to MI.
Lymphocyte: 11.2% (low)
Monocyte: 1.2
Basophils: 0.3%
WBC: 16.9 (high)
Neutrophils: 13.2 (high)
 12-Lead ECG
Sinus rhythm with T wave inversion in the inferior and the lateral leads
 Other investigations
Echocardiography Chest X-ray
2
1 Revealed good LV systolic function, mild left
ventricular hypertrophy, the ejection fraction =
Peribronchial cuffing in parahilar regions, probably
secondary to bronchitis
68%, no regional wall motion abnormalities, no LV
apical thrombus, mild mitral regurgitation, good Presence of interstitial shadowing in both lung, could be
RV function, no PE. reactive pulmonary congestion status

Ultrasound of the abdomen X-ray of the cervical spine

3 Mild hepatomegaly with fatty infiltration. Mild 4 No abnormality was
splenomegaly with mild increase in the echogenicity of shown
the splenic parenchyma. Debris was found in the urinary
bladder. Urinalysis was advised to rule out cystitis.
Provisional
Diagnosis
Non ST-segment elevation
Myocardial Infarction
 MY TREATMENT PLAN
So once the patient arrives to the emergency department, the initial therapy should focus on stabilising the patient's condition,
relieving ischemic pain, and providing antithrombotic therapy to reduce myocardial damage and prevent further ischemia.
I’d give Morphine for pain control, oxygen, sublingual or IV nitroglycerin, soluble aspirin 325 mg, and clopidogrel with a 300- to
600-mg loading dose as initial treatment.
I will do 12-lead ECG to rule out STEMI, as it is an emergency and if I saw an ST-segment elevation the patient should be taken
to the cath lab within 90 minutes
If the 12-lead ecg is negative;no ST-segment elevation, Then i'll check for cardiac biomarkers (Troponins) to rule in or out
NSTEMI. As it was high in our patient, along with the ECG findings, she was diagnosed with NSTEMI.
Then I would take the patient to cath; urgently. Since the best test to diagnose ACS is the invasive coronary angiogram. So as
soon as the patient crosses high risk they go to cath, until that the patient should get worked up. We repeat ECG and troponins,
if there is elevation in the ST-segment on two or more contiguous leads, this is a risk, or if the troponin keeps elevating, this is
also a risk. If there were negative we rule out myocardial ischemia, if they failed to rule out so this is high risk and I would do a
cath.
We should also determine how many vessels are involved to decide if the patient should undergo PCI or CABG. If less than 3
vessels are involved we go with PCI, if more CABG.
The goal is to re-supply blood flow. We do that by percutaneous coronary
intervention (PCI). We should revascularize in 24 hours from the symptoms onset,
preferably before 12 hours.
PCI: It enters the ostia to reverse the vessel where it will cross the lesion and expand
the ballon where it will smash all the atherosclerotic plaques into the wall of the
vessels and then a stent would be placed.
There are two type of stents, we could give either bare metal stent or drug eluding
stent - then the patient would be placed on Dual anti platelet therapy. It will be for
life, but for BMS we give it every month, and for DES we give it every year. Then we
could shift to a monotherapy; either aspirin or P2y12.
Coronary artery angiogram and percutaneous coronary intervention was done
It showed:
- Left main coronary artery: Normal and arises from the right coronary cusps
- Left anterior descending artery: Normal
- Left circumflex artery: Non dominant and normal
- Right coronary artery: Super dominant and the proximal RCA has 70% unstable plaque with
haziness, patent ductus arteriosus (PDA) and posterior left ventricle (PLB) has mild disease.
In the same setting, intravascular ultrasound (IVUS) to the right coronary artery was done, and it showed that the
proximal right coronary artery has severe stenosis with plaque burden 85%,
It was directly stented the lesion using 4 x 28 Xience Sierra DES (15 atm); which is a drug eluding stent, and post
dilated the stent using 5x15 (20 atm) with good end result.
Then the patient was shifted to the recovery area for closed observation, she complained of heaviness and pain in the
chest. And was given an injection of Premosan 10 mg and morphine 300 mg.
And we support this intervention by a MONABASH2
Morphine treat pain it is actually associated with an increase in infarct size
Oxygen treat hypoxemia, but we should never over oxygenate the patient, because more oxygen means more free radicals in the plasma and
reperfusion injury could occur.
Nitroglycerin it can be used as a diagnostic to see if it is anginal, and also to reduce pain but in ACS reducing the work isn’t gonna work
because that’s supply. But it can still be tried except when there’s a inferior wall infarct.
Aspirin 325 mg, once
Beta blockers prevents ventricular arrhythmia
ARB/ ACE reduce the infarct size, improve ejection fraction (prevent it from falling as a result of the infarct) - however I would use ARBs
over ACE because they are actually the same except that ACE causes dry cough and edema.
Statins high potency
Heparin
P2y12 inhibitors is given as a loading dose, and IV is better that oral
Aspirin and beta-blockers are life saver!

And as this patient has essential thrombocytosis; I would increases the dose of hydroxyurea since her platelets were severely high.
And she also has hypothyroidism so I will continue giving her Levothyroxine.

Subjective
The patient's symptoms has subsided,
she no longer complains of chest pain
or any discomfort. She reports feeling
well and not anxious. No shortness of
breath or light headedness anymore.
Follow-up
Objective
1 2 The patient is not in pain or acute
distress anymore. She is lying
comfortably in the bed with no
complains. She is breathing on room
air. A full cardiovascular examination
was done again and no abnormalities
were noted.

Assessment 3 4
The patient’s symptoms and overall condition has
improved since the day she arrived at the hospital in
which she was in acute distress. She has corresponded
to the treatment, the operation went well and was
uneventful. Her platelets count dropped from 1284 to
985, and her creatine kinase dropped to 3.51, indicating
that she is corresponding to the treatment. Her post
procedure ECG was good as well.
Plan
The patient was planned on increasing the
dose of Hydroxyurea to 1000 mg to manage
her essential thrombocytosis and then she
was discharged as she was stable and no
longer have any complaints, before
discharge she was given several medications
 Learning points:
● Patients with suspected acute coronary syndrome must be evaluated rapidly. The objectives of the initial evaluation are first to
identify signs of immediate life-threatening instability, and then to ensure that the patient is moved rapidly to the most
appropriate setting for the level of care needed, based on diagnostic criteria and an estimation of the need for intervention.
● Vital signs and appearance are two of the most important aspects of the physical exam. These two components of the physical
exam can be assessed quickly and allow for immediate stratification into patients at higher or lower risk for death or nonfatal
myocardial infarction.
● It is recommended that patients with a suspected ACS with chest discomfort or other ischemic symptoms at rest for more than
20 min, hemodynamic instability, or recent syncope or presyncope to be referred immediately to an emergency room or a
specialized chest pain unit
● NSTEMI patients presents with clinical features of UA along with the evidence of myocardial necrosis like elevated serum levels
of cardiac biomarkers (i.e., creatine kinase, MB isoenzyme of CK and Troponins I and T). Troponins are fairly sensitive and
specific for myocardial necrosis. For the diagnosis of NSTEMI to be made, the troponin elevation must occur in the context of
ischemic chest pain, however the diagnosis should not be made based on laboratory findings alone, as there are other possible
etiologies for elevated troponins.
●
 Learning points cont…
● Unstable angina and NSTEMI are at different ends of the spectrum of the same disease. While there is no way
to determine which patients presenting with unstable angina will ultimately progress to NSTEMI, the
distinction between the two entities is clear. Often, for patients presenting prior to the four hour window
before cardiac biomarkers are positive (namely CK-MB), the EKG in context of the patient's chest pain will be
marker for whether patient has STEMI versus UA/NSTEMI and needs to urgently undergo percutaneous
revascularization.
● Coronary artery disease, although rare, can occur in patients without risk factors.
● The presence of traditional cardiovascular risk factors alone is an insufficient way of assessing risk of CAD in
women. Risk assessment in women should therefore be modified.13
● Regardless of a lack of traditional cardiovascular risk factors, a history of typical angina should prompt
referral and appropriate investigation.

●
 Thank you
Aisha Alyassi
Fourth year medical student
University Of Sharjah - College Of Medicine
U18105466@sharjah.ac.ae