School of Medicine

Bachelor of Medicine; Bachelor of Surgery

Internal Medicine 2
Case Write-Up
Name: Loga Tharshini
Student ID: 0329763
Date of Posting: 15th March 2021
Case write-up number: 1

Item Marks Allocated Marks Awarded

Patient’s data 5
History 15
Physical Examination 20
Diagnosis/Differential Diagnosis with Discussion 15
Investigation with Discussion 10
Management 15
Discussion including EBM and references 20
Total 100

Name of Lecturer: Dr Benjamin Date: 4th April 2021 Signature:

Patient identification
Name : Mr R

Age : 65 years

Gender : Male

Marital status : Married

Ethnicity : Malay

Nationality : Malaysian

Occupation : Retired Felda Worker

Address : Bentung, Pahang

R/N : 56068

Date of Admission : 30 March 2021

Source of History : Patient

Chief Complaint

Mr. R, a 65-year-old Malaysian gentleman, presented with a mild shortness of breath that
lasted for about 20 minutes. This is the second episode within 2 days.

History of Presenting illness

Mr. R was well until suddenly he experienced dyspnea. He described his dyspnea as mild,
and still being able to breathe and speak but had general discomfort. The onset of the
symptom was at night when he just about to sleep. He was still sitting up and was about to lie
down when the episode had started. He had no pain, but some chest tightness and diaphoresis.

This episode was similar to the dyspnea he had the night before, which had resolved
spontaneously after 15 minutes.

He did not have symptoms of paroxysmal nocturnal dyspnea as he did not wake up in after
few hours of sleep, due to breathlessness. He did not have any chest pain, chest heaviness or
radiating pain on his jaw or shoulders. He denied any chest pain during the episodes, and
prior to the recent episodes.

Mr R did not notice any breathlessness while lying down, but has recently, for the past 3
years, started sleeping with 2 pillows as he felt more comfortable that way.

He did not have any symptoms of heart burn, nausea or vomiting. There was no exacerbating
or precipitating factors to these episode, as it was sudden on onset. Mr. R rated the severity of
dyspnea as 3 out of 10, as 10 being the most severe shortness of breathing. He claims to be
compliant to his medications and never misses his heath check up appointments. He also
mentioned that he did not have any change in medication or increased medication dosage.

Past Medical History

Patient has underlying dyslipidemia and hypertension which was diagnosed 8 years ago and
is on medications for it. He has been hospitalized 3 years ago due to dengue fever, which
resolved within a week. He also had a kidney stone that was removed 4 years ago. No other
hospitalization or surgeries was done in the past.

Drug History

Patient was on amlodipine 10 mg, oral dose, for hypertension and atorvastatin 10 mg for oral
dose for dyslipedemia. He is also on allupurinol 100mg, oral dose, which is medication for
gout, to prevent urate crystals formation.

Family History

Mr. R is a married man with 4 children. His wife is diabetic and is on oral hypoglycemics.
His children are well and healthy with no medical illness. His parents died due to old age, and
suspected cardiac arrest, but he is not aware if they had any underlying medical illnesses. His
3 siblings are alive and well, but he is not sure if they have any underlying medical
conditions. No history of malignancies or congenital anomalies in his family. However,
cardiac diseases cannot be ruled out.

Social History

Mr. R does not smoke, consume alcoholic beverages or abuse recreational drugs. He is a
retired FELDA worker and has a sedentary lifestyle, which does not include exercising. He
also does not follow a healthy or nutritious diet to control to control his dyslipidemia. He
lives with his son in an apartment in the first floor and does not have difficulty or dyspnea
while climbing the stairs.

Physical examinations

I did not have consent of the patient for systemic examination.

General examinations

Patient is conscious, comfortable with no sign of breathlessness, in pain or distress and

afebrile. His orientation to time, place and person is good. He has a good recent memory and
past memory. On general examination, patient is sitting up on his bed and is able to walk to
the bathroom by himself. He maintains a healthy and normal weight and, appears generally
well, alert and has no sign of respiratory distress or dehydration.
On the examination of the face, he has no conjunctival pallor and no yellow discolouration of
sclera. Corneal arcus and senile cataracts was evident on patient’s eyes. No xanthelasma seen.
There is no sign of dehydration on his lips or skin. No glossitis, coated tongue, oral
candidiasis and ulcers are seen. There is no central cyanosis and the oral hygiene is good with
normal dentition. His face looks normal and symmetrical while talking, smile and there is
wrinkling of forehead. Upon examination of the neck, no signs of engorged vessels
I was not able to examine the patient, because I was not given consent, as he was
feeling dizzy and tired.
However, I would like to look for lymphadenopathy, elevation of jugular venous
pulse. I would also check if the carotid pulses were regular in rhythm and of good pulse
volume. There is abnormal swelling seen in the region of thyroid or around the neck,
clavicles and sub-clavicular region. No lymph node enlargement on suboccipital, submental,
submandibular, sub-clavicular, supraclavicular lymph nodes that was visible, but I would like
to examine the patient’s lymph nodes, by palpation, including the axillary and inguinal lymph
nodes.
In chest and abdomen examination, I would like to check if the skin looked normal, I
would check for presence of skin rashes, deformities or surgical scars seen. Patient seems to
have normal chest and axillary distribution.
 He has an identification tag on his right wrist. His forearms is bruised with formation
ecchymosis from several attempts to withdraw his blood. He did not have a urinary catheter
but had intravenous fluid drips at the time of examination. He had a winged infusion
(butterfly) needle on his left cubital fossa.
On the examination of the lower limb, I would check for scars. I would check his
toenails look had for signs of infections, gangrene, ulcer or any signs or ischemic limb. His
lower limbs were not grossly swollen, but patient did mention that he had mild swelling
sometimes. I would like to check for pitting oedma and determine the level of dependent
oedema of the patient. I want to also check for signs of cellulitis. I would palpate his medial,
lateral malleolus and dorsalis pedis arterial pulse.
I would also examine all his other peripheral pulses to check its rhythm, volume and
character. I would check for collapsing pulse or radio-radio delay. His respiratory rate was 24
breaths per minute. His blood pressure was recorded at 150/90 mmHg. His oxygen saturation
was unknown and temperature at 37˚C. Patient was not having a fever at the time of clerking.
Upon examination of the hands, his palms are warm and moist. Capillary refilling
time is normal (< 2seconds). No signs on palmar pallor was noticed in the palm. There is no
yellowish discolouration, no finger clubbing, no peripheral cyanosis or any scars and
deformities seen. There are no rashes on her hands, forearms and arms of both left and right
side. There is no signs of IV drug abuse or tattoos. Splinter haemorrhages and Osler’s nodes
are not present hence, no sign of infective endocarditis. Flapping tremors are not present, and
he is able to lift his arm and hold it without deviation when his eyes were closed . No fine or
coarse tremors was observed. No tendon xanthomas or swollen interphalangeal joints. His
nails look normal and healthy with no pitting or any deformities. IV line was still intact.

Systemic examinations
1. Cardiovascular system
a. Inspection: I would like to examine for visible pulsation or heave over the chest wall.
I would also feel for the apex beat at the left 5th intercostal space in the midclavicular
line. If the apex beat if shifted, we could suspect mediastinal mass or cardiomegaly. I
would check for precordial bulge, chest deformities, visible mass, swellings or
surgical scars are seen.
 b. Palpation: I would palpate for heaves or thrills over the chest and for the apical
impulse is at the left 5th intercostal space in the midclavicular line. I would check if
the apex beat is only felt at one intercostal space.
c. Auscultation: I would examine for abnormal heart sounds, murmurs or additional
sounds were heard over the heart region.

2. Respiratory system

a. Inspection: I would examine for deformities of the chest wall and any use of
accessory muscles during breathing. Chest wall rise and fall was symmetrical. Patient
was able to speak. Patient was not tachypneic. No signs of severe respiratory distress.
b. Palpation: No evidence of deviation of trachea. Chest wall movement is
symmetrical. I would examine for increased vocal fremitus over both lungs and local
tenderness over the chest wall palpation. I would also check for increased vocal
fremitus to rule out fluid accumulation or mass in the lungs, in supraclavicular,
infraclavicular, mammary, axillary, infra axillary, suprascapular, infrascapular and
interscapular areas.

c. Percussion: I would also examine for reduced resonance over the lungs. Region of
cardiac dullness should be appreciated. I would check for at supraclavicular,
infraclavicular, mammary, axillary, infra axillary, suprascapular, infrascapular and
interscapular areas.
d. d. Auscultation: I would auscultate at supraclavicular, infraclavicular, mammary,
axillary, infra axillary, suprascapular, infrascapular and interscapular areas. I would
mainly look for inspiratory course crackles to rule out pulmonary edema in the lower
lobes of the lungs.

. Gastrointestinal system
a. Inspection: Patient is at a normal weight and not obese. I would examine if his skin
had any abnormal pigmentation or discoloration, to rule out jaundice and skin infections.
 I would check if his abdominal wall were symmetrical with no surgical scars. I would
also examine the umbilicus and check for swellings that can be appreciated on any
quadrants of the abdomen. I would check of movements of all quadrants of the
abdominal wall with respiration was normal. No striae, hernias, engorged veins or
lesions were seen. I would also check for presence of generalized or localized distention,
that may suggest ascites or herniation.

b. Palpation: Upon palpation, I would check for tenderness or masses felt while doing
the superficial and deep palpation of the abdomen, to ensure no guarding or rebound
tenderness, to rule out peritonitis. I would also check if patient was comfortable
throughout the palpation progress. I would do a renal punch and bimanual palpation of
the kidney was done to detect the enlargement or pain over of the flank, as he already had
history of kidney stone removal. I would palpate for tenderness over the liver. I would also
do a hepatojugular reflux to check raised jugular venous pulsation that may indicate right
heart failure. I would also palapte to check for hepatomegaly to rule out fatty liver. Next
I would examine the spleen to check for splenomegaly and any pulsating mass.

c. Percussion: I would examine for fluid thrill to check if there is free fluid in the
peritoneum to rule out ascites. I would percuss the bowels for general tympanic sound, to
ensure no obstruction. I would expect left hypochondriac region, right lumbar region,
umbilical region, left lumbar region, right iliac fossa region, hypogastric region
left iliac fossa region to be tympanic. Psoas sign and obturator sign would also be done
for rule out appendicitis and completion of the examination.
Auscultation: I would auscultate for absence or increased bowel sounds over the
quadrants of the abdomen. I would check for renal bruits to rue out renal artery stenosis.

Examination of the genitalia and rectal: I would complete the with examination of
genitalia and rectum. Patient however reported no abnormalities, rash, pain or mass
present around the area of rectum and genitalia.

4. Central Nervous System

a. Patient has a Glasgow Coma Score of 15. Patient is capable of opening his eyes
spontaneously (4/4), his verbal response is oriented (5/5), his motor response is good as
he obeys command (6/6).
b. Patient has no slurring of speech or weakness of any side of the body. He has no
headaches or triggering migraine factors. He no history of seizures, or abnormal
movements. He has no tremors, and no loss of consciousness or orientation.
c. Patient did not report any psychiatric illnesses or hallucinations.

Provisional Diagnosis

Provisional Supporting factors Factors Against

Unstable Angina  No precipitating factors  No history of cardiac
or activities done prior to disease
the episode of dyspnea.  No chest pain
 Has been diagnosed  No palpitations
hypertension and
dyslipidemia for the past
8 years
 Diaphoresis with mild
dyspnea
 Sedentary lifestyle
 Older age group

Differential diagnosis
Disease Supporting factors Factors Against
Pulmonary Sudden onset dyspnea No chest pain
Embolism sweating No leg pain or claudication
No signs of deep vein
thrombosis or reduced
movement
Pleural effusion Dyspnea No pain upon inspiration or
expiration.
No signs heart failure
No signs of kidney failure
Pulmonary Dyspnea No congestive heart failure or
edema severe pitting edema
No raised jugular venous pulse
Myocardial Dyspnea No palpitation
infarction Dyslipidemia No sharp chest pain or
Hypertension radiating pain

Nephrotic Dyspnea No polyuria

syndrome Edema of leg No frothy urine
History of kidney pathology No infection (due to loss of
immunoglobulin in urine)
No orbital edema

Investigations and Results

1. Haematology
a. Full blood count (FBC)
I would like to do a full blood count and compare with the value range given below,
to rule out infectious cause.
White blood cell (4.08 – 11.37)

Red blood cell (3.86 – 5.62)

Haemoglobin (11.8 – 16.9)

Haematocrit (35.7 – 48.9)

Mean cell volume (80.6 – 95.5)

Mean cell hemoglobin (26.9 – 32.3)

Mean cell hemoglobin concentration (31.9 – 35.3)

Red cell distribution width (12.0 – 14.8)

Platelet (142 – 350)

Mean platelet volume (9.4 - 12.3)

Percentage of neutrophil

Percentage of lymphocyte

Percentage of monocyte

Percentage of eosinophil

Percentage of basophil

Absolute neutrophil (3.93 – 7.15)

Absolute lymphocyte (1.85 – 4.81)

Absolute monocyte (0.39 – 1.14)

Absolute eosinophil (0.00 – 0.83)

 Absolute basophil (0.00 – 0.10)

Close monitoring of potassium and magnesium levels is important in patients with acute
coronary syndrome because low levels may predispose them to ventricular arrhythmias.
Routine measurement of serum potassium levels and prompt correction are recommended.

b. Renal profiling
I would also do a renal profile to check the kidney function, as the patient mentioned he
sometimes had oedema in his lower limbs, which may suggest nephrotic syndrome. The
bilirubin levels help in determining presence of haemolysis. The normal value ranges are
given below.
A creatinine level is also needed, particularly if cardiac catheterization is considered. Use of
N -acetylcysteine and adequate hydration can help prevent contrast material–induced
nephropathy.

Urea (3.0 – 9.2)

Sodium (136 – 145)

Potassium (3.50 – 4.50)

Chloride (98.0 – 107.0)

Creatinine (65.0 – 111.0)

Total bilirubin (3.4 – 20.5)

Direct bilirubin (0.0 – 8.6)

Indirect bilirubin (0.0 – 8.6)

c. Liver function test (LFT)

Total Protein (65.0 – 83.0)

Alkaline Phosphatase (40 – 150)

Alanine Transaminase (7-55)

Aspartate Transaminase (5 – 34)

 I would also do a liver function test to check for any liver pathology.

d. Lipid profile
I would do a lipid profile to check if the patient’s dyslipidaemia is controlled or needs
intervention. High triglycerides and LDL cholesterol may suggest impending or may
support diagnosis of cardiovascular or cerebrovascular diseases.
Triglycerides (0.00 – 1.70)

LDL Cholesterol (0.00 – 1.95)

HDL Cholesterol (>1.04)

Cholesterol (0.00 – 5.20)

Cardiac Biomarkers
I would obtain a cardiac biomarker tests, that include creatine kinase, CK-MB, and troponin.
Absolute elevations of creatine kinase and its MB isoenzyme (CK-MB) or troponin levels are
highly specific evidence of myocardial cell death and distinguish non−ST-elevation MI
(NSTEMI) from unstable angina. Besides that, I would also do brain natriuretic peptide to
check for significant cardiac dysfunction like heart failure due to increased stress on
myocardium.

Imaging

X- ray

I would do an X ray to have a clear view of the heart and lung fields. It is important to rule
out lung pathology as it could present with similar symptoms.
Electrocardiography (ECG)

Figure 1

Figure 1 shows the results of electrocardiogram (ECG) procedure done for Mr.A on 30th
march 2021. This ECG shows sinus rhythm but sinus bradycardia, which is usually seen in
acute angina. All the waves have smaller amplitude compared to a normal healthy ECG of the
heart. There is no suggestion of cardiomegaly or myocardial infarction as there is no right or
left axis deviation (> 90 degrees). No tall R-waves in RV leads or deep S-waves in LV leads.
No increase in QRS duration. No changes in ST segment or changes directed opposite to
QRS direction. All the p wave are present before the QRS complex, which rules out
arrythmia and heart failure related arrythmia.

Echocardiography

I would also do echocardiography to provide a quick evaluation of left ventricular function

either for prognosis or for diagnosis, as when new segmental wall motion abnormality is
detected. However, small infarcts may not be apparent on the echocardiogram. Important
causes of chest pain, such as aortic stenosis and hypertrophic obstructive cardiomyopathy
(HOCM), can be readily detected by echocardiography.

Angiogram
I would also do a coronary angiogram to view the coronary vessels which may possibly cause
ischemia to the myocardium.

Exercise testing
I would not perform this test on this patient as he is in an acute state of unstable angina, and
this test might predispose another episode of angina. However, if the patient is already
stabilized, this test could be done before discharging the patient to ensure check their stress
tolerance.

Discussion

Unstable angina belongs to the spectrum of clinical presentations referred to collectively as

acute coronary syndromes, which range from ST-segment elevation myocardial infarction
(STEMI) to non-STEMI (NSTEMI). Unstable angina is an acute coronary syndrome in which
there is myocardial ischemia without detectable myocardial necrosis as, cardiac biomarkers
of myocardial necrosis, such as creatine kinase MB isozyme, troponin, myoglobin that are not
released into the circulation.

The term unstable angina was meant to signify the intermediate state between myocardial
infarction (MI) and the more chronic state of stable angina. Patients with angina are generally
categorized by presentation, diagnostic test results, or course over time. These categories
include new-onset angina, accelerating angina, rest angina, early postinfarct angina, and early
post revascularization angina.
The patient’s history and diagnostic testing are generally more sensitive and specific for
unstable angina than the physical examination, which may be unremarkable. The patient
however has symptoms of diaphoresis and ECG findings shows sinus bradycardia which is
suggestive of unstable angina. This is due to transient myocardial dysfunction (eg, systolic
blood pressure < 100 mm Hg. Some patients may also present with tachycardia and chest
pain which is absent in this patient.

Laboratory studies for the evaluation of a patient with unstable angina are, 12 lead
electrocardiogram, serial cardiac biomarker assays (eg, creatine kinase MB isoenzyme [CK-
MB], troponin I or T), complete blood count (CBC) with hemoglobin level, serum chemistry
panel (including magnesium and potassium), and lipid panel are vital. However, these reports
are inaccessible in this patient.

Management

Management is directed toward reducing myocardial oxygen demands; improving myocardial

oxygen supply; and assessing the patient's risk of progression to myocardial infarction or
having a complication related to treatment.

Patients with unstable angina require admission to the hospital for bed rest with continuous
telemetry monitoring. One should obtain intravenous (IV) access, and provide supplemental
oxygen if evidence of desaturation is noted. Because the course of unstable angina is highly
variable and potentially life-threatening.

Use of cardiac catheterization with possible revascularization can be done with constant
monitoring of ECG. The therapy should target causes of the unstable angina, such as
increased myocardial rate-pressure product, coronary vasoconstriction, platelet aggregation,
and thrombosis.

Medications that provide symptomatic relief include nitrates (eg, nitroglycerin IV), calcium
channel blockers (eg, diltiazem, verapamil), and low molecular weight heparin. Medications
that have been convincingly shown to be capable of reducing short- or long-term adverse
events are aspirin, clopidogrel, beta-adrenergic blocking agents, lipid-lowering agents
(statins), angiotensin-converting enzyme (ACE) inhibitors, glycoprotein (GP) IIb/IIIa
antagonists.

Diet and Exercise

A healthy diet low in cholesterol and saturated fat is recommended in patients with unstable
angina. Diet modification with adequate intake of fruits and vegetables, exercise, and
behavioral modification and counseling are indicated. They should also exercise to correct
dyslipidemia, but they also should avoid sudden strenuous physical activity. Sodium
restriction should be instituted for patients with heart failure or hypertension. Patients who
are smoking should immediate stop smoking, but this patient is a non – smoker. Patients
should also be advised to reduce their waist circumference, to less than 90cm.
Evidence Based Medicine

How does epicardial adipose tissue thickness (EAT) affect the prognosis of unstable angina?

Despite the growing number of patients discharged from hospital with a diagnosis of unstable
angina, the diagnostic procedures and treatment of unstable angina are still greatly debated,
as they have been for patients with myocardial infarction.

Some studies have shown that significant prognosticators for poor outcome in patients with
unstable angina are ongoing chronic heart failure, presence or history of poor left ventricular
ejection fraction (LVEF), hemodynamic instability, recurrent angina despite intensive anti-
ischemic therapy, new or worsening mitral regurgitation, and sustained ventricular
tachycardia.

Epicardial adipose tissue (EAT) is part of visceral adipose tissue localized between the heart
and pericardium, particularly in the atrioventricular and interventricular sulcus, lateral wall of
the right ventricle, and around the coronary arteries. EAT has endocrine, paracrine, vasocrine,
and inflammatory characteristic and is associated with metabolic syndrome, insulin
resistance, coronary artery disease, and hypertension. Therefore, measurement of EAT
thickness has gained importance. EAT thickness can be measured by transthoracic
echocardiography, cardiac computed tomography (CT), and cardiac magnetic resonance
imaging (MRI) methods. Evaluation by transthoracic echocardiography has many
advantages, such as easy availability, low cost, no radiation exposure and it is fast.

More recent studies indicate that epicardial adipose tissue thickness (EAT) can also be used
to predict major adverse cardiac events. EAT thickness measured during end-systole to be
minimum 1 mm and maximum 22.6 mm with a mean value of 7 mm in males and 6.5 mm in
females among individuals evaluated by echocardiography for standard clinical indications.

In a study of 200 patients hospitalized with stable angina pectoris, unstable angina pectoris,
or acute myocardial infarction who underwent coronary angiography, patients with a baseline
EAT of more than 7 mm suffered significantly more revascularizations, non-fatal myocardial
infarction, and cardiovascular death. While interpreting these threshold limit values, it should
be kept in mind that EAT thickness could be influenced by age, gender, and race and whether
the measurement was done during end-systole or end- diastole

Differentiating EAT from pericardial effusion is of great importance. Even though the EAT is
viewed as a hypoechoic area, it has different features from pericardial effusion. EAT has
specific echo-density that comprises echo-lucent areas and whitish-speckled appearance.
However, pericardial effusion has more hypoechoic appearance. In addition, although EAT is
limited to the front of the right ventricle, pericardial effusion reveals wider spread, and
usually it is more prominent in the posterolateral aspect of the left ventricle while the patient
is left lateral decubitis position.

There are several limitations to the measurement of EAT thickness by transthoracic

echocardiography. First, we only partially measure EAT by transthoracic echocardiography.
In contrast, both EAT thickness and volume can be measured by cardiac CT and MRI
precisely and more accurately than echocardiography. Echocardiographic measurements are
not as reproducible as cardiac CT and MRI. Another limitation is the lack of certain threshold
values to predict in pathologies. EAT thickness appears to increase with age, and it could be
influenced with gender and ethnicity. Although EAT measurement by echocardiography has
some limitations, it has the advantage of being an easy, readily available, repeatable, and low-
cost modality without radiation exposure.
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