Challenges in Diagnosing Acute Coronary Syndrome at

Emergency Department
Nik Ahmad Shaiffudin*, Nurin Natasha Binti Mohd Razali, Nurul Aqilah Binti Mohd
Nasir, Siti Nurizah Binti Ishak

Department of Emergency Medicine, Faculty of Medicine, UniSZA Medical Campus,

20400, Kuala Terengganu, Terengganu, Malaysia

ABSTRACT
Acute coronary syndrome (ACS) refers to a spectrum of clinical presentations ranging
from those for ST-segment elevation myocardial infarction (STEMI) to presentations found
in non–ST-segment elevation myocardial infarction (NSTEMI) or in unstable angina. The
patient with undifferentiated chest pain often presents as a diagnostic challenge in the ED.
Many conditions may mimic ACS, from cardiopulmonary pathology to
gastrointestinal disease. ECG findings of T wave inversion in precordial and inferior leads
and lab findings of troponinemia may be seen in both PE and ACS, further confounding the
diagnosis.(Fedullo et al., 2003) It is crucial to distinguish aortic dissection from ACS, as the
two are managed very differently. Furthermore, improperly diagnosing aortic dissection as
ACS can have devastating consequences if the patient were to receive anticoagulation or
thrombolytic therapy. (Klompas & MD Michael, 2002) ECG of patients with myocarditis
may show nonspecific ST segment and T wave abnormalities and may even mimic an acute
myocardial infarction. (S C Smith et al., 1997) Mucosal disorders including peptic ulcer
disease and gastritis may mimic ACS due to overlapping symptoms of vague epigastric pain,
pain in the lower half of the chest, nausea, and vomiting. ACS cannot reliably be
differentiated from gastrointestinal pathology on the basis of history and physical exam.
(S.W. Goodacre et al., 2003). ECG findings of DKA causing hypokalemia may mimic the
findings seen in acute coronary syndrome and should be differentiated in critically ill patient.
(Özkaya et al., 2010) Suspicion of ACS should never delay the investigation of other life-
threatening disorders. History and physical exams alone cannot reliably rule out ACS.
Physicians must perform a focused history, physical exam, and risk stratification for
appropriate evaluation.
Patient delay is among the longest in the pre-hospital chain of ACS patients. Patients
with chest pain most often contact the general practitioner (GP) instead of the recommended
EMT, increasing delays as well. To decrease the delays by referring all patients promptly and
without restriction to the emergency department (ED) is not feasible. Up to 80% of the
patients with chest pain do not have a cardiac diagnosis and thus referral of all these patients
would result in overcrowding of the ED. Triage is therefore crucial. Triage of patients with
chest pain is therefore imperative and there is a great need for validated triage tools. (Mol et
al., 2016)

KEYWORDS : Acute coronary syndrome; clinical presentations; Emergency

Department; challenges
INTRODUCTION:

Careful assessment and risk stratification are important because these guide the use of
more complex pharmacological and interventional treatments which can improve outcome. It
has been demonstrated that the use of multivariate models as scores represent the most
accurate means of risk prediction, superior to that obtained subjectively through clinical
impression (Yan et al., 2009). The thrombolysis in myocardial infarction (TIMI) risk score is
a tool used to predict the chances of having or dying from a heart event for people with
unstable angina and non-ST-segment elevation myocardial infarction (NSTEMI). The TIMI
risk score is calculated by taking seven factors into account. Some of these are determined by
performing specialised heart tests or asking about a person’s medical history. The Braunwald
classification is conceptually useful, in that it factors in the clinical presentation (new or
progressive vs rest angina), context (primary, secondary, or post-MI), and intensity of
antianginal therapy. The New York Heart Association (NYHA) Classification provides a
simple way of classifying the extent of heart failure. It classifies patients in one of four
categories based on their limitations during physical activity; the limitations/symptoms are in
regards to normal breathing and varying degrees in shortness of breath and or angina pain.

Routine use of validated risk scores may enhance risk stratification and facilitate more
appropriate tailoring of intensive therapies toward high-risk patients. (Yan et al., 2009)
Routine risk stratification as soon as possible after presentation will determine the clinical
pathway, and that this practice should be embedded in the hospital system. This is a
challenging change in approach for the hospital system, but bound to be fruitful in reducing
decision time when early revascularization is needed, and avoiding unnecessary intervention
when it is not. Risk stratification is infrequently applied and, as a consequence,
undertreatment of higher-risk patients is common. Ensuring routine application of risk
stratification across hospitals may improve treatment of patients who have the most to gain
from evidence-based therapies. This requires embedding standard practices into complex
clinical environments, and includes the routine implementation of treatment algorithms in a
permissive environment with clinical champions and support from the hospital
administration. The implementation of routine systems of care defining prehospital,
interhospital and individual hospital practice is challenging, but essential to minimise deficits
in care. (Brieger, 2014)

The classification of acute coronary syndromes as STEMI or NSTEMI is not always

straightforward; misclassification commonly occurs. The patients with STEMI need
emergency percutaneous coronary intervention, while in those with NSTEMI, the therapeutic
strategy depends on the clinical circumstances. On some occasions, the ECG pattern of
evolving STEMI in the hyperacute phase shows only peaked positive T waves with or
without ST‐segment deviation, and in other casewith STEMI,
spontaneous reperfusion occurs, and the ECG may show negative T waves. Evolving ACS is
a dynamic process, which sometimes may present as an NSTEMI pattern, but evolves to an
STEMI pattern or vice versa. If the dynamic nature of the disease is not taken into account,
the ECG changes may be misinterpreted. (Fiol-Sala et al., 2019)

Many patients with ACS are misdiagnosed. Between 2% and 5% of patients are
inappropriately discharged from the ED. (Barstow, 2020) Discharging patients with acute
myocardial infarction or unstable angina from the emergency department because of missed
diagnoses can have dire consequences. Misinterpretation of an ECG and overreliance on a
normal ECG have also been reported as causes of misdiagnosis of ACS. Higher rates of
atypical symptoms or presentations, such as abdominal pain, shortness of breath, and
congestive heart failure, might contribute to missed diagnoses.. (Brieger, 2014) Accurate
recognition of the symptoms of MI in both patients and physicians is crucial. The patient's
inability to recognize MI symptoms will inevitably lead to delay in receiving timely therapy,
which in turn may lead to a larger infarct and worse prognosis (Canto et al., 2007). The
inability of health care providers to recognize an evolving MI may lead to an incorrect
diagnosis and delays in treatment. Young age and the absence of chest discomfort are among
the strongest predictors of a missed diagnosis of MI and inappropriate discharge from the
emergency department. (Canto et al., 2007)
Patients who experience ACS present with heterogeneous clinical manifestations. In
the emergency department, risk assessment should immediately identify patients with STEMI
who are in need of emergency reperfusion. In patients with NSTEMI, the focus is on
identifying those at higher risk of recurrent infarction or death. This then guides the
application of evidence-based therapies such as angiography and appropriate
revascularisation, powerful antithrombotic therapy and comprehensive secondary prevention.
Evaluations of clinical practice have consistently shown underuse of risk stratification and
consequent inappropriate application of evidence-based practice. This is particularly true for
patients at higher risk of adverse events, who are often undertreated yet have the most to gain
from evidence-based therapy.Because risk stratification should be one of the first objectives
when assessing an ACS patient, it provides the earliest opportunity to define care.
Application of a risk-stratification tool provides an unambiguous definition of the patient at
high risk, who has the most to gain from evidence-based care, and this strategy is
recommended in local and international ACS guidelines. (Brieger, 2014)

In this case series, we present 4 different cases of acute coronary syndromes among
patients that come with different clinical presentations.

METHODS:

Retrospective study through case series.

CASE SERIES:

CASE REPORT 1

A 49 years old Malay man presented to the Emergency Department (ED) due to
worsening epigastric pain for 2 days, radiating to the tip of left shoulder, left arm, back and
neck. The pain was pricking in nature, exaggerated by activities and relieved after resting. He
did take antacid, as he suspected that the pain was due to dyspepsia, but the pain did not
resolve. The pain score was 8/10, and was associated with dizziness. Otherwise, the patient
denied orthopnea, paroxysmal nocturnal dyspnea and profuse sweating. He has a family
history of hypertension, in which 2 of his siblings were diagnosed at a young age. He is also a
chronic active smoker with 30 pack years.
On examination, he was alert, conscious, lethargic-looking, but not tachypnoeic. His
neck vein was not distended, his peripheries were warm, and there was no pedal edema. As
for his vital signs upon arrival at ED, his temperature was 37°C, blood pressure was 131/91
mmHg, pulse rate was 56 bpm, respiratory rate was 20 breaths per minute and oxygen
saturation was 99% under room air. Otherwise there were normal findings on cardiovascular,
respiratory and abdominal examinations.
12-lead ECG that was done upon his arrival at ED showed sinus bradycardia and T
wave inversion over lead V1 with no significant ST changes. His chest x-ray was normal as
there was no signs of cardiomegaly, in which the cardiothoracic ratio was less than 0.5. There
were also no signs of heart failure such as pulmonary edema. For the cardiac biomarker, his
blood was sent for CK and CK-MB levels, and the result came out normal as well.

Upon arrival at ED, he was triaged to the yellow zone after his vital signs were noted,
investigations were done and he was treated as Unstable Angina (UA). Sublingual glyceryl
trinitrate (GTN) to relieve the angina, 300 mg tablet plavix and 300 mg subcutaneous
fondaparinux as the definitive treatment. He was then referred to the cardiology department
for further evaluation and management.

CASE REPORT 2

A 65-year old Malay man with underlying ischemic heart disease presented to the
Emergency Department with central chest pain for one day duration. It was sudden in onset
and heaviness in nature. It lasted about 5 to 6 minutes during resting and was relieved by
taking GTN. The pain then radiated to his back and left shoulder and the pain score given by
the patient was 5/10. It was associated with fatigue, shortness of breath with reduced effort
tolerance, paroxysmal nocturnal dyspnea and orthopnea, Otherwise , the patient denied
having fever, coughing, profuse sweating , palpitation, nausea, vomiting or syncope. Patient
was an active smoker , who smokes about 5-6 cigarettes a day. He lived a sedentary lifestyle
and rarely did exercise .
On physical examination, he was alert, conscious and not tachypnoeic. Upon arrival at
ED, his temperature was 37.0℃, blood pressure was 101/67 mmHg, pulse rate was 90 bpm,
respiratory rate was 17 breath per minute and oxygen saturation
was 99% under room air. Bibasal crepitation was heard. There was bilateral pitting oedema
on the leg up to mid shin. In the cardiovascular examination, the apex beat was displaced to
the lateral mid clavicular line (MCL). Otherwise there were no other remarkable findings on
respiratory and abdominal examinations.

ECG was done and it showed sinus tachycardia with ST depression in lead V5 and V6
and T wave inversion in lead V4 and V6. On chest radiograph, there was cardiomegaly,
opacity on the lower zone of both lungs and blunting of costophrenic angle resulting from
accumulation of fluid in the pleural space .There was presence of kerley B line in the right
lower zone of the lung. Cardiac marker results showed elevated creatine kinase (879U/L) and
CK-MB level (45U/L). C-reactive protein (CRP) was also elevated.

He was diagnosed with non STEMI with acute decompensated congestive cardiac
failure. The patient was resuscitated with oxygen and given pain medication to
relieve his symptoms He was treated with double antiplatelet agent (t. aspirin 300mg and t.
plavix 300mg), IV lasix 40 mg and IV heparin 4000 iu bolus and 5 cc/hr. He was referred to
the medical ward for further management.

CASE REPORT 3

A 61yo malay male, active smoker 45 pack years, ex-pensioner with underlying
Diabetes Mellitus, hypertension, hypercholesterolemia and ischemic heart disease, presented
with history of chest pain for 3 days that worsening today, its occur at the left sided,
throbbing in nature, radiated to the left shoulder, left arm and at the back, for duration 3-4
minutes per episode. It was exaggerated by exertion and relieved by rest and taking
sublingual GTN. The severity was 6/10. It was associated with palpitation, profuse sweating,
shortness of breath, nausea, orthopnea, paroxysmal nocturnal dyspnea, dizziness, reduce
effort tolerance. There was no history of fever, vomiting. He also complained that slight
limitations of physical activities result in fatigue.

Past medical history, he was diagnosed with Diabetes Mellitus in 2013 with history of
polyuria, currently on insulin and oral hypoglycemic agent. He was diagnosed with
hypertension and hypercholesterolemia in 2014, during the follow up. Currently follow up at
KK Seberang Takir. He was not compliant to the medications. He was diagnosed with
ischemic heart disease in 2017, with coronary angiogram and percutaneous coronary
intervention done in august 2019. He had last admission for ACS in 2020 at hospital JB.

On physical examination, he was alert and conscious, not tachypneic, warm

peripheries, good pulse volume. Vital sign: BP 147/80 hypertensive, pulse rate 80 normal,
SPo2 98% and temperature 37C. CVS, RS and GIT examination was unremarkable. No pedal
edema.

For investigation, ECG showed premature ventricular contractions at lead

II and III, ST elevation V1-V5. Chest X-ray showed evidence of redistributive pulmonary
vessels, but no cardiomegaly
FBC: WBC, HB and platelet normal. BUSEC normal, CK and CKMB high. Prothrombin
time was normal. Medication given was tablet aspirin 300mg stat, tablet Plavix 300 mg stat,
subcutaneous fondaparinux 2.5mg stat. Continuous vital sign monitoring and refer cardiology
department for admission

CASE REPORT 4

A 36 years old malay male with major cardiovascular risk factors (ischemic
heart disease, hypertension, hyperlipidemia, diabetes mellitus) presented with left-sided chest
pain 3 hours prior to admission. He developed chest pain while he was sleeping, left-sided
chest pain and the pain score was 9/10. The pain was heavy in nature. The pain was
continuous, with increased intensity, gradually in onset. It radiated to the left shoulder, jaw
and back. The pain was not relieved after he took the sublingual medication. The pain was
aggravated by breathing. It was associated with shortness of breath, profuse sweating,
orthopnea, paroxysmal nocturnal dyspnea. However, no palpitation, nausea or vomiting.
However there is no limitation of physical activities.

He was a known case of ischemic heart disease, hypertension and hyperlipidemia

diagnosed in 2014 with symptoms of chest pain. He has had diabetes mellitus for 10 years.
He had 1-2 history of hospitalisation earlier every year. Currently, the patient was on
anti-hypertensive, anticoagulant, lipid-lowering agent, antiplatelet drug, antianginal and anti-
diabetic drugs. He was not compliant to medication. He is anactive smoker who smoked 23
pack years. He also had cocaine drug abuse and had poor diet control.

On physical examination, he was alert and conscious, not tachypneic, warm

peripheries, good pulse volume. Vital sign: BP 134/80, pulse rate 80, RR 17, SPo2 98% and
temperature 37C. CVS, RS and GIT examination was unremarkable. No pedal edema.

For investigation, ECG showed ST elevation V1-V4. Chest X-ray cardiomegaly but
no pulmonary oedema, FBC normal. BUSEC normal, CK and CKMB high, Lipid profile
high cholesterol. He was given iv streptokinase 1.5mu/H, t aspirin 300mg, t plavix 300 mg s/l
GTN 1 tablet, iv tramadol 50mg. Continuous vital sign monitoring and refer medical for
admission
RESULTS:

C Description
a
s
e

1 Diagnosis: Unstable Angina

Historical:
● Age 49 years old (not more
than 65)
● Active smoker, no known
medical illness ( not more
than 3 CAD risks)
● No known case of CAD
● ASA not used in 7 days
Presentation:
● Recent (<24 hours) severe
angina
 ● No ST changes
● No raised cardiac marker TIMI risk score: 1 (low risk) Braunwald score: Class
1 - new onset, severe and accelerated

2 Diagnosis: Non-STEMI with decompensated congestive heart failure

Historical:
● Age 65 years old
● Active smoker
● Known case of CAD
● ASA not used in 7 days Presentation:
● Recent (<24 hours) severe angina
● ST depression
● Raised cardiac marker
TIMI risk score: 6 (high risk) Braunwald score: Class 2 – rest angina without recent
episode (<48 hours)
NYHA: Class III – marked limitation of physical activities. Although patient
comfortable at rest, less than ordinary activities lead to symptom

3 Diagnosis: STEMI Presentation:

● underlyingDiabetes
Mellitus, hypertension, hypercholesterolemia and ischemic heart disease
● He was not compliant to the medications.
● Had undergone percutaneous coronary intervention
● Develop left sided heart
failure
Investigation:
 ● ECG - ST elevation V1-V5
● Cardiac marker - CK-MB high
● Chest X-ray - evidence of redistribution pulmonary vessels, but no
cardiomegaly

4 Diagnosis: STEMI Presentation:

● Underlying ischemic heart
disease, hypertension, hyperlipidemia
● Smoker with 23 pack years
● Had cocaine drug abuse
● Develop left sided heart
failure
Investigation:
● ECG show ST elevation V1-V4
● Cardiac marker - CK-MB high
● CXR - cardiomegaly, no pulmonary oedema

DISCUSSION

CASE 1

Unstable Angina (UA) is a clinical diagnosis based on history, physical examination

findings, and diagnostic testing that does not reveal a STEMI or NSTEMI. It is a broad
clinical diagnosis that includes patients at different levels of risk for an unfavourable
outcome. (Betriu et al., 1992, 1). The first case involves a patient with no known medical
illness, presented with a complaint of epigastric pain radiating to the left shoulder and arm.
That was his first time ever experiencing such pain in his life, and it occurred in less than 48
hours upon presentation at ED.
Although chest pain is the most common symptom for patients with ACS, 20-30% of all
patients diagnosed with ACS report atypical symptoms, for instance, abdominal pain, and
their chief complaint may not include chest pain. (Cline et al., 2017, 131). Patients with
UA/NSTEMI have an increased risk of death, recurrent MI, recurrent symptomatic ischemia,
serious arrhythmias, heart failure and stroke. Risk stratification scores for UA/NSTEMI have
been developed and validated in large patient population. TIMI risk score is commonly used
in clinical practice, is simple and widely accepted. (Malaysian Ministry of Health, 2011). For
this patient, according to his presentation, he scored 1/7, in which the risk of him developing
complications would be 4.7%. Unstable angina itself can be classified according to clinical
circumstances using Braunwald's Classification. (Malaysian Ministry of Health, 2011). This
case is classified as Class 1, as the patient had a new onset of accelerated angina.

ECG should be done for all patients presented with chest pain, or symptoms
suggesting cardiac problems. ECG features suggestive of UA/NSTEMI are: 1) dynamic ST/T
changes; 2) ST depression ≥ 0.5 mm in 2 or more contiguous leads; 3) deep symmetrical T
wave inversion. (Malaysian Ministry of Health, 2011). For patients with suspected ACS,
serum troponin, chest radiograph, FBC, electrolytes and PT/APTT should be obtained. (Cline
et al., 2017, 132). Cardiac biomarkers, such as cardiac troponins (troponin T or I) are
recommended as they are highly specific and sensitive for myocardial injury and/or necrosis.
(Malaysian Ministry of Health, 2011). However, in this patient, only Creatine Kinase (CK)
and CK-MB were done. The cardiac biomarkers levels were not elevated and therefore he
was treated as UA. Like troponins, CK and CK-MB are also important indicators of
myocardial necrosis, however, they are less specific compared to cardiac troponins.
(Malaysian Ministry of Health, 2011).

CASE 2

Risk factors of ACS for this patient include male sex, older age (65 years old),
smoking, personal history of coronary artery disease / IHD. The differential diagnosis of
acute coronary syndrome is wide and includes most causes of central chest pain or collapse.
Patient was presented with central chest pain with heaviness in nature, occuring at rest and
relieved by taking GTN. The pain then radiated to his back and left shoulder and it was
associated with fatigue, shortness of breath with reduced effort tolerance, paroxysmal
nocturnal dyspnea and orthopnea, On physical examination, bibasal crepitation was heard.
There was bilateral pitting oedema on the leg up to mid shin. In cardiovascular examination,
the apex beat was displaced to the lateral mid clavicular line (MCL).

According to the TIMI risk score, this patient has a score of 5, therefore he has a
26.2% risk of having or dying from a heart event. Following Braunwald score, this patient is a Class 2
as he has rest angina without a recent episode (<48 hours). The New York Heart Association
(NYHA) Classification classifies the patient into Class III as the patient has marked
limitation in activity due to symptoms, even during less-than-ordinary activity
such as walking short distances (20—100m) and he is comfortable only at rest. (New York
Heart Association (NYHA) Classification, n.d.)
The standard 12-lead ECG is central to confirming the diagnosis. (Ralston et al.,
2018) In non-STEMI, there is partial occlusion of a major vessel or complete occlusion of a
minor vessel, causing unstable angina or partial-thickness MI. This is associated with ST-
segment depression and T-wave changes. The ECG changes are best seen in the leads that
‘face’ the ischaemic or infarcted area. (Ralston et al., 2018) In this patient, ECG was done
and it shows sinus tachycardia with ST depression in lead V5 and V6 and T wave inversion in
lead V4 and V6, indicating this patient has anterolateral NSTEMI, as it produces changes
from V4 to V6. The T wave becomes inverted because of a change in ventricular
repolarization. Serial measurements of serum troponin should be taken. MI causes a rise in
plasma troponin T and I concentrations and other cardiac muscle enzymes. Levels of
troponins T and I increase within 3–6 hours, peak at about 36 hours and remain elevated for
up to 2 weeks(Ralston et al., 2018). For this patient, cardiac marker results show elevated
creatine kinase (879U/L) and CK-MB level (45U/L). C-reactive protein (CRP) is also
elevated. A chest X-ray should be performed since this may demonstrate pulmonary oedema
that is not evident on clinical examination. The heart size is often normal but there may be
cardiomegaly due to pre-existing myocardial damage(Ralston et al., 2018). On chest
radiograph of this patient, there was cardiomegaly, opacity on the lower zone of both lungs
and blunting ofcostophrenic angle resulting from accumulation of fluid in the pleural space.
There is presence of kerley B line in the right lower zone of the lung. The CXR showed
evidence of heart failure such as cardiomegaly, pulmonary edema and pleural effusion.

From the symptoms and clinical presentations as well as investigation results, we can
conclude that this patient has both left sided heart failure (with features cardiomegaly,
pulmonary edema, pleural effusion (CXR), dyspnea, PND, orthopnea and fatigue) and right
sided heart failure (due to finding of bilateral pedal edema up to shin).

Supplemental oxygen is recommended in patients with oxygen saturation less than

90%, those with respiratory distress, or when high-risk features of hypoxemia are present. In
patients where NSTEMI has been definitively diagnosed or is highly likely, anticoagulation
should be initiated. Unfractionated heparin with bolus dosing and a continuous infusion is
commonly used, with most institutions having protocols available. Diuretics reduce
extracellular fluids, filling pressures and cardiac cavities, with a consequent improvement of
performance, thus promoting fast symptomatic relief of congestion. The use of diuretics must
be aimed to preserve renal function (the lowest possible dose with the best result). The loop
diuretic furosemide (Lasix) is used in this patient. Other strategies may include the use of
enoxaparin, bivalirudin, fondaparinux, and dual antiplatelet therapies. Fibrinolytic therapies
should not be used in NSTEMI.
CASE 3

In this patient, with risk factors male, age more than 65yo, active smoker,
diabetes mellitus, hypertension, hypercholesterolemia and ischemic heart disease. He
presented with common case of ACS which are left sided chest pain that radiates to the left
shoulder, left arm and at the back. He also has undergone percutaneous coronary intervention
in august 2019. He also not compliant to medication. After balloon dilatation with or without
stent implantation, stenoses can form outside the area of intervention; there can also be
restenosis in the treated area. Restenosis is defined as an angiographically demonstrated
reduction of vessel diameter by at least 50% (“angiographic restenosis”). Less than half of all
patients with angiographically documented restenosis develop clinical
manifestations (clinically relevant restenosis) within one year. This may be because
angiographically demonstrable vascular narrowing is not necessarily associated with impaired
distal myocardial perfusion. The most common manifestation of clinically relevant restenosis
is exercise-induced angina, followed by unstable angina (25%) and acute myocardial
infarction (5–10%)
As recommended in the National Disease Management Guidelines, patients with
coronary heart disease and those who have undergone stent implantation should be followed
up regularly (every three to six months) by their primary care physicians, independently of
any additional visits that may be necessitated by worsening symptoms, comorbidities, or any
other tests that need to be done (recommendation grade B, evidence level2). In these regular
follow-up visits, the physician should take a clinical history focusing particularly on current
symptoms (specific cardiac symptoms, but also fatigue or diminished performance),
endurance level, and functional status, including effects on family life, occupation, everyday
activities, sports, and sexual activity (recommendation grade B, evidence level 2). Further
questions should be asked about emotional aspects
(depression, anxiety, worries, disappointment) and the patient’s psychosocial situation,
conception of illness, and behavior patterns, e.g., excessive caution. The goal is to
communicate an optimistic attitude about
the possibilities for treatment (recommendation grade 0, evidence level 3/4). The patient’s
tobacco use, physical activity, nutrition, and regular taking of medications should be
assessed, and, if necessary, the patient should be encouraged to change his or her behavior
in health-promoting ways (recommendation grade A, evidence level 1). At each visit, a
physical examination should also be carried out, including the heart, lungs, limbs (peripheral
pulses, edema), weight (BMI), blood pressure, and heart rate (recommendation grade B,
evidence level 2).

In the first year after PCI, the patient should be cared for both by his or her primary
care physician/internist in primary care and by a cardiologist. The primary care physician
should refer the patient to the cardiologist whenever symptoms and signs arise that might be
due to CHD and cannot be adequately evaluated by the primary care physician alone.
Referral to the cardiologist may also
be indicated if the primary care physician cannot achieve adequate symptomatic relief or
cannot implement the treatments (drugs and other measures) that are indicated to improve the
prognosis, e.g., because of adverse effects, interactions, or non-compliance, where a specialist
might be able to address these problems more effectively. Finally, referral is indicated when
preexisting heart failure worsens, when the new onset of heart failure is suspected, or when
new, clinically relevant arrhythmia is documented.

So for this patient, investigation that had done during this admission were ECG
showed premature ventricular contractions at lead II and III, ST elevation V1-V5, CK and
CKMB high indicate he has STEMI. Chest X-ray showed evidence of redistributive
pulmonary vessels, but no cardiomegaly suggest suspected develop acute heart failure.
Medication given was antiplatelet and anticoagulant. He was classified into NYHA Class II
because there is a slight limitation of physical activities resulting in fatigue,
palpitation, dyspnea or angina. This patient has left sided heart failure because he
presents with dyspnea, PND, orthopnea by evidence of CXR that show redistribution
of pulmonary vessels, no cardiomegaly, no pulmonary edema.

CASE 4

In this patient, the risk factors are smoking, ischemic heart disease, hypertension,
hyperlipidemia and cocaine drug abuse. This patient has common symptoms of ACS,
complains of pain at his left side of chest and radiated to his left arm and back. Patient also
complained of sweating which is also one of the symptoms of ACS due to increased sympathetic
activity. Cocaine use is known to be associated with ACS and/or AMI. Cocaine is a potent
sympathomimetic agent that not only prevents pre‐synaptic re‐uptake of norepinephrine and
dopamine, but also stimulates secretion of catecholamines. This increase in catecholamine
concentrations leads to an excessive stimulation of both α and β adrenergic receptors, which in
part explains the increased risk of ACS and AMI following cocaine use. There is an increase in
the heart rate leading to an increased myocardial oxygen demand, as well as coronary artery
vasospasm which leads to a reduction in blood flow to the myocardium. In addition to this,
cocaine has been shown to cause platelet activation and platelet aggregation, increase endothelin
concentrations and reduce nitric oxide production, all of which are additive to the cocaine‐
induced coronary vasoconstriction and can worsen myocardial ischaemia.

Classical management of AMI in patients with atheromatous coronary artery disease,

in whom the mechanism of coronary occlusion is thrombus formation, is to administer
aspirin, clopidogrel, and thrombolysis to reduce platelet aggregation and treat any underlying
coronary artery thrombosis. β‐blockers are also used to reduce myocardial oxygen demand in
the presence of reduced oxygen delivery and reduce the risk of arrhythmias. In cocaine‐
induced AMI/ACS, the pathophysiology isdifferent—the decrease in coronary artery blood
flow is secondary to coronary artery vasospasm rather than plaque rupture and formation of
coronary artery thrombus, and therefore the management required is different. High‐dose
benzodiazepines and vasodilators, such as intravenous nitrates and calcium channel blockers,
are the first line management in those patients with cocaine induced AMI and ACS. These
help to reverse the cocaine‐induced coronary artery vasospasm and reduce the cocaine‐
induced sympathetic nervous system stimulation which leads to a reduction in heart rate and
therefore myocardial oxygen demand. β‐blockers have no role since they can lead to
unopposed α‐stimulation and therefore worsen cocaine‐induced hypertension. Cocaine is a
relative contraindication to the use of thrombolysis, due to cocaine‐induced hypertension and
therefore an increased risk of intracranial
haemorrhage. Patients with cocaine‐induced AMI, who are not responding to
benzodiazepines and vasodilator drugs, should have coronary angiography and either
angioplasty and stenting or intracoronary artery drug treatment to reverse vasoconstriction.

Diagnosis of cocaine‐induced ACS/AMI is based on a positive history of cocaine use

in the context of chest pain, changes in 12 lead electrocardiogram (ECG) and elevations in
specific cardiac enzymes. Often rises in cardiac enzymes occur after a number of hours and
therefore cardiac enzymes may not be useful in the early acute management of patients with
ACS/AMI. Additionally, the ECG has been shown to be abnormal in up to 85% of patients
presenting with chestpain following cocaine use, even without subsequent biochemical
evidence of AMI. Therefore obtaining an accurate history on presentation, which includes a
history of recent cocaine use or non‐use, is essential in the diagnosis of ACS/AMI since usual
routine investigations may not provide timely conclusive evidence.

The investigations that were done for this patient showed ST elevation in ECG and
elevation of CK-MB so indicated that he developed STEMI. Cholesterol levels were high and
increased the risk of ACS. However, X-ray show signs of heart failure which is
cardiomegaly, but no pulmonary oedema. For the management of this disease, patient should
be given oral antiplatelet therapy such as aspirin or clopidogrel for those with confirmed ACS
as a second antiplatelet agent. Patients also should be given anticoagulants, beta-blockers in
higher-risk patients with no contraindications, nitrates for recurrent chest pain and lipid
management. Patient should be advised on the benefits and the importance of lifestyle
changes. These lifestyle measures include cessation of smoking, dietary or weight control and
regular exercise. For this patient, since he is non-compliant to the given medication, he was
advised on the importance of continuing his medications as prescribed. He was classified into
NYHA Class I as there is no limitation of physical activities. Ordinary physical activities do
not cause dyspnea or angina. He has left sided HF as presence of orthopnea, PND, dyspnea.
CXR shows cardiomegaly, no pulmonary edema

Based on these 4 case reports, we can conclude that different patients will have
different presentations and different outcomes according to their risk factors and development
of complications from ACS. In Case 1, the patient presented with epigastric pain, which is an
atypical presentation of ACS. He took antacid medication as he thought his condition was
due to dyspepsia. As the symptoms worsen, he seeks medical attention, and ECG and other
investigations done, leads to diagnosis of Unstable Angina. In Case 2, the patient’s
presentation is an example of typical angina, in which it was central, exaggerated by activity
and relieved after taking GTN. Upon examination and as the investigations result came out,
he was diagnosed with NTEMI with development of decompensated congestive cardiac
failure, which is a complication of ACS. In Case 3, this patient has had comorbidities that
predispose him to ACS and eventually, heart failure. Considering the risk factors,
presentations, and investigations result, he was diagnosed with NSTEMI, with high suspicion
of acute heart failure. In Case 4, the patient is a young man with a history of cocaine abuse,
which is one of the etiologies of ACS. It is quite rare for young patients to develop ACS.
Cocaine is a potent sympathomimetic agent that not only prevents pre‐synaptic re‐uptake of
norepinephrine and dopamine, but also stimulates secretion of catecholamines. This increase
in catecholamine concentrations leads to an excessive stimulation of both α and β adrenergic
receptors, which in part explains the increased risk of ACS and AMI following cocaine use.
(Wood et al., 2007).

Based on retrospective case series that had been done, it has become clear that these
ACS patients present with typical and atypical complaints for ACS.Especially for the atypical
presentation, at first glance, one might simply treat them as non cardiac cases, which can
result in future problems for patients when they start to have complications. Early detection
of ACS may give better outcomes as patients will be treated early before they even get
complications. Always raise a suspicion of ACS for patients who complain of chest pain, for
old-age patients, and patients with strong risk factors for ACS.

CONCLUSION

To conclude, it is important for the clinical practitioner to detect symptoms of Acute

Coronary Syndrome (ACS), whether the patient presented with typical presentations or atypical
presentations. Therefore, we have to know what are the possible presentations that can lead to
diagnosis of ACS. A thorough and complete history taking, physical examination and
investigations should be done in all patients suspected to have ACS, since they can be presented
at different stages of ACS, and they might already develop complications such as heart failure.
Despite the presentations, history taking also comprises of evaluating any risk factors
predisposing patients in developing ACS. Important risk factors for ACS would include; age 65
years old or older, strong family history of Coronary Artery Disease (CAD), other comorbidities
(Hypertension, Hypercholesterolemia, Diabetes Mellitus) and active smoker. TIMI risk score
is widely used in clinical settings to predict the chances of having or dying from a heart event
for people diagnosed with UA/NSTEMI.Braunwald’s classification is another scoring
method in classifying patients with Unstable Angina based on their severity.

Most cases of ACS, patients have no obvious signs upon physical examination,
unless they start to develop complications. For example, patients with congestive heart
failure will have bilateral lower limb pitting edema, and signs of pulmonary edema. The
New York Heart Association (NYHA) classification is used to stage heart failure. It
provides a simple way of classifying the extent of heart failure. It classifies patients in one
of four categories based on their limitations during physical activity; the
limitations/symptoms are in regards to normal breathing and varying degrees in shortness
of breath and or angina pain. (The Joint Commission, 2018).

The obvious difference between UA/NSTEMI and STEMI is the finding in ECG.
There will be ST elevation in STEMI, but not in UA/NSTEMI. To distinguish UA and
NSTEMI, is the level of cardiac biomarkers, such as troponin I and T, and CK-MB. In
UA, the cardiac biomarkers are not raised, while in NSTEMI, these cardiac biomarkers
levels will be elevated.

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