Case Report

A FOURTY-NINE YEARS OLD MALE PATIENT WITH

STEMI ANTEROLATERAL, LV DILATED AND MR MILD IN
CUT MEUTIA REGIONAL GENERAL HOSPITAL
LHOKSEUMAWE

Composed by:

1. Siti Faizah S.Ked (2006112002)

2. Elsa Nur Salsabila, S.Ked (2006112044)
3. Jihan Haura, S.Ked (2106111012)
4. Fadhilah Amirah Nasution, S.Ked (2106111032)
5. Cut Desy Diana Sari, S.Ked (2106111031)

Preceptor:

dr. Yuri Savitri, M.Ked(Cardio), Sp.JP, FIHA

DEPARTMENT OF CARDIOLOGY
MEDICAL FACULTY OF MALIKUSSALEH UNIVERSITY
CUT MEUTIA REGIONAL GENERAL HOSPITAL
NORTH ACEH
2022
 I. PRELIMINARY
Acute Coronary Syndrome is a major cardiovascular problem and it causes
high hospitalization and mortality rates. Acute Coronary Syndrome is a term used
to describe a state of acute partial to total disruption of coronary blood flow to the
myocardium (1).
Acute coronary syndrome is divided into ST-segment elevation myocardial
infarction (STEMI), non-ST-segment elevation myocardial infarction (NSTEMI),
and unstable angina pectoris (UAP). Myocardial infarction is a rapidly progressing
myocardial necrosis. It will be the imbalance between the supply and demand for
oxygen in the heart muscles. The symptoms are influenced by the component of
arterial vasospasm and the size of the thrombus depending on the degree of
narrowing (1) .
One million people in the United States have acute myocardial infarction
each year. As many as 300,000 people die of acute myocardial infarction before
reaching the hospital (2). According to WHO in 2004, acute myocardial infarction
is one of the leading causes of death in the world. A total of 7,200,000 (12.2%)
deaths occur due to this disease worldwide. This disease is also one of causes of
death in adults (3).
In low-income countries, acute myocardial infarction is the second leading
cause of death with a mortality rate of 2,470,000 (9.4%) (3). Indonesia in 2002 the
acute myocardial infarction was the first cause of death, with a mortality rate of
220,000 (14%). According to research by the Directorate General of Health and
Medical Indonesia in 2007, the number of heart disease patients undergoing
inpatient and outpatient hospitalization in Indonesia was 239,548 people. It was
found that the most cases were ischemic heart disease, which was around 110,183
cases. The highest case fatality rate (CFR) occurred in acute myocardial infarction
(13.49%), heart failure (13.42%) and other heart diseases (13.37%) (4).
STEMI is an indicator of the incidence of total coronary artery occlusion.
This situation requires revascularization to restore blood flow and myocardial
reperfusion as soon as possible, either medically using fibrinolytic agents or
mechanically through primary percutaneous coronary intervention. The diagnosis

1
of STEMI is made if there is a complaint of acute angina pectoris with persistent
ST-segment elevation in two adjacent leads. The initiation of revascularization
treatment does not need to wait for the results of elevated cardiac biomarkers (1).

2
 II. CASE REPORT

A 49-years-old male patient, domiciled in Matang Anoe, North Aceh,

admitted to emergency department of Cut Mutia hospital, the patient was brought
to the hospital by his family at 22.47 pm on February 11st, 2022. Patient was
admitted to the hospital with complaints of chest pain. Six hours before go to
hospital patient had left sided chest pain like a pressure or heaviness and radiating
to the shoulder, left arm and back. The chest pain was intermittent with a duration
of <5 minutes, the patient also complained of pounding and easily fatigued with
moderate or mild activity since 5 days ago. The patient was vomiting and nausea.
Past medical history such hypertension and diabetes mellitus are denied.
Physical examination before treatment was obtained the patient looked
restless and weakness, BP: 130/80 mmHg, HR: 112x/m, RR: 20x/m, T: 36,5 OC,
SpO2: 99%. Chest examination show breath sounds were vesicular. In this case on
physical examination showing tachycardia.
TABEL 1. Laboratory On February, 11st 2022
Test Result Unit Normal
Range
Hematology
Complete Blood Count
Hemoglobin 15.43 g/dl 13.0-18.0
Erythrocytes 5.33 juta/uL 4.5-6.5
Hematocrit 42.40 % 37.0-47.0
MCV 79.57 fL 79-99
MCH 28.96 Pg 27.0-31.2
MCHC 36.39 g/dl 33.0-37.0
Leukocyte 17.32 ribu/uL 4.0-11.0
Thrombocyte 229 ribu/uL 150-450
RDW-CV 10.31 % 11.5-14.5
White Blood Cell (WBC) Count
Basophil 0.26 % 0-1.7
Eosinophil 0.54 % 0.60-7.30
Neutrophil Segmen 79.56 % 39.3-73.7
Lymphocyte 19.03 % 18.0-48.3
Monocyte 0.61 % 4.40-12.7
NLR 4.18 Cutoff 0-3.13
ALC 3296.00 Juta/L 0-1500
Renal Function Test (RFT)

3
Ureum 25 mg/dl <50
Creatinine 0.22 mg/dl 0.6-1.1
Uric Acid 4.4 mg/dl 3.4-7.0
Blood Glocose Level
Blood Glucose 142.0 mg/dl <180

TABEL 2. Laboratory On February, 12nd 2022

Test Result Unit Normal
Range
Hematology
Complete Blood Count
Hemoglobin 16,22 g/dl 13.0-18.0
Erythrocytes 5.62 juta/uL 4.5-6.5
Hematocrit 44.84 % 37.0-47.0
MCV 79.83 fL 79-99
MCH 28.87 Pg 27.0-31.2
MCHC 36.16 g/dl 33.0-37.0
Leukocyte 19.27 ribu/uL 4.0-11.0
Thrombocyte 237 ribu/uL 150-450
RDW-CV 10.32 % 11.5-14.5
Blood Type B - -
Coagulation
Troponin 33.13 ng/mL 0-0.5
Renal Function Test (RFT)
Ureum 24 mg/dl <50
Creatinine 0.97 mg/dl 0.6-1.1
Uric Acid 4.0 mg/dl 3.4-7.0
Blood Glocose Level
Blood Glucose 116.0 mg/dl <180
Electrolyte
Na 131 mmol/L 136-146
K 3.3 mmol/L 3.5-5.0
Cl 127 mmol/L 98-106
Ca 0.42 mmol/L 1.12-1.32
Chemical Blood Test (Lipid)
Kolesterol total 178 mg/dl ≤190
HDL 37 mg/dl >40
LDL 97 mg/dl <130
Trigliserida 65 mg/dl <150

4
 Figure 1. ECG Findings
The electrocardiogram examination showed that elevation of ST Segmen in
V2 (0,3 mV), V3 (0,2 mV) and V4 (0,1 mV) and Q patologis in lead
I,avL,V1,V2,V3 and V4. T inverted in lead I, avL,V2,V3,V4,V5 and V6. The
conclusion was Stemi Anterolateral.

Figure 2. ECG Findings

The second electrocardiogram examination showed that elevation of ST Segmen in
V2, V3, V4, V5 and V6. Q patologis in lead I,avL,V1,V2,V3, V4, V5 and V6. The
conclusion was Stemi Anterolateral.

Figure 2. X-Ray Findings

5
 COR
 The apex of the heart shifts to the laterocaudal
PULMO
 Increase of bronchovascular pattern
 Spots appear in right pericardial
 Right hemidiphragma at 10th rib posterior
 Right and left costophrenic sinus are sharp
Result
 Cardiomegaly
 Bronchopneumonia

Figure 3. Echocardiography Findings

Echocardiography examination showed that the MR mild and LV Dilated
with EF was 49%.
The patient was given initial treatment in Cut Mutia General Hospital. We
administrate injection of arixtra /24h, injection of furosemide 1 amp/12h, Concor
1x 2.5 mg, CPG 1x75 mg, NKR 2x2.5 mg, Aptor 1x100 mg, lansoprazole 2x30mg
and simvastatin 1x20mg

6
 III. DISCUSSION
An acute ST-elevation myocardial infarction occurs due to occlusion of one
or more coronary arteries, causing transmural myocardial ischemia which in turn
results in myocardial injury or necrosis. This activity reviews the presentation,
evaluation, and management of patients with with ST-elevation myocardial
infarctions and highlights the role of the interprofessional team in caring for these
patients (5)(6).
Patient was admitted to the hospital with complaints of chest pain. Six
hours before go to hospital patient had left sided chest pain like a pressure or
heaviness and radiating to the shoulder, left arm and back. The chest pain was
intermittent with a duration of <5 minutes, the patient also complained of
pounding and easily fatigued with moderate or mild activity since 5 days ago.
The patient was vomiting and nausea. Past medical history such hypertension
and diabetes mellitus are denied.
The classic symptom of acute myocardial ischemia is precordial or
retrosternal discomfort, commonly described as a pressure, crushing, aching, or
burning sensation. Radiation of the discomfort to the neck, back, or arms frequently
occurs, and the pain is usually persistent rather than fleeting. The discomfort
typically achieves maximum intensity over several minutes and can be associated
with shortness of breathe, nausea, diaphoresis, generalized weakness, and a fear of
impending death. Some patients, particular the elderly, may also present with
syncope, unexplained nausea and vomiting, acute confusion, agitation, or
palpitations. Symptoms in the advanced elderly (>75 years old) are more likely to
be atypical than in younger patients and can lead to a missed diagnosis if a medical
professional is not vigilant in the initial assessment (5).
Approximately 20% of AMI patients are asymptomatic or have atypical
symptoms that are not initially recognized. Painless myocardial infarction occurs
more frequently in the elderly, women, diabetics, and postoperative patients (7)(8).
Myocardial infarction occurs due begins with the formation of
atherosclerosis which then ruptures and clogs blood vessels. Atherosclerosis is
characterized by the gradual formation of fatty plaques in the arterial walls. Over

7
time, these plaques continue to grow into the lumen, so that the lumen diameter
narrows. The narrowing of the lumen interferes with blood flow to the arteries.
distal to where the blockage occurred (9)(10).
In this case, patient feeling chest pain occurs due to narrowing of the
segmental coronary arteries caused by plaque. These events can temporarily worsen
the condition of obstruction, reduce coronary blood flow so that it can cause clinical
manifestations in the form of chest pain. Site of the chest pain gives important clue
to the diagnosis of ACS/AMI. Pain which is located in the center of chest is more
likely to be ischemic than a peripherally located chest pain. Most common site
where AMI pain radiates is left shoulder and arm. This is because of presence of
heart on the left of chest, so pain radiates along left sided cervical nerve roots (11).
Physical examination before treatment was obtained the patient looked
restless and weakness, BP: 130/80 mmHg, HR: 112x/m, RR: 20x/m, T: 36,5 OC,
SpO2: 99%. Chest examination show breath sounds were vesicular. In this case
on physical examination showing tachycardia. In this case, HR patient is 112x/i.
Several extrinsic factors, such as fever, anemia, thyrotoxicosis, hypotension,
tachycardia, can be a trigger for ACS in patients who have have atherosclerotic
plaques.
In this case on laboratory examination on February 12th, 2022 results
increased cardiac troponin: 33,13 ng/mL. Serum cardiac biomarkers (creatine
kinase [CK], CK-MB, cardiac specific troponins, myoglobin) are useful for
confirming the diagnosis of MI and estimating infarct size. Serum cardiac
biomarkers also provide valuable prognostic information. For patients with ST-
segment elevation, the diagnosis of STEMI is secure; initiation of reperfusion
therapy should not be delayed while awaiting the results of a cardiac biomarker
assay. In contrast, because cardiac troponin I (cTnI) and cardiac troponin T (cTnT)
are not normally detected in the blood of healthy people, the definition of an
abnormally increased level is a value that exceeds that of 99% of a reference control
group (1).
The electrocardiogram examination showed that elevation of ST
Segmen in V2 (0,3 mV), V3 (0,2 mV) and V4 (0,1 mV) and Q patologis in lead

8
I,avL,V1,V2,V3 and V4. T inverted in lead I, avL,V2,V3,V4,V5 and V6. The
conclusion was Stemi Anterolateral. That means acute anterolateral ST‐elevation
myocardial infarction (STEMI) is defined by ST‐elevation (STE) in the precordial
leads V1–V6 in addition to leads I and aVL. STE in lead aVL has been associated
with infarct‐ related occlusion proximal to the first diagonal branch (D1) of the left
anterior descending coronary artery (12).
The result by x-ray findings showed that cardiomegaly. That means
cardiomegaly occurs when the heart muscle pumps blood with more effort than
normal. This excessive workload over time will cause thickening of the heart
muscle, so that the size of the heart becomes larger.
Echocardiography examination showed that the MR mild and LV
Dilated with EF was 49%. Echocardiography is the available modality widely and
cheaply and has great benefits in establishing the diagnosis of ventricular infarction,
as well as evaluating ventricular shape, size and function. Echocardiography can
show abnormalities that can appear on the ventricular infarction. For example, these
disorders ventricular dilatation, atrial dilatation, changes in wall motion (akinesis,
dyskinesis) of the ventricles and changes in the curved shape of the septal wall (13).
Mitral regurgitation is known to be a frequent complication of AMI (14).
Mild mitral regurgitation may not have any symptoms. When regurgitation is more
severe, a person may have palpitations, often due to atrial fibrillation. If
regurgitation is severe enough, the heart may enlarge to maintain forward flow of
blood, causing heart failure (when the heart does not pump enough blood to the
body). This may produce symptoms ranging from shortness of breath during
exertion, coughing, congestion around the heart and lungs and swelling of the legs
and feet (edema) (15)(16).
Left ventricular systolic dysfunction (LVSD) with an ejection fraction
<50% is one of the complications that quite often occurs after acute coronary
syndrome (ACS). LVSD after ACS will give a poor prognosis. Approximately 40%
of patients with acute coronary syndromes will develop LVSD with or without
symptoms of heart failure (17).

9
 The treatment is patients should undergo percutaneous coronary
intervention (PCI) within 90 minutes of presentation at a PCI capable hospital or
within 120 minutes if transfer to a PCI capable hospital is required (18). If PCI is
not possible within the first 120 minutes of first medical contact, fibrinolytic
therapy should be initiated within 30 minutes of patient arrival at the hospital. It is
important to rule out conditions that can mimic an acute coronary syndrome like
acute aortic dissection or acute pulmonary embolism (19)(20).
All patients with an acute myocardial infarction should be started on a beta
blocker, high intensity statin, aspirin, and a P2Y12 inhibitor as soon as possible,
with certain exceptions. Nitroglycerin administration can reduce anginal pain
however it should be avoided in patients who have used phosphodiesterase
inhibiting medication within the last 24 hours and in cases of right ventricular
infarction. Further pain relief with morphine can be given for patients that continue
report discomfort after nitroglycerin administration however judicious use is not
recommended as it may adversely affect outcomes. P2Y inhibiting antiplatelet
medication choice depends on whether the patient underwent PCI or fibrinolytic
therapy. Ticagrelor and prasugrel are preferred to clopidogrel in patients who
undergo PCI due to recent trials showing superiority. Patients undergoing
fibrinolytic therapy should be started on clopidogrel. It is important to be careful
about relative contraindications of P2Y12 inhibitors. Prasugrel is contraindicated in
pateints with Transient Ischemic attack and stroke. Anticoagulation should also be
started among side with unfractionated heparin, low-molecular-weight heparin,
bivalirudin, or fondaparinux (19)(21).

10
 REFERENCES

1. PERKI. Pedoman Tata Laksana Sindrom Koroner Akut. Indonesian Heart

Association. 2018. p. 76.
2. Brian P. Griffin MD FACC. Manual of Cardiovascular Medicine 5th Edition.
LWW; 5th edition; 2018. 1172 pages.
3. World Health Organization. The top 10 causes of death. 2014.
4. Kementerian Kesehatan Republik Indonesia. Profil Kesehatan Indonesia
2020. Vol. 48, IT - Information Technology. 2020. 6–11 p.
5. Valentin Fuster, Richard A RA. Hurst’s The Heart. 13th ed. New York:
McGraw Hill-Medical; 2011. 1354 p.
6. Roffi M. Patrono C. Collet JP et al. ESC Guidelines for the management of
acute coronary syndromes in patients presenting without persistent ST-
segment elevation: Task Force for the Management of Acute Coronary
Syndromes in Patients Presenting without Persistent ST-Segment Elevation
of the E. Eur Hear J. 2016;37:267–315.
7. Hartikainen TS, Sörensen NA, Haller PM, Goßling A, Lehmacher J, Zeller
T, Blankenberg S, Westermann D NJ. Clinical application of the 4th
Universal Definition of Myocardial Infarction. Eur Hear J. 2020;2209–16.
8. Alpert JS, Thygesen K, Antman E BJ. Myocardial infarction redefined--a
consensus document of The Joint European Society of Cardiology/American
College of Cardiology Committee for the redefinition of myocardial
infarction. J Am Coll Cardiol. 2000;959–69.
9. Manning J. “Fluid and Blood Resuscitation” in Emergency Medicine: A
Comprehensive Study Guide. New York: McGraw-Hill; 2004. 227 p.
10. Wilson PW. Established risk factors and coronary artery disease: the
Framingham Study. Am J Hypertens. 1994;7S-12S.
11. Everts B, Karlson B, Wahrborg P, Hedner T HJ. Localization of pain in
suspected acute myocardial infarction in relation to final diagnosis, age and
sex, and site and type of infarction. Hear Lung. 1996;25(6):430–7.
12. Arbane, M., & Goy J. Prediction of the site of total occlusion Admission, in
the left anterior descending coronary artery using Infarction.,
electrocardiogram in anterior wall acute myocardial. Am J Cardiol.
2000;85(4):487–491.
13. Inohara T, Kohsaka S, Fukuda K, Menon V. The Challenges in the
management of ventricular infarction. Eur Hear J Acute.
14. Tcheng JE, Jackman JD, Nelson CL, Gardner LH, Smith LR, Rankin JS,
Califf RM SR. Outcome of patients sustaining acute ischemic mitral
regurgitation during myocardial infarction. Ann Intern Med. 1992;18–24.
15. barzilai B, Gessler C, Perez JE, Schaab C, Jaffe AS. Significance of Doppler-

11
 detected mitral regurgitation in acute myocardial infarction. 1988;61:220–3.
16. American Heart Association. Mitral Valve Regurgitation. Sci Med Advis.
2020;
17. Laura A, Giuspee C, Egle C, Eluisa L.F, Antonio R, Pasquale A. Diagnosis
and Treatment of Asymptomatic Left Ventricular Systolic Dysfunction After
Myocardial Infarction. 2013;
18. Armstrong PW. Gershlick AH. Goldstein P et al. Fibrinolysis or primary
PCI in ST-segment elevation myocardial infarction. N Engl J Med.
2013;368:1379–87.
19. O’Gara PT, Kushner FG, Ascheim DD, Casey DE, Chung MK, de Lemos
JA, Ettinger SM, Fang JC, Fesmire FM, Franklin BA, Granger CB,
Krumholz HM, Linderbaum JA, Morrow DA, Newby LK, Ornato JP, Ou N,
Radford MJ, Tamis-Holland JE, Tommaso CL, Tracy CM, Woo YJ, Zh.
American College of Cardiology Foundation/American Heart Association
Task Force on Practice Guidelines. 2013 ACCF/AHA guideline for the
management of ST-elevation myocardial infarction: a report of the American
College of Cardiology Foundation/American He. Circulation. 2013;
20. James SK et al. ESC Guidelines for the management of acute myocardial
infarction in patients presenting with ST-segment elevation. Eur Hear J.
2012;33:2569–619.
21. Sabatine MS, Cannon CP, Gibson CM, López-Sendón JL, Montalescot G,
Theroux P, Claeys MJ, Cools F, Hill KA, Skene AM, McCabe CH BE.
Addition of clopidogrel to aspirin and fibrinolytic therapy for myocardial
infarction with ST-segment elevation. N English J Med. 2005;

12