Karaganda Medical University

Department of Medicine
Name:- Ananya Basu
Group:- 4017
Patient profile
Name:- William
Age:- 32
Gender:- Male
Clinical Case
William was evaluated in the emergency department of this hospital for the abrupt onset of
postprandial chest pain. Several hours before presentation, the patient had eaten pizza in his
apartment. Less than 1 hour later, while he was at rest and watching television, “crushing” pain,
diaphoresis, dyspnea, and nausea developed. He rated the pain at 7 on a scale of 0 to 10 (with 10
indicating the most severe pain), and he noted that the pain did not radiate or worsen with
respiration. He attempted to induce vomiting and took calcium carbonate tablets, but his
condition did not improve. After 2 hours of constant pain, he presented to the emergency
department of this hospital. The patient had no medical history and took no medications. His
father had had a myocardial infarction when he was 51 years of age. The patient was allergic to
penicillin (unknown reaction). He lived with his girlfriend, who had recently had streptococcal
pharyngitis. He had been under a great deal of stress because of a new job as a sales manager, a
move to a new apartment, and the recent death of a family pet. He consumed a six-pack of beer
daily. He had used cocaine (most recently 3 months earlier) but did not report using other illicit
substances. On examination, the temperature was 36.3°C, the heart rate 83 beats per minute, the
blood pressure 158/81 mm Hg, the respiratory rate 28 breaths per minute, and the oxygen
saturation 100% while the patient was breathing ambient air. The body-mass index (the weight in
kilograms divided by the square of the height in meters) was 26.9. He appeared to be anxious
and uncomfortable and had diaphoresis. The jugular venous pressure was 6 cm of water with a
normal waveform. There was no evidence of a heart murmur or rub. When the patient was asked
to indicate the location of the pain, he pointed to the subxiphoid area; there was some tenderness
in that area on palpation. The stool was guaiac negative. The remainder of the examination was
normal. Urinalysis revealed a specific gravity of greater than 1.040 and was otherwise normal. A
urine toxicology screen revealed cannabinoids, and a blood toxicology screen was negative;
other laboratory test results are shown in Table 1. An electrocardiogram showed concave ST-
segment elevations (1 to 2 mm) in the inferior leads and V3 through V6 precordial leads, along
with a PR-segment elevation in lead aVR and possible subtle PR-segment depressions (Figure 1).
Imaging studies were obtained. A chest radiograph was normal. The lungs were clear, and there
was no evidence of pneumothorax, cardiomegaly, or mediastinal widening.
Ans:-
Based on the provided clinical information, the leading syndrome in this case is acute coronary
syndrome (ACS). ACS refers to a spectrum of conditions characterized by a decrease in blood
flow to the heart due to the obstruction of coronary arteries. The differential diagnosis for ACS
includes:
1.Unstable angina: This is a form of ACS characterized by transient and reversible myocardial
ischemia without myocardial necrosis. The patient's symptoms of chest pain, diaphoresis, and
dyspnea, which developed shortly after a meal, are consistent with unstable angina. The absence
of ST-segment elevation on the ECG supports this diagnosis.
2.Non-ST-segment elevation myocardial infarction (NSTEMI): NSTEMI occurs when there is
partial occlusion of a coronary artery leading to myocardial ischemia and necrosis without
complete blockage. The patient’s symptoms, such as severe chest pain, diaphoresis, and dyspnea,
along with the presence of ST-segment depressions on the ECG, suggest NSTEMI as a
possibility.
3.Variant (Prinzmetal’s) angina: Variant angina is caused by coronary artery vasospasm, resulting
in temporary vessel constriction and myocardial ischemia. Although the patient’s symptoms and
ECG findings are more indicative of unstable angina or NSTEMI, variant angina should be
considered as a differential diagnosis.
Now, let’s formulate and justify each fragment of the diagnosis:
1.Unstable angina: The patient’s symptoms of abrupt-onset chest pain, diaphoresis, dyspnea, and
relief attempts through vomiting, along with the absence of ST-segment elevation on the ECG,
suggest unstable angina. The presence of risk factors such as a family history of myocardial
infarction and daily alcohol consumption further support this diagnosis.
2.Non-ST-segment elevation myocardial infarction (NSTEMI): The patient’s symptoms of severe
chest pain, diaphoresis, and dyspnea, along with the presence of ST-segment depressions on the
ECG, raise suspicion for NSTEMI. The negative urine toxicology screen, absence of cardiac
murmurs, and normal chest radiograph help rule out other potential causes.
3.Variant (Prinzmetal’s) angina: Although less likely based on the clinical presentation and ECG
findings, variant angina should be considered due to the possibility of coronary artery
vasospasm. However, further investigations are necessary to confirm this diagnosis.
The principles of therapy for the leading syndrome, which is likely unstable angina or NSTEMI,
include:
1.Goal of treatment: The primary goal is to relieve the patient's symptoms, stabilize the coronary
artery disease, prevent further ischemic events, and reduce the risk of complications.
2.Non-drug treatment methods: The patient should be advised to rest, preferably in a cardiac care
unit, to reduce myocardial oxygen demand. Continuous cardiac monitoring and supplemental
oxygen should be provided as necessary.
3.Drug treatment methods:
 Nitroglycerin: Sublingual nitroglycerin should be administered to relieve chest pain.
Nitroglycerin can also be given intravenously if the symptoms persist.
 Aspirin: Immediate administration of chewable aspirin (325 mg) is recommended, as it
acts as an antiplatelet agent and reduces the risk of further thrombotic events.
 Beta-blockers: These should be initiated early unless contraindicated. Beta-blockers help
reduce heart rate, blood pressure, and myocardial oxygen demand, thereby improving
ischemic symptoms.
 Heparin or low-molecular-weight heparin (LMWH): These anticoagulants are often
administered to prevent further clot formation and reduce.