Pharmacotherapy Case Study 8: ST-Elevation Myocardial Infarction (STEMI) By: Dr. Nehad Ahmed

 

Chief Complaint:

A 62-year-old male presents to the emergency department with severe, crushing chest pain that started approximately 45 minutes ago while he was at rest. The pain radiates to his left arm and jaw and is associated with shortness of breath and sweating. He is extremely anxious and appears in distress.

Subjective Data:

History of Present Illness (HPI):
The patient reports the sudden onset of severe, squeezing chest pain that started while he was sitting at rest. The pain is located in the center of his chest and radiates to his left arm and jaw. The pain is not relieved by changing position or resting. It has been constant and severe, rated as 9/10 on the pain scale. The patient describes the pain as the "worst chest pain" he has ever experienced. He also feels short of breath and has been sweating profusely.

He denies any recent trauma, cough, or fever. The patient is frightened and anxious about the severity of his symptoms. He has not taken any medication for the pain.

Past Medical History (PMH):

Hypertension (diagnosed 12 years ago)

Hyperlipidemia (diagnosed 5 years ago)

Type 2 Diabetes Mellitus (diagnosed 8 years ago)

Obesity (BMI 32 kg/m²)

Coronary Artery Disease (CAD) (diagnosed 2 years ago, previous stress test showing reduced coronary flow but no prior myocardial infarction)

Chronic Kidney Disease (CKD) (stage 2, creatinine 1.2 mg/dL)

Gastroesophageal Reflux Disease (GERD)

Medications:

Lisinopril 10 mg daily

Aspirin 81 mg daily

Atorvastatin 40 mg nightly

Metformin 1000 mg twice daily

Hydrochlorothiazide 25 mg daily

Omeprazole 20 mg daily

Allergies:

No known drug allergies.

Family History:

Father had a myocardial infarction at age 60.

Mother had hypertension and died of a stroke at age 70.

Social History:

Smoking history: 1 pack/day for 25 years, quit 2 years ago.

Occasional alcohol use (3-4 drinks per week).

Sedentary lifestyle, no regular exercise.

Diet high in processed foods, low in fruits and vegetables.

 

Review of Systems:

Cardiovascular: Severe chest pain radiating to left arm and jaw, shortness of breath, and diaphoresis.

Respiratory: No cough or wheezing.

Gastrointestinal: No nausea or vomiting.

Neurological: No dizziness or syncope.

Musculoskeletal: No recent trauma or injuries.

Objective Data:

Vital Signs upon Arrival:

Blood Pressure: 90/55 mmHg (hypotension)

Heart Rate: 110 bpm (tachycardia)

Respiratory Rate: 22 breaths/min

Temperature: 36.6°C

Oxygen Saturation: 94% on room air

Weight: 100 kg (BMI 32 kg/m²)

Height: 175 cm

Physical Exam:

General: Patient appears anxious, diaphoretic, and in distress.

Cardiovascular:

Tachycardia noted, with a heart rate of 110 bpm.

Blood pressure 90/55 mmHg, indicating hypotension.

Regular rhythm, no murmurs, but signs of possible shock (weak peripheral pulses).

Respiratory:

Slightly labored breathing, no wheezes or crackles.

No signs of pulmonary edema.

Abdomen: Soft, non-tender, no hepatomegaly.

Extremities: Peripheral edema absent, pulses weak but present in both feet.

Skin: Diaphoretic, pale, cool to touch.

Laboratory Results:

Electrolytes: Sodium 138 mEq/L, Potassium 3.8 mEq/L, Chloride 102 mEq/L

Creatinine: 1.2 mg/dL (stable)

Blood Glucose: 150 mg/dL (elevated, stress hyperglycemia)

Troponin I: 2.5 ng/mL (elevated, indicating myocardial injury)

B-type Natriuretic Peptide (BNP): 550 pg/mL (elevated, possibly indicating heart strain)

Complete Blood Count (CBC): Normal white blood cell count, hemoglobin 13.5 g/dL, hematocrit 40%.

Lipid Profile:

Total Cholesterol: 220 mg/dL

LDL: 145 mg/dL

HDL: 35 mg/dL

Triglycerides: 200 mg/dL

Electrocardiogram (ECG):

ST-Elevation in leads II, III, and aVF, confirming acute inferior wall STEMI.

T-wave inversion and Q-waves in leads I, aVL, V5, and V6.

No significant arrhythmias observed at the time of the ECG.

Chest X-ray:

No acute pulmonary findings.

No signs of cardiomegaly or pulmonary edema.

Assessment:

The patient is experiencing an acute ST-elevation myocardial infarction (STEMI), likely due to acute thrombotic occlusion of a coronary artery. The clinical presentation, including severe chest pain, shortness of breath, diaphoresis, hypotension, and elevated troponin levels, aligns with an acute myocardial infarction. The ECG confirms ST elevation in the inferior leads, a hallmark of STEMI affecting the inferior wall of the heart.

Risk factors such as hypertension, hyperlipidemia, diabetes, smoking, and obesity significantly contribute to the patient's current presentation. The patient’s hypotension and elevated BNP levels suggest significant strain on the heart, and the elevated troponin levels indicate myocardial injury.

 

 

Plan:

Immediate Management:

Administer aspirin 325 mg orally (chewable) to inhibit platelet aggregation.

Administer clopidogrel 300 mg orally as a loading dose (unless contraindicated) to further inhibit platelet aggregation.

Initiate IV heparin (or enoxaparin if preferred) to prevent further clot formation. Monitor activated partial thromboplastin time (aPTT).

Administer nitroglycerin IV (5 mcg/min) for pain relief and to reduce myocardial oxygen demand. Monitor blood pressure closely.

Administer morphine 2-4 mg IV for pain control if chest pain persists, with monitoring for hypotension.

Oxygen: Administer 4 L/min via nasal cannula to maintain oxygen saturation > 94%.

Administer beta-blocker (metoprolol 5 mg IV) to reduce heart rate and myocardial oxygen consumption, unless contraindicated (e.g., hypotension).

Pain management: Continue analgesia with morphine if necessary, along with nitroglycerin.

Percutaneous Coronary Intervention (PCI):

Emergency coronary angiography and possible stenting to restore coronary blood flow. The patient should be transferred to a catheterization lab as soon as possible for evaluation of the coronary arteries.

If PCI is not immediately available, consider thrombolytic therapy (alteplase or tenecteplase) within 30 minutes of arrival if PCI is not an option.

 

Pharmacotherapy upon Stabilization:

Aspirin 81 mg daily for long-term antiplatelet therapy.

P2Y12 inhibitor (clopidogrel 75 mg daily) for at least 12 months post-PCI.

Beta-blocker (metoprolol 50 mg daily) to reduce mortality and re-infarction risk.

Statin therapy (atorvastatin 40-80 mg daily) to reduce cholesterol and prevent further plaque rupture.

ACE Inhibitor (lisinopril 10 mg daily) to reduce mortality and improve left ventricular remodeling.

Aldosterone antagonist (eplerenone 25 mg daily) if ejection fraction is reduced or heart failure develops.

Monitor for Complications:

ECG: Repeat to monitor for resolution of ST elevation and for potential arrhythmias.

Hemodynamics: Continuous monitoring of blood pressure and heart rate, with adjustments to medications as needed.

Cardiac enzymes: Monitor troponin and CK-MB levels to assess for further myocardial injury.

Lifestyle Modifications:

Smoking cessation: Strongly encourage complete cessation.

Dietary changes: Refer for a heart-healthy diet (low in saturated fats, high in fruits and vegetables).

Exercise: Gradual increase in physical activity after hospital discharge (walking 30 minutes daily).

Weight loss: Encourage weight reduction to BMI <25 to reduce cardiovascular risk.

Follow-up:

Cardiology follow-up in 1-2 weeks to assess post-PCI recovery and medication adherence.

Monitor for depression, as patients post-STEMI can be at increased risk for mental health issues.

Routine follow-up appointments with primary care for diabetes and hypertension management.

Discussion:

STEMI occurs due to a ruptured atherosclerotic plaque and subsequent thrombotic occlusion of a coronary artery, leading to a significant reduction in myocardial blood flow. This case highlights the importance of early recognition and aggressive pharmacological and procedural intervention. Aspirin, clopidogrel, heparin, beta-blockers, and nitroglycerin are vital to manage the acute phase. Percutaneous coronary intervention (PCI) is the gold standard treatment for STEMI and should be performed as soon as possible to improve survival and reduce complications. Long-term therapy with statins, beta-blockers, ACE inhibitors, and antiplatelet therapy is essential to prevent further events and promote recovery.

Prognosis:
With timely and appropriate intervention, including PCI, pharmacotherapy, and lifestyle modifications, the patient’s prognosis can be improved, though careful follow-up is necessary to address risk factors and prevent recurrent events.