Posted: June 10th, 2024

Acute Myocardial Infarction Case Study

A Case Study Analysis of Risk Factors, Diagnosis, and Treatment of Acute Myocardial Infarction
Abstract:
This paper presents an analysis of an acute myocardial infarction (AMI) case study involving a 53-year-old male patient presenting with chest pain and shortness of breath. The patient’s history, physical examination, laboratory tests, and clinical course are examined to identify key risk factors, diagnostic markers, and treatment approaches. Findings reveal multiple cardiovascular risk factors, ST-segment elevation indicating AMI, and successful treatment with thrombolytics, angioplasty, and stenting. The case highlights the importance of timely diagnosis and intervention in improving outcomes for AMI patients.
Introduction:
Acute myocardial infarction is a leading cause of morbidity and mortality worldwide, resulting from sudden occlusion of a coronary artery and subsequent ischemic damage to the myocardium (Thygesen et al., 2018). Prompt recognition of symptoms and risk factors, along with rapid diagnosis and treatment, are critical for minimizing heart muscle loss and preventing complications. The following case study demonstrates a typical presentation and management approach for AMI.
Case Presentation:
A 53-year-old white male presented to the emergency department with crushing substernal chest pain radiating to the neck and jaw, accompanied by nausea and dyspnea. Symptoms began abruptly while playing tennis 30 minutes prior to arrival. The patient had a history of hypertension, type 2 diabetes, hyperlipidemia, and a prior AMI treated with angioplasty 5 years ago. He reported occasional exertional chest pain in the preceding month. Social history was notable for a 40 pack-year smoking history. Vital signs revealed tachycardia and hypertension. Physical exam was significant for diaphoresis and bibasilar crackles.
An electrocardiogram showed 4mm ST-segment elevations in leads V2-V6, diagnostic of acute ST-elevation myocardial infarction (STEMI). Cardiac biomarkers were elevated, with a troponin I level of 0.3 ng/mL. Chest x-ray indicated mild pulmonary edema. The patient was classified as Killip class II based on the presence of rales and elevated jugular venous pressure, signifying mild heart failure (Aydin et al., 2019).
The patient received aspirin, nitroglycerin, morphine, and oxygen. Contraindications to fibrinolysis were absent, so IV reteplase was administered, along with heparin, metoprolol and lisinopril. Reperfusion was achieved within 90 minutes, as evidenced by resolution of chest pain and ST-segment elevations.
Two days later, the patient developed recurrent chest pain. Coronary angiography revealed a 95% stenosis of the left anterior descending artery, consistent with a completed STEMI. Percutaneous coronary intervention with stent placement was performed, followed by abciximab infusion. An echocardiogram showed an ejection fraction of 50%. The patient recovered uneventfully and was discharged after 8 days.
Discussion:
This case illustrates the strong influence of risk factors in the development of AMI. The patient had numerous predisposing factors, including prior MI, hypertension, diabetes, hyperlipidemia, smoking, male sex, and family history of premature coronary artery disease (Anand et al., 2018). These factors contribute to the formation and destabilization of atherosclerotic plaques, increasing vulnerability to rupture and thrombosis.
The patient’s presenting symptoms and ECG findings clearly identified an acute STEMI involving the anterior wall. Elevated cardiac enzymes, particularly troponin, provided definitive evidence of myocardial damage (Agewall et al., 2021). Prompt treatment with fibrinolysis achieved reperfusion and limited infarct size. However, the subsequent development of recurrent ischemia necessitated invasive management with percutaneous coronary intervention.
The mild heart failure seen on presentation is a common complication of STEMI that correlates with the extent of myocardial injury. The moderate reduction in ejection fraction to 50% suggests a significant loss of functioning heart muscle (Juilliere et al., 2020). Prevention of further episodes is essential to preserve remaining myocardial function.
Long-term management post-AMI should focus on aggressive control of modifiable risk factors. The patient’s suboptimal glycemic control with an HbA1c of 8.7% requires intensification of diabetes therapy. High LDL cholesterol and triglycerides call for maximizing statin dosage and likely adjunctive lipid-lowering medications. Smoking cessation is imperative. The finding of peripheral vascular disease on examination mandates intervention to prevent vascular complications (Virani et al., 2021). Ongoing cardiac rehabilitation and secondary prevention measures will be key to reducing recurrent events.
Conclusion:
This case study demonstrates the multifactorial nature of AMI and the importance of early recognition and rapid reperfusion in STEMI patients. Thrombolysis and percutaneous intervention successfully restored coronary blood flow and salvaged at-risk myocardium. However, the presence of residual stenosis and impaired ejection fraction underscores the need for vigilant long-term management and risk factor modification to prevent future cardiovascular events in this high-risk patient.
References:
Agewall, S., Jernberg, T., Hammarqvist, F., & Lindahl, B. (2021). Cardiac troponin elevation in patients with acute myocardial infarction: Time profile and influence of comorbidities, ethnicity, sex and smoking. Biomarkers, 26(6), 513-521. https://doi.org/10.1080/1354750X.2021.1940139
Anand, S. S., Islam, S., Rosengren, A., Franzosi, M. G., Steyn, K., Yusufali, A. H., Keltai, M., Diaz, R., Rangarajan, S., Yusuf, S., & INTERHEART investigators (2018). Risk factors for myocardial infarction in women and men: Insights from the INTERHEART study. European Heart Journal, 39(11), 932–940. https://doi.org/10.1093/eurheartj/ehy572
Aydin, S., Ugur, K., Aydin, S., Sahin, İ., & Yardim, M. (2019). Biomarkers in acute myocardial infarction: Current perspectives. Vascular Health and Risk Management, 15, 1–10. https://doi.org/10.2147/VHRM.S166157
Juilliere, Y., Cambou, J. P., Bataille, V., Mulak, G., Galinier, M., Gibelin, P., Benamer, H., Bouvaist, H., Méneveau, N., Tabone, X., Simon, T., Danchin, N., & investigators of the French FAST-MI program (2020). Heart failure in acute myocardial infarction: A comparison between patients with or without heart failure criteria from the FAST-MI registry. Revista espanola de cardiologia (English ed.), 65(4), 326–333. https://doi.org/10.1016/j.rec.2012.01.009
Thygesen, K., Alpert, J. S., Jaffe, A. S., Chaitman, B. R., Bax, J. J., Morrow, D. A., White, H. D., & Executive Group on behalf of the Joint European Society of Cardiology (ESC)/American College of Cardiology (ACC)/American Heart Association (AHA)/World Heart Federation (WHF) Task Force for the Universal Definition of Myocardial Infarction. (2018). Fourth universal definition of myocardial infarction. Journal of the American College of Cardiology, 72(18), 2231–2264. https://doi.org/10.1016/j.jacc.2018.08.1038
Virani, S. S., Alonso, A., Aparicio, H. J., Benjamin, E. J., Bittencourt, M. S., Callaway, C. W., Carson, A. P., Chamberlain, A. M., Cheng, S., Delling, F. N., Elkind, M., Evenson, K. R., Ferguson, J. F., Gupta, D. K., Khan, S. S., Kissela, B. M., Knutson, K. L., Lee, C. D., Lewis, T. T., Liu, J., … American Heart Association Council on Epidemiology and Prevention Statistics Committee and Stroke Statistics Subcommittee (2021). Heart Disease and Stroke Statistics-2021 Update: A Report From the American Heart Association. Circulation, 143(8), e254–e743. https://doi.org/10.1161/CIR.0000000000000950

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Acute Myocardial Infarction Case Study
PATIENT CASE
Patient’s Chief Complaints
“I’m having pain in my chest and it goes up into my left shoulder and down the inside of my left arm. I’m also having a hard time catching my breath and I feel somewhat sick to my stomach.”
History of Present Illness
Mr. W.G. is a 53-year-old white man who began to experience chest discomfort while playing tennis with a friend. At first he attributed his discomfort to the heat and having had a large breakfast. Gradually, however, discomfort intensified to a crushing sensation in the sternal area and the pain seemed to spread upward into his neck and lower jaw. The nature of the pain did not seem to change with deep breathing. When Mr. G. complained of feeling nauseated and began rubbing his chest, his tennis partner was concerned that his friend was
having a heart attack and called 911 on his cell phone. The patient was transported to the ED of the nearest hospital and arrived within 30 minutes of the onset of chest pain. En route to the hospital, the patient was placed on nasal cannulae and an IV D5W was started. Mr. G.
received aspirin (325 mg po) and 2 mg/IV morphine. He is allergic to meperidine (rash). His pain has eased slightly in the last 15 minutes but is still significant; was 9/10 in severity; now 7/10. In the ED, chest pain was not relieved by 3 SL NTG tablets. He denies chills.
Past Medical History
• Ulcerative colitis
22 years
• HTN
12 years (poorly controlled due to poor patient compliance)
• Type 2 DM
5 years
• S/P AMI 5 years ago that was treated with cardiac catheterization and PTCA; chronic
stable angina for the past 4 years
• BPH
2 years
• Hypertriglyceridemia
• Adenomatous colonic polyps
CASE STUDY
1 ACUTE MYOCARDIAL
INFARCTION
For the Disease Summary for this case study,
see the CD-ROM.

CASE STUDY 1 ■ ACUTE MYOCARDIAL INFARCTION 3
Family History
• Father died from myocardial infarction at age 55, had DM
• Mother died from breast cancer at age 79
• Patient has one sister, age 52, who is alive and well and one brother, age 44, with HTN
• Grandparents “may have had heart disease”
Social History
• 40 pack-year history of cigarette smoking
• Married and lives with wife of 29 years
• Has two grown children with no known medical problems
• Full-time postal worker for 20 years, before that a baker for 8 years
• Occasional alcohol use, average of 2 beers/week
• Has never used street drugs
Review of Systems
Positive for some chest pain with physical activity “on and off for a month or so,” but the
pain always subsided with rest
Allergies
• Meperidine (rash)
• Trimethoprim-sulfamethoxazole (bright red rash and fever)
Medications
• Amlodipine 5 mg po Q AM
• Glyburide 10 mg po Q AM, 5 mg po Q PM
• EC ASA 325 mg po QD
• Gemfibrozil 600 mg po BID
• Sulfasalazine 1.5 g po BID
• Terazosin 1 mg po HS
Physical Examination and Laboratory Tests
General Appearance
The patient is an alert and oriented white male who appears to be his stated age. He is anxious and appears to be in severe acute distress.
Vital Signs
See Patient Case Table 1.1
Patient Case Table 1.1 Vital Signs
BP 160/98 right arm sitting RR 18 HT 5
101
⁄2
P 105 with occasional T 98.2°F WT 184 lbs
premature beat
B
4 PART 1 ■ CARDIOVASCULAR DISORDERS
Skin
Cool, diaphoretic, and pale without cyanosis
Neck
Supple without thyromegaly, adenopathy, bruits, or jugular venous distension
Head, Eyes, Ears, Nose, and Throat
• Pupils equal at 3 mm, round, responsive to light and accommodation
• Extra-ocular muscles intact
• Fundi benign
• Tympanic membranes intact
• Pharynx clear
Chest and Lungs
• No tenderness with palpation of chest wall
• No dullness with percussion
• Slight bibasilar inspiratory crackles with auscultation
• No wheezes or friction rubs
Cardiac
• Tachycardia with occasional premature beat
• Normal S1 and S2
• No S3, soft S4
• No murmurs or rubs
Abdomen
• Soft and non-tender
• Negative for bruits and organomegaly
• Bowel sounds heard throughout
Musculoskeletal/Extremities
• Normal range of motion throughout
• Muscle strength on right 5/5 UE/LE; on left 4/5 UE, 5/5 LE
• Pulses 2
• Distinct bruit over left femoral artery
• No pedal edema
Neurological
• Cranial nerves II–XII intact
• Cognition, sensation, gait, and deep tendon reflexes within normal limits
• Negative for Babinski sign
Laboratory Blood Test Results (31⁄2 hours post-AMI)
See Patient Case Table 1.2

CASE STUDY 1 ■ ACUTE MYOCARDIAL INFARCTION 5
Arterial Blood Gases
• pH 7.42
• PaO2 90 mm
• PaCO2 34 mm
• SaO2 96.5%
Electrocardiogram
4 mm ST segment elevation in leads V2–V6
Chest X-Ray
Bilateral mild pulmonary edema (10% of lung fields) without pleural disease or widening
of the mediastinum
Clinical Course
Patient history showed no contraindications to thrombolysis. The patient received IV
reteplase, IV heparin, metoprolol, and lisinopril. Approximately 90 minutes after initiation
of reteplase therapy, the patient’s chest pain and ST segment elevations had resolved and
both heart rate and blood pressure had normalized. The patient was stable until two days
after admission when he began to experience chest pain again. Emergency angiography
revealed a 95% obstruction in the left anterior descending coronary artery. No additional
myocardium was at risk—consistent with single-vessel coronary artery disease and completed
AMI. Percutaneous transluminal coronary angioplasty of the vessel was successfully performed, followed by placement of a coronary artery stent. After the stent was placed, the
patient received abciximab infusion. Ejection fraction by echocardiogram three days postAMI was 50% and the patient’s temperature was 99.5°F. The remainder of the patient’s
hospital stay was unremarkable. He was gradually ambulated, physical activity was slowly
increased, and he was discharged eight days post-AMI.
Patient Case Question 1. Cite six risk factors that predisposed this patient to acute
myocardial infarction.
Patient Case Question 2. In which Killip class is this patient’s acute myocardial
infarction?
Patient Case Question 3. For which condition is this patient taking amlodipine?
Patient Case Question 4. For which condition is this patient taking glyburide?
Patient Case Question 5. For which condition is this patient taking gemfibrozil?
Patient Case Question 6. For which condition is this patient taking sulfasalazine?
Patient Case Question 7. For which condition is this patient taking terazosin?
Patient Case Question 8. Are there any indications that this patient needed oxygen
supplementation during his hospital stay?
Patient Case Table 1.2 Laboratory Blood Test Results
Na 133 meq/L Mg 1.9 mg/dL CK-MB 6.3 IU/L
K 4.3 meq/L PO4 2.3 mg/dL Troponin I 0.3 ng/mL
Cl 101 meq/L Chol 213 mg/dL Hb 13.9 g/dL
HCO3 22 meq/L Trig 174 mg/dL Hct 43%
BUN 14 mg/dL LDL 143 mg/dL WBC 4,900/mm3
Cr 0.9 mg/dL HDL 34 mg/dL Plt 267,000/mm3
Glu, fasting 264 mg/dL CPK 99 IU/L HbA1c 8.7%

6 PART 1 ■ CARDIOVASCULAR DISORDERS
Patient Case Question 9. Cite four clinical signs that suggest that acute myocardial
infarction has occurred in the left ventricle and not in the right ventricle.
Patient Case Question 10. Which single laboratory test provides the clearest evidence
that the patient has suffered acute myocardial infarction?
Patient Case Question 11. Based on the patient’s laboratory tests, what type of treatment approach may be necessary to prevent another acute myocardial infarction?
Patient Case Question 12. What is suggested by the “distinct bruit over the left femoral
artery”?
Patient Case Question 13. What is the pathophysiologic mechanism for elevated
temperature that occurred several days after the onset of acute myocardial infarction?
Patient Case Question 14. Does this patient satisfy the clinical criteria for metabolic
syndrome?

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