Medical Writing : Mock Project 1 : Acute Anterolateral ST-Elevation Myocardial Infarction in a 58-Year-Old Man
Patient Presentation
A 58-year-old man presented to the emergency department with a 2-hour history of severe chest pain. The pain was described as a heavy, crushing pressure in the center of his chest, radiating to his left arm and jaw. He also experienced associated shortness of breath, nausea, and diaphoresis (profuse sweating). The symptoms began at rest early in the morning and did not resolve with rest or sublingual antacid, prompting him to seek urgent medical care. On arrival, he appeared anxious and in obvious distress due to ongoing chest pain rated 10/10 in intensity.
History
The patient’s history revealed multiple cardiac risk factors. He had long-standing hypertension and hyperlipidemia, for which he was on intermittent treatment. He was an active smoker with a 30 pack-year history, and his BMI was approximately 30 (obese). He denied having diabetes mellitus. He reported no prior episodes of chest pain or known coronary artery disease, although he recalled a few weeks of mild exertional chest discomfort that he had attributed to heartburn and not medically evaluated. There was a family history of premature coronary disease — his father had a myocardial infarction in his 50s. He was not on any daily medications aside from occasional use of a thiazide diuretic for blood pressure, and he had no known drug allergies.
Clinical Findings
On examination, the patient was pale and diaphoretic. Vital signs on admission showed a blood pressure of 145/90 mmHg and a heart rate of 100 beats/min (sinus rhythm). He was tachypneic with a respiratory rate of 22/min, and oxygen saturation was 95% on room air. Cardiac auscultation revealed a regular rhythm with normal S1 and S2 heart sounds. Notably, a fourth heart sound (S4 gallop) was present at the apex, which often accompanies acute myocardial ischemia. No murmurs were heard (in particular, no murmur of papillary muscle rupture or ventricular septal defect). There were a few fine crackles at the lung bases, suggesting mild pulmonary congestion. Extremities were warm with intact pulses, and there were no signs of peripheral edema.
Investigations
An immediate 12-lead electrocardiogram (ECG) was performed within minutes of arrival. It showed ST-segment elevations in the anterior and lateral leads (most prominently in V2–V5, and leads I and aVL), with reciprocal ST depressions in inferior leads, consistent with an extensive anterior wall ST-elevation myocardial infarction (STEMI).
Figure: The patient’s electrocardiogram on presentation demonstrates marked ST-segment elevation in the anterior chest leads (V2–V6) and lateral leads (I, aVL), indicative of an acute anterolateral STEMI. This pattern corresponds to an occlusion of the left anterior descending (LAD) coronary artery, which typically supplies the anterior wall of the left ventricle. The ECG findings confirmed the need for urgent reperfusion therapy given the ongoing infarction.
Laboratory cardiac biomarkers were markedly abnormal. The initial high-sensitivity troponin-I level was elevated to 2.8 ng/mL (normal <0.04) and continued to rise on serial measurements, confirming myocardial injury. Other labs showed a mild leukocytosis (12×10^9/L) and modestly elevated serum glucose (9 mmol/L), likely stress-induced. Electrolytes and renal function were within normal limits. A chest X-ray revealed a normal cardiac silhouette with no acute pulmonary edema or widening of the mediastinum (helping to exclude aortic dissection as a cause of chest pain). After the acute intervention (described below), a transthoracic echocardiogram was performed, which showed akinesia of the anterior septum and apex with a moderately reduced left ventricular ejection fraction of 45%. No valvular abnormalities or ventricular septal defect were noted on echo.
Diagnosis
The clinical picture was diagnostic of an acute myocardial infarction involving the anterior wall of the left ventricle. In particular, the patient fulfilled criteria for an acute anterior STEMI (ST-elevation myocardial infarction). This diagnosis was supported by the classic triad of ischemic chest pain, characteristic ECG changes, and elevated cardiac biomarkers. The ECG localization (anterolateral ST elevations) and subsequent angiography (see below) pointed to an occlusion in the proximal LAD artery as the culprit lesion. There was no evidence that this was a secondary (Type 2) MI; rather, the findings were consistent with a Type 1 MI due to acute plaque rupture and coronary thrombosis in an epicardial artery.
Management Plan
Acute management: The patient was immediately started on guideline-directed medical therapy for acute coronary syndrome upon recognition of the STEMI. He was given a chewable aspirin (300 mg) loading dose promptly, as recommended for all patients with suspected MI. He was also loaded with a P2Y₁₂ platelet inhibitor (ticagrelor 180 mg) to achieve dual antiplatelet therapy. Sublingual nitroglycerin was administered for pain and blood pressure control, and morphine was given for analgesia due to continued severe pain. Intravenous heparin bolus and infusion were initiated for anticoagulation. He was placed on cardiac monitors and supplemental oxygen was reserved since his saturation remained ≥95%. The on-call interventional cardiology team was activated immediately. The patient was quickly transferred to the cardiac catheterization lab for primary percutaneous coronary intervention (PCI), the preferred reperfusion strategy in STEMI.
Intervention: Urgent coronary angiography was performed about 60–90 minutes from symptom onset (well within guideline targets for door-to-balloon time). Angiography confirmed a 100% occlusion of the proximal LAD artery with thrombus. The other major coronary vessels had only mild atherosclerosis. The LAD was successfully opened by balloon angioplasty, and a drug-eluting stent was deployed in the proximal LAD with restoration of normal TIMI-3 flow. Post-stenting, the ST elevations on ECG gradually resolved and the patient’s chest pain completely abated. No acute complications occurred during PCI; the patient did not have any sustained arrhythmias or hemodynamic instability throughout the procedure.
In-hospital care: After PCI, the patient was admitted to the coronary care unit for monitoring. He was started on a high-intensity statin (atorvastatin 80 mg nightly) and an ACE inhibitor (lisinopril) the next morning, given anterior wall involvement, to help prevent adverse remodeling. A beta-blocker (bisoprolol) was initiated once he was stable and pain-free to reduce myocardial oxygen demand (avoiding early beta-blocker in the very acute phase due to initial hemodynamic stress). These medications — aspirin, beta-blocker, ACE inhibitor, and statin — are standard evidence-based therapies after MI to improve long-term outcomes. The patient’s risk factors were addressed: his home antihypertensive regimen was optimized, and he received counseling for smoking cessation, diet, and exercise. Over 48 hours of observation, he remained free of chest pain. Telemetry monitoring detected only occasional premature beats; no sustained ventricular arrhythmias were noted. His blood pressure and urine output remained stable, and the mild basal crackles resolved, suggesting no progression of heart failure. By hospital day 3, repeat labs showed down-trending cardiac enzymes and stable hemoglobin and creatinine.
Outcome
The patient had an excellent outcome following timely reperfusion. He was discharged on hospital day 4. At discharge, he was pain-free and ambulatory, with instructions to avoid strenuous activity until cleared. His discharge medications included dual antiplatelet therapy (aspirin plus ticagrelor) to continue for 12 months, along with long-term statin, ACE inhibitor, and beta-blocker – a regimen aligned with standard post-MI secondary prevention guidelines. He was also prescribed a short course of high-dose proton-pump inhibitor for gastroprotection due to dual antiplatelet use. The patient was referred to outpatient cardiac rehabilitation and received extensive education on lifestyle modifications (smoking cessation, low-salt heart-healthy diet, weight loss, and regular exercise as tolerated).
On follow-up at 1 month, the patient was doing well. He reported no anginal chest pain or dyspnea with daily activities. He had stopped smoking and was adhering to his medications without side effects. In cardiac rehab sessions, his exercise capacity was gradually improving. A clinic follow-up echocardiogram at 6 weeks showed left ventricular ejection fraction improved to 50%. This positive recovery was attributed to the early reperfusion and ongoing optimal medical therapy. The patient continues under regular cardiology follow-up, and he remains committed to risk factor management to prevent recurrence.
Discussion
This case illustrates a classic presentation of acute myocardial infarction (MI) and highlights the crucial importance of prompt recognition and management. Acute MI (heart attack) refers to the irreversible necrosis of heart muscle due to prolonged ischemia[8]. It is a common but serious cardiac condition — cardiovascular disease is the leading cause of death globally, with ischemic heart disease (including MI) accounting for millions of deaths each year. Our patient had several major risk factors for coronary artery disease, including hypertension, smoking, hyperlipidemia, obesity, and a positive family history. These are well-established contributors to atherosclerosis; in fact, studies indicate that modifiable risk factors account for ~90% of myocardial infarction cases in men. This underlines the importance of aggressive risk factor modification (smoking cessation, blood pressure control, lipid management, etc.) in the prevention of MI.
The patient’s presentation with typical ischemic chest pain and diaphoresis allowed an early clinical suspicion of MI. The ECG changes were immediately diagnostic of STEMI, which expedited reperfusion therapy. Rapid identification of ST-elevation myocardial infarction and triage to primary PCI is life-saving. Guidelines recommend administering aspirin and achieving coronary reperfusion as quickly as possible (ideally by primary PCI within 90 minutes of first medical contact) for STEMI patients. In this case, door-to-balloon time was well within the recommended window. Timely restoration of coronary blood flow limits the size of the infarct and improves outcomes – evidence shows that early reperfusion (within hours of symptom onset) significantly improves survival and cardiac function. Conversely, delays in treatment are associated with larger infarcts and higher mortality.
Our patient’s clinical course demonstrates the benefits of adherence to evidence-based acute management. He received prompt PCI, which is the preferred reperfusion strategy and has been shown to reduce mortality compared to fibrinolysis in STEMI. Fortunately, he did not develop any of the common complications of acute MI, such as arrhythmias, cardiogenic shock, or significant heart failure. (It is worth noting that complications like ventricular arrhythmias, myocardial rupture, or acute heart failure can occur in MI, especially with large or delayed-treatment infarcts; close monitoring in a CCU is thus warranted for early complication management.) His left ventricular function was moderately reduced but improved with revascularization and therapy, which is a favorable sign – patients with preserved or recovering ejection fraction post-MI have better prognoses than those with severe impairment.
Long-term management is focused on secondary prevention of another cardiac event. Our patient was discharged on the appropriate medical regimen of dual antiplatelets, beta-blocker, ACE inhibitor, and high-intensity statin, which is standard after MI to prevent reinfarction and improve survival. Enrollment in cardiac rehabilitation was arranged, as supervised rehab has been shown to improve exercise capacity, enhance quality of life, and even reduce mortality in post-MI patients. Patient education was reinforced regarding recognizing symptoms and calling emergency services promptly if symptoms recur, given that a significant proportion of MI fatalities occur before reaching the hospital.
In summary, this case study of an acute anterior STEMI showcases the importance of rapid diagnosis, immediate reperfusion therapy, and comprehensive multidisciplinary care in achieving a positive outcome. Through timely intervention and diligent post-MI care, the patient was able to make an excellent recovery. The case underscores fundamental principles in cardiology: “time is muscle” in myocardial infarction, and long-term management of cardiovascular risk factors is key to improving prognosis and preventing future cardiac events.
