{
  "proficient_health_literacy": "A 23-year-old male presented to the emergency department with a sudden onset of severe frontal headache lasting two hours, accompanied by nausea, vomiting, and chest heaviness. His medical history was unremarkable, with no known illicit drug use; however, he had a significant smoking history of 23 pack-years and denied alcohol consumption. Physical examination revealed acute distress, full consciousness, and orientation to time, place, and person. Chest auscultation demonstrated normal vesicular breath sounds, while cardiovascular and abdominal examinations were non-specific. Neurological assessment identified neck stiffness, bilateral dilated pupils with intact light reflexes, normal plantar responses, and no focal neurological deficits. Vital signs showed hypertension (blood pressure 178/103 mmHg), tachypnea (respiratory rate 26 breaths/min), fever (temperature 38.9°C), heart rate of 87 beats/min, and oxygen saturation of 94%.\n\nEmergency evaluation included an electrocardiogram (ECG), which demonstrated ST-segment elevation greater than 2 mm in leads V2–V5, consistent with acute ST-elevation myocardial infarction (STEMI) as the primary differential diagnosis. This prompted immediate referral to a tertiary cardiac center for percutaneous coronary intervention (PCI). Prior to transfer, a 300 mg aspirin loading dose was administered. Cardiac biomarkers revealed markedly elevated troponin levels (1.48 mg/dL, normal <0.16 mg/dL), confirming myocardial injury. PCI via the femoral artery was performed, with coronary angiography showing normal coronary artery anatomy and TIMI flow grade 3, indicating patent vessel flow. Post-procedure ECG showed normal sinus rhythm with evidence of left ventricular hypertrophy (LVH). Echocardiography confirmed preserved left ventricular systolic function with no regional wall motion abnormalities (RWMA), suggesting no acute ischemic injury to myocardial segments.\n\nFollowing PCI, the patient was admitted to the medical ward for further workup. Laboratory tests included complete blood count (CBC), random blood glucose, renal function tests, and C-reactive protein (CRP), which revealed lymphocytosis and a mildly elevated CRP, suggestive of inflammatory or infectious processes. A non-contrast head CT was performed to evaluate the cause of the headache, which identified a cisternal subarachnoid hemorrhage (SAH) extending anterior to the right temporal lobe. Abdominal ultrasound was conducted to exclude polycystic kidney disease, which was negative. Cerebral CT angiography was planned to assess for the presence of a cerebral aneurysm, a common source of spontaneous SAH. Nimodipine 60 mg every 4 hours was initiated to prevent cerebral vasospasm, with a target mean arterial pressure of 160/100 mmHg to optimize cerebral perfusion.\n\nOn day two, the patient experienced a rapid clinical deterioration, culminating in in-hospital cardiac arrest. Cardiopulmonary resuscitation (CPR) was initiated, resulting in a Glasgow Coma Scale (GCS) score of 6, indicating severe neurological impairment. The patient was intubated and placed on mechanical ventilation in the intensive care unit (ICU). Due to hemodynamic instability and deteriorating neurological status, repeated neuroimaging and the planned cerebral CT angiography were not performed.\n\nOver the subsequent seven days, the patient was managed with a multidisciplinary approach, including nasogastric tube placement for enteral nutrition and fluid resuscitation. Medications administered included intravenous fluids, broad-spectrum antibiotics (to rule out systemic infection), proton pump inhibitors (to prevent stress-induced gastric mucosal injury), and continued nimodipine therapy.\n\nOn day eight, the patient developed sudden ventricular fibrillation, which persisted despite multiple defibrillation attempts (greater than five shocks). Despite aggressive resuscitation efforts, return of spontaneous circulation was not achieved, and the patient died. The case highlights the diagnostic challenge of differentiating between acute coronary syndrome and subarachnoid hemorrhage in a young patient with non-classic risk factors, where initial ECG findings may misdirect early management. The presence of SAH in a young individual without known vascular pathology or hypertension underscores the importance of neuroimaging in the evaluation of acute headaches with systemic symptoms, particularly when cardiovascular findings are initially suggestive of myocardial infarction. The coexistence of SAH and STEMI in this patient may reflect a rare, potentially shared pathophysiological mechanism, such as vasospasm or microvascular injury, though no direct causal link has been established. The absence of coronary atherosclerosis in this patient further emphasizes that STEMI in young individuals can arise from non-atherosclerotic etiologies, including coronary vasospasm, thrombosis, or