Cardiac Cephalalgia: A Rare Case of STEMI Presenting Without Chest Pain

This case report highlights a rare presentation of myocardial infarction as a severe headache, known as cardiac cephalalgia, in a 47-year-old man with diabetes and tobacco use history. Despite the absence of chest pain, ECG revealed an inferior STEMI, and coronary angiography confirmed critical blockages, successfully treated with stenting. The headache resolved immediately after revascularization. The report emphasizes the importance of considering cardiac causes in people presenting with sudden, intense headaches—especially those having cardiovascular risk factors—to avoid misdiagnosis and ensure timely intervention.

• A 47-year-old male driver presented with a sudden-onset, intense generalised headache lasting 4 hours, which had awakened him from sleep. The headache was most intense in the frontotemporal region, continuous, tightening in nature, and linked with nausea, 2 episodes of vomiting, and a feeling of faintness.
• He denied diaphoresis (excessive sweating), photophobia (light sensitivity), phonophobia (fear of sound), chest pain, dyspnoea, and arm or neck pain. At home, he took 1 gram of paracetamol and applied an ayurvedic balm to his forehead, but experienced no relief.
• Notably, 2 days prior to presentation, he had throat irritation and mild fever and was given paracetamol (1 g as needed), diclofenac sodium (50 mg twice daily), amoxicillin (500 mg three times a day), and omeprazole (20 mg twice daily). His throat symptoms and fever resolved by the day prior to presentation.
• His diabetes was initially controlled with metformin, but for the past 4 years, it was managed with Mixtard 30 insulin. He was non-adherent to his insulin therapy, had irregular clinic follow-ups, and often procured medications over the counter. There was no prior screening for diabetes-associated complications.

Introduction

Worldwide, coronary heart disease continues to be one of the primary contributors to illness and mortality. In 2020, nearly 244.1 million people were affected by ischaemic heart disease, with men displaying a higher prevalence when compared to women. Myocardial ischaemia's classic symptoms encompass chest pain or discomfort, which may extend to the arms, jaw, or upper abdomen and can manifest either at rest or during physical activity. Nonetheless, less common signs like palpitations or even symptom-free (silent) ischaemia are also well-documented.

Cardiac cephalalgia represents a rare but notable atypical presentation of myocardial ischaemia, where the person experiences a migraine-like headache during an ischaemic episode. Given its uncommon and vague nature, especially when chest pain is absent, this ailment may be misdiagnosed or overlooked, leading to delays in appropriate care.

This case report describes a middle-aged man who presented with a headache as the only symptom of an inferior ST-segment elevation myocardial infarction, highlighting the need to consider cardiac cephalalgia as an atypical but important sign of acute coronary syndrome (ACS).

Medical History

• The patient had a 15-year history of diabetes mellitus and a 20-year history of smoking, amounting to nearly 5 pack-years.
• Past surgeries included drainage of abscesses located on the left leg and right groin.
• Both of his parents were diabetic, and his father had passed away due to complications related to alcoholic liver cirrhosis.

• On hospitalization, the patient was afebrile but hemodynamically unstable. He exhibited a pulse rate of 50 beats per minute (bpm) and blood pressure of 88/50 mmHg. On room air, his oxygen saturation was 100%.
• Respiratory and cardiovascular examinations were unremarkable. Neurological examination illustrated no focal deficits.
• Electrocardiography (ECG) illustrated ST-segment elevation in leads II, III, and augmented voltage foot (aVF), with reciprocal ST depression in leads V2–V4. This indicated an inferior ST-elevation myocardial infarction (STEMI) with first-degree atrioventricular block.
• Transthoracic echocardiography showed a left ventricular ejection fraction of 55%, along with impaired wall motion in the inferior region and no signs of fluid accumulation in the pericardial space. Serum troponin I was considerably elevated at 6.14 ng/mL (reference: 0.00–0.04 ng/mL), confirming myocardial injury.
• At the time of admission, his serum creatinine was raised to 1.85 mg/dL (normal range: 0.72–1.25 mg/dL). By the 2nd day, it had dropped to 1.1 mg/dL, pointing to an episode of acute kidney injury, probably caused by dehydration and decreased blood flow to the kidneys.
• Liver enzymes (aspartate aminotransferase [AST] 128 U/L and alanine aminotransferase [ALT] 123 U/L) were also elevated and decreased to 38 U/L and 65 U/L, respectively, by day 2. Abdominal ultrasound was unremarkable.

• The patient was given loading doses of aspirin (300 mg), clopidogrel (300 mg), and atorvastatin (80 mg), together with atropine (1.2 mg in segregated doses) and an isoprenaline infusion (5 µg/min).
• Nearly 30 minutes after the initiation of treatment, his headache began to subside.
• After being transferred to the cardiology unit, he was alert and fully oriented. His vital signs were as follows: oxygen saturation at 98% on room air, blood pressure at 100/60 mmHg, pulse rate of 84 bpm, and respiratory rate of 20 breaths per minute.
• Isoprenaline infusion was continued. Insulin therapy was optimized. Coronary angiography depicted total thrombotic occlusion of the mid-right coronary artery. Furthermore, 80% long-segment stenosis of the proximal to mid-left anterior descending artery was also noted.
• Stents were deployed successfully in both vessels. Post-revascularisation, the patient’s headache subsided completely. ECG was also normalised. The isoprenaline infusion was gradually tapered and discontinued.
• He was discharged 3 days later on dual antiplatelet therapy (clopidogrel and aspirin), enalapril, atorvastatin, bisoprolol, and Mixtard 30 insulin.
• At his 2-week review and during subsequent monthly follow-ups, the patient remained asymptomatic and had recommenced his routine work activities.

Discussion

ACS typically manifests as left-sided, tightening chest pain radiating to the arms, neck, or jaw. However, atypical presentations like cardiac cephalalgia—headache as the primary or sole symptom—require a high level of clinical suspicion, especially in those with cardiovascular risk factors such as diabetes mellitus. This case corresponds with previously documented reports of cardiac cephalalgia. Kobata et al. described 4 people with headaches either prior to or concurrent with myocardial ischaemia.

All had common risk factors including hypertension, diabetes, hyperlipidaemia, and smoking. Similarly, a review of 30 cases by Wei and Wang found migraine-like headaches, often frontotemporal or occipital, as typical presentations. This was frequently the only symptom, especially in men over 50 with known cardiovascular risks. Headaches were accompanied by autonomic symptoms, and diagnosis was supported by ECG changes and elevated cardiac enzymes. Most cases illustrated symptom resolution following coronary intervention.

In the present case, a 47-year-old man experienced a sudden, severe headache that woke him from sleep—an uncommon presentation of ACS. Although subarachnoid haemorrhage is a primary concern in such presentations, myocardial ischaemia must also be considered in high-risk individuals after ruling out neurological causes. Non-contrast computed tomography is the preferred initial test for excluding subarachnoid haemorrhage. However, this patient’s ECG changes and haemodynamic instability confirmed STEMI, obliging urgent coronary intervention.

The abrupt onset and severity of headache ruled out post-febrile headache. Absence of neurological deficits, together with ECG findings, pointed towards cardiac cephalalgia (a rare but recognized form of myocardial ischaemia). As per the International Classification of Headache Disorders (ICHD-3), it typically presents with migraine-like headache exaggerated by exertion, occurring during ischaemia, and ameliorated by nitrates. In this case study, the patient had multiple risk factors for coronary artery disease, encompassing poorly controlled longstanding diabetes and a past history of tobacco consumption.

Diabetes is linked to exaggerated atherosclerosis and autonomic neuropathy, that may blunt typical anginal symptoms and arouse unusual manifestations like headache. Cardiac autonomic neuropathy triggers sensory denervation, which may explain why chest pain is absent in diabetic patients. Histological and imaging studies, such as m-Iodobenzylguanidine scintigraphy, have shown evidence of sympathetic denervation and altered pain perception in such individuals. Also, the lack of a circadian pattern of cardiac events in diabetics further supports the presence of autonomic dysfunction.

Differentiating cardiac cephalalgia from migraine is critical. Common migraine treatments like triptans and ergot derivatives are vasoconstrictors and contraindicated in those suffering from myocardial ischaemia. Therefore, ECG should be part of the initial assessment of any acute headache in patients with cardiovascular risk factors. Serial ECGs and cardiac biomarkers can additionally assist in identifying ischaemia. Though the exact mechanism behind cardiac cephalalgia is unclear, several hypotheses have been proposed:

• Referred pain theory: Convergence of afferent cardiac vagal fibers with cranial pain pathways.
• Neurotransmitter release: Substances such as bradykinin, histamine, adenosine, and serotonin released during ischaemia may cause cerebral vasodilation and trigger headache.
• Venous congestion theory: Headache may arise from cerebral venous congestion during acute heart failure.

In this case, the referred pain mechanism is likely, given the patient’s poorly controlled diabetes and resulting autonomic neuropathy, which likely masked chest pain and allowed headache to emerge via alternative neural pathways. An additional factor was a recent upper respiratory tract infection with throat irritation—an acknowledged risk factor for ACS, particularly within 2 weeks of infection.

The inflammatory and pro-thrombotic response may destabilize atherosclerotic plaques. Furthermore, the patient had been taking 50 mg twice daily diclofenac sodium for 2 days before admission. NSAIDs, particularly diclofenac, are associated with elevated cardiovascular risk and can trigger ACS in those with existing risk factors.

Learning

Cardiac cephalalgia is a rare but underrecognized manifestation of acute myocardial ischemia. Clinicians should include ACS in the differential diagnosis when high-risk individuals—such as those with diabetes or a smoking history—present with a sudden, intense headache even in the absence of neurological deficits or migraine history. Simple diagnostic tools like ECG and cardiac biomarkers can be lifesaving. Early recognition is key to preventing misdiagnosis and ensuring timely treatment of potentially fatal cardiac events.