ischemia, frequently underdiagnosed due to low awareness and its unconventional presentation. Unlike typical angina, which is characterized by oppressive chest pain radiating to the arm and jaw, cardiac headache can occur in isolation, triggered by physical exertion [5]. Therefore, a detailed clinical approach—based on medical history, cardiovascular risk factor assessment, and complementary exams such as stress tests and coronary angiography—is essential for differential diagnosis and appropriate treatment of these patients [2, 3, 6–10].

The third and last hypothesis suggests that inammatory mediators are impli­cated in cardiac cephalalgia. Acute myocardial injury triggers the release of pro­inammatory substances from the cardiac muscle, such as bradykinin, serotonin, substance P, histamine, and adenosine. These mediators can induce cerebral edema, cerebral artery vasodilation, and cerebral cortical hypoperfusion, ultimately mani­festing as a headache [2, 5].

A 61-year-old male with a history of hypertension, managed with regular antihyper­tensive therapy, and obesity presented to the emergency department with acute pre­cordial pain. The pain began approximately 30minutes prior while the patient was at rest at home. He described the pain as oppressive, retrosternal, and radiating to the left shoulder and upper limb, accompanied by dyspnea, nausea, and a single episode of emesis. Concurrently, the patient experienced a severe, acute-onset head­ache localized to the vertex, characterized as oppressive and increasing in intensity with the worsening chest pain. Upon arrival, vital signs revealed a blood pressure of 145/80 mmHg; other vital signs were unremarkable. Neurological examination revealed no focal decits or abnormalities. An electrocardiogram (ECG) demon­strated ST-segment elevation greater than 1.5mm in leads II, III, and aVF.An ultra­sensitive troponin level was elevated at 1500 ng/L. Laboratory investigations showed inammatory markers within normal limits and no evidence of autoimmune or infectious etiologies. A computed tomography (CT) scan of the head revealed normal anatomical ndings, without evidence of hemorrhage, mass lesions, or other abnormalities. The patient was transferred to the cardiac catheterization laboratory, where primary percutaneous coronary intervention (PCI) revealed a 90% occlusion of the right coronary artery. Following PCI, the patient reported signicant improve­ment in both chest pain and headache.

The rarity of cardiac cephalalgia makes its diagnosis complex, given its varied clini­cal presentation [3]. The literature suggests a patient prole typically over 50years old male exhibiting established cardiovascular risk factors including systemic arte­rial hypertension, dyslipidemia, obesity, and a smoking history [14–19]. However, this is not absolute, as cases have been reported in younger individuals and in patients without cardiovascular risk factors [13, 20, 21].

Although age is a relevant factor in the anamnesis, other characteristics must be carefully assessed for proper patient identication. Gathering information about headache presentation, similarity to previous typical headache episodes, and response to commonly used headache medications is crucial [28]. Additionally, investigating the presence of comorbidities, as previously mentioned, should be part of the patient’s evaluation.

The assessment of these patients involves stress testing, which usually reveals recurrent headaches associated with ST-segment depression, and coronary angiog­raphy [2, 3, 7–10]. A review, involving 30 patients, reinforced the importance of performing brain magnetic resonance imaging (MRI) to exclude other underlying pathological conditions [6]. Regarding treatment, the triptans, as selective 5-HT