Upon arriving to the emergency department, the patient was tachycardic but normotensive, with generalized urticaria. Electrocardiography showed supraventricular tachycardia which resolved with vagal maneuvers and adenosine, as well as ST elevation in leads I and aVL, and T-wave inversions in the inferolateral leads. He received diphenhydramine and epinephrine, which produced mild symptom relief.
Troponin levels rose from 0.174 ng/mL to 7.4 ng/mL. Point-of-care ultrasound demonstrated reduced left ventricular ejection fraction (LVEF), and chest radiography showed worsening pleural effusions requiring diuresis. Cardiac catheterization demonstrated unobstructed coronary arteries but marked global systolic impairment of left ventricular systolic function. Right heart catheterization showed normal pulmonary pressures and a cardiac index less than two.
During hospitalization, the patient developed hypoxemia requiring high-flow nasal cannula and treatment with dopamine, norepinephrine, and dobutamine, followed by a steroid taper. Viral and parasitic serologies were negative, while elevated immunoglobulin E levels suggested an allergic mechanism. Serum tryptase remained low at 2.2 ng/mL. Cardiac imaging indicated an LVEF of 30% with basal wall motion abnormalities and apical sparing. No inflammation or edema was shown on cardiac magnetic resonance imaging. By hospital day 4, LVEF had improved to 45%, and the patient was discharged with cardiology and immunology follow-up.
Diagnosis
The patient was diagnosed with acute cardiomyopathy and cardiogenic shock secondary to scombroid (histamine) fish poisoning, a reaction likely caused by improperly stored fish. Differential diagnoses included Kounis syndrome, an allergic acute coronary syndrome.
Discussion
Researchers described cardiogenic shock mediated by acute histamine release in scombroid poisoning. Catecholamines typically mediate acute stress-induced cardiomyopathy, particularly in older adults, but histamine toxicity represents an uncommon alternative pathway.
Differential diagnoses included eosinophilic, lymphocytic, or hypersensitivity myocarditis; Kounis syndrome; and histamine-mediated ischemic injury. However, the absence of eosinophilia, lack of new medication exposure, and normal coronary arteries favored an allergic or histamine-induced mechanism. The patient was managed with levalbuterol, famotidine, and montelukast, alongside conservative cardiac care.
No relevant relationships were reported.
Source: Chest 2025