Zollinger-Ellison syndrome may represent a novel metabolic trigger for Takotsubo cardiomyopathy, expanding the differential for stress-induced cardiomyopathy.
Case Report (n=1)
Zollinger-Ellison syndrome may represent a novel metabolic trigger for Takotsubo cardiomyopathy.
Abstract Background Takotsubo cardiomyopathy (TC) is classically precipitated by emotional or physical stress. Zollinger-Ellison syndrome (ZES), a gastrin-secreting neuroendocrine tumor, causes severe metabolic stress through hypergastrinemia and acid hypersecretion. We present the first reported case of hypergastrinemia-induced Takotsubo cardiomyopathy secondary to ZES, highlighting a novel neuroendocrine-gastrocardiac connection. Case Presentation A 70-year-old woman with COPD (on 5 L home O2), type 2 diabetes, and chronic tobacco use was found collapsed after lying on the floor for three days. On presentation, she was dehydrated and hypothermic. ECG showed deep anterolateral T-wave inversions with QTc ≈ 520 ms; troponin peaked at 5.54 ng/mL and BNP 41 000 pg/mL. Coronary angiography revealed no obstructive coronary artery disease, but left ventriculography demonstrated apical ballooning with ejection fraction 40-45% and dynamic LVOT obstruction, consistent with Takotsubo cardiomyopathy. Soon after, she developed coffee-ground emesis and epigastric pain. EGD demonstrated Grade D esophagitis, a pyloric channel ulcer with adherent clot, and numerous duodenal ulcers extending beyond the ampulla. Gastrin 131 pg/mL (off PPI; ref 100) and chromogranin A 1477 ng/mL confirmed hypersecretory physiology consistent with Zollinger-Ellison syndrome. CT abdomen/pelvis with contrast showed no pancreatic or duodenal mass, no lymphadenopathy. Infectious evaluation was negative despite leukocytosis and elevated procalcitonin (8.3 ng/mL). The patient received aggressive IV fluid resuscitation, high-dose IV pantoprazole, electrolyte correction, and initiation of octreotide infusion for symptomatic acid suppression. Ga-68 DOTATATE PET/CT has been ordered for tumor localization and is pending at the time of this report. She remains hemodynamically stable, on baseline oxygen, and will undergo repeat echocardiography to assess recovery of systolic function. Continued proton-pump inhibition, octreotide, nutritional support, and endocrinology follow-up are planned. Discussion This case highlights a previously unreported neuroendocrine-cardiac interaction. Severe vomiting, hypovolemia, electrolyte derangements, and catecholamine surge from gastrinoma-related hypergastrinemia likely triggered myocardial stunning via sympathetic overactivation and microvascular dysfunction. While emotional and neurologic stressors are typical, this presentation demonstrates that gastrointestinal-endocrine stress can precipitate Takotsubo physiology. Conclusion Zollinger-Ellison syndrome may represent a novel metabolic trigger for Takotsubo cardiomyopathy. Awareness of this association can expand the differential for stress-induced cardiomyopathy and prompt evaluation for occult gastrinoma when TC coexists with refractory peptic ulcer disease or unexplained hypergastrinemia. This abstract is funded by: None
Inturi et al. (Fri,) conducted a case report in Takotsubo cardiomyopathy and Zollinger-Ellison syndrome (n=1). Zollinger-Ellison syndrome may represent a novel metabolic trigger for Takotsubo cardiomyopathy, expanding the differential for stress-induced cardiomyopathy.