A 56-year-old woman developed stress-induced cardiomyopathy with an LVEF of 30-35% following severe vomiting, which improved to 60-65% after guideline-directed supportive therapy.
Case Report (n=1)
Severe vomiting can precipitate stress-induced cardiomyopathy, which closely mimics acute coronary syndrome and requires careful diagnostic evaluation to prevent unnecessary interventions.
Abstract Introduction Stress-induced cardiomyopathy (SICM), also known as Takotsubo syndrome (TTS), is a transient left ventricular dysfunction precipitated by physical or emotional stress. While emotional distress is a recognized trigger, SICM can also be induced by severe nausea and vomiting, likely mediated by excessive catecholamine release and myocardial stunning. We present a case in which recurrent retching led to SICM in a patient without prior cardiovascular disease, mimicking acute coronary syndrome (ACS) and necessitating thorough evaluation to distinguish between the two conditions. Case Presentation A 56-year-old woman with hypertension, rheumatoid arthritis, controlled hyperthyroidism (on methimazole and propranolol), prior alcohol use disorder (sober for six months), tobacco use, and mood disorders presented with sudden, severe chest pain following multiple episodes of non-bloody vomiting after dinner. On arrival, high-sensitivity troponin was 2,086 ng/L, decreasing to 1,884 ng/L after six hours. Electrocardiogram (ECG) demonstrated inferolateral T-wave inversions, prolonged QTc (531 ms), and a left anterior fascicular block. Laboratory testing revealed hypokalemia (3.3 mmol/L) and leukocytosis (13,550/µL). Urine drug screen was positive for cannabinoids and opiates. Despite treatment with nitroglycerin, morphine, ketorolac, and antiemetics, her symptoms persisted. Given concern for acute coronary syndrome, she was anticoagulated and underwent urgent coronary angiography, which revealed no obstructive coronary artery disease (CAD). Transthoracic echocardiogram (TTE) showed severe mid-to-apical hypokinesis with a left ventricular ejection fraction (LVEF) of 30-35%, consistent with SICM. She was treated with guideline-directed supportive therapy GDMT including metoprolol succinate and losartan as tolerated, electrolyte correction, optimized antiemetics, and continuous telemetry monitoring. Repeat echocardiogram after discharge demonstrated improvement in LVEF to 60-65% and she remained asymptomatic. Discussion This case underscores a diagnostic pitfall: prolonged vomiting can mimic NSTEMI with elevated troponin and ischemic ECG changes yet represent SICM. Although uncommon, prior reports describe SICM secondary to severe vomiting in conditions such as hyperemesis gravidarum, gastroparesis, and chemotherapy-induced nausea. Diagnosis requires exclusion of obstructive CAD and application of standardized criteria, such as the International Takotsubo (InterTAK) Diagnostic Score (67 in our patient), indicating a high likelihood of TTS (Table 1). Clinicians should promptly correct electrolyte abnormalities, avoid or use QT-prolonging antiemetics cautiously, and monitor for arrhythmias or left ventricular thrombus. Conclusion Severe vomiting can precipitate SICM, closely resembling ACS. Early recognition, appropriate imaging, and aggressive symptom control are critical to prevent misdiagnosis and unnecessary interventions. This abstract is funded by: None
Tency et al. (Fri,) conducted a case report in Stress-induced cardiomyopathy (SICM) (n=1). Guideline-directed supportive therapy was evaluated. A 56-year-old woman developed stress-induced cardiomyopathy with an LVEF of 30-35% following severe vomiting, which improved to 60-65% after guideline-directed supportive therapy.
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