Grayanotoxin poisoning, commonly known as "mad honey" intoxication, is a rare but potentially life- threatening condition primarily affecting the cardiovascular system. It is characterized by bradycardia, hypotension, and, in rare cases, extreme QT interval prolongation, which predisposes patients to malignant arrhythmias. We report a 62-year-old male with no prior cardiac history who developed dizziness, nausea, and cold sweats 30 min after ingesting a tablespoon of mad honey. On admission, he exhibited sinus bradycardia, hypotension (70/40 mmHg), and marked QTc prolongation with giant inverted T waves on electrocardiogram. Laboratory and echocardiographic evaluations were unremarkable. The patient was managed with intravenous hydration and magnesium sulfate, resulting in rapid clinical and electrocardiographic recovery within 24 h. Grayanotoxins exert their toxic effects by modulating voltage-gated sodium channels, leading to sustained depolarization and impaired cardiac conduction. While bradycardia and hypotension are well-documented manifestations, extreme QT prolongation remains a rare but critical complication due to its association with ventricular arrhythmias such as torsades de pointes. This case underscores the importance of vigilant cardiac monitoring and electrolyte management in mad honey poisoning. Early recognition and appropriate supportive treatment can prevent fatal outcomes. Mad honey intoxication should be considered in patients presenting with unexplained bradycardia and hypotension, especially in endemic regions. Extreme QT prolongation, although rare, is a significant electrophysiological disturbance that necessitates prompt intervention to mitigate arrhythmic risk.

Gitelman syndrome is an inherited renal tubulopathy characterized by hypokalemia and hypomagnesemia, which can increase susceptibility to cardiac arrhythmias. Although ventricular arrhythmias have been reported, ventricular tachycardia (VT) storm triggered by atrial tachyarrhythmia with recurrent implantable cardioverter-defibrillator (ICD) therapies is uncommon. A 68-year-old woman with Gitelman syndrome, chronic kidney disease stage IIIa, long-QT physiology, and sinus bradycardia status post pacemaker implantation with subsequent dual-chamber ICD placement presented after palpitations followed by over 35-40 ICD therapies. Initial laboratory evaluation showed profound hypokalemia (2.2 mmol/L) and hypomagnesemia (1.6 mg/dL). Electrocardiography demonstrated a narrow-complex atrial tachyarrhythmia most consistent with atrial flutter, while device interrogation revealed a rapid atrial tachyarrhythmia preceding ventricular tachyarrhythmic events. The episode was clinically interpreted as atrial flutter degenerating into sustained VT. After intravenous potassium, magnesium, and metoprolol, she converted to an atrial-paced rhythm but subsequently developed transient rebound hyperkalemia necessitating temporizing therapy. Echocardiography showed preserved left ventricular systolic function. This report highlights a trigger-mediated VT storm in the absence of structural left ventricular dysfunction. Key management strategies included strict electrolyte control, avoidance of proarrhythmic triggers, optimization of ICD programming, and consideration of an electrophysiology study with potential ablation.

Drug-induced QT prolongation (diQTP) can lead to rare, but potentially fatal adverse effects of many medications, yet individual susceptibility varies due to both clinical and genetic factors. SDHAF3 p.F53L (rs62624461) is a genetic variant that plays a role in mitochondrial function and was previously associated with diQTP in one small prior study. Therefore, the objective of this retrospective pharmacogenetic study was to evaluate whether SDHAF3 p.F53L is associated with clinically significant diQTP. Data were obtained from the Michigan Genomics Initiative, which links genotype information with electronic health records at Michigan Medicine. Adult patients with available genotype and electrocardiogram data who received at least one high-risk QT-prolonging drug between 2001 and 2022 were included. The analysis was limited to 5848 patients of European ancestry, of whom 320 (5.5%) were carriers of the SDHAF3 p.F53L variant. QT prolongation was defined as a QTc greater than or equal to 500 ms or an increase greater than 60 ms from baseline during high-risk QT-prolonging drug prescription. Logistic regression under a dominant genetic model assessed associations between variant carrier status and diQTP, with and without propensity score adjustment. Baseline demographics and comorbidities were similar between carriers and noncarriers. No significant association was observed between SDHAF3 p.F53L and diQTP [unadjusted odds ratio (OR) = 1.06, 95% confidence interval (CI) = 0.76-1.48, P = 0.742; adjusted OR = 1.05, 95% CI = 0.74-1.51, P = 0.773]. These results suggest that SDHAF3 p.F53L does not meaningfully influence diQTP risk in a large, real-world clinical cohort. Future studies should examine this variant across diverse populations.