Aconitine poisoning presenting as atrial fibrillation with slow ventricular rate: A case report

Abstract

Aconitine is a diterpenoid diester alkaloid primarily found in traditional Chinese herbs. It is rapidly absorbed through the upper gastrointestinal tract and exhibits some beneficial effects. However, due to its toxicity, improper use of aconitine can easily lead to poisoning, primarily characterized by cardiovascular and neurological toxicity. Most cases of aconitine poisoning involve multiple types of arrhythmias, with rapid ventricular arrhythmias being the most common. However, it can also result in bradyarrhythmias. We report a case of aconitine poisoning manifesting as atrial fibrillation with slow ventricular rate and an ST-segment resembling a fishhook pattern on the electrocardiogram, detailing its clinical presentation and treatment approach. This case report highlights the importance of healthcare professionals thoroughly reviewing patients' medical history and medication use to identify and address adverse drug reactions.

Learning objectives

• 1.Recognize that aconitine poisoning, while commonly presenting with rapid ventricular arrhythmias, can also manifest as bradyarrhythmias, including atrial fibrillation with slow ventricular response.
• 2.Identify the potential electrocardiographic finding of a fishhook-shaped ST-segment as a clue in suspected aconitine toxicity.
• 3.Emphasize the critical importance of a thorough review of a patient's medication history and use of traditional herbs in the evaluation of unexplained arrhythmias.

Introduction

Aconitine is a diterpenoid bis-ester alkaloid found in herbs such as Aconitum, Caowu, and Fuzi. It is rapidly absorbed by the upper gastrointestinal tract and exhibits analgesic, anti-inflammatory, circulation-promoting, and anti-tumor effects [1,2]. However, due to its significant toxicity to humans, improper use can lead to cardiovascular and neurological toxicity. Patients often experience symptoms such as nausea, vomiting, numbness of the tongue and extremities, ataxia, and arrhythmia after excessive intake of aconitine. In some cases, symptoms may only manifest after a long latency period [3]. Most patients develop multiple types of arrhythmias, with rapid ventricular arrhythmias being the most common. Here, we report a case of aconitine poisoning presenting as atrial fibrillation with a slow ventricular rate, featuring ST segment changes resembling a fishhook pattern, and discuss the clinical manifestations and treatment approach.

Case report

A 67-year-old female patient was admitted with a 20-year history of recurrent palpitations and chest tightness, which had worsened over the past week. The patient initially experienced palpitations and chest tightness over two decades previously without any apparent trigger, and an electrocardiogram (ECG) performed at a local hospital revealed atrial fibrillation. In 2011, due to exacerbation and prolongation symptoms, she underwent catheter ablation for atrial fibrillation at another hospital. Despite occasional recurrence of palpitations and chest discomfort postoperatively, no further treatment was sought as the symptoms were milder.

One week prior to admission, the patient reported worsening palpitations and chest tightness accompanied by poor appetite and vomiting. On March 23, 2024, she presented to our hospital and was subsequently admitted for further evaluation and management. Her medical history included type-2 diabetes mellitus, hypertension, and sequelae from a past cerebrovascular accident. Physical examination revealed a heart rate of 46 beats per minute, an irregular rhythm, accentuated second heart sound in the pulmonary area, and moderate lower extremity edema.

At 20:00 on the day of admission, the patient suddenly lost consciousness while in the restroom, regaining it approximately 5 s later without any incontinence of bladder or bowel. Immediate cardiac monitoring showed a blood pressure of 149/60 mmHg, pulse rate of 49/min, respiratory rate of 22/min, and oxygen saturation at 98 %. A 12 lead ECG showed atrial fibrillation with a slow ventricular rate (44/min), QRS duration < 120 ms, ST-T changes (downsloping ST segments with biphasic T waves in leads I, II, III, aVF, V4-V6, and ST segment elevation in lead aVR), and a shortened QT interval of 300 ms (< 320 ms), with the longest R-R interval of 1. 87 s (Fig. 1). Telemetry later showed a 3.3 s long R-R interval. Further history revealed that two weeks prior, the patient had self-administered a traditional Chinese medicine concoction containing 10 g of Fupian, among other herbs, twice daily for a week, due to perceived “deficiency of qi and blood.” However, the total intake of aconitine was difficult to estimate due to large interindividual variability. She denied taking medications such as metoprolol, digoxin, or amiodarone for atrial fibrillation.

Fig. 1.

The 12‑lead electrocardiogram (2024-03-23 20:48:20)

(1) Atrial fibrillation with a slow ventricular rate (44/min);

(2) Downsloping ST-segment depression with biphasic T waves (in leads I, II, aVF, V4 ∼ V6);

(3) ST-segment elevation with a convex upward curve (in lead aVR);

(4) Shortened QT interval 300 ms (<320 ms);

(5) The longest R-R interval (1.87 s).

During hospitalization, telemetry consistently showed atrial fibrillation with a ventricular rate fluctuating between 38 and 60/min. Supportive therapy led to the gradual resolution of vomiting, with notable improvements in the patient's mental state and appetite. The ventricular rate associated with atrial fibrillation gradually increased. A follow-up ECG on March 28th showed atrial fibrillation with a ventricular rate of 74/min, normal QRS duration, and a normalized QT interval, with the ST segment and T waves returning to normal (Fig. 2). The patient was discharged on April 2nd.

Fig. 2.

The 12‑lead electrocardiogram (2024-03-28 20:54:59).

Atrial fibrillation (ventricular rate 74/min), QRS <120 ms, normal QT interval, and normalized ST segments and T waves.

Discussion

Acute aconitine poisoning typically presents with cardiovascular symptoms such as hypotension, sinus bradycardia, palpitations, chest pain, ventricular tachycardia, and ventricular fibrillation [2]. Aconitine causes arrhythmias through abnormal vagal stimulation, altered ion channel function in cardiomyocytes, gap junction protein dephosphorylation, mitochondrial energy metabolism disorders, and oxidative damage to cardiomyocytes. Additionally, gastrointestinal adverse reactions such as severe nausea, vomiting, and diarrhea can also occur, often leading to electrolyte imbalances such as hypokalemia and hypomagnesemia, which further increase myocardial excitability and ectopic pacemaker automaticity. High doses (1–10 μmol/L) of aconitine induce calcium dysregulation and calcium transients in cardiomyocytes, while low doses (5–20 nmol/L) enhance mitochondrial energy metabolism, indicating a dose-dependent toxic effect [4]. The toxic dose of aconitine in humans is 0. 2 mg, with a lethal dose ranging from 2 mg to 5 mg.

Ventricular tachycardia and ventricular fibrillation, which are life-threatening arrhythmias, are leading causes of death in aconitine poisoning, with an in-hospital mortality rate of approximately 5.5 % [1,5]. There is no specific antidote for aconitine poisoning, but symptomatic treatment with antiarrhythmic drugs such as amiodarone and lidocaine can be effective [6]. Aconitine also activates the ventromedial nucleus of the hypothalamus, which is associated with circulatory inhibition, leading to hypotension and sinus bradycardia. Sinus bradycardia typically responds well to atropine, while hypotension can be effectively managed with intravenous fluids and vasopressor infusions, such as dopamine [7]. Previous research has established a rat model of bradycardia and hypotension using aconitine [8], and clinical reports of aconitine poisoning leading to sinus bradycardia and hypotension exist [9]. However, slow ventricular arrhythmias in the context of aconitine poisoning have not been reported in the literature.

This case report details a patient with altered mental status, vomiting, and anorexia. Upon admission, the ECG showed atrial fibrillation with a slow ventricular rate. However, a review of previous medical records revealed that the patient had atrial fibrillation with a rapid ventricular rate (108/min) in December 2023. The significant reduction in ventricular rate in the absence of rate-slowing medications suggested an alternative mechanism. Further inquiry about recent medication uncovered the patient's ingestion of a Fuzi-containing herbal medicine. The combination of neurological and gastrointestinal symptoms suggested aconitine poisoning as the underlying cause. It should be noted that serum aconitine concentrations were not measured, so direct confirmation of exposure was not possible. Supportive treatment led to symptom improvement and an increase in ventricular rate, supporting the diagnosis.

The patient's admission ECG (2024-03-23 20:48) (Fig. 1) showed: (1) atrial fibrillation with a slow ventricular rate (44/min), (2) downsloping ST segments with biphasic T waves (leads I, II, aVF, V4-V6), (3) ST segment elevation in lead aVR, (4) a shortened QT interval of 300 ms (< 320 ms), and (5) the longest R-R interval of 1. 87 s. Five days later, a follow-up ECG on March 28, 2024 at 20:54:59 (Fig. 2) showed improvement: atrial fibrillation with a ventricular rate of 74/min, normal QRS duration, and a normal QT interval, with normalized ST segment and T waves. Notably, the patient's initial ECG, without the use of digitalis, showed a fishhook-like ST segment pattern, which was hypothesized to be related to aconitine poisoning. The downsloping ST segments with biphasic T waves and shortened QT interval resembled the fishhook effect of digitalis (Fig. 3).

Fig. 3.

The ST segment of the electrocardiogram slopes down and resembles a ladle handle, which is referred to as a ladle-like or fishhook-like ST-segment change.

The electrocardiographic manifestation of aconitine poisoning has not been reported in the literature. It is hypothesized that the mechanism of the fishhook-like ST segment is due to aconitine's delaying effect on myocardial repolarization, resulting in specific ST-T changes. The ST segment slopes downward and merges with the front slope of the T wave, forming a straight downward incline, while the rear slope of the T wave is short and rises abruptly, creating an inverted and asymmetric waveform (fishhook-like). In lead aVR, the QRS complex has a downward main wave, and the ST segment is elevated. The Q-T interval is shortened due to enhanced myocardial contractility. This heightened myocardial activity can also lead to arrhythmias. Early recognition of ECG changes that resemble fishhook-like patterns can aid in the early diagnosis and treatment of aconitine poisoning.

Conclusion

As China's international influence continues to expand, traditional Chinese medicine, rooted in thousands of years of practices, is gaining recognition and adoption in many Western countries, offering significant potential to improve health. However, a single Chinese herbal medicine can be either a therapeutic drug or a lethal poison, depending on the dosage and form, making it crucial to determine the optimal drug dosage for specific diseases. In daily clinical practice, healthcare workers should thoroughly inquire about patients' medical and medication histories, continuously update their knowledge to make accurate diagnosis, and deliver evidence-based treatments promptly when adverse drug reactions occur.

Declaration of competing interest

The authors report no financial relationships or conflicts of interest regarding the contents of the manuscript.