Propafenone Overdose: From Cardiogenic Shock to Brugada Pattern

Gil, Júlio; Marmelo, Bruno; Abreu, Luís; Antunes, Hugo; Santos, Luís; Cabral, José Costa

doi:10.5935/abc.20180033

Cited by 5 publications

(6 citation statements)

References 7 publications

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“…As TC can occur due to high catecholamines and positive inotropic agents, using these agents as they were merely needed is crucial. Brugada pattern and acute ST-segment elevation myocardial infarction-like ECG development secondary to propafenone intake has been reported (12)(13)(14)(15)(16)(17)(18). The detection of the Brugada pattern and acute inferior ST-segment elevation myocardial infarction-like ECG in the ECG follow-ups of our case supports the current publications.…”

Section: Discussionsupporting

confidence: 89%

“…Therefore, these changes were attributed to propafenone-induced Brugada phenocopy. Due to the first-pass hepatic elimination effect, bioavailability is not predictable and the elimination half-life of propafenone varies depending on whether the patient's metabolizing pathways are weak or vigorous (18)(19)(20). These individual differences and important clinical changes necessitate close ECG follow-up after propafenone initiation.…”

Section: Discussionmentioning

confidence: 99%

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Propafenona Bağlı Gelişen Takotsubo Kardiyomiyopatisi: Sadece Bir Tesadüf mü, Yeni Bir Nedensel İlişki mi?

ÇAKAN,

ADAR

2023

Düzce Tıp Fakültesi Dergisi

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Propafenone is a class 1C antiarrhythmic drug that blocks sodium channels and is used in the treatment of arrhythmia. Because of its rapid effect on terminating paroxysmal episodes of atrial fibrillation, it can be used as a pill-in-the-pocket. In patients with structural heart disease, it is less preferred due to cardiotoxic effects in long-term use. Although propafenone use is known to cause several cardiovascular side effects, the development of Takotsubo cardiomyopathy is unknown. Propafenone toxicity at standard doses is a rare condition. Propafenone plasma concentrations may increase through inhibition of cytochrome P450 2D6 and complete inhibition of 2D6 metabolism can increase propafenone levels by up to 3 to 10 times. In this case report, we aimed to present a 37-year-old female patient who developed Takotsubo cardiomyopathy and cardiogenic shock after the first dose of propafenone use and recovered with medical treatment.

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Section: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 99%

Propafenona Bağlı Gelişen Takotsubo Kardiyomiyopatisi: Sadece Bir Tesadüf mü, Yeni Bir Nedensel İlişki mi?

ÇAKAN,

ADAR

2023

Düzce Tıp Fakültesi Dergisi

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“…However, we corroborated collateral history from the spouse with that of the patient, and it is highly likely that the toxicity was from propafenone and propranolol ingestion, rather than just a single agent. The presence of type-1 Brugada pattern, seen in both propranolol toxicity and propafenone toxicity 9,11 and the presence of generalized tonic-clinic seizures (also a clinical sign of toxicity caused by both agents) support this. 12 In summary, patients suffering from an overdose of combined therapy have been used.…”

Section: Discussionmentioning

confidence: 82%

“…Lipid emulsion therapy has been successfully used in treating lipophilic drug poisoning (eg, from propranolol) by acting as a “lipid‐sink” that attracts substances away from the brain and heart and toward the lipid‐sink preventing toxic accumulation of the substances in those tissues 14 . In addition to the aforementioned treatments, we believe that early administration of NaHCO 3 should take place in patients exhibiting signs of Na‐channel blockade, due to its ability to prevent cardiac dysrhythmias by reversing Na‐channel blockade 11 …”

Section: Discussionmentioning

confidence: 99%

Propafenone and propranolol dual toxicity

et al. 2020

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Propranolol is a highly lipid‐soluble beta‐receptor antagonist and propafenone is a potent class 1c anti‐arrhythmic agent with strong Na‐channel blockade effect. We describe a novel case of dual overdose of propafenone and propranolol resulting in hypotension, generalized seizures, and reduced level of consciousness that was successfully treated. A 52‐year‐old female ingested 500 mg of propranolol and 1.5 g of propafenone. The patient was brought to the emergency department (ED) and exhibited signs of systemic toxicity and reduced level of consciousness. The patient was treated as a case of combined β‐blocker and propafenone toxicity using high dose insulin, NaHCO 3 , glucagon, atropine, and dopamine. She started improving and becoming more alert, with subsequent ECGs revealing normal sinus rhythm. The patient was discharged 4 days later. We believe that early administration of NaHCO 3 should be administered in patients exhibiting signs of Na‐channel blockade.

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“…The toxic effect (poisoning) of PPF occurs mainly in the case of intentional self-harm when higher doses of PPF are administered, which may or may not result in death. In these cases, symptoms such as collapse, vomiting and unresponsiveness, different levels of the Glasgow Coma Scale, a ventricular escape rhythm and intraventricular conduction, delayed bradycardia, hypotension, QRS prolongation and a corrected QT interval, generalized tonic-clonic seizures and cardiac arrest have been observed [13][14][15][16]. Fatal cases of PPF intoxication (five were intentional suicides and one was accidental) are rarer, characterized by significantly higher PPF concentrations in the blood than during therapy [17][18][19][20][21].…”

Section: Introductionmentioning

confidence: 99%

A Tissue Distribution Study of Propafenone in an Intentional Fatal Poisoning Case

Nižnanská,

Hengerics Szabó,

Masár

et al. 2024

IJMS

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Propafenone (PPF) belongs to the class 1C antiarrhythmics and can cause electrocardiogram-associated adverse/toxic effects. Cases of PPF intoxication are rarely investigated. We developed a novel and selective GC-MS/MS method for the determination of PPF and its tissue distribution in an intentional fatal poisoning case, which is applicable to PPF quantification in the range of therapeutic to lethal concentrations in complex post-mortem samples. A simple and effective sample pretreatment was applied to all analyzed samples. PPF was determined without the need for dilution, even in highly complex samples containing a wide range of analyte concentrations. Quantification was performed using the standard addition method, developed and validated according to the ICH M10 guidelines. The obtained results indicated that the PPF concentration in the serum from blood taken while alive, before therapy, was the highest ever reported in the literature. Despite the intensive therapy after the patients’ admission, the PPF concentrations in the lungs, spleen, femoral blood and cardiac blood were fatal or abnormally high. On the other hand, the concentrations in the liver and skeletal muscle were lower or approximately the same as observed in cases with therapeutic doses. To the best of our knowledge, the distribution of PPF has not been investigated in fatal intoxication cases and can be helpful in clinical or forensic toxicology.

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Propafenone Overdose: From Cardiogenic Shock to Brugada Pattern

Cited by 5 publications

References 7 publications

Propafenona Bağlı Gelişen Takotsubo Kardiyomiyopatisi: Sadece Bir Tesadüf mü, Yeni Bir Nedensel İlişki mi?

Propafenona Bağlı Gelişen Takotsubo Kardiyomiyopatisi: Sadece Bir Tesadüf mü, Yeni Bir Nedensel İlişki mi?

Propafenone and propranolol dual toxicity

A Tissue Distribution Study of Propafenone in an Intentional Fatal Poisoning Case

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