Torsades de pointes medicamentos

Torsade de pointes

The proposed cellular mechanism of drug-induced prolonged QT interval involves inhibition of the rapid component of the delayed rectifier potassium current IKr. This excess of positively charged ions leads to an extended repolarization phase, resulting in a prolonged QT interval and causing arrhythmias such as TdP. This TdP trigger is seen as a premature ventricular complex PVC that is generated during the prolonged repolarization phase, also known as the R-on-T phenomenon.

Similarly, prior to the availability of fexofenadine, astemizole was approved by the FDA in , but its manufacturer voluntarily withdrew it from the market in due to safety issues, most notably QT prolongation following inhibition of hepatic metabolism by other drugs. Many distinct genetic mutations and polymorphisms lead to congenital long QT syndrome, which occurs in about 0.

Risk Factors for Torsades de Pointes 1 , There is an extensive list of medications that can prolong the QT interval and cause TdP, some of which are listed in Table 2. Drug interactions involving the inhibition of metabolism have contributed to the removal of a number of medications from the U. Terfenadine was removed from the market in early , once the safer, nonsedating antihistamine fexofenadine became available; it did not prolong the QT interval.

CredibleMeds develops educational and research programs and provides resources for medical professionals, researchers, and consumers. Droperidol Inapsine, Taylor Pharmaceuticals was approved by the FDA in as an injectable antiemetic for patients undergoing surgical and diagnostic procedures. Many of these drugs are common in clinical practice, such as antiarrhythmics, antimicrobials, antipsychotics, antihistamines, and antiemetics.

However, it is possible for TdP to degenerate to ventricular fibrillation and cause sudden cardiac death.

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The authors describe the causes, risk factors, symptoms, diagnosis, and treatment of TdP. This column strays a bit from its regular format no patient case is included to discuss a drug-related adverse event that often goes undiagnosed or underdiagnosed. Every medication has the potential to cause disease, but clinicians are often slow to recognize drug therapy as an etiological factor.

Drugs by themselves can cause them in patients with underlying risk to be discussed , and also in the setting of polypharmacy. Subsequently, safer antiemetics were approved by the FDA and utilized. Sometimes TdP is self-limiting and can spontaneously resolve. Some medication classes, notably anti-arrhythmics and fluoroquinolones, indirectly affect the heart via heterogeneity of transmural ventricular repolarization among the three principal cell types of the heart: endocardial, myocardial, and epicardial cells.

All pharmaceuticals carry a risk of ADRs, whether they are new and improved, generic agents, older brand products, complex biologics, or biosimilars. Drug-induced QT prolongation is defined as a QTc of ms or greater or an increase of 60 ms or greater in the QT interval compared with the premedication baseline interval. As noted above, a number of medications have been withdrawn from the U. Medications that directly affect the electrophysiology of the heart can prolong the QT interval.

QTc prolongation may be acquired secondary or congenital primary. Other times, it can degenerate into ventricular fibrillation and death.

Torsades de Pointes: Symptoms, Causes, Treatment, and More

I encourage anyone with a potential case or related idea to contact me at moc. A list of the risk factors for TdP can be seen in Table 1. In addition, any patient who presents to the emergency department following an overdose of a QT-prolonging drug should be evaluated for TdP. Other conditions to consider in the differential diagnosis for drug-induced TdP include: atrial fibrillation, atrial flutter, atrial tachycardia, atrioventricular node re-entrant tachycardia, monomorphic ventricular tachycardia, non-TdP polymorphic ventricular tachycardia, and sinus tachycardia.

Drug-induced QT prolongation and torsades de pointes TdP are probably more prevalent than clinicians might think. QT prolongation is one of the most infamous adverse drug reactions taught in pharmacy curricula because it can lead to sudden cardiac death. Cisapride Propulsid, Janssen , a pro-kinetic agent used as a treatment for gastroesophageal reflux disease, was approved by the FDA in and withdrawn from the market worldwide in January due to the occurrence of QT prolongation, ventricular arrhythmia, and sudden cardiac death due to inhibition of cisapride metabolism by CYP3A4 from other drugs.

The development of TdP is multi-factorial.

Federal government websites often end in. Welcome to the Pharmacovigilance Forum, where we report on interesting adverse drug reactions ADRs , including drug-induced disease. Torsades de pointes TdP —an uncommon but life-threatening polymorphic ventricular tachycardia—is almost always drug induced. It has built and utilizes a novel, risk-stratification—based approach to reducing medication harm and drug—drug interactions, particularly for those drugs that prolong the QT interval and increase the risk for TdP.

The symptoms of TdP are similar to other tachyarrhythmias related to heart rate, blood pressure, and cardiac output. A patient presenting with any of the above symptoms should be evaluated for TdP. Drug-induced TdP can occur at different times while the patient is receiving the offending oral agent s. TdP, an uncommon polymorphic ventricular tachycardia, is characterized by a gradual change in the amplitude and twisting of the QRS complexes around the isoelectric line on an electrocardiogram.

There is no threshold of QTc prolongation at which TdP is certain to occur. The site is secure.