Why do Torsades de Pointes (TdP) have a sinusoidal appearance, and what is the underlying physiopathological mechanism?

From the Guidelines

Torsades de Pointes (TdP) has a sinusoidal appearance due to its characteristic twisting pattern of QRS complexes around the isoelectric line, resembling a spindle or "twisting of the points," which occurs as a result of early afterdepolarizations (EADs) developing in the setting of prolonged ventricular repolarization (long QT interval) 1. The pathophysiological mechanism involves abnormal calcium handling in cardiac cells during phase 2 and 3 of the action potential, where delayed repolarization allows calcium channels to reactivate, triggering premature depolarizations. Some key points to consider in the context of TdP include:

• The role of medications that prolong the QT interval, such as certain antiarrhythmics, antipsychotics, and antibiotics, in triggering TdP 1
• The importance of electrolyte abnormalities, particularly hypokalemia and hypomagnesemia, in the development of TdP 1
• The potential for bradycardia and congenital long QT syndromes to contribute to the risk of TdP 1
• The use of intravenous magnesium sulfate as a first-line agent to terminate TdP, regardless of the serum magnesium level 1 The sinusoidal pattern of TdP reflects the continuous change in ventricular activation sequence as the arrhythmia circulates through the myocardium, with varying amplitudes creating the spindle-shaped appearance on ECG. Key factors to consider in the prevention and management of TdP include:
• Awareness of individual risk factors and ECG signs of drug-induced long QT syndrome (LQTS) 1
• Recognition of ECG harbingers of TdP, such as marked QTc prolongation, QT-U prolongation and distortion, and episodes of polymorphic ventricular tachycardia 1
• The importance of correcting electrolyte abnormalities and other exacerbating factors, including the prevention of bradycardia and long pauses with temporary pacing if necessary 1

From the Research

Torsades de Pointes (TdP) Characteristics

• TdP is a polymorphic ventricular tachycardia associated with QT interval prolongation 2, 3, 4, 5, 6
• It is characterized by a sinusoidal appearance on the surface electrocardiogram 4
• TdP episodes are usually short-lasting and terminate spontaneously, but may recur and persist, leading to syncope or sudden death 4

Underlying Physiopathological Mechanism

• The underlying mechanism of TdP involves abnormalities of ventricular repolarization, which can be congenital or acquired 4, 6
• Acquired factors that contribute to TdP include pause-dependent torsades, paroxysmal bradycardia, drugs that prolong repolarization, and potassium and magnesium deficiencies 4
• The electrophysiological mechanisms of TdP comprise reentry and afterdepolarization-induced activity, with genetic factors playing a role in some cases 4

Precipitating Factors

• Precipitating factors for TdP include electrolyte imbalance (hypokalemia, hypomagnesemia), slow heart rate, and certain drugs (e.g. type IA antiarrhythmic agents, methadone, cocaine) 2, 3, 5, 6
• Other factors that may contribute to TdP include cardiac disease, hypoxia, and starvation 5, 6

Treatment

• Treatment of TdP aims to shorten the QT interval and prevent recurrence of the arrhythmia 2, 5
• Effective treatments include intravenous magnesium sulfate, isoproterenol infusion, cardiac pacing, and correction of underlying electrolyte abnormalities 2, 3, 4, 5