An electrocardiogram (EKG) translates the heart’s electrical activity into a series of waves and segments. The ST segment is a specific portion of this tracing, representing the period between the end of ventricular depolarization (contraction) and the beginning of ventricular repolarization (recovery). This segment should normally appear flat or “isoelectric” on the EKG. A “long” ST segment indicates an abnormal delay in the heart’s electrical recovery time, suggesting an underlying issue with the flow of ions that regulate the heart’s rhythm.
The ST Segment and the Prolonged QT Interval
The phrase “long ST segment” points toward the more clinically relevant measurement known as the QT interval. The QT interval spans from the start of the Q wave to the end of the T wave, encompassing the entire period required for the ventricles to depolarize and repolarize. Since the ST segment occurs between these two electrical events, a longer ST segment effectively lengthens the entire QT interval. Because heart rate affects the QT interval duration, clinicians use the corrected QT interval (QTc) for standardized measurement. A prolonged QTc interval signals that heart muscle cells are taking too long to reset their electrical charge after each beat, creating a state of electrical vulnerability.
Inherited and Acquired Causes of Extended Repolarization
The underlying reasons for this extended electrical recovery fall into two primary categories: acquired and inherited. Acquired causes are the most common, frequently involving exposure to medications that interfere with the heart’s ion channels.
- Antibiotics (e.g., azithromycin)
- Antiarrhythmics
- Antipsychotic medications
- Antidepressants
Another frequent acquired cause is an imbalance in the body’s electrolytes, specifically low levels of potassium (hypokalemia), magnesium (hypomagnesemia), or calcium (hypocalcemia). These minerals are necessary for the proper functioning of the ion channels that govern the flow of electrical current across the heart muscle cell membrane. Conditions such as severe bradycardia or significant structural heart disease can also contribute to this acquired form of extended repolarization.
Inherited causes, though less common, are often more severe and are collectively known as congenital Long QT Syndrome (LQTS). This condition is caused by genetic mutations that affect the structure or function of the ion channels responsible for potassium and sodium flow within the heart cells. These channel defects prevent the heart from repolarizing efficiently, leading to a chronically prolonged QT interval. LQTS can be present from birth and may cause symptoms in childhood or adolescence.
The Risk of Life-Threatening Arrhythmias
The central danger posed by extended repolarization is the creation of an unstable electrical environment within the ventricles. When the heart muscle takes too long to reset, it becomes susceptible to an abnormal electrical trigger that can initiate a chaotic rhythm. This electrical instability is due to early afterdepolarization, where a second electrical impulse fires before the heart is fully recovered.
The most serious arrhythmia associated with a prolonged QTc is Torsades de Pointes (TdP), a specific type of polymorphic ventricular tachycardia. TdP, which translates to “twisting of the points,” is characterized on the EKG by QRS complexes that oscillate and twist around the baseline. This rapid, disorganized rhythm can cause dizziness or fainting, but it frequently degenerates into ventricular fibrillation, leading to sudden cardiac arrest. The risk of developing TdP increases once the QTc measurement exceeds 500 milliseconds.
Confirmation and Treatment Approaches
The evaluation of a prolonged ST segment begins with a careful review of the patient’s EKG and a comprehensive assessment of all medications and supplements. If the initial EKG shows a prolonged QTc, further monitoring may involve a Holter monitor to capture electrical activity, especially if symptoms like syncope or palpitations are present. Genetic testing can be used to confirm a diagnosis of congenital LQTS when acquired causes are ruled out.
Management for acquired prolonged QTc focuses on immediately removing the precipitating factor. This includes discontinuing the offending medication, which typically allows the QTc interval to return to a normal range. It is also necessary to quickly correct any electrolyte abnormalities, focusing on raising low levels of potassium and magnesium.
In contrast, the management of inherited LQTS or high-risk acquired cases requires long-term intervention. Pharmacological treatment typically involves beta-blockers, such as nadolol or propranolol, which help stabilize the heart’s electrical activity by blocking sympathetic stimulation. For patients who have experienced cardiac arrest or have recurrent symptoms despite medication, an Implantable Cardioverter-Defibrillator (ICD) may be necessary to deliver an electrical shock to terminate TdP and prevent sudden death.