Why Are Beta Blockers Used In Long QT Syndrome?

Like an electrical appliance, heart also works on the proper conduction of electricity in the form of electrical signals. However, heart is more complex than any other man-made machine and as it is a vital organ, any abnormality in the electric conductivity will have a life-threatening repercussion. Long QT Syndrome (LQTS) is one such event that emerges when there is an abnormal electrical conductivity. There is no proper rhythm in the conduction of electrical impulses thus leading to long QT interval, which is diagnosed by an Electrocardiograph. The LQTS may be congenital i.e. the condition may be present from birth or acquired i.e. the disease is acquired after birth. Causes of the condition may include electrolytic imbalance and drugs. Further, people having family history of having long QT syndrome are at greater risk than those who do not have family history.

Why Are Beta Blockers Used In Long QT Syndrome?

Beta blockers are the most common therapy in the management of long QT syndrome. It is appropriate to state that these drugs are currently the mainstay of the LQTS management. Nadolol is the preferred choice in the treatment of LQTS when the patient can tolerate this drug. Beta blockers are recommended to the patients of LQTS as these drugs are effective in reducing the symptoms related to long QT syndrome such as syncope. Beta blockers reduce the tachycardia-induced effects in patients with LQTS. These drugs are also effective in shortening the QT and QTc interval in the exercise induced faster heart rates. Beta blockers decrease the QT interval when the heart rate is high while increasing the QT interval at the lower heart rate. In the research studies, nadolol is found to highly effective in risk reduction in the patients with LQT2.

It has been noted that in cases where a beta blocker is prescribed to patients, in almost all the cases of beta blocker therapy failure, the reason is non-adherence to the therapy and administration of the drug inducing prolong QT interval. Further, use of beta blocker is also advised to patients who are asymptomatic. The mechanism of action, through which beta blockers exerts their action is the blockage of adrenergic receptors which reduces the risk of cardiac arrhythmia. However, the efficacy of beta blockers differs when it comes to the type of long QT syndrome to be treated. For instance, in LQT1, metoprolol is noneffective while propranolol and nadolol are effective. Further, in LQT2, only nadolol is effective. This may be due to the differences in their pharmacokinetic as well as pharmacodynamic parameter. Metoprolol has no or very little effect on the ion conduction. Nadolol is a long acting drug thus provides its effect for a longer period of time. Further it does not have intrinsic sympathomimetic activity. It also exerts effect on the ion conduction. The reason why propranolol is not effective in LQT2 is not conclusively known but the proposed mechanism is that it blocks Ikr at higher concentration.

As the electrical conduction of the heart is not up to the mark, the net result is the reduced flow of blood to the organs. Thus, the patient may experience fatigue. Further, if the brain does not have the proper supply of blood, the patient may also experience syncope. The symptoms of the condition are more pronounced when the patient exposes himself to energy-demanding tasks such as strenuous exercises. In many cases, the condition remains undiagnosed and only comes in knowledge when the patient undergoes a routine checkup. If the long QT syndrome is not properly managed, the patient may experience a cardiac arrest which may be fatal.


Long QT syndrome is a condition of abnormal conduction of electrical impulses, which leads to cardiac arrhythmia and may lead to fatal cardiac arrest. Beta blockers remain the mainstay of treatment due to their adrenergic blocking activity, which reduces the cardiac arrhythmia and also reduces mortality and syncope. Nadolol is the preferred choice and should be considered as first line therapy due to its beneficial effect on both LQT1 and LQT2.

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