Long QT syndrome

Nearly half of patients with LQTS never have a symptom - SADS Foundation

Long QT syndrome
Long QT syndrome

image by: Rachel's Long QT Foundation

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Why parents must know about Long QT Syndrome

On August 30th, 1997, my seemingly healthy 22 -year-old daughter, Emilie, died suddenly in her sleep from sudden cardiac arrest (SCA). How could a beautiful, healthy young woman just go to bed and die in such a mysterious manner? It’s an understatement to say we were in shock, or grief-stricken. Losing a child was the hardest thing I’ve ever faced.

An autopsy showed only “Acute Cardiac Arrhythmia.” Emilie’s toxicology report was totally negative and the Medical Examiner offered our family no other information about the cause of death.

We had only a few clues. On Emilie’s second day of life she had been observed having a “seizure,” and a nurse told us she appeared somewhat…

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 Why parents must know about Long QT Syndrome

Emilie saw cardiologists. Her tests were interpreted as normal. The cardiologist’s explanation was that she was tall and thin, and that she was just feeling irregular heartbeats that we all have at times (but which are not clinically significant and which we may not feel). Unfortunately, we accepted this diagnosis. We now know that she should have seen a pediatric cardiologist, even in 9th grade.

Long QT Syndrome australia

Long QT syndrome is usually diagnosed after a person has a cardiac event (eg, syncope, cardiac arrest). In some situations, this condition is diagnosed after a family member suddenly dies. In some individuals, the diagnosis is made when an electrocardiogram shows QT prolongation. A history of cardiac events is the most typical clinical presentation in patients with LQTS.


RhythmFirstTM and RhythmNextTM are multi-gene panels for patients with long QT syndrome (LQTS) that can be ordered individually or on a reflex basis.

British Heart Foundation

LQTS may be genetically inherited, but it can also be caused by certain medications you may be taking for other medical conditions. There are two types of LQTS. In most cases, the condition delays the flow of potassium ions out of heart muscle cells. However, for a small number of people, the sodium channels are affected and too many sodium ions are allowed into the cells.


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Heart & Stroke

If you have LQTS, your heart’s structure is perfectly normal, but you may have fast, chaotic heartbeats. The fast heartbeats may cause a sudden fainting spell or a seizure. In some cases, the heart can stop and cause sudden death. Long QT is treatable.

SADS Foundation

LQTS is a disturbance of the heart’s electrical system. It is caused by abnormalities of microscopic pores (proteins) in the heart cells called ion channels. Nearly half of patients with LQTS NEVER have a symptom!

Life in The Fastlane

normal QT = < 440ms (two large squares) – prolonged QT > 450ms produces prolonged ventricular repolarisation -> predisposes to malignant ventricular arrhythmias


You can be born with a genetic mutation that puts you at risk of long QT syndrome. In addition, certain medications and medical conditions might cause long QT syndrome. Long QT syndrome is treatable.


Long QT syndrome causes problems with the electrical activity of the heart. It's uncommon, occurring in around 1 in every 2,000 people. Long QT syndrome is often the result of a faulty gene that's inherited from one of your parents. The abnormal gene causes an imbalance in the chemicals that create the electric impulses in your heart. The syndrome can also be caused by medicines for other conditions.


Beta blockers are medicines that prevent the heart from beating faster in response to physical or emotional stress. Most people who have LQTS are treated with beta blockers. Doctors may suggest that people who have LQTS 3 take sodium channel blockers, such as mexiletine. These medicines make sodium ion channels less active.


The causes of QT interval prolongation can be divided into congenital or acquired. Congenital causes are usually a result of mutations in ion channels (potassium, calcium, or sodium) with more than 15 identified mutations. In contrast, acquired QT interval prolongation may be a result of electrolyte abnormalities, and/or drugs that affect those ion channels.

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