Instruct: Given a question, retrieve relevant documents that can help answer the question.
Query: What else can cause Long QT?
There are several subtypes of long QT syndrome. These can be broadly split into those caused by genetic mutations which those affected are born with, carry throughout their lives, and can pass on to their children (inherited or congenital long QT syndrome), and those caused by other factors which cannot be passed on and are often reversible (acquired long QT syndrome).
A sudden death in a young person can be caused by heart disease (including cardiomyopathy, congenital heart disease, myocarditis, genetic connective tissue disorders, or conduction disease), medication-related causes or other causes. Rare diseases called channelopathies may play a role such as long QT syndrome (LQTS), Brugada syndrome (BrS), CPVT (catecholaminergic polymorphic ventricular tachycardia), PCCD (progressive cardiac conduction defect), early repolarisation syndrome, mixed sodium channel disease, and short QT syndrome. No cause of death is found, even after extensive examination in 5% of cases.
Jervell and Lange-Nielsen syndrome (JLNS) is a type of long QT syndrome associated with severe, bilateral sensorineural hearing loss. Long QT syndrome causes the cardiac muscle to take longer than usual to recharge between beats. If untreated, the irregular heartbeats, called arrhythmias, can lead to fainting, seizures, or sudden death. It was first described by Anton Jervell and Fred Lange-Nielsen in 1957.
The symptoms of this condition are:
The clinical signs are:
Loss of function mutations in this channel may lead to long QT syndrome (LQT2), while gain of function mutations may lead to short QT syndrome. Both clinical disorders stem from ion channel dysfunction (so-called channelopathies) that can lead to the risk of potentially fatal cardiac arrhythmias (e.g., "torsades de pointes"), due to repolarization disturbances of the cardiac action potential. There are far more hERG mutations described for long QT syndrome than for short QT syndrome.
Inherited or sporadic KCNE gene mutations can cause Romano-Ward syndrome (heterozygotes) and Jervell Lange-Nielsens syndrome (homozygotes). Both these syndromes are characterized by Long QT syndrome, a delay in ventricular repolarization. In addition, Jervell and Lange-Nielsen syndrome also involves bilateral sensorineural deafness. Mutation D76N in the KCNE1 protein can lead to long QT syndrome due to structural changes in the KvLQT1/KCNE1 complex, and people with these mutations are advised to avoid triggers of cardiac arrhythmia and prolonged QT intervals, such as stress or strenuous exercise.
Long QT syndrome (LQTS) is a condition which affects repolarization of the heart after a heartbeat.[4] This results in an increased risk of an irregular heartbeat which can result in palpitations, fainting, drowning, or sudden death.[1] These episodes can be triggered by exercise or stress.[5] Other associated symptoms may include hearing loss.[1]
Hypothyroidism, a condition of low function of the thyroid gland, can cause QT prolongation at the electrocardiogram. Acute hypocalcemia causes prolongation of the QT interval, which may lead to ventricular dysrhythmias.
Clarithromycin can lead to a prolonged QT interval. In patients with long QT syndrome, cardiac disease, or patients taking other QT-prolonging medications, this can increase risk for life-threatening arrhythmias.
Anderson-Tawil syndrome affects the heart by prolonging the QT interval, a measure of how long it takes the heart to relax after each heart beat. This, as in other forms of long QT syndrome, can lead to abnormal heart rhythms such as ventricular ectopy or ventricular tachycardia causing palpitations. The ventricular tachycardia seen in Anderson-Tawil syndrome often takes a form known as bidirectional ventricular tachycardia. The arrhythmias seen in association with the condition can cause sudden cardiac death, but the risk of this is lower than in other forms of Long QT syndrome. 
Common causes for torsades de pointes include diarrhea, low blood magnesium, and low blood potassium. It is commonly seen in malnourished individuals and chronic alcoholics, due to a deficiency in potassium and/or magnesium. Certain combinations of drugs resulting in drug interactions can contribute to torsades de pointes risk. QT prolonging medications such as clarithromycin, levofloxacin, or haloperidol, when taken concurrently with cytochrome P450 inhibitors, such as fluoxetine, cimetidine, or particular foods including grapefruit, can result in higher-than-normal levels of medications that prolong the QT interval in the bloodstream and therefore increase a person's risk of developing torsades de pointes. In addition, inherited long QT syndrome significantly increases the risk of episodes of TdP.
The ECG tracing in torsades demonstrates a "polymorphic ventricular tachycardia" with a characteristic illusion of a twisting of the QRS complex around the isoelectric baseline (peaks, which are at first pointing up, appear to be pointing down for subsequent "beats" when looking at ECG traces of the "heartbeat"). It is hemodynamically unstable and causes a sudden drop in arterial blood pressure, leading to dizziness and fainting. Depending on their cause, most individual episodes of torsades de pointes revert to normal sinus rhythm within a few seconds; however, episodes may also persist and possibly degenerate into ventricular fibrillation, leading to sudden death in the absence of prompt medical intervention. Torsades de pointes is associated with long QT syndrome, a condition whereby prolonged QT intervals are visible on an ECG. Long QT intervals predispose the patient to an , wherein the R-wave, representing ventricular depolarization, occurs during the relative refractory period at the end of repolarization (represented by the latter half of the T-wave). An R-on-T can initiate torsades. Sometimes, pathologic T-U waves may be seen in the ECG before the initiation of torsades.
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Inherited, or congenital Long QT syndrome, is caused by genetic abnormalities. LQTS can arise from mutations in several genes, leading in some cases to quite different features.[19] The condition is most commonly inherited in an autosomal dominant manner, or rarely in an autosomal recessive fashion.[20] The autosomal recessive forms of LQTS tend to have a more severe phenotype. Genetic testing for LQTS is clinically available and may help to direct appropriate therapies.
Genetic variants causing LQTS tend to prolong the duration of the ventricular action potential (APD), thus lengthening the QT interval. The most common causes of LQTS are mutations in the genes KCNQ1 (LQT1), KCNH2 (LQT2), and SCN5A (LQT3). [4] The following is a list of genes associated with LQTS:
Almost half the sudden deaths of previously healthy children have no findings on autopsy. These children are referred to as having sudden unexplained death syndrome (SUDS). In the Olmsted County population study, six of the twelve cases died of unknown causes of SUDS. A lot of forensic pathologists blame a fatal arrhythmia of the heart to be the cause of SUDS due to the lethal disorders like long QT syndrome (LQTS). This is a prolonged QT interval in the heart’s natural rhythm. This is can leave no trace for an autopsy. The clinical signs of LQTS are syncope, seizures, or sudden death.
Andersen–Tawil syndrome, also called Andersen syndrome and Long QT syndrome 7, is a rare genetic disorder affecting several parts of the body. The condition is associated with a disturbance of the electrical function of the heart, specifically a long QT interval recorded on an electrocardiogram, which increases the risk of abnormal heart rhythms. It can be distinguished from other forms of Long QT syndrome by the characteristic physical features often seen in Andersen–Tawil syndrome including low-set ears and a small lower jaw, as well as intermittent periods of muscle weakness known as hypokalaemic periodic paralysis.
Polymorphic ventricular tachycardia, on the other hand, is most commonly caused by abnormalities of ventricular muscle repolarization. The predisposition to this problem usually manifests on the ECG as a prolongation of the QT interval. QT prolongation may be congenital or acquired. Congenital problems include long QT syndrome and catecholaminergic polymorphic ventricular tachycardia. Acquired problems are usually related to drug toxicity or electrolyte abnormalities, but can occur as a result of myocardial ischemia. Class III anti-arrhythmic drugs such as sotalol and amiodarone prolong the QT interval and may in some circumstances be pro-arrhythmic. Other relatively common drugs including some antibiotics and antihistamines may also be a danger, in particular in combination with one another. Problems with blood levels of potassium, magnesium and calcium may also contribute. High-dose magnesium is often used as an antidote in cardiac arrest protocols.
Romano-Ward syndrome can be distinguished clinically from other forms of Long QT by affecting only the electrical properties of the heart, while other forms of long QT can also affect other parts of the body. The condition may be treated using medication such as beta-blockers, an implantable cardioverter-defibrillator, or surgery to disrupt the sympathetic nervous system. 
This channel is also sensitive to drug binding, as well as decreased extracellular potassium levels, both of which can result in decreased channel function and drug-induced (acquired) long QT syndrome. Among the drugs that can cause QT prolongation, the more common ones include antiarrhythmics (especially Class 1A and Class III), anti-psychotic agents, and certain antibiotics (including quinolones and macrolides).
The company is conducting research with Columbia University and the Mayo Clinic to determine if the KardiaBand can identify early warning signs of Long QT syndrome, a cause of sudden death, especially in young people.
An abnormally prolonged QT interval could be due to long QT syndrome, whereas an abnormally shortened QT interval could be due to short QT syndrome.
Caution should be taken in people with a history of interstitial lung disease (ILD) were excluded from clinical trials, as the drug can cause severe ILD or pneumonia. Caution should also be taken in people with a predisposition to long QT syndrome as the drug can provoke this.
The QT interval is a measurement made on an electrocardiogram used to assess some of the electrical properties of the heart. It is calculated as the time from the start of the Q wave to the end of the T wave and approximates to the time taken from when the cardiac ventricles start to contract to when they finish relaxing. An abnormally long or abnormally short QT interval is associated with an increased risk of developing abnormal heart rhythms and sudden cardiac death. Abnormalities in the QT interval can be caused by genetic conditions such as Long QT syndrome, by certain medications such as sotalol, by disturbances in the concentrations of certain salts within the blood such as hypokalaemia, or by hormonal imbalances such as hypothyroidism.
The QT interval is often corrected for heart rate and is shown as QTc. Some conditions that can prolong the QTc interval are ischemic heart disease, autonomic dysfunction, bradycardia, electrolyte abnormalities, cardiac remodeling, and dehydration medications that interfere with the cardiac potassium ion channels. Which of these factors are seen in long-duration astronauts?The environment created by the combination of factors listed above might cause or exacerbate the prolongation of the QT interval.
Although Long QT syndrome is often a genetic condition, a prolonged QT interval associated with an increased risk of abnormal heart rhythms can also occur in people without a genetic abnormality, commonly due to a side effect of medications. Drug-induced QT prolongation is often a result of treatment by antiarrhythmic drugs such as amiodarone and sotalol, antibiotics such as erythomycin, or antihistamines such as terfenadine.[14] Other drugs which prolong the QT interval include some antipsychotics such as haloperidol and ziprasidone, and the antidepressant citalopram. [15] [13] Lists of medications associated with prolongation of the QT interval such as the QTdrugs database can be found online. [16]