Multifocal atrial tachycardia

Multifocal atrial tachycardia Microchapters
Overview
Historical Perspective
Pathophysiology
Causes
Epidemiology and Demographics
Natural History, Complications and Prognosis
Diagnosis
Treatment
Prevention
Differentiating Multifocal Atrial Tachycardia from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor-In-Chief: Sara Mohsin, M.D.[2], Cafer Zorkun, M.D., Ph.D. [3], Syed Hassan A. Kazmi BSc, MD [4]

Synonyms and keywords: MAT, Chaotic atrial tachycardia, Supraventricular tachycardia

Overview

Multifocal atrial tachycardia (MAT) is a cardiac arrhythmia which is specifically a type of supraventricular tachycardia with an irregular, rapid atrial rhythm arising from multiple ectopic foci within the atria with a heart rate exceeding 100 beats per minute. It is characterized by an organized atrial activity yielding three or more different non-sinus P wave morphologies in the same lead with variable or irregular PP, PR and RR intervals. There's an isoelectric baseline between P waves with the most P waves being conducted to the ventricles and some R waves being aberrantly conducted. This variability pattern makes MAT look irregular on the surface ECG, thus oftenly leading to misinterpretion as atrial fibrillation. It is typically seen in elderly patients with a variety of underlying comorbidities, the most common being chronic obstructive pulmonary disease (COPD) and congestive heart failure (CHF) and eventually it develops into atrial fibrillation. A rhythm with similar ECG characteristics but at a slow rate is referred to as multifocal atrial rhythm (MAR). The pathogenesis of MAT is not well understood and the patients are generally asymptomatic with mostly being hemodynamically stable. Typically, no treatment is required beyond treatment of underlying conditions in the majority of the MAT patients. However, it is very important to evaluate such patients as this arrhythmia is a poor prognostic sign in the setting of an acute illness.

Historical Perspective

• In the late 1960s, the term ''MAT'' became a commonplace terminology.
• In 2001, Bradley et al reported the clinical course of MAT in infants and children.

Pathophysiology

• The exact pathology behind production of MAT is not well understood, however, the multiple discrete p wave morphologies along with variable PR intervals suggest an atrial pacemaker activity most likely originating from multiple ectopic foci within the atria. Hence, each unique P wave corresponds to a different site of atrial origin.
• The possible underlying mechanism for MAT includes:
  • Right atrial enlargement
  • Hypoxia
  • Hypercapnia
  • Adrenergic stimulation in pulmonary disease
• MAT has been reported in >20% of the pediatric patients and up to 60% of the adult patients with coexisting pulmonary disease.
• The following factors are considered to be responsible for the infant-predominant age distribution of MAT and its favorable outcome in idiopathic infant cases:
  • The immaturity of both the lungs and the heart in infants.
  • The growth and development of bronchopulmonary system and pulmonary vessels in infants continues for at least 2 years (unlike that in adults).
  • Immature and vulnerable atrium in utero is considered as an important contributor for fetal MAT detected in utero.
• The following table shows the proposed theories explaining the underlying mechanism of MAT but none of these theories has yet been demonstrated conclusively.

Proposed theories suggesting the underlying mechanism of MAT

Theory	Description
Theory of re-entry	This theory centers upon the idea that automaticity foci having different exit pathways or electrical circuits with abnormal intra-atrial conduction can produce tachycardia with several discrete P wave morphologies. However, the role of re-entrant pathways is still not clear and needs to be explained in detail. According to different studies, programmed electrical stimulation which both triggers and terminates reentrant rhythms has not been found to have any effect on multifocal atrial tachycardia or to reproduce it. According to one of the electrophysiological studies including patients of multifocal atrial tachycardia, following three abnormal conduction pathways were found out: Intra-atrial Atrionodal Atrioventricular
Theory of abnormal automaticity	The main focus of the theory of abnormal automaticity is on an increase in the ability of atrial myocytes to spontaneously depolarize and thus triggering an action potential. Many of the underlying conditions associated with MAT support this theory. Pulmonary diseases such as COPD can cause any of the following pathological conditions known to be associated with an increase in automaticity: Hypoxia Hypercapnia Acidosis Increased adrenergic stimulation Pulmonary hypertension associated with pulmonary diseases can also result in right atrial enlargement, in turn, causing right atrial hypertension leading to an increase in automaticity. Ventricular dysfunction associated with coronary artery disease and congestive heart failure can lead to atrial enlargement and atrial hypertension which can also increase the automaticity. Medications and electrolyte abnormalities associated with MAT are also known to increase the automaticity.
Theory of triggered activity	This theory involves the spontaneous action potentials which are generated from afterdepolarizations due to the instability of the myocardial cell membrane. It states that a normal stimulus such as an action potential generated by a sinoatrial node leads to afterdepolarizations due to the membrane potential changes which can achieve threshold and “trigger” the spontaneous action potentials. Intracellular calcium overload can also lead to afterdepolarization which can result in the triggered activity. This theory of triggered activity still needs to be explained clearly, however, the effectiveness of calcium channel blockers, such as verapamil acting to reduce the intracellular calcium overload, supports this theory.

Multifocal Atrial Tachycardia.

Multifocal atrial tachycardia (MAT) [https://en.wikipedia.org/wiki/Multifocal_atrial_tachycardia#/media/File:Multifocal_atrial_tachycardia_-_MAT.png

Causes

Following is a list of potential causes of multifocal atrial tachycardia:

Life Threatening Causes

Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated and include the following:

• Aminophylline toxicity
• Theophylline toxicity
• Isoproterenol toxicity
• Congestive heart failure
• Hypokalemia
• Hypoxia
• Myocardial infarction
• Pulmonary embolism
• Sepsis
• Pneumomediastinum (is a complication of surgical emphysema, the MAT gets reverted to sinus rhythm after aspiration of air from mediastinum).

Common Causes

• Chronic obstructive pulmonary disease is the most common cause, as MAT is associated with:
  • 60% cases of significant lung disease
  • 20% patients of acute respiratory failure
  • 17% patients hospitalized with COPD
• Chronic renal failure
• Congestive heart failure
• Coronary artery disease
• Diabetes mellitus
• Major surgery
• Hypokalemia
• Hypoxia
• Myocardial infarction
• Valvular heart disease
• Pneumonia
• Pulmonary embolism
• Sepsis

Causes by Organ System

Cardiovascular	Congestive heart failure, myocardial infarction,
Chemical/Poisoning	No underlying causes
Dental	No underlying causes
Dermatologic	No underlying causes
Drug Side Effect	Aminophylline,, theophylline
Ear Nose Throat	No underlying causes
Endocrine	Diabetes mellitus
Environmental	No underlying causes
Gastroenterologic	No underlying causes
Genetic	No underlying causes
Hematologic	No underlying causes
Iatrogenic	Postoperative complication
Infectious Disease	Pneumonia, sepsis
Musculoskeletal/Orthopedic	No underlying causes
Neurologic	No underlying causes
Nutritional/Metabolic	No underlying causes
Obstetric/Gynecologic	No underlying causes
Oncologic	Lung cancer
Ophthalmologic	No underlying causes
Overdose/Toxicity	Aminophylline
Psychiatric	No underlying causes
Pulmonary	Chronic obstructive pulmonary disease, hypoxia, lung cancer, pneumonia, pulmonary embolism
Renal/Electrolyte	Chronic renal failure, hypokalemia, hypomagnesemia
Rheumatology/Immunology/Allergy	No underlying causes
Sexual	No underlying causes
Trauma	No underlying causes
Urologic	No underlying causes
Miscellaneous	No underlying causes

Causes in Alphabetical Order

• Aminophylline
• Chronic obstructive pulmonary disease
• Chronic renal failure
• Congestive heart failure
• Diabetes mellitus
• Hypercapnia
• Hypokalemia
• Hypomagnesemia
• Hypoxia
• Isoproterenol
• Lung cancer
• Myocardial infarction
• Pneumonia
• Postoperative complication
• Pulmonary embolism
• Sepsis
• Valvular heart disease

Epidemiology and Demographics

• Multifocal atrial tachycardia is a relatively uncommon arrhythmia with low incidence.
• It is seen only in 0.05% to 0.32% of electrocardiograms in general hospital admissions.
• The average age of patients affected by MAT is approximately 70 years.
• Prevalence of pulmonary disease in MAT has been well established in adult MAT patients with up to 60% of the adult patients having a coexisting pulmonary disease, particularly those with chronic obstructive pulmonary disease.
• MAT is a relatively rare condition with clinical features not well established in pediatric ages.
• It accounts for less than 1% of supraventricular tachycardia in infants and children and is reported to affect >20% of the pediatric patients.
• Multifocal atrial tachycardia though rare in neonates, can be diagnosed prenatally by cardiotocography.
• MAT is difficult to treat in infancy but it resolves frequently and spontaneously within the first year of life.

Natural history, Complications and Prognosis

• Multifocal atrial tachycardia is considered to be a relatively benign arrhythmia with likely good outcome in the absence of a severe underlying illness.
• MAT can be well controlled if treated with appropriate drugs along with a suggested long follow-up period.
• In the case of a required pharmacologic intervention, amiodarone is suggested as an excellent choice.
• Baek et al reported in a study that:
  • Usually, MAT affects infants with a favorable prognosis especially the idiopathic infant group.
  • But in the presence of other comorbidities with MAT, it may have a variable clinical course.
• Although most patients with multifocal atrial tachycardia are hemodynamically stable, still MAT is a poor prognostic sign in the setting of an acute illness.
• MAT is associated with a 60% in-hospital mortality rate.
• The mean survival of patients with MAT is just over one year.

Diagnosis

The diagnosis of MAT is usually not clinical rather the following electrocardiographic diagnostic criteria is used:

Electrocardiography

ECG of MAT has following characteristics:

• Atrial rate of greater than 100 beats per minute (although some also suggest a threshold of 90 beats per minute for MAT diagnosis)
• Irregularly irregular rhythm
• There are P waves of varying morphology from at least three different foci.
• There is an absence of one dominant atrial pacemaker.
• Variable or irregular PP intervals, RR intervals, and PR intervals (however, variation in PR intervals is not yet included in the diagnostic criteria because of the variation of PR interval depends on the length of the preceding RP interval).
• Can be mistaken for atrial fibrillation if the p waves are of low amplitude.

Other diagnostic workup

• As multifocal atrial tachycardia is mostly associated with the underlying medical conditions such as cardiac and pulmonary disease, so its diagnosis does not typically warrant any additional workup, other than the workup required for the suspected underlying conditions.
• If the arrhythmia persists despite of treating the underlying medical conditions, following tests should be done to check for any signs of infection, anemia, or electrolyte abnormalities such as hypokalemia and hypomagnesemia:
  • Complete blood count
  • Serum chemistry panel

Challenges in MAT pediatric patients

• Pediatric practitioners usually face the following four challenges regarding MAT in children:

Challenges faced by pediatric practitioners while treating children with multifocal atrial tachycardia

Challenges	Details
How to detect MAT early	Early detection of MAT is very important in order to prevent the worse outcome in the case of infantile-onset MAT. Usually, tachycardia is first detected during the newborn period and the incidental detection of MAT not based on the clinical suspicion is rather high. Clinical suspicion of the infantile-onset of MAT is very important for its early detection. MAT lasting longer over several days without any proper management can lead to myocardial dysfunction which can further cause congestive heart failure due to tachycardia-induced cardiomyopathy. Hence, it is necessary to detect MAT early and immediately treat it with appropriate management to prevent CHF.
How to control MAT	Complete control of the MAT is not easily achievable even with high-dose combinations of multiple antiarrhythmic medications. A more realistic treatment goal is to initially reduce the percentage of MAT by achieving ventricular rate control. Various drugs such as beta-blockers, digoxin, and amiodarone have been used for the purpose, but there is not enough data to support the superiority of any one of these approaches.
How deep to investigate etiologies of MAT	As there are many varieties of etiologies of MAT in children, these etiologies should be described in detail in order to treat the underlying problems and get a better clinical outcome. Idiopathic infantile-onset group shows a favorable outcome compared to the other groups such as syndromic disease. RASopathy has been reported to be associated with a high incidence of atrial arrhythmias hence, MAT in children should be checked for the association of RASopathy and vice versa.
How to predict another arrhythmia and outcome	Atrial premature beats, atrial fibrillation (AF), or atrial flutter are known to accompany MAT in both adults and pediatric patients. MAT may be an early manifestation of catecholaminergic polymorphic ventricular tachycardia (CPVT) with additional findings of atrioventricular nodal reentrant tachycardia. Phenotypical progression of MAT into CPVT and an association between the RyR2 mutation and AF and ectopic atrial tachycardia have been reported. MAT in young children may be the initial manifestation of a potentially life-threatening arrhythmia of CPVT. Hence, aggressive evaluations and close follow-ups might be required for the non-infantile form of MAT with a structurally normal heart.

History and Symptoms

• Mostly patients with multifocal atrial tachycardia are asymptomatic.
• MAT is often incidentally found during the routine electrocardiogram.
• Once the diagnosis of MAT is made, a thorough history should be obtained with main focus on commonly associated conditions such as cardiac and pulmonary diseases particularly congestive heart failure and chronic obstructive pulmonary disease respectively.
• The clinical manifestations of MAT differ from those of other tachyarrhythmias in that symptoms predominantly relate to the underlying precipitating illness rather than the arrhythmia itself.
• Patients usually present with:
  • Irregular heart rate greater than 100 beats per minute (mostly identified only during the physical examination by the health care provider)
  • Palpitations (rare)
  • Presyncope (rare)
  • Syncope (rare)
• Picture of a typical MAT patient is as follows:
  • Elderly patient
  • Decompensated pulmonary disease
  • Decompensated heart failure
  • Postoperative
  • Usually hemodynamically stable (no severe hemodynamic compromise associated with MAT)
• High mortality ECG features in MAT patients include:
  • P waves with ≥3 forms
  • Atrial rate usually 100 to 200 bpm
  • Irregular atrial rate
  • Variable PR interval
  • Isoelectric baseline between P waves
  • May progress to atrial fibrillation

Physical Examination

• Physical examination findings of patients with multifocal atrial tachycardia include:
  • Elevated heart rate usually greater than 100 bpm
  • Irregularly irregular rhythm
  • Hemodynamically stable (mostly)
• As MAT is associated with underlying medical conditions, hence, it is suggested to carry out a general assessment for the signs of cardiopulmonary disease, especially because MAT can trigger the decompensation of underlying cardiac and pulmonary disease.

Treatment

Treatment options for multifocal atrial tachycardia

Treatment option	Description
Treat underlying medical condition	The treatment of multifocal atrial tachycardia should be focused on treating the underlying medical conditions as most episodes of the MAT resolve with the treatment of underlying conditions. Specific treatment of MAT is indicated if the patient develops symptomatic decompensation of their underlying cardiac or pulmonary disease or in the rare setting of persistent symptomatic arrhythmia despite adequate treatment of underlying conditions.
Magnesium repletion	If treatment is indicated in a MAT patient, therapy should first start with correcting any underlying electrolyte abnormalities with the repletion of potassium or magnesium. According to studies, magnesium suppresses ectopic atrial activity, and thus, can be beneficial even if magnesium levels are within the normal range. Intramuscular and continuous intravenous magnesium sulfate regimens used in pre-eclampsia can be used for MAT treatment. Both routes of administration are proven to be successful in causing reversion to sinus rhythm. However, a higher and more sustained serum magnesium concentration can be attained by the intramuscular regimen, leading to the conversion of MAT associated arrhythmia to normal sinus rhythm in a shorter period of time (1-2 hours) as compared to the intravenous regimen (4-8 hours). Intravenous magnesium sulfate is considered to be superior to amiodarone in the conversion of acute atrial tachyarrhythmias, while initial slowing of ventricular response rate in nonconverters appears to be equally efficacious with both agents.
Potassium repletion	Parenteral potassium administered together with serum magnesium stabilizes the ionic balance of atrial cells and thus prevents spontaneous ectopy.
Non-dihydropyridine calcium channel blockers	Once all the electrolyte abnormalities have been corrected, possible treatment options include non-dihydropyridine calcium channel blockers. If the MAT patient has an underlying pulmonary disease, the first-line agent is a non-dihydropyridine calcium channel blocker such as verapamil or diltiazem. These drugs suppress the atrial rate and decrease conduction through the atrioventricular node thus, slowing the ventricular rate, with an average reduction in the ventricular rate of 31 beats per minute and reversion of 43% of the MAT patients to normal sinus rhythm. Calcium channel blockers (CCB) should be used with caution in patients with preexisting heart failure or hypotension due to negative inotropic effects and peripheral vasodilation. CCB should also be avoided in patients with atrioventricular blocks unless a pacemaker has already been implanted.
Beta blockers	Beta-blockers are the first-line agents in the treatment of MAT patients with no underlying pulmonary disease. Beta-blockers act by suppressing the ectopic foci and thus, reduce the sympathetic stimulation leading to a decrease in conduction through the atrioventricular node, ultimately slowing the ventricular response. They cause an average decrease in heart rate of 51 beats per minute and reversion of 79% of the MAT patients to normal sinus rhythm. Only 20% of the MAT patients require long-term therapy with beta-blockers. Beta-blockers should be used with caution in patients with an underlying pulmonary disease such as COPD and decompensated heart failure due to an increased risk for bronchospasm and decreased cardiac output. Beta-blockers should be avoided in patients with atrioventricular blocks unless a pacemaker has already been implanted.
Antiarrhythmic drugs	Combined flecainide and sotalol therapy is proven efficacious for multifocal atrial tachycardia patients with the cardio-facio-cutaneous syndrome. The successful treatment of MAT with ibutilide is also demonstrated. Treatment with a Class III antiarrhythmic agent opposes the frequently accepted mechanism of triggered activity in causing this arrhythmia. Antiarrhythmics such as quinidine, procainamide, lidocaine, and phenytoin are not yet proven successful. Digitalis has also not been proven to be beneficial in MAT treatment.
Radiofrequency AV nodal ablation	In a few selected cases of refractory multifocal atrial tachycardia, AV nodal ablation has been proven beneficial. According to studies, an average reduction of 56 beats per minute in the ventricular rate is found with adequate control of ventricular response in 84% of the patients. However, AV nodal ablation causes a complete heart block and requires the placement of a permanent pacemaker.

Prevention

Primary Prevention

• Patients with chronic obstructive pulmonary disease and congestive heart failure, both conditions associated with magnesium deficiency and MAT, should be treated with magnesium-sparing diuretics in order to prevent magnesium deficiency leading to MAT.

Differentiating Multifocal Atrial Tachycardia from other Diseases

Multifocal atrial tachycardia must be differentiated from the following:

• Atrial fibrillation (has discrete P wave morphologies)
• Atrial flutter with variable AV node conduction (has regular PP intervals and flutter waves)
• Atrioventricular nodal reentry tachycardia (AVNRT)
• Paroxysmal supraventricular tachycardia
• Premature atrial contractions (PAC)
• Wolff-Parkinson-White syndrome (WPW)
• Ventricular fibrillation (VF)
• Ventricular tachycardia (VT) with frequent premature atrial contractions (has regular PP intervals)
• Wandering atrial pacemaker (has heart rate less than 100 beats per minute)

Arrhythmia	Rhythm	Rate	P wave	PR Interval	QRS Complex	Response to Maneuvers	Epidemiology	Co-existing Conditions
Atrial fibrillation (AFib)	Irregularly irregular	On a 10-second 12-lead EKG strip, multiply number of QRS complexes by 6	Absent Fibrillatory waves	Absent	Less than 0.12 seconds, consistent, and normal in morphology in the absence of aberrant conduction	Does not break with adenosine or vagal maneuvers	2.7–6.1 million people in the United States have AFib 2% of people younger than age 65 have AFib, while about 9% of people aged 65 years or older have AFib	Elderly Following bypass surgery Mitral valve disease Hyperthyroidism Diabetes Heart failure Ischemic heart disease Chronic kidney disease Heavy alcohol use Left chamber enlargement
Atrial flutter	Regular or Irregular	75 (4:1 block), 100 (3:1 block) and 150 (2:1 block) beats per minute (bpm), but 150 is more common	Sawtooth pattern of P waves at 250 to 350 bpm Biphasic deflection in V1	Varies depending upon the magnitude of the block, but is short	Less than 0.12 seconds, consistent, and normal in morphology	Conduction may vary in response to drugs and maneuvers dropping the rate from 150 to 100 or to 75 bpm	Incidence: 88 per 100,000 individuals	Elderly Alcohol
Atrioventricular nodal reentry tachycardia (AVNRT)	Regular	140-280 bpm	Slow-Fast AVNRT: Pseudo-S wave in leads II, III, and AVF Pseudo-R' in lead V1. Fast-Slow AVNRT P waves between the QRS and T waves (QRS-P-T complexes) Slow-Slow AVNRT Late P waves after a QRS Often appears as atrial tachycardia. Inverted, superimposed on or buried within the QRS complex (pseudo R prime in V1/pseudo S wave in inferior leads)	Absent (P wave can appear after the QRS complex and before the T wave, and in atypical AVNRT, the P wave can appear just before the QRS complex)	Less than 0.12 seconds, consistent, and normal in morphology in the absence of aberrant conduction QRS alternans may be present	May break with adenosine or vagal maneuvers	60%-70% of all supraventricular tachycardias	Structural heart disease Atrial tachyarrhythmias
Multifocal atrial tachycardia	Irregular	Atrial rate is > 100 beats per minute	Varying morphology from at least three different foci Absence of one dominant atrial pacemaker, can be mistaken for atrial fibrillation if the P waves are of low amplitude	Variable PR intervals, RR intervals, and PP intervals	Less than 0.12 seconds, consistent, and normal in morphology	Does not terminate with adenosine or vagal maneuvers	0.05% to 0.32% of electrocardiograms in general hospital admissions	Elderly Chronic obstructive pulmonary disease (COPD)
Paroxysmal supraventricular tachycardia	Regular	150 and 240 bpm	Absent Hidden in QRS	Absent	Narrow complexes (< 0.12 s)	Breaks with vagal maneuvers, adenosine, diving reflex, oculocardiac reflex	Prevalence: 0.023 per 100,000	Alcohol Caffeine Nicotine Psychological stress Wolff-Parkinson-White syndrome
Premature atrial contractrions (PAC)	Regular except when disturbed by premature beat(s)	80-120 bpm	Upright	> 0.12 seconds May be shorter than that in normal sinus rhythm (NSR) if the origin of PAC is located closer to the AV node Ashman’s Phenomenon: PAC displaying a right bundle branch block pattern	Usually narrow (< 0.12 s)	Breaks with vagal maneuvers, adenosine, diving reflex, oculocardiac reflex		Infants Cardiomyopathy Myocarditis Elderly Coronary artery disease Stroke Increased atrial natriuretic peptide (ANP) Hypercholesterolemia
Wolff-Parkinson-White Syndrome	Regular	Atrial rate is nearly 300 bpm and ventricular rate is at 150 bpm	With orthodromic conduction due to a bypass tract, the P wave generally follows the QRS complex, whereas in AVNRT, the P wave is generally buried in the QRS complex.	Less than 0.12 seconds	A delta wave and evidence of ventricular pre-excitation if there is conduction to the ventricle via ante-grade conduction down an accessory pathway A delta wave and pre-excitation may not be present because bypass tracts do not conduct ante-grade.	May break in response to procainamide, adenosine, vagal maneuvers	Worldwide prevalence of WPW syndrome is 100 - 300 per 100,000	Ebstein's anomaly Mitral valve prolapse: This cardiac disorder, if present, is associated with left-sided accessory pathways. Hypertrophic cardiomyopathy: This disorder is associated with familial/inherited form of WPW syndrome. Hypokalemic periodic paralysis Pompe disease Tuberous sclerosis
Ventricular fibrillation (VF)	Irregular	150 to 500 bpm	Absent	Absent	Absent (R on T phenomenon in the setting of ischemia)	Does not break in response to procainamide, adenosine, vagal maneuvers	3-12% cases of acute myocardial infarction (AMI) Out of 356,500 out of hospital cardiac arrests, 23% have VF as initial rhythm	Myocardial ischemia / infarction Cardiomyopathy Channelopathies e.g. Long QT (acquired / congenital) Electrolyte abnormalities (hypokalemia/hyperkalemia, hypomagnesemia) Aortic stenosis Aortic dissection Myocarditis Cardiac tamponade Blunt trauma (Commotio Cordis) Sepsis Hypothermia Pneumothorax Seizures Stroke
Ventricular tachycardia	Regular	> 100 bpm (150-200 bpm common)	Absent	Absent Initial R wave in V1, initial r > 40 ms in V1/V2, notched S in V1, initial R in aVR, lead II R wave peak time ≥50 ms, no RS in V1-V6, and atrioventricular dissociation	Wide complex, QRS duration > 120 milliseconds	Does not break in response to procainamide, adenosine, vagal maneuvers	5-10% of patients presenting with AMI	Coronary artery disease Aortic stenosis Cardiomyopathy Electrolyte imbalances (e.g., hypokalemia, hypomagnesemia) Inherited channelopathies (e.g., long-QT syndrome) Catecholaminergic polymorphic ventricular tachycardia Arrhythmogenic right ventricular dysplasia Myocardial infarction Torsades de pointes is a form of polymorphic VT that is often associated with a prolonged QT interval

References

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