Supraventricular tachycardia (SVT) is a tachycardia involving the atrium and/or the atrioventricular node (AV node). SVT is caused by a reentry pathway in about 90% of patients and an irritable focus due to abnormal automaticity or triggered activity in the remaining 10% of patients.
Symptoms of SVT
Usually, patients with SVT see a physician first in their teens, twenties, thirties or forties, but SVT can begin at any age. Patients usually have “spells” consisting symptoms of palpitations or out right tachycardia. Associated symptoms may include chest pain, pulsations in the neck, dyspnea, light-headedness, fatigue, sweating, etc. After a spell of SVT, the patient may have urinary frequency (due to release of ANF from the atria) or may feel fatigued for hours to days.
Diagnosis of SVT
SVT can be documented by a regular ECG performed at the time that the patient’s heart is racing if the patient goes to the emergency room. Patients who have daily episodes of SVT can have a 24-hour holter monitor placed to document the SVT. More commonly, patients may have monthly episodes and can use an external event monitor to record episodes and call them in on a toll-free telephone number. More rare episodes are difficult to document unless the patient waits until an episode occurs and then seeks medical attention at an emergency room or physician’s office. Patients who call 911 may have their episode of SVT documented by the paramedics en route to the hospital. Patients who are in the hospital wearing a telemetry monitor may have their SVT documented. Internal looped monitors are not usually deployed just to document SVT. However when such monitors are inserted in patients with syncope, SVT is occasionally documented. The heart rate of SVT can be from just over 100 beats per minute to nearly 300 beats per minute. Usually, the heart rate is between 160 and 220 beats per minute.
Acute care of SVT at home
Patients frequently ask what to do when they have an episode of SVT. The most important factor is for them to use common sense. If they feel very bad (severe chest pain, severe dyspnea) then calling 911 is prudent. Lesser degrees of symptoms give the patient the opportunity to try vagal maneuvers to see if they can get their heart rhythm back to normal. The only maneuvers that are safe to try at home are the Valsalva maneuver or the Muller maneuver. Other maneuvers are not recommended. Eyeball pressure has resulted in retinal injuries. Immersing the face in ice water has rarely caused cardiac arrest. Gagging seldom works to restore normal rhythm. Patients that tolerate their SVT without significant symptoms may elect to wait at home or even try to fall asleep in hopes that the episode will resolve on its own. Most patients will eventually go to the emergency room after waiting at home for a while if SVT persists.
Care of SVT in the emergency room
Doctors after recording and ECG and assessing the patients vital signs will decide whether the patient is really in danger (hypotension, severe chest pain, dyspnea, etc,) or not. If the patient is unstable, the doctor will sedate the patient and perform external cardioversion. If the patient seems stable, the doctor may ask the patient to perform vagal maneuvers to see if sinus rhythm can be restored. If this is ineffective, then medications can be given intravenously such as adenocard, verapamil, diltiazem or beta blockers. If these are ineffective other medications such as ibutilide, procainamide or rarely even amiodarone can be tried. If nothing succeeds in restoring normal rhythm, then eventually external cardioversion is performed. Usually once sinus rhythm is restored, the patient can be discharged rather than admitted to the hospital. The typical cost for such a visit to the emergency room can exceed $2,000.
Workup of SVT
Patients with a history of SVT should be seen by a cardiologist or even better by an electrophysiologist. The typical workup of patients with SVT involves having an echocardiogram done to search for structural heart disease. Patients with prominent symptoms of angina, or risk factors for coronary artery disease, may need stress testing or even a coronary angiography. Patients who might be treated with antiarrhythmic drugs need blood tests done to assess renal and hepatic function.
Prognosis of SVT
Unless structural heart disease is present, the prognosis of patients with SVT is excellent. As mentioned above, SVT does not shorten life – it does not lead to death, stroke or myocardial infarction. Should an episode of SVT arise while the patient is sleeping, they will be awakened by the symptoms. However, SVT will recur at some point in nearly all patients who do not die of another cause. For patients who have just experienced their first episode of SVT, it is impossible to say when the next episode will occur. For this reason, many of such patients take a wait and see approach to their SVT. As years and decades pass, nearly every patient experiences more frequent and/or more long-lasting episodes. It is also common for the patients to feel worse physically with their SVT as they get older.
Treatment of SVT
Usually structural heart disease is not present in patients with SVT. Unless WPW is present, SVT is a nuisance and not life-threatening. Because of this, the treatment of SVT does not prolong life. The only other reason to treat SVT then is to prevent the patient from having symptoms from their tachycardia. There are rare patients who are in SVT at least 90% of the day with heart rates over 130 beats per minute. Such patients may develop a tachycardiomyopathy in which case treatment is mandatory.
Patients with SVT have four general options for therapy:
- Doing nothing to prevent or cure SVT
- Taking medications
- Having a percutaneous ablation for cure performed
- Having open-heart surgery.
Practically, patients needing open-heart surgery for another reason may have a surgical approach to their SVT, but this is quite rare. For the remainder, it is living with SVT, taking heart rhythm medications, or having an ablation for cure.
Living with SVT (no therapy)
This is a good option for patients with rare episodes that are associated with lower heart rates (usually less than 150 beats per minute) and only minor symptoms. Such patients when they experience SVT can try vagal maneuvers at home or even try to fall asleep in hopes that the SVT will go away on its own. After some period of time, such patients eventually must go to the emergency room if their SVT does not go away. Usually intravenous medicines are required to terminate SVT. Frequent visits to the emergency room are inconvenient and expensive, such that many patients eventually decide on some form of therapy.
Heart rhythm medications can be given either only when SVT occurs or on a daily basis to prevent SVT. The so-called “pill in the pocket” approach involves the patient taking a large single dose of an antiarrhythmic drug and then waiting for a few hours to see if SVT goes away. Flecainide or propafenone are the most common medications used. This approach is only safe for patients who tolerate their SVT well with minimal symptoms.
Daily antiarrhythmic medication is a better option if SVT is not as well tolerated by the patient. The physician starts a medication and asks the patient to notify them if any side effects occur. If none occur, the dose of the medication is increased until there is a good chance that it might work for the patient. If SVT never recurs, the patient takes that medication the rest of their life. If SVT recurs, the physician has the option of increasing the dose or trying another medication. Milder medications (digitalis, beta blockers, calcium channel blockers) are the safest and the least expensive, but they tend to have more side effects are not very effective. However some patients need to be on such medications for other reasons such as hypertension or migraine headaches. In these patients, such medications should generally be tried before considering other medications or ablation.
There are stronger medications for patients who fail the above medications. These medications consist of flecainide, propafenone, and sotalol. Flecainide and propafenone can not be given to patients with any significant abnormalities on the echocardiogram or any degree of coronary artery disease. Sotalol, however, is safe in such patients. These three medications are less likely to cause side effects and more likely to prevent SVT. However, rarely in SVT patients, such medications will cause a cardiac arrest. Estimates of this risk are in the 1% range, but many physicians consider this to be too high of an estimate.
If several medications are tried, 50-70% of patients can be successfully treated and take the medications the rest of their lives. Careful follow up is required to be sure that these medications continue to be safe and effective. Amiodarone, the most potent of all heart rhythm medications is too risky for the vast majority of patients.
Ablation for SVT
Ablation is the option selected by the majority of patients, and most ablations are done with RF energy. Curative ablation for SVT is performed about 150,000 times annually in the US. In the past, this was the most common ablation performed. However today, in many centers, SVT ablations are not as commonly performed. Some very experienced doctors now do predominantly one type of ablation e.g. for atrial fibrillation. Almost always an invasive diagnostic procedure called electrophysiology study or EPS can be performed in which SVT can be started and stopped multiple times to determine whether it is caused by a short circuit or an irritable spot. EPS will determine that SVT is one of three main types.
In slightly more than half of SVT patients, the mechanism is atrioventricular nodal reentry (AVNRT). In AVNRT, the short circuit is produced by a process of longitudinal dissociation of the AV node. This produces an extra part of the AV node called the slow pathway that is usually about 2-3 cm below the bundle of His. The SVT usually utilizes the slow pathway for conduction toward the ventricle and then the fast pathway back up to the atrium in a reentry circuit. Accessory pathways (APs) comprise the second-most common mechanism for SVT. These abnormal pathways are present since birth and result from incomplete separation of the atrium from the ventricle. An ectopic beat can block in the AP, conduct down the AV node and then back to the atrium over the AP leading to SVT. The least common type of SVT involves one or more irritable spots that have formed after birth in one of the atria. These spots usually form around the valves that separate the top from the bottom of the heart. They can suddenly usurp control of the heart rhythm through abnormal automaticity or triggered activity causing SVT.
Success with SVT RF ablation
The chance of ending the procedure with no SVT inducible is at least 90% in experienced EP labs. The success depends on what type of SVT is present and how many SVTs are present. The highest chance of success is with AVNRT and approaches 98%. The chance of success with ablation of an accessory pathway is about 95%. The chance of success with ablation of atrial tachycardia is about 90%. The recurrence rates are also dependent upon the type of SVT. With AVNRT, the chances are typically 2% or less. With accessory pathways, the chance of recurrence is about 5%, and with atrial tachycardia, the chance is about 10%.
Risk of SVT ablation
The risk of the procedure in experienced hands is about 1% being slightly less than this for ablations on the right side of the heart and slightly greater with ablation on the left side of the heart. Possible risks include minor events such as bleeding, infection, pain, nausea/vomiting, etc. More serious side effects include stroke, perforation of the heart, myocardial infarction, complete heart block requiring a permanent pacemaker, damage to heart valves, damage to blood vessels/nerves requiring an extended hospital stay, open-heart surgery, or even death. The risk of the procedure is not dependent to any great extent on patient characteristics: younger patients have a similar risk as elderly patients. There certainly are some patient characteristics that an experienced electrophysiologist can identify placing the patient at increased risk. Some these factors include the following:
- Pathway/Focus location near important normal heart structures/nerves
- Previous ablation procedures that may have damaged such structures
- Problems with excessive bleeding or blood clotting problems
- High risk for anesthesia/prolonged procedure
Cryoablation for AVNRT
The most common cause of SVT is AV node reentry (AVNRT). This represents about 60% of all SVT, even more in women. This type of SVT involves a short circuit close to the normal pathway, the AV node. Therefore ablation of AVNRT with RF energy carries a risk of damage to the AV node and therefore a permanent pacemaker. This risk was 1% in a large series of over 1000 patients, which included 373 patients with AVNRT (1). In another series of 4463 patients including 880 with AVNRT, the risk of a permanent pacemaker was 2% in all centers but over 6% in centers with less experience (2). The risk of a permanent pacemaker or new heart rhythm problems is even higher if longer term follow up occurs (3). RF ablation was compared with cryoablation in 2 randomized European trials using the smallest cryoablation catheter: with a 4 mm tip. This catheter is known to make smaller lesions that an RF catheter with the same sized tip. Nevertheless, cryoablation and RF ablation proved to be equally effective at the end of the ablation procedure. Cryoablation, in one study, was accomplished with fewer lesions but with equal efficacy (4). In the other study, the success at the end of the ablation procedure was equal comparing cryoablation with RF ablation, but recurrent SVT was more common in the cryoablation group (5). This was probably because of the smaller lesion size with the cryoablation catheter. In a Swedish registry when a larger cryoablation catheter was used in over a thousand consecutive patients with AVNRT, the success rates were excellent with no long term heart block and no permanent pacemakers required. (6). This study involved only a single freeze at the successful site – a strategy known to result in a smaller lesion than the freeze-thaw-refreeze strategy used in other institutions. In rare cases of AVNRT the optimal site of ablation is inside the coronary sinus (7,8). Trying to ablate too far inside the vein with RF is risky (see below). Cryoablation, in my opinion, is the procedure of choice in patients with AVNRT.
Cryoablation for accessory pathways
The second-most common cause of SVT is caused by accessory pathways (AP). There are three AP locations (comprising nearly half of all pathways) that may be more suitable for CrA than RFA. Firstly, the 10% of pathways close to the AV node called septal pathways are ideal for CrA. When the electrophysiologist has placed the cryoablation catheter where she/he believes the septal pathway to be, gentle cooling is delivered through the catheter (cryomapping). If the AV node starts to be affected, the cooling is immediately turned off and the AV node can recover fully. The catheter is then repositioned to a different location and cryomapping is repeated. Finally a site will be found where cooling causes the pathway to loose function without affecting the AV node. At this site, freezing the tissue will cause the septal AP to be destroyed without affecting the AV node. On the other hand if a septal AP is subjected to RF ablation, the only approach is to make the burn hoping to come off with power if an untoward effect is seen. Unfortunately, research on RF ablation has shown that lethal temperatures can persist for up to 12 seconds after power is turned off (9). The chance of inadvertent damage to the AV node requiring a permanent pacemaker after RF ablation of septal APs in a large series was 3% (1). There was also an 11% chance of recurrence of heart racing after RF ablation in this same study. The initial use of RF ablation in patients with septal APs highlighted the risk of CHB requiring a PPM (10). The safety and efficacy of CrA for septal APs in case reports (11-13) and small series (14-16) was excellent making this the ablation modality of choice for these APs. A larger series of 35 adolescent patients showed acute success rates comparable to what would have been expected with RF ablation, but with slightly higher recurrence rates (17).
The second pathway location where CrA has an advantage is the rare pathway located inside the coronary sinus. Animal studies have suggested that if these APs are within 5 mm of a coronary artery, there is a high chance of RF ablation damaging the artery, which could cause a myocardial infarction (18). CrA delivered close to such arteries is much less likely to damage the artery. Also if such pathways are in very small veins, not enough power can be given with RF ablation to make a big enough lesion to kill the AP (19). There are also cases of getting the RF catheter stuck in the small vein when RF energy ‘welds’ the catheter to the vein. CrA in small vein locations with low blood flow allows the CrA catheter to make a bigger lesion than normal, and welding does not occur. The use of cryoablation inside the coronary sinus in children has been shown to be safe (20)
Thirdly, APs on the right side of the heart cross the tricuspid valve, which tends to move vigorously during right ventricular contraction. Often it is difficult for the electrophysiologist to get a RF ablation catheter to stay in contact with the AP long enough to kill it. With CrA, the catheter sticks to the heart tissue within 10 seconds or so and will not move after freezing starts to occur. In a large series using RF ablation for right sided APs, the success at the end of the first procedure was only 84% with 7% of patients requiring a second procedure. 14% of patients had recurrence of their heart racing (1). These results with RF ablation are not encouraging. One study of CrA in 3 patients with right-sided APs has been published showing efficacy in all 3 patients (21).
Cryoablation for atrial tachycardia
Atrial tachycardia, the least common mechanism of SVT may also require CrA, a safer alternative in some patients than RF ablation. First of all, the site of the irritable focus causing the atrial tachycardia may be close to the AV node or the Sinus node in which case RF ablation will invariably result in a higher risk of a permanent pacemaker than cryoablation. Secondly, the irritable focus may be close to the right phrenic nerve. Injury to the right phrenic nerve diminishes the patient’s breathing capacity by 55% resulting in significant disability in most cases. Preliminary information suggests that CrA may be safer in such cases. Thirdly, the irritable focus may be within a vein where low blood flow renders RF energy incapable of delivering sufficient energy to kill the focus. Cryoablation, in contrast, works better in areas of low blood flow. Lastly, if the irritable focus is close to a coronary artery, it will almost certainly be better approached with cryoablation (18).
Ganz L, Friedman P. Medical Progress: Supraventricular Tachycardia. N Engl J Med. 1995; 332: 162-173
A good review of the basics of SVT but somewhat outdated with regards to practices such as 3-dimensional mapping and cryoablation.
Thornton A, and Jordaens L. Advances in the approaches to ablation of complex arrhythmias. J Cardiovasc Electrophysiol 2007;18:S2-S10.
A good review of the latest techniques and technologies.
Insulander P, Andersson M, Bergfeldt L et.al. Ablation of AVNRT and AVRT. Current results in 1310 consecutive patients. Poster from Stockholm, Sweden
Cryoablation was more effective for paraseptal pathways than RF ablation. It was safer and more effective for AVNRT slow pathway ablation than RF.
- Calkins H, Yong P, Miller J. etal. Catheter ablation of accessory pathways, atrioventricular nodal reentrant tachycardia, and the atrioventricular junction: final results of a prospective, multicenter clinical trial. Circulation. 1999; 99: 262-270
- Hindricks G on behalf of the MERFS Investigators. Incidence of complete atrioventricular block following attempted radiofrequency catheter modification of the atrioventricular node in 880 patients. Eur Heart J. 1996; 17: 82-88.
- Kimman G, Bogaard , Van Hemel N, etal. Ten-year follow-up after radiofrequency catheter ablation for atrioventricular nodal reentrant tachycardia in the early days forever cured, or a source for new arrhythmias? Pacing and Clinical Electrophysiology. 2005; 28: 1302-1309
- Kimman G, Theuns D, Szili-Torok T. etal. CRAVT: a prospective, randomized study comparing transvenous cryothermal and radiofrequency ablation in atrioventricular nodal re-entrant tachycardia. European Heart Journal. 2004; 25: 2232-2237.
- Zrenner B, Dong J, Schreieck J etal. Transvenous cryoablation versus radiofrequency ablation of the slow pathway for the treatment of atrioventricular nodal re-entrant tachycardia: a prospective randomized pilot study. European Heart Journal. 2004; 25: 2226-2231
- Cryoablation of substrates adjacent to the atrioventricular node: safety of 1303 ablation procedures. Europace (2013) doi:10.1093/Europace/eu 215
- Otomo K, Okamura H, Noda T. etal. “Left-variant” atypical atrioventricular nodal reentrant tachycardia: electrophysiological characteristics and effect of slow pathway ablation within the coronary sinus. J Cardiovasc Electrophysiol. 2006; 17: 1177-1183
- Nam G, Rhee K, Kim J. Left atrionodal connections in typical and atypical atrioventricular nodal reentrant tachycardias: activation sequence inside the coronary sinus and results of radiofrequency catheter ablation. J Cardiovasc Electrophysiol. 2006; 17: 171-177.
- Bunch T, Bruce K, Johnson S etal. Analysis of catheter-tip (8-mm) and actual tissue temperatures achieved during radiofrequency ablation at the orifice of the pulmonary vein. Circulation 2004; 110: 2988-2995
- Schulter M and Kuch K. Catheter ablation form right atrium of anteroseptal accessory pathways using radiofrequency current. Journal of the American College of Cardiology. 1992; 19: 663-670
- Kimman G, Szili-Torok T et.al. Transvenous cryothermal catheter ablation of a right anteroseptal accessory pathway. Journal of Cardiovascular Electrophysiology. 2001; 12: 1415-141
- Lanzotti M, DePonti R, Tritto M et.al. Successful treatment of anteroseptal accessory pathways by transvenous cryomapping and cryoablation. Italian Heart Journal. 2002; 3: 128-13
- Idris F, Green M, Tang A, et.al. A cool ablation. Journal of Cardiovascular Electrophysiology. 2002; 13: 299
- Atienza F, Arenal A, Torrecilla et.al. Acute and long-term outcome of transvenous cryoablation of midseptal and parahissian accessory pathways in patients at high risk of atrioventricular block during radiofrequency ablation. American Journal of Cardiology. 2004; 93:1302-1305
- Gaita F, Riccardi R, Hocini M et.al. Safety and efficacy of cryoablation of accessory pathways adjacent to the normal conduction system. Journal of Cardiovascular Electrophysiology. 2003; 14: 825-829
- Gaita F, Montefusco A, Riccardi R, et.al. Cryoenergy catheter ablation: a new technique for treatment of permanent junctional reciprocating tachycardia in children. Journal of Cardiovascular Electrophysiology. 2004; 15: 263-268
- Bar-Cohen Y, Cecchin F, Alexander M et. al. Cryoablation for accessory pathways located near normal conduction tissues or within the coronary venous system in children and young adults. Heart Rhythm. 2006; 3: 253-258
- Aoyama H, Nakagawa H, Pitha J et.al. Comparison of cryothermia and radiofrequency current in safety and efficacy of catheter ablation within the canine coronary sinus. J Cardiovascular Electrophysiology. 2005;16:1218-122
- Morady F. Catheter Ablation of Supraventricular Arrhythmias: State of the Art. Pacing and Clinical Electrophysiology. 2004; 27:125-142
- Collins K, Rhee K, Kirsh J et.al. Cryoablation of accessory pathways in the coronary sinus in young patients: a multicenter study fron the pediatric and congenital electrophysiology society’s working group on cryoablation. J Cardiovasc Electrophysiol 2007;18:592-597.
- Rodriguez L, Geller J, Tse H etal. Acute results of transvenous cryoablation of supraventricular tachycardia (atrial fibrillation, atrial flutter, wolff-parkinson-white syndrome, atrioventricular nodal reentry tachycardia). Journal of Cardiovascular Electrophysiology. 2002; 13:1082-1089.