Catheter Ablation for Cardiac Arrhythmias
http://www.100md.com
《新英格兰医药杂志》
Cardiac arrhythmias are common; some are life-threatening, others merely a nuisance. They are caused by abnormalities in impulse formation or conduction that lead to slow or fast, regular or irregular heart rhythms. It is not difficult to treat patients with slow rhythms: currently available pacemakers are able to adapt their function to the needs of the body.
The situation is different, however, for patients with rapid rhythms. Such rhythms may originate anywhere in the heart and result from a variety of mechanisms. They may be focal, meaning that the abnormal impulse formation is confined to a small area, or they may be the result of an impulse running in a circuit composed of several interconnected cardiac cells. Such a circuit may be small (measuring a few millimeters) or large, as in atrial flutter and in arrhythmias in which both the normal atrioventricular conduction system and an extra connection between the atrium and the ventricle are incorporated into the circuit of the arrhythmia.
Historically, pharmacologic interventions were used in attempts to terminate and prevent rapid rhythms. During the past two decades, however, it has become clear that antiarrhythmic drugs may have serious side effects and may sometimes even facilitate the occurrence of life-threatening arrhythmias and sudden death. The recognition of these effects has led to increasing interest in developing techniques for localizing the site of origin or pathway of an arrhythmia and then isolating or destroying the tissue that is responsible. Today, these tasks can be accomplished with the use of intracardiac catheter techniques. With the help of intracardiac catheters, one may not only determine the site of origin or pathway of an arrhythmia but also cure the rhythm disturbance by applying, through the catheter, radiofrequency, laser, ultrasound, or microwave energy or freezing temperatures to the tissue causing the arrhythmia.
When should catheter ablation be performed? As the Table shows, there are different classes of indications. The decision is easy when the arrhythmia is severe or life-threatening — as, for example, in the case of a ventricular tachycardia or atrial fibrillation in a patient with the Wolff–Parkinson–White syndrome who has an extra connection between the atrium and the ventricle (outside the normal atrioventricular conduction system) with a very short anterograde refractory period.
Table. Patients with Cardiac Arrhythmias That Are Currently Treated by Catheter Ablation.
During atrial fibrillation in such a patient, the ventricular rate can reach more than 300 beats per minute, leading to ventricular fibrillation and sudden death. Catheter ablation is also indicated when a rapid rhythm is present most of the day, severely impairing cardiac function and resulting in a so-called tachycardiomyopathy. When the tachycardia is not life-threatening but interferes with physical and social well-being, the risk of complications from catheter ablation has to be weighed against the possibility of a definite cure.
Apart from the general risks associated with cardiac catheterization, such as bleeding and infection, there are specific risks related to the site where catheter ablation has to be performed, especially when that site is close to the atrioventricular conduction system, a coronary artery, or the valvular apparatus. For example, catheter ablation for a tachycardia in the atrioventricular node carries the risk of creating atrioventricular block and necessitating the implantation of a pacemaker. The possibility of complications has to be thoroughly discussed with the patient. At this time, there are several centers that have had excellent long-term success and a low complication rate with catheter ablation for arrhythmias. The patients who have been treated at these centers to date, however, have had symptomatic arrhythmias. At present, prophylactic ablation of a potential arrhythmia-inducing structure is rarely performed. In this issue of the Journal, Pappone et al. (pages 1197–1205) report the use of catheter ablation in a subgroup of asymptomatic children who had the electrocardiographic pattern of the Wolff–Parkinson–White syndrome but no additional heart disease.
In these children (ranging in age from 5 to 12 years), whose electrocardiogram revealed the presence of an extra connection between the atrium and the ventricle, an intracardiac study was performed to determine which children were at high risk for life-threatening arrhythmias. The children in whom such an arrhythmia could be induced during the study were randomly assigned to catheter ablation of the extra connection or to no treatment. Follow-up showed that a serious arrhythmia later developed in a substantial proportion of the children in the control group. The authors therefore suggest that catheter ablation be performed in asymptomatic children with the Wolff–Parkinson–White syndrome diagnosed on electrocardiography if the electrophysiological properties of the extra connection are such that a sustained, serious tachycardia, possibly leading to sudden death, may occur.
There are a few potential problems with such an approach. First, how are these high-risk but asymptomatic children to be identified? The incidence of electrocardiographic findings indicative of the Wolff–Parkinson–White syndrome (whether symptomatic or asymptomatic) is estimated to be about 0.15 percent in the general population. This means that in order to identify 165 asymptomatic children between 5 and 12 years of age who have the syndrome (the number reported in the study), approximately 200,000 electrocardiograms would have to be obtained in asymptomatic children. Electrocardiography is apparently performed in asymptomatic children frequently in Italy, but this practice is unusual in other countries.
Second, the stratification of risk was based on the outcome of the electrophysiological study, with the induction of a sustained arrhythmia proving to be the most important marker of high risk. Less attention was paid to the anterograde refractory period of the accessory connection. This value, when short, may become more important, however, during middle age, when atrial fibrillation develops. In addition, the electrophysiological properties of the components of a tachycardia pathway may change over time. It is well known that accessory connections are subject to such change, which may occur not only early but also later in life. The inability to induce an arrhythmia in an eight-year-old child does not guarantee that induction will not be possible in the future. Another important marker of risk in the Wolff–Parkinson–White syndrome is the patient's sex: several studies, including the current one, have shown that sudden death in this syndrome usually occurs in boys and men, typically during situations of sympathetic stimulation such as exercise, anxiety, or illicit drug use.
Third, in balancing the risks and benefits of catheter ablation in asymptomatic patients, the experience of the center is extremely important, especially in the case of children. In the current study, all ablation procedures were performed by the same person, who is considered by his peers to be an extremely gifted operator. It remains to be shown whether his results and complication rate can be generalized to operators in other institutions.
This study is important because it indicates that a Wolff–Parkinson–White electrocardiogram in an asymptomatic child is not necessarily a benign finding and that a procedure can be performed to prevent an adverse outcome. But the identification and treatment of high-risk children would require not only a large number of electrocardiograms, but also the availability of centers with sufficient experience to perform intracardiac studies and ablative procedures in children with minimal risk and no long-term adverse effects. This approach will also have major consequences for the cost of health care. All these aspects require further study before general advice can be given regarding the treatment of children with asymptomatic Wolff–Parkinson–White syndrome.
Source Information
From the Cardiovascular Research Institute, Maastricht, the Netherlands.(Hein J.J. Wellens, M.D.)
The situation is different, however, for patients with rapid rhythms. Such rhythms may originate anywhere in the heart and result from a variety of mechanisms. They may be focal, meaning that the abnormal impulse formation is confined to a small area, or they may be the result of an impulse running in a circuit composed of several interconnected cardiac cells. Such a circuit may be small (measuring a few millimeters) or large, as in atrial flutter and in arrhythmias in which both the normal atrioventricular conduction system and an extra connection between the atrium and the ventricle are incorporated into the circuit of the arrhythmia.
Historically, pharmacologic interventions were used in attempts to terminate and prevent rapid rhythms. During the past two decades, however, it has become clear that antiarrhythmic drugs may have serious side effects and may sometimes even facilitate the occurrence of life-threatening arrhythmias and sudden death. The recognition of these effects has led to increasing interest in developing techniques for localizing the site of origin or pathway of an arrhythmia and then isolating or destroying the tissue that is responsible. Today, these tasks can be accomplished with the use of intracardiac catheter techniques. With the help of intracardiac catheters, one may not only determine the site of origin or pathway of an arrhythmia but also cure the rhythm disturbance by applying, through the catheter, radiofrequency, laser, ultrasound, or microwave energy or freezing temperatures to the tissue causing the arrhythmia.
When should catheter ablation be performed? As the Table shows, there are different classes of indications. The decision is easy when the arrhythmia is severe or life-threatening — as, for example, in the case of a ventricular tachycardia or atrial fibrillation in a patient with the Wolff–Parkinson–White syndrome who has an extra connection between the atrium and the ventricle (outside the normal atrioventricular conduction system) with a very short anterograde refractory period.
Table. Patients with Cardiac Arrhythmias That Are Currently Treated by Catheter Ablation.
During atrial fibrillation in such a patient, the ventricular rate can reach more than 300 beats per minute, leading to ventricular fibrillation and sudden death. Catheter ablation is also indicated when a rapid rhythm is present most of the day, severely impairing cardiac function and resulting in a so-called tachycardiomyopathy. When the tachycardia is not life-threatening but interferes with physical and social well-being, the risk of complications from catheter ablation has to be weighed against the possibility of a definite cure.
Apart from the general risks associated with cardiac catheterization, such as bleeding and infection, there are specific risks related to the site where catheter ablation has to be performed, especially when that site is close to the atrioventricular conduction system, a coronary artery, or the valvular apparatus. For example, catheter ablation for a tachycardia in the atrioventricular node carries the risk of creating atrioventricular block and necessitating the implantation of a pacemaker. The possibility of complications has to be thoroughly discussed with the patient. At this time, there are several centers that have had excellent long-term success and a low complication rate with catheter ablation for arrhythmias. The patients who have been treated at these centers to date, however, have had symptomatic arrhythmias. At present, prophylactic ablation of a potential arrhythmia-inducing structure is rarely performed. In this issue of the Journal, Pappone et al. (pages 1197–1205) report the use of catheter ablation in a subgroup of asymptomatic children who had the electrocardiographic pattern of the Wolff–Parkinson–White syndrome but no additional heart disease.
In these children (ranging in age from 5 to 12 years), whose electrocardiogram revealed the presence of an extra connection between the atrium and the ventricle, an intracardiac study was performed to determine which children were at high risk for life-threatening arrhythmias. The children in whom such an arrhythmia could be induced during the study were randomly assigned to catheter ablation of the extra connection or to no treatment. Follow-up showed that a serious arrhythmia later developed in a substantial proportion of the children in the control group. The authors therefore suggest that catheter ablation be performed in asymptomatic children with the Wolff–Parkinson–White syndrome diagnosed on electrocardiography if the electrophysiological properties of the extra connection are such that a sustained, serious tachycardia, possibly leading to sudden death, may occur.
There are a few potential problems with such an approach. First, how are these high-risk but asymptomatic children to be identified? The incidence of electrocardiographic findings indicative of the Wolff–Parkinson–White syndrome (whether symptomatic or asymptomatic) is estimated to be about 0.15 percent in the general population. This means that in order to identify 165 asymptomatic children between 5 and 12 years of age who have the syndrome (the number reported in the study), approximately 200,000 electrocardiograms would have to be obtained in asymptomatic children. Electrocardiography is apparently performed in asymptomatic children frequently in Italy, but this practice is unusual in other countries.
Second, the stratification of risk was based on the outcome of the electrophysiological study, with the induction of a sustained arrhythmia proving to be the most important marker of high risk. Less attention was paid to the anterograde refractory period of the accessory connection. This value, when short, may become more important, however, during middle age, when atrial fibrillation develops. In addition, the electrophysiological properties of the components of a tachycardia pathway may change over time. It is well known that accessory connections are subject to such change, which may occur not only early but also later in life. The inability to induce an arrhythmia in an eight-year-old child does not guarantee that induction will not be possible in the future. Another important marker of risk in the Wolff–Parkinson–White syndrome is the patient's sex: several studies, including the current one, have shown that sudden death in this syndrome usually occurs in boys and men, typically during situations of sympathetic stimulation such as exercise, anxiety, or illicit drug use.
Third, in balancing the risks and benefits of catheter ablation in asymptomatic patients, the experience of the center is extremely important, especially in the case of children. In the current study, all ablation procedures were performed by the same person, who is considered by his peers to be an extremely gifted operator. It remains to be shown whether his results and complication rate can be generalized to operators in other institutions.
This study is important because it indicates that a Wolff–Parkinson–White electrocardiogram in an asymptomatic child is not necessarily a benign finding and that a procedure can be performed to prevent an adverse outcome. But the identification and treatment of high-risk children would require not only a large number of electrocardiograms, but also the availability of centers with sufficient experience to perform intracardiac studies and ablative procedures in children with minimal risk and no long-term adverse effects. This approach will also have major consequences for the cost of health care. All these aspects require further study before general advice can be given regarding the treatment of children with asymptomatic Wolff–Parkinson–White syndrome.
Source Information
From the Cardiovascular Research Institute, Maastricht, the Netherlands.(Hein J.J. Wellens, M.D.)