Incessant ventricular tachycardia (VT) occurs infrequently. Management is challenging because of the arrhythmia's resistance to treatment with antiarrhythmic drugs and repeated external cardioversions. In addition to being generally ineffective, antiarrhythmic drugs may cause proarrhythmia and myocardial depression. The use of an implantable cardioverter/defibrillator (ICD) is contraindicated because of the multiple shocks it delivers and because of its inability to prevent recurrences. Therefore, therapeutic options have to be aimed at the arrhythmia substrate. Currently, transcatheter radiofrequency ablation and surgical cryoablation are the only available options. We present the case report and long-term follow-up of a patient who had refractory incessant VT that was successfully treated with surgical cryoablation.

A 52-year-old man was admitted to our institution in December 1996. His medical history included chronic renal failure, and 2 renal transplants (1976 and 1989), and an inferolateral myocardial infarction in 1984. Coronary angiography at the time of the myocardial infarction revealed 90% stenosis in the right coronary artery and a 30% left ventricular ejection fraction. The patient continued on medical treatment until November 1993, when he began to experience exertional chest discomfort and palpitations. Repeat coronary angiography showed findings similar to those of 1984, except that the left ventricular ejection fraction had decreased to 20%. The patient was found to be in heart failure. During 1996, he was admitted to local hospitals 6 times for sustained VT that required cardioversion on each occasion. Amiodarone therapy (600 mg/day) was instituted in various combinations with other antiarrhythmic agents; however, the VT continued to be refractory to medical management. In November 1996, the patient was referred to a European center for further evaluation and treatment. He was found to have 4 different types of inducible VT: 3 were noted to have left bundle-branch block morphology, and 1 had right bundle-branch block morphology. Radiofrequency ablation attempts were unsuccessful; therefore, a Medtronic ICD (Medtronic; Minneapolis, Minn) was implanted in November 1996. Antitachycardia pacing was also unsuccessful in converting the VT, and the patient returned to the hospital for recurrence of VT not controlled by ICD and amiodarone combined. In December, the patient was transferred to our institution.

Following admission, the patient continued to be in incessant ventricular tachycardia that remained refractory to the various parenteral combinations of antiarrhythmic medications. A nuclear perfusion study (technetium-99 sestamibi) showed a large scar on the inferior wall of the left ventricle (presumably from the previous myocardial infarction) and no evidence of stress-induced ischemia. The electrocardiogram indicated normal sinus rhythm (Fig. 1).

Fig. 1 12-lead electrocardiogram showing ventricular tachycardia manifesting a second morphology of QR waves.

Electrophysiologic studies showed 3 types of inducible VT (Figs. 2–4), all hemodynamically stable. Meanwhile, multiple ineffective shocks and numerous antitachycardia overdrive pacing attempts were ineffective. A repeat attempt at radiofrequency catheter ablation was unsuccessful, despite extensive mapping of both ventricles and guidance by transesophageal echocardiography to direct the mapping catheter to the area of the left ventricular inferior wall aneurysm.

Fig. 2 12-lead electrocardiogram during sustained ventricular tachycardia with left bundle-branch morphology and atrioventricular dissociation. Tachycardia cycle length is 580 ms.

Fig. 3 12-lead electrocardiogram during ventricular tachycardia. Cycle length is 450 ms; very wide QRS complexes manifest left bundle-branch block morphology and left-axis deviation.

Fig. 4 12-lead electrocardiogram in sinus rhythm. There is evidence of left ventricular hypertrophy and inferior wall myocardial infarction. The presence of ST-segment elevation in inferior leads suggests left ventricular aneurysm.

On 31 December 1996, the patient underwent surgery, during which a large area of scar tissue was noted in the inferior wall of the left ventricle. The heart was 1st mapped externally, which showed that arrhythmic foci were entering the epicardium along the anterior border of the septum. The left ventricle was then opened and mapped internally. The arrhythmias were emanating from the rim of the scar tissue caused by the previous myocardial infarction. A CryoProbe (Bruker Instruments, Inc.; Billerica, Mass) was used on multiple areas along the border of the scar tissue; eventually, the heart converted to sinus rhythm. The patient tolerated the procedure well. After surgery, he had no further episodes of VT or even single premature ventricular contractions. He did, however, manifest transient left bundle-branch block during sinus rhythm. The ICD was programmed to detect the VF at more than 200 beats/min and to defibrillate the ventricle at 34 J. Bradycardia pacing backup was programmed at the rate of 40 beats/min.

During his most recent follow-up visit on 7 July 1998, the patient was in stable condition. He reported substantial improvement in his daily functioning. Echocardiography showed an ejection fraction of approximately 30%, indicating an improvement in left ventricular function, and he was in New York Heart Association functional class II. The patient continues to take 200 mg of amiodarone daily.

Incessant VT is an uncommon arrhythmia that is refractory to antiarrhythmic drugs and to repeated external cardioversion. This type of VT is a therapeutic challenge, in that antiarrhythmic agents can cause myocardial depression or vasodilation, thus aggravating the condition. ¹ Such medications might even encourage the incessant mechanism itself by slowing cardiac conduction and assisting reentry. Moreover, antiarrhythmic agents, separately or in combination, can initiate torsades de pointes and subsequent hemodynamic decline. Use of an ICD is also ineffective; its relatively slow rate is not particularly effective for tachycardias, and it is not suited to incessant arrhythmias. ¹ In fact, because an ICD delivers multiple shocks and does not prevent recurrences, its use is contraindicated as a sole therapeutic option. ²

Transcoronary chemical (alcohol) ablation ² is a new treatment for VT that is still in the experimental stage. The 1st step of this technique is precise endocardial mapping. Then the smallest tachycardia-related coronary vessel is cannulated, and intracoronary cold saline or antiarrhythmic agents are injected to test whether the tachycardia will terminate. If that is successful, a small amount of pure ethanol is injected into the vessel. In our patient, this approach was not possible because of long-term occlusion of the right coronary artery.

The treatment of choice for incessant tachyarrhythmia is direct intervention to alter the substrate; however, safety must be the foremost consideration. ¹ The available options are radiofrequency catheter ablation or ablative surgery; of these, radiofrequency ablation is preferred. ³ Its success rate in patients who have ventricular tachycardia with structural heart disease ranges from 45% to 75%. Recently, Greenspon and coworkers ⁴ reported their development and use of a multielectrode “basket” catheter for endocardial recording and pacing. This catheter may decrease the length of time required for VT analysis and enhance the postoperative outcome of radiofrequency ablation. ⁴ Even after successful radiofrequency ablation, the use of an ICD is generally advisable because recurrence of the arrhythmia occurs so frequently. ³ It has been shown that with the use of a hand-held probe, ⁵ freezing in the area of an old scar can ablate the associated arrhythmogenic substrate of VT permanently. In addition, the use of reversible “ice mapping” allows electrophysiologic properties to be overridden, thereby enabling examination of the arrhythmogenic area before definitive ablation is performed.

In a study by Lee and colleagues, ⁶ the operative mortality rate of patients undergoing ventricular surgery was 8%; an age of more than 65 years was the most important risk factor. Postoperative programmed electrical stimulation showed 63% of the patients to have noninducible tachycardia and the other 37% to have inducible tachycardia. Shumway's group ⁷ reported similar results. In a postmortem examination, Watanabe and associates ⁸ performed a histologic examination of chronic cryolesions in a case involving ventricular tachycardia. A homogenous fibrous scar was found, with sinusoid capillary proliferation all around. The boundary between the area of fibrosis and the healthy myocardium was distinct. Those authors concluded that cryothermia, by clearly defining lesions unlikely to cause arrhythmias, constitutes an effective surgical technique for correcting arrhythmias.

In summary, our patient had incessant ventricular tachycardia despite treatment with a combination of antiarrhythmic medications. A cardioverter/defibrillator was implanted, and several attempts of programmed electrical stimulation and radiofrequency ablation were unsuccessful. Finally, intraoperative arrhythmia mapping and application of cryoablation halted the ventricular tachycardia. At an 18-month follow-up, the patient was free of arrhythmia, with a satisfactory left ventricular ejection fraction and functional class.