Surgery for ventricular tachycardia. The view from Paris

International Journal of Cardiologv, Elsevier Biomedical Press

1 (1982) 351-359

351

Editorial

Review

Surgery for ventricular tachycardia. The view from Paris Guy Fontaine Centre de Stimulation

Cardiaque et de Rythmologie,

H6pital Jean-Rostond,

Ivysur-Seme,

France

The traditional surgical management of ventricular tachycardia (VT) was based on two principles, the excision of post-infarction scar tissue (aneurysmectomy) and myocardial revascularization by aorto-coronary bypass [ 1.21. Recurrences of VT were observed with both techniques suggesting that these surgical procedures were far from ‘optimal’ [3]. In the first case, the ‘border zone’ between the scar tissue and adjacent healthy myocardium, now known to be the point of origin of arrhythmias, could have been inadvertantly resected [4], and in the second it is easy to think that the revascularization procedure could only be truly effective when bypassing a coronary stenosis responsible for paroxysmal acute ischemia [5,6]. Our group has developed new approaches based on data obtained in patients with VT unrelated to ischemic heart disease [7]. The first case was a patient with primary cardiomyopathy with attacks of life-threatening tachycardia resistant to all available anti-arrhythmic drugs. Peroperative epicardial mapping performed during VT localized the epicardial breakthrough of the abnormal activation. Simple ventriculotomy at this point in the search for underlying anatomical changes did not reveal any abnormality but the patient remained free of VT thereafter. Two other important features were demonstrated during the same operation: the arrhythmia could be induced and terminated at will by programmed pacing (the patient underwent emergency surgery without preoperative electrophysiological investigations), and post-excitation potentials were recorded [8]. These findings suggested that an intramyocardial reentry phenomenon was responsible for the arrhythmia [9]. Good results with the same surgical technique in the following cases of VT unrelated to myocardial infarction led us to suppose that simple ventriculotomy at the point of epicardial breakthrough of the abnormal activation could interrupt a possible intramyocardial reentry pathway [lo].

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Guy

Fontaine.

Hbpital

Jean-Rostand.

0 Elsevier Biomedical

Press

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rue Jean

Le Galleu,

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352

Ventricular tachycardia not related to myocardial infarction

We have classified VT unrelated to myocardial infarction into a number of groups based on the data available at that time. This led us to the definitions of new pathologic condition concepts. Arrhythmogenic right ventricular dysplasia

The results of surgery in the so-called arrhythmogenic right ventricular dysplasia syndrome have been very favorable [ 11,121. The explanation probably lies in the fact

Fig. 1. Epicardial mapping of the right ventricle in two instances of ventricular tachycardia in a case of arrhythmogenic right ventricular dysplasia. The point of epicardial emergence suggests that the origin of the abnormal rhythm could be situated in the interventricular septum. This could explain difficult management of the arrhythmia during operation, and the recurrences of ventricular tachycardia during the early phase and the follow up. This patient has been finally correctly treated by drugs and leads a normal life.

353

that left ventricular function is hardly affected by this condition. Recurrent VT can be attributed to a septal point of origin of the arrhythmia (Fig. l), or to a deviated point of epicardial breakthrough caused by intramyocardial block within the pathological right ventricular wall. However, when postoperative relapses occurred it was generally possible to treat them with antiarrhythmic therapy which had been ineffective preoperatively. Idiopathic

left ventricular

aneurysm

Excellent results have been observed in idiopathic left ventricular aneurysm as the left ventricular lesions were very limited [lo]. The classification and significance of these cases is still unclear. Idiopathic

ventricular

tachycardia

In the group of patients with idiopathic VT originating high up in the interventricular septum, the striking feature was the quasi-total failure of surgery in preventing the arrhythmia which recurred with virtually the same configuration and rate. We were only able to reduce the frequency of attacks of VT in one case using cryosurgery at several points on the upper part of the interventricular septum, the arrhythmia being reduced to a few runs of a dozen or so complexes at the most, which were asymptomatic and detected on Holter monitoring [ 131. Surgical management of such cases seems to be limited by the anatomical site of origin of the arrhythmia for which a more appropriate method is still awaited. In the remaining patients of non-ischemic ventricular tachycardia. diminished left ventricular reserve was a major limiting factor; this was observed in congestive cardiomyopathy, idiopathic left ventricular tachycardia, cardiac tumor and Uhl’s anomaly. In Uhl’s anomaly a more appropriate surgical technique could have prevented myocardial failure [ 141. Mortality The overall early mortality rate during the first month in these 26 cases of VT unrelated to myocardial infarction was 15% and the relapse rate in the same period was also 15%. The overall mortality with 7 years follow-up was 31% and the relapse rate 35%. However, it must be emphasized that the majority of these cases were easily treated medically with all patients leading normal lives. A more detailed analysis of these cases has been published elsewhere [ 151.

Ventricular tachycardia related to myocardial infarction We tried to use the same technique of simple ventriculotomy in VT complicating myocardial infarction but the results were less satisfactory [16]. This was partially due to the fact that the lesions were severe, leading to the excision of myocardial

354

tissues which was incompatible with normal left ventricular function. The other problem was that most of these arrhythmias arose within the interventricular septum whilst mapping limited to the epicardium often revealed the earliest point of breakthrough of VT at distance from the site of origin [16-181. Encircling

endocardial ventriculotomy

The underlying concept of encircling endocardial ventriculotomy introduced by our surgeon G. Guiraudon [19] was the suppression of the arrhythmogenic activity of the border zone between the infarcted and normal tissues by the interruption of the reentry pathways. This new approach was not based on electrophysiological data recorded during surgery, but on the macroscopical appearances of the infarction scar on the endocardial surface. An incision from the endocardium to the epicardium all around the ischemic zone would then interrupt the intramyocardial reentry pathways. This technique was adapted to the underlying anatomical changes; when severe left ventricular dilatation was present, classical aneurysmectomy would be completed by encircling endocardial ventriculotomy before closing the ventricle. Simple ventriculotomy had few indications in these patients. Aorto-coronary bypass was not chosen for its anti-arrhythmic potential in the few cases in which it was performed. The surgical results in this group of VT complicating myocardial infarction have to be interpreted with caution because of the small number of patients treated and great interpatient variability. Patients with a previous history of one or more infarcts were classified with the other cases despite the aggravating nature of this association [20]. Furthermore, two cases were operated in a low output state and had been considered high operative risks because of the reduced myocardial contractility. Two patients died during follow-up due to recurrent myocardial infarction, one of which was confirmed by autopsy. The therapeutic benefit of surgery was lost in other cases. In one patient with VT in the months following aorto-coronary bypass surgery in whom the endocardial appearances were diffuse, surgery guided by endocardial mapping [21] effectively prevented the arrhythmia but refractory cardiac failure occurred a few months later. On the other hand, a case of myocardial infarction due to chest wall trauma and a case of an abnormal left anterior descending artery were included in this series. In both these cases the short- and especially long-term prognosis could well have been different to that of patients with progressive coronary artery disease. Despite these reservations, the use of these new surgical techniques in VT complicating myocardial infarction has led to a clear improvement in the prevention of the arrhythmia. As with all new techniques, encircling endocardial ventriculotomy has been improved upon with experience and better results obtained, particularly since November, 1978 [20]. Even in patients with early recurrent VT after surgery (3 cases) anti-arrhythmic therapy effectively controlled the arrhythmia whereas the same drugs at higher doses had been ineffective before operation. In one of these patients (Fig. 2), anti-arrhythmic therapy was only necessary for 6 months, after which treatment was stopped with no further recurrence of VT.

355

Fig. 2. Epicardial mapping in sinus rhythm in a case of recurrent ventricular tachycardia after anteroseptal myocardial infarction. A delay of conduction is visible at the apex of the left ventricle (minus sign). A large aneurysm was found at the opening of the left cavity. The encircling endocardial ventriculotomy prevented most of the arrhythmias but antiarrhythmic therapy was necessary during a period of six months. After that period the drug was discontinued without recurrences; however, cardiac glycosides were necessary.

An experimental study at Duke University [22] seems to have shown that the changes that result from this procedure are related more to alterations in vascularisation increasing the ischemia of the partially degenerated fibers situated in the border zone, making reentry impossible. The procedure would therefore lead to some loss in myocardial contractility but this has not been evaluated quantitatively as yet. Furthermore, iatrogenic complications may arise with this technique. In one of our cases, a small ventricular septal defect was demonstrated on postoperative angiography ~231. Of the 41 cases of VT related to myocardial infarction, 27 underwent encircling endocardial ventriculotomy; the mortality rate in the first month was 15% with 8% recurrences. The global mortality rate over the 5-year period was 33% with 24%

356

recurrences.

A more detailed

analysis

of these cases has been published

elsewhere

[201Ventridar

function

The principal problem found in the surgical treatment of chronic ventricular tachycardia whether or not related to myocardial infarction lies in the altered left ventricular function whether present before or after surgery. The cases of peroperative death, some of which were considered to be very high operative risks before surgery, demonstrate that surgery cannot be undertaken when myocardial dysfunction is severe. Surgical approach in the treatment of VT involves three independant but complementary procedures. All, with a probable ‘exception for the first, could have deleterious effect on the cardiac function. Thorucotomy. This can be performed even in patients with severe hemodynamic disturbances as in one of our cases, not included in the general series, in whom the peroperative findings of ischemic cardiomyopathy prevented any anti-arrhythmic surgical procedure. This patient was later controlled by anti-arrhythmic drugs and is still alive after several months follow-up. Cardiopulmonary bypass. Without taking its duration into account, the trauma of cardiopulmonary bypass and the changes it produces generally and in particular on myocardial contractility in patients already weakened by the disease process, may well affect the short and long-term prognosis. The specific procedure. This depends, as explained above, on the underlying anatomical changes; but even if simple encircling endocardial ventriculotomy is selected, under ideal conditions, it is still difficult to determine the exact depth of the incision and its precise position with respect to the subendocardial scar and the adjacent healthy tissues. Recurrences The second special problem is the interpretation of recurrences of VT after surgery. Early recurrences, according to our definition, are those occurring in the first post-operative month [20]. In cases of VT of septal origin the exact similarity with attacks recorded before surgery suggests that the same mechanism is operative. Early recurrences occurring in other clinical settings such as VT complicating myocardial infarction or arrhythmogenic right ventricular dysplasia are more difficult to interpret. The configuration of the QRS complexes during tachycardia are usually different after operation, but it is impossible to determine whether it is the same arrhythmia which has been distorted by the surgical action or a different VT originating from another zone.

351

Pathophysiology

of ventricular tachycardia

The results of surgery may be more easily understood when viewed in the light of modern concepts of the pathophysiology of VT [24]. If we admit that VT is caused by slow conduction in diseased fibers connected in ‘bridges’ to the healthy myocardium fulfilling the critical conditions for the initiation of intramyocardial reentry, it may be deduced that surgery results in irreversible damage to the diseased fibers in some zone indispensable for the reentry phenomenon. However, in other areas the same surgical action causes fibers which were previously far from fulfilling these critical conditions to become arrhythmogenic. This could explain why recurrent postoperative VT is easier to treat medically. We can speculate that amongst all the forms of VT, only a small percentage are life-threatening due to the rapidity of the rhythm. When refractory to medical therapy, surgery may be envisaged. If the surgical procedure definitely interrupts the reentry pathway, a possible recurrent form of VT is statistically more likely to be of a slower and less dangerous type and more sensitive to conventional anti-arrhythmic treatment. Another possibility is that surgery might only partially alter the reentry pathway, directly or indirectly and that the same tachycardia could then recur at a slower rate, making it more accessible to anti-arrhythmic drug therapy. These explanations only deal with the pathophysiological situation at a given moment in the patient’s life. They do not take into account spontaneous progression of the illness or ageing of the myocardium, two factors which may play a role in either direction. An arrhythmogenic zone may spontaneously become less dangerous whilst another more normal zone may become arrhythmogenic. This is probably the operative mechanism in the majority of late recurrences, occurring several years after surgery. This reasoning could also explain why ventricular tachycardia could occur abruptly several years after myocardial infarction without a new acute event.

Conclusion Cardiovascular surgery has provided new information in our understanding of the mechanisms and treatment of VT in man. We believe, however, that the procedures in practice at present are out of proportion to their objectives. If the intraventricular reentry concepts are correct, it will only be necessary to alter the rate of activation slightly in the zones of slow conduction to make the unidirectional blocks bidirectional. These zones can be approached in two ways: the recording of the epicardial breakthrough of the abnormal activation by mapping during VT, providing this is centered on the actual point of origin of the arrhythmia, and by the detection of post-excitation potentials. However, their sites may be much more widespread than those found in the critical situations allowing the initiation and maintenance of intraventricular reentry [25]. The treatment of VT, not only by surgery but also by any other therapeutic means, may therefore entail changing perhaps only slightly the dynamic properties of conduction in certain regions of the myocardium, in order to alter the critical

358

conditions essential for the initiation of reentry. These hypotheses are only valid in the context physiopathological mechanisms may well be operative arrhythmias.

of chronic VT as different in other forms of ventricular

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