(Circulation. 1997;96:4307-4313.)
© 1997 American Heart Association, Inc.
Articles |
Ventricular Tachycardia in Valvular Heart Disease
Facilitation of Sustained Bundle-Branch Reentry by Valve Surgery
From the Electrophysiology Laboratories, University of Wisconsin–Milwaukee Clinical Campus, Sinai Samaritan and St Luke's Medical Centers, Milwaukee, Wis.
Correspondence to Zalmen Blanck, MD, 2901 West Kinnickinnic River Pkwy, Suite 470, Milwaukee, WI 53215.
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Abstract |
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Background The clinical characteristics of sustained monomorphic ventricular tachycardia (SMVT), when it develops after valve surgery, have not been described.
Methods and Results Between 1985 and 1996, 31 patients (30 men and 1 woman) who had undergone valve surgery were found to have inducible SMVT. Nine patients (29%) had sustained VT due to bundle-branch reentry (BBR) (group 1). Four of these patients had normal left ventricular function, and VT with a right bundle-branch morphology was inducible in 4 patients. Group 2 included 20 patients with inducible myocardial (ie, non-BBR) VT. Coronary artery disease was present in 15 group 2 patients (75%) due to atherosclerotic (n=12) and nonatherosclerotic (n=3) causes. Two patients had both inducible sustained BBR and myocardial VT (group 3). Sustained BBR VT occurred significantly earlier after valve surgery (median, 10 days) than the onset of postoperative myocardial VT (median, 72 months; P<.005).
Conclusions Myocardial VT was the most common type of inducible SMVT in patients with valvular heart disease. The majority of these patients had underlying coronary artery disease and significant left ventricular dysfunction. However, in almost one third of the patients, sustained BBR VT was the only type of inducible SMVT. This type of VT was facilitated by the valve procedure occurring within 4 weeks after surgery in most patients. In these patients, left ventricular function was relatively well preserved, and the right bundle-branch block type of BBR was frequently induced. Because a curative therapy can be offered to these patients (ie, bundle-branch ablation), BBR should be seriously considered as the mechanism of VT in patients with valvular heart disease, particularly if the arrhythmia occurs soon after valve surgery.
Key Words: ablation • valves • heart disease • tachycardia • bundle-branch reentry
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Introduction |
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Valve replacement is frequently performed in patients with severe valvular heart disease. However, after surgery, patients continue to be at risk for untoward events from progressive myocardial dysfunction, prosthetic valve–related problems, and sudden cardiac death.1 In a large series of 1533 patients who underwent aortic or mitral valve replacement, 20% of the deaths were sudden, and 6% of the deaths were directly attributed to arrhythmias.2 Among patients with aortic valve disease, VT has been documented as a cause of sudden death.3 Furthermore, ventricular arrhythmias seem to increase in frequency soon after valve surgery.4
Myocardial stretch, ischemia, and excess catecholamines are some of the postulated mechanisms for ventricular arrhythmias in patients with valvular heart disease.5 Few data exist on the clinical characteristics and electrophysiological mechanisms of inducible sustained VT in patients with valvular heart disease. Although VT due to BBR has been reported in patients with valvular heart disease,6 the prevalence and characteristics of this arrhythmia have not been addressed. The purposes of this study therefore were (1) to describe the clinical and electrophysiological characteristics of SMVT in a cohort of patients who had undergone valve surgery and (2) assess the prevalence of BBR as the mechanism of inducible sustained VT. To our knowledge, this is the first study to systematically analyze the characteristics of SMVT in this clinical setting.
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Methods |
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We reviewed the clinical, electrophysiological, and surgical records of 96 consecutive patients who had undergone valve surgery and were subsequently referred for electrophysiological evaluation of documented or suspected ventricular arrhythmias between 1985 and 1996. Only patients with inducible SMVT were included in this study. Patients underwent a right and left heart catheterization to assess the hemodynamic severity of their valve disease, presence of coronary artery disease, and left ventricular function. The severity of valvular lesions was also assessed by Doppler echocardiography. Patients with acute mitral regurgitation due to myocardial infarction were excluded.
Electrophysiological Study
Electrophysiological evaluation was
performed in the postabsorptive state according to previously described
methods.7 When possible, the baseline
electrophysiological evaluation was
performed in the absence of antiarrhythmic drugs. Several multipolar
electrode catheters were introduced through central and/or
peripheral veins. These were positioned under fluoroscopic
guidance in the high right atrium, across the tricuspid valve to
record His-bundle and/or right bundle-branch electrograms, and in
the right ventricle.
Programmed electrical stimulation was performed from the right ventricular apex or outflow tract using constant or short-to-long basic drives, and up to three extrastimuli were introduced. Intravenous isoproterenol was used if patients were on antiarrhythmic drugs or VT was not inducible at baseline. In patients not taking oral antiarrhythmic drugs, intravenous procainamide8 (up to 10 mg/kg) was administered if VT was not inducible, and the pacing protocols were repeated. Surface ECG leads (I, II, and V1), intracardiac electrograms, and time lines were displayed simultaneously on an oscilloscope and printed on a thermal recorder. Electrical stimulation was performed using a digital stimulator (Bloom Associates).
Diagnostic criteria for BBR VT have been previously reported9,10 and include (1) the QRS morphology of the tachycardia exhibits a typical RBBB or LBBB pattern; (2) the onset of ventricular depolarization is preceded by His-bundle (H), right bundle-branch, or left bundle-branch potentials with an appropriate sequence of H-RB-LB activation and relatively stable HV (ventricle), RB-V, or LB-V intervals; (3) spontaneous variations in VV intervals are preceded by similar changes in HH intervals; (4) the induction of tachycardia during programmed stimulation is consistently dependent on achieving a critical conduction delay in the His-Purkinje system; and (5) BBR is noninducible after successful RBB ablation. If the VT was induced by programmed stimulation but did not fulfill these criteria, it was considered to originate in the myocardium (ie, non-BBR VT or myocardial VT).
Ablation of the RBB was performed using previously described techniques.9 A 7F deflectable quadripolar catheter with a 4-mm tip was positioned across the tricuspid valve to record the RBB potential. Radiofrequency energy was delivered when a stable RBB potential was obtained from the distal electrodes of the ablation catheter. The end point of the procedure was the appearance of complete RBBB on the surface ECG and noninducibility of BBR tachycardia. In patients treated with an ICD, discharges were considered appropriate if they were preceded by syncope or the electrograms were indicative of a ventricular arrhythmia (ie, the morphology of the electrograms was different from those of sinus rhythm).
Follow-up information was obtained from the hospital records and by contacting the patients or the referring physicians by telephone. We compared the clinical and electrophysiological characteristics of patients with BBR (group 1) and non-BBR VT (group 2).
Statistical Analysis
Data are expressed as the mean±1 SD for all continuous
variables. The mean values of the two groups were compared using
the Student's t test (unpaired). Fisher's exact test was
used to compare the categorical variables. A value of
P<.05 was considered statistically significant.
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Results |
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Ninety-six patients with valvular heart disease and previous valve surgery underwent an electrophysiological study for a documented or suspected ventricular arrhythmia. Patients were excluded (n=65) if they had polymorphic VT or ventricular fibrillation (n=8), nonsustained VT (n=8), or no inducible sustained VT (n=49) during programmed electrical stimulation. There were 31 patients (30 men and 1 woman; mean age, 64±13 years) with inducible SMVT that developed after valve surgery. Nine of the 31 patients (29%) had sustained BBR VT (group 1), and 20 patients (65%) had non-BBR, myocardial VT (group 2). Two patients (6%) had inducible VT due to both mechanisms (group 3). Cardiac arrest, syncope, or presyncope was the presenting symptom in >70% of these patients (7 patients in group 1 and 15 patients in group 2). The left ventricular ejection fraction of the 31 patients was 36±16% (range, 13% to 68%). Four of the 9 patients (44%) in group 1 had normal left ventricular function (ie, ejection fraction,
55%) compared with 1 of the 20 patients (5%) in group 2
(P
.05). The baseline clinical characteristics of both
groups are summarized in Table 1
.
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Underlying Valvular Disease
Of the 31 patients, 29 (94%) had undergone prosthetic
valve replacement. The remaining 2 patients underwent mitral valve
repair for mitral regurgitation (n=1) and aortic
valvotomy for aortic stenosis (n=1), respectively (Table 2).
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Group 1
All 9 patients (29%) with inducible sustained BBR VT (Figs 1 and 2)
had previously undergone valve replacement (metallic
prosthesis, n=7; bioprosthetic valve, n=2). The
indication for valve replacement was aortic valve disease in 7 patients
(23%) (aortic regurgitation, n=5; aortic
stenosis, n=2) and mitral regurgitation in 2
patients (6%).
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Group 2
Among the 20 (65%) patients with myocardial VT (Fig 3), 18
patients had undergone valve replacement (metallic prosthesis,
n=16; bioprosthetic valve, n=2). The indication for valve
replacement was aortic valve disease in 9 patients (29% (aortic
stenosis, n=4; aortic regurgitation, n=5),
mitral regurgitation in 6 patients (19%), and the
involvement of both aortic and mitral valves in 3 patients (10%). One
patient with mitral regurgitation had undergone mitral
valve repair, and 1 patient with aortic stenosis had undergone
aortic valvotomy.
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Group 3
In 2 patients (6%), both BBR VT and myocardial VT were inducible;
they developed VT 3 and 8 years after aortic valve replacement for
aortic stenosis.
Concomitant Coronary Artery Disease
Group 1
Two of the 9 patients had three-vessel coronary artery
disease (patients 3 and 9; Table 3).
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Group 2
Fifteen of the 20 patients (75%) had significant coronary
artery disease: atherosclerotic coronary artery disease in 12
and nonatherosclerotic coronary occlusion in 3
(coronary embolism, n=2; surgical injury to the circumflex
artery, n=1). Two of these 3 patients developed a
perioperative myocardial infarction. The other patient
was suspected of having a coronary embolism 15 years after
valve replacement (Table 4).
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Group 3
Both of the group 3 patients had prior myocardial infarction due
to coronary artery disease.
Electrophysiological Findings
The HV interval was 82±13 ms in group 1 and 51±15 ms in group 2
(P<.001). During right ventricular programmed
stimulation, SMVT was induced in all 31 patients. Five patients were on
antiarrhythmic therapy for recurrent VT before
electrophysiological testing.
In group 1, the cycle length of the induced tachycardia was 276±46 ms (versus 260±39 ms for the clinical VT in 4 patients). The morphology of the induced BBR tachycardia was LBBB in 5 patients, RBBB in 1 patient, and both RBBB and LBBB in 3 patients (the spontaneous VT was documented by ECG only in 2 patients, both of whom with an LBBB morphology).
Among the group 2 patients, the tachycardia cycle length was 304±47 ms (P=NS compared with group 1). The morphology of the VT was RBBB pattern (n=13), LBBB pattern (n=4), and multiple VT morphologies (n=3).
In the group 3 patients, the BBR VT cycle length was 300±113 ms, and the morphology was RBBB in 1 patient and LBBB in the other. The myocardial VT cycle length was 350±28 ms, and the morphology was RBBB in 1 patient and LBBB in the other.
Facilitation of BBR VT by Valve Replacement Surgery
Among the 9 group 1 patients who had undergone valve replacement
surgery, sustained BBR VT occurred in the early postoperative period
(median, 10 days) in 7 patients (range, 1 to 27 days). In another
patient with an episode of VT a few days before aortic valve
replacement, the tachycardia became incessant and
refractory 24 hours postoperatively, requiring multiple cardioversions
and emergent electrophysiology study and catheter ablation of the RBB.
Therefore, in 8 of 9 patients, the tachycardia developed
for the first time or worsened in the immediate postoperative period.
In the remaining patient, the VT occurred 4 years after the valve
surgery. None of the group 1 patients had intramyocardial VT inducible
before or after ablation of the RBB.
Myocardial VT and Valve Replacement Surgery
Among the 20 group 2 patients, VT developed after a
median duration of 72 months (range, 1 day to 23 years) after valve
surgery. Five patients with myocardial VT had no associated
coronary artery disease. In this subgroup of patients, the VT
cycle length was 295±47 ms; the morphology was LBBB in 2 and RBBB in 3
patients. Of these 5 patients, 3 had severe left
ventricular dysfunction with left ventricular
ejection fractions of <30%. Eight of 9 patients in group 1 (89%)
presented with VT in the first postoperative month versus 3 of
20 patients (15%) in group 2 (P<.01) (Table 5).
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Treatment and Follow-up
Group 1
Eight patients were treated with catheter ablation of the RBB, and
1 patient received an ICD at another institution. The mean follow-up
was 30±29 months. Two patients treated with RBB ablation died from
progressive heart failure. The other 7 patients are alive and well.
Only 1 patient is on antiarrhythmic therapy (amiodarone for
atrial fibrillation).
Group 2
Of the 20 patients, 19 received ICDs (95%) and 1 patient was
treated with amiodarone. The mean follow-up of this group was
38±28 months. There were 7 deaths: 6 patients died of cardiac failure,
and 1 patient died from recurrent VT (the implanted defibrillator was
turned off at the patient's request). One patient with progressive
left ventricular dysfunction is being considered for
cardiac transplantation. Among the patients treated with ICDs, 10
received appropriate discharges for recurrent VT. Two patients were
lost to follow-up.
Group 3
Both patients received appropriate ICD discharges for recurrent
VT. One patient subsequently underwent cardiac transplantation for
progressive heart failure. Both are alive and well.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Two types of SMVT were seen in patients with valvular heart disease: myocardial VT, the most common type, was usually associated with underlying coronary artery disease (75% of the patients), and/or significant left ventricular dysfunction (mean left ventricular ejection fraction, 33%). The other type of SMVT was BBR, which accounted for about one third of all inducible SMVTs. Although the prevalence of BBR VT in this study was similar to that in patients with idiopathic dilated cardiomyopathies, several unique features of BBR VT were seen in those patients with valvular heart disease, as discussed below.
Role of Anatomic Substrate in the Mechanism of VT
Inducible SMVT is unusual in the absence of a prior myocardial
infarction or ventricular
dysfunction.11 Patients with valvular
heart disease but without the above-mentioned substrates are,
therefore, less likely to have VT due to reentry in the
myocardium. Because these patients frequently have disease
in the His-Purkinje system, BBR may emerge as an important mechanism of
SMVT in this population, regardless of their underlying
ventricular function. The proximity of the bundle of His
and proximal bundle branches to the aortic and mitral valve
annuli12 makes them vulnerable to the
pathological processes involving either of these valve structures and
accounts for the frequent occurrence of conduction abnormalities in
these patients.13,14
Prior Studies
Sudden death due to ventricular arrhythmia has
been reported in patients with aortic valve
disease,3 and ventricular
arrhythmias have been documented before sudden death in
patients with mitral valve disease.15 As seen in
this and prior studies, surgical correction of the valve lesion does
not eliminate the risk of ventricular arrhythmias
or sudden death.2 In studies based on Holter
monitoring, VT was observed in 
10% of patients after aortic
valvulotomy and in 13% after aortic valve
replacement.16
Sustained BBR in the Setting of Valvular Heart
Disease
Although sustained BBR VT is known to occur in patients with
valvular heart disease, only isolated cases have been
previously reported.17,18 In this series of
patients with BBR VT due to valvular heart disease, we describe
several previously unreported features.
First, sustained BBR VT occurred a median of 10 days after valvular surgery compared with myocardial VT that occurred a median of 72 months after valve surgery. Given the long natural history of valvular heart disease before valve replacement, it is striking that the onset of BBR VT clustered in the immediate postoperative period in most patients (89%). This is in sharp contrast to myocardial VT, which occurred a median of 72 months after surgery. Valve surgery may worsen the His-Purkinje system conduction abnormalities known to be a prerequisite for sustained BBR.10 Conduction abnormalities are common in valvular heart disease13,14 due to the associated ventricular dilatation and the calcification of the valvular annuli. Because the valvular annuli are in close proximity to the specialized conduction system,12 the conduction abnormalities may worsen by the excision of the native valve and its replacement.19,20 In this context, hemorrhagic lesions involving the His bundle and bundle branches among patients who died early after valve replacement have been reported.21,22 These factors, along with the heightened adrenergic state of the postoperative period, could facilitate BBR VT. It is notable that among 13 patients with valvular heart disease and sustained BBR VT,6,17,18,23 BBR VT occurred in 11 of these patients (85%) after valve replacement, a finding almost identical to ours. In a report by Touboul et al,17 a patient developed sustained BBR VT in the immediate postoperative period (ie, within 48 hours) after aortic valve replacement. Mehdirad et al18 reported 8 patients with valvular heart disease and BBR tachycardia. All these 8 patients developed BBR VT after valve replacement surgery, but the interval was not reported.
A high incidence of sudden death in the first 2 years after valve
surgery has been reported particularly in those with
intraventricular conduction
abnormalities.24 Interestingly, the risk for
sudden death peaked at 3 weeks after mitral or aortic valve
replacement surgery.2 The temporal relationship
of BBR tachycardia and valve surgery documented in this
study and the postoperative sudden deaths reported in the literature
are very similar. Our data suggest that sustained BBR VT may be a more
common cause of postoperative mortality than is usually suspected in
this setting.
(2) Forty percent of patients with sustained BBR VT had normal
left ventricular function. In the present study, the
ejection fraction was 43±19% and 4 patients had ejection fractions
55%. As in other settings where sustained BBR may occur, significant
left ventricular dilatation and/or dysfunction is not
essential,25 and the HV interval is significantly
prolonged.22 The mere presence of conduction
abnormalities in the His-Purkinje system may create the appropriate
electrophysiological milieu for the
development of sustained BBR VT.
(3) Forty percent of the patients had inducible BBR VT with an RBBB configuration. In contrast to patients with dilated cardiomyopathies in whom LBBB-BBR is, by far, the most common type of BBR and RBBB-BBR is rarely seen (ie, 6% of all BBR VTs in the absence of valvular heart disease [unpublished observations]), BBR associated with valvular heart disease frequently manifests an RBBB QRS configuration. BBR VT with RBBB has been previously reported in patients with valvular heart disease.26 In this study, >40% of the patients had RBBB-BBR. The reason for this is not clear. However, the different underlying substrate and trauma associated with valve surgery may result in different types or degrees of His-Purkinje system conduction abnormalities. Nevertheless, this morphology could allow this mechanism of VT to go unrecognized, particularly if the left ventricular function is normal.
Intramyocardial VT in Valvular Heart Disease
Intramyocardial SMVT was the most common type of VT in this study
and accounted for 70% of all inducible VTs in this patient population.
In contrast to BBR VT, there was no temporal relationship between the
onset of myocardial VT and the valve surgery. There were no significant
conduction abnormalities in the His-Purkinje system as evidenced by
normal HV intervals. The most common underlying substrate for
myocardial VT was coronary artery disease and prior myocardial
infarction or associated left ventricular dysfunction.
Clinical Outcome
In contrast to a prior study of patients with sustained BBR VT and
dilated cardiomyopathies,23
in which the cardiovascular mortality was 40% during a
15-month follow-up, the long-term survival in this study was 78%
during a follow-up period of >2 years. This may be related to the
different degrees of left ventricular dysfunction (mean
ejection fraction, 23% versus 40% in this study) and the potential
improvement of underlying ventricular function after valve
surgery.
Unlike patients with BBR VT, patients with myocardial VT have a high recurrence rate of VT (up to 52% in those with ICDs), because of the palliative nature of the chosen therapy. Although ICDs prevented sudden death in many of these patients with appropriate ICD discharges, the rate of deterioration of left ventricular function ultimately determined longevity in this group.
Study Limitations
The study group was a selected population. For example, the number
of patients with severe valvular disease with arrhythmic sudden
death before valve surgery is unknown. Furthermore, patients in whom
clinical VT was not documented or who presented with
ventricular fibrillation did not show clear evidence that
the induced VT triggered the episode of cardiac arrest or syncope.
Conclusions
Sustained BBR accounts for 30% of all SMVT after valve
surgery, and it emerges as the most common type of VT in the early
postoperative period. In this setting, the underlying
ventricular function may be preserved, and the VT may have
an RBBB morphology. Because bundle-branch ablation eliminates BBR, this
mechanism should be seriously considered when SMVT occurs early after
valve surgery. Myocardial VT usually occurs with underlying
coronary artery disease (due to atherosclerotic and
nonatherosclerotic causes) and/or ventricular
dysfunction.
Addendum
Since the original submission, another patient developed incessant
BBR VT (with both RBBB and LBBB QRS morphology) at 240 bpm 3 days after
aortic valve replacement for critical aortic stenosis. He had
normal left ventricular function and no coronary
artery disease. Because of multiple cardioversions, he underwent
emergent electrophysiological evaluation
and catheter ablation of the RBB, which successfully eliminated the
VT.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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We would like to thank Brian Schurer for preparation of the figures.
Received April 17, 1997; revision received August 25, 1997; accepted September 12, 1997.
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