© 2005 The European Society of Cardiology. Published by Elsevier Ltd. All rights reserved.
Sustained ventricular tachycardia induced by dobutamine stress echocardiography: A prospective study
Department of Cardiology, Athens Euroclinic Athens, Greece
Manuscript submitted 4 January 2005. Revision received 25 July 2005. Accepted after revision 7 May 2005.
*Corresponding author. Athens Euroclinic, 9 Athanassiadou Street, Athens 11521, Greece. Tel.: +210 6416600; fax: +210 6416661, +210 6819779. E-mail address: dkatrits{at}otenet.gr (D.G. Katritsis).
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Abstract |
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AIMS: To investigate the prognostic significance and electrophysiological characteristics of dobutamine stress echo (DSE)-induced sustained monomorphic ventricular tachycardia (VT).
METHODS: In our department, 3022 DSE studies were carried out on 2688 patients, aged 54.7±11.8 years, over a 3.5 year period. Patients with DSE-induced VT were studied by means of coronary angiography and electrophysiological testing, and were followed-up for 17.8±9.3 months.
RESULTS: During DSE, nine patients (0.3%) developed sustained monomorphic VT. Four patients had coronary artery disease, one developed spontaneous right coronary artery (RCA) dissection during DSE, one patient had peripartum cardiomyopathy and the remainder had normal coronary arteries. Logistic regression analysis did not identify clinical parameters such as left ventricular ejection fraction, documentation of an ischaemic response or the presence of non-viable myocardial segments during DSE, that could predict the occurrence of DSE-induced VT. Monomorphic VT was inducible by electrophysiological testing in two patients with CAD and reduced LVEF. During follow-up, only these two patients developed VT.
CONCLUSION: Sustained monomorphic VT is a rare complication of DSE, with no predictive value for the identification of patients with coronary artery disease and no prognostic significance in patients with normal coronary arteries. No predictors of its occurrence were identified.
Key Words: dobutamine stress echocardiography, sustained ventricular tachycardia
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Introduction |
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The reported incidence of ventricular tachyarrhythmias such as frequent ventricular ectopic beats, non-sustained or sustained ventricular tachycardia, and ventricular fibrillation, during dobutamine stress echocardiography (DSE) varies between 0.02 and 4% [1
–5]. Sustained monomorphic ventricular tachycardia (VT) has been reported to occur in 0–0.3% of DES but its prognostic significance is unknown [1–9], and the detection of clinical predictors of its occurrence has been controversial [3,4]. No longitudinal studies on patients with DSE-induced sustained VT exist. Furthermore, no electrophysiological data for the characterization of this entity have been reported. We report on an extensive series of consecutive patients subjected to DSE for investigation of chest pain. Patients with DES-induced sustained monomorphic ventricular tachycardia were prospectively studied by means of coronary angiography and electrophysiological testing, and were followed-up for a period of 11–32 months.
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Methods |
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Patients
All patients undergoing DSE at Athens Euroclinic between July 2001 and February 2004, were considered for the study. All patients with DSE-induced sustained monomorphic VT, during this period, were recruited and subjected to coronary angiography, electrophysiological testing, and follow-up with 24-h ambulatory ECG monitoring at 3-month intervals. The trial was approved by our Institutional Review Board and all patients with DSE-induced VT had provided written, informed consent.
Dobutamine stress echocardiography
All stress echocardiography studies were performed by an experienced operator with dobutamine infusion for the assessment of myocardial viability, as previously described [10,11]. Dobutamine was administered intravenously with an infusion rate of 10 µg kg–1 min–1 for 3 min, increasing by 10 µg kg–1 min–1 every 3 min, up to a maximum of 50 µg kg–1 min–1. In patients not achieving 90% of their age- and gender-predicted maximal heart rate and without symptoms or signs of myocardial ischaemia, atropine was administered, starting with 0.25 mg intravenously and repeated up to a maximum of 2.0 mg with continuation of dobutamine infusion [11]. The left ventricle was divided into 16 myocardial segments according to the model proposed by the American Society of Echocardiography [12]. Throughout the dobutamine infusion the ECG was continuously monitored (three leads) and recorded (12 leads) at 1 min intervals. Reasons for interruption of the test were: severe angina with extensive wall thickening abnormalities and/or ST-segment elevation more than 2 mm at an interval of 80 ms after the J point compared with baseline in patients without previous myocardial infarction, symptomatic reduction in systolic blood pressure <70 mmHg, significant increase of blood pressure >240/120 mmHg, or sustained ventricular tachycardia. Intravenous (IV) atenolol was available to reverse the effects of dobutamine. Dobutamine-atropine stress echocardiography was considered non-diagnostic when the peak heart rate was at least 85% of maximal in the absence of new or worsening wall thickening abnormalities.
Arrhythmia definitions
Ventricular tachycardia was defined as five or more consecutive beats arising below the atrioventricular node with an RR interval of <500 ms (>120 beats min–1) [13]. Sustained ventricular tachycardia lasted >30 s (unless requiring termination because of haemodynamic collapse), whereas non-sustained tachycardia terminated spontaneously within 30 s [14].
Coronary angiography and electrophysiological testing
Coronary angiography was performed according to standard techniques. For electrophysiological testing (EPS), patients were studied in the post-absorptive state, under sedation with diazepam and diamorphine, and after beta-blockers or other antiarrhythmic agents had been discontinued for at least 5 days. No patient was receiving amiodarone. Local anaesthesia was administered, and under fluoroscopic control multipolar electrodes were introduced into the right atrium and the His-bundle area, the coronary sinus, and the right ventricle. Bipolar electrograms were recorded from the distal pair of electrodes, filtered at 30–500 Hz, amplified at gains of 20–80 mm mV–1 and displayed and acquired on a Bard, LabSystem Duo, together with surface electrocardiogram. Programmed electrical stimulation was accomplished according to the standard Wellens protocol [15]. Initiation of ventricular tachycardia was facilitated by isoprenaline infusion of 2–5 µg min–1 aiming at a target heart rate of 120 beats min–1.
Statistical analysis
Continuous variables are presented as mean value±standard deviation. We assessed the assumption of normality in all investigated measurements by the application of Shapiro–Wilk criterion. Continuous variables in our study proved to be of not normal distribution, so comparisons of means of continuous variables were performed with the use of non-parametric Mann–Whitney test. Associations between categorical variables were tested by the use of contingency tables and the calculation of Fisher's chi-squared test. Logistic regression analysis was applied to check for any explanatory predicting variables of a dichotomous variable. All reported P-values are based on two-sided tests and compared with a significance level of 5%. SPSS 11.0 software (SPSS Inc. 2002, Illinois, USA) was used for all the statistical calculations.
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Results |
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Patient characteristics
In total, 2688 patients, aged 54.75±11.8 years, 2334 (74.93%) males and 679 (25.07%) females, underwent 3022 pharmaceutical stress echocardiographic studies with administration of dobutamine and atropine. The study population comprised two groups: group A, which included 1571 (51.9%) patients without a previous history of coronary artery disease, and group B, which included 1451 (48.1%) patients with a preexisting history of coronary artery disease (Table 1). Group A patients were investigated for chest pain. In group B, 217 patients (14.9%) had a history of aortocoronary by-pass surgery, whereas 325 patients (84.6%) had been previously submitted to percutaneous coronary intervention. Group B patients were investigated either for recurrent symptoms (1117 patients, 76.9%), or as part of their routine post-intervention follow-up (334 patients, 23.01%).
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Although 271 (8.9%) patients had poor acoustic windows, the DSE study reached a clear diagnostic result. Of the total number of DSE studies, 997 studies (32.9%) were positive, while 2025 studies (67.1%) were negative for myocardial ischaemia.
Patients with DSE-induced VT
In total, 28 cases of ventricular tachycardia were recorded. Nineteen patients had NSVT (0.6%), whereas nine patients had sustained monomorphic VT (0.3%). Clinical characteristics of patients who developed DSE-induced sustained monomorphic VT are provided in Table 2.
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Four patients with DSE-induced VT suffered ischaemic heart disease. In two of them, the clinical VT was induced at EPS. One patient developed acute chest pain and ST elevation in the inferior leads during DSE that responded to IV nitrates and atenolol. Subsequent coronary angiography revealed a non-obstructing dissection of the RCA that was successfully treated with conservative therapy. At EPS no tachycardia was induced. Three patients had DSE-induced VT in the absence of coronary artery disease or cardiomyopathy; monomorphic sustained VT was not induced at EPS. Magnetic resonance imaging failed to detect evidence of arrhythmogenic right ventricular dysplasia or other form of cardiomyopathy. Finally, one patient had DSE-induced VT in the context of a history of postpartum cardiomyopathy.
Predictors of DSE-induced VT
Patients with DSE-induced VT did not differ from the rest of the population, regarding age, 54.7±11.8 vs 54.3±14.1 years respectively (P=0.95), and sex, 3 (33.3%) females vs 679 (22.5%) females respectively (P=0.43). Left ventricular ejection fraction was lower in patients with DSE-induced VT, but the difference did not reach statistical significance (47.22±14.97% vs 53.13±14.72 respectively, P=0.14). Logistic regression analysis revealed that no clinical parameter, including left ventricular ejection fraction (P=0.23), documentation of an ischaemic response (P=0.21), and presence of at least one non-viable myocardial segment (P=0.37) during DSE study could predict the occurrence of DSE-induced VT. However, two patients with documented VT before the echocardiography study developed DSE-induced VT. Logistic regression analysis showed that DSE-induced VT could not predict the presence of significant coronary artery disease on coronary angiography (P=0.08).
EPS-induced VT
Sustained monomorphic VT with a similar morphology to that seen during DSE was induced in two patients (Table 2). Both of them had ischaemic heart disease with reduced left ventricular ejection fraction and had received an implantable cardioverter-defibrillator (ICD) in the past for ventricular tachycardia and/or fibrillation. Non-sustained polymorphic VT was also detected in two patients during the delivery of three extrastimuli; this response was considered non-specific. In the remainder, no VT could be induced despite the use of three extrastimuli and co-administration of isoprenaline.
Follow-up
Patients were followed-up for 17.8±9.3 months (range 11 to 32 months, Table 3). At follow-up, only two patients had sustained or non-sustained monomorphic ventricular arrhythmia. Both had significant coronary artery disease, were treated with implantable ICDs, and at EPS monomorphic ventricular tachycardia was inducible. No other patient had experienced episodes of palpitations or had any evidence of non-sustained VT on Holter. A patient with a history of peripartum cardiomyopathy and re-attempted pregnancy refused any further investigations but at follow-up remained asymptomatic and free of VT on Holter, having been subjected to successful caesarean section.
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Discussion |
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Clinical significance of DSE-induced VT
The clinical significance and prognostic ability of DSE-induced VT have not been so far clarified. In accordance with previous studies [1–
5] we found that VT induced during DSE in a population investigated for chest pain is not related to induction of ischaemia. Stambler et al. have recently shown that dobutamine-induced ischaemia facilitates the induction of VT during EPS, but their study included only patients with known ischaemic heart disease and a history of previous myocardial infarction [16]. Bigi et al. [9] in a cohort of 377 post-MI patients failed to establish a relationship between DSE-induced ventricular tachycardia and electrical instability of the heart 11 days after the acute event. Similarly, our results indicate that DSE-induced VT does not indicate an adverse prognosis in the absence of established risk factors for sudden cardiac death. In patients with apparently normal hearts, exercise-induced VT that is usually not inducible by programmed electrical stimulation may be seen and has been attributed to catecholamine-sensitive enhanced automaticity [17] or catecholamine-related delayed afterdepolarizations [18]. Our data suggest that DSE-induced sustained VT in the absence of heart disease has a favourable short-term prognosis. Patients with a negative EPS did not experience clinical VT in follow-up despite a lack of antiarrhythmic or other medication.
Predictors of DSE-induced VT
Poldremans et al. [3] have identified left ventricular dysfunction as well as a history of ventricular arrhythmias as predictors of the occurrence of VT/VF during stress echocardiography. However, Secknus et al. [4] in a series of 3011 tests have failed to identify such clinical predictors. Our results also indicate that coronary artery disease and reduced left ventricular ejection fraction cannot serve as predictors of DSE-induced VT. However, they also provide evidence that a history of previous VT and inducibility of clinical VT at EPS can identify patients with arrhythmia recurrence at follow-up. The additional use of echo contrast agents in order to facilitate endocardial border visualization has also been reported to enhance the arrhythmogenic effect of dobutamine in the absence of inducible myocardial ischaemia [19] but no contrast agents were used in our studies.
Study limitations
The main limitation of our study is the small number of patients with VT. However, the rarity of this condition makes such a limitation difficult to avoid, since the number of our DSE studies is amongst the largest reported in the literature. Second, in patients with DSE-induced VT in the context of an apparently normal heart, no conclusions may be drawn regarding the long-term prognosis. Although we failed to detect any deterioration of left ventricular function or symptoms, undetected genetic abnormalities predisposing to the development of ventricular arrhythmia [20,21] cannot be ruled out. Furthermore, the long-term prognostic implications of exercise-induced ventricular arrhythmias may be adverse [22,23].
In conclusion, DSE-induced VT is a rare event with no predictive value for the identification of patients with coronary artery disease. No clinical predictors of its occurrence can be identified. It carries prognostic significance only when it occurs in the context of coronary artery disease with impaired left ventricular function. In this respect, EPS is useful in identifying patients prone to tachycardia recurrences. DSE-induced VT in patients with negative DSE studies and apparently normal hearts does not appear to carry adverse prognostic significance.
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