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Table of Contents
ORIGINAL ARTICLE
Year : 2022  |  Volume : 12  |  Issue : 4  |  Page : 168-172

Etiology, clinical profile, and 1-year outcome of patients presenting with nonischemic ventricular tachycardia: An observational study


Department of Cardiology, Nizam's Institute of Medical Sciences, Hyderabad, Telangana, India

Date of Submission06-Mar-2022
Date of Decision04-Apr-2022
Date of Acceptance05-Apr-2022
Date of Web Publication19-Dec-2022

Correspondence Address:
Dr. Oruganti Sai Satish
Department of Cardiology, Nizam's Institute of Medical Sciences, Hyderabad - 500 082, Telangana
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jicc.jicc_7_22

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  Abstract 


Background: Although ventricular tachycardia and the ventricular fibrillation occur more often in adults with coronary artery disease, These ventricular arrhythmias may appear in young people, often early and late after surgery for congential heart disease or in association with a variety of cardiac disease ,autonomic imbalance, drugs, as well as in the absence of detectable cardiac desease, when serious ventricular tachyarrhythmias occur in the young they may be misdiagnosed as aberrantly conducting supraventricular tachycardias because of their presumed infrequency. Information on clinical characteristics and outcome of patients with NIVT in our patient population is limited. Aims and Objectives: This prospective observational study was aimed at patients presenting with NIVT to our tertiary care center and to analyze their clinical features, electrocardiogram (ECG) characteristics, underlying disease, management and clinical outcome at one year of follow up. Methods: It is an observational prospective study of 50 patients who presented with nonischaemic VT (NIVT) to our tertiary care center. History , physical examination ,chest X-RAY, electrocardiogram (ECG) and echocardiography were done. Details of electrophysiological studies and radio frequency ablation were collected. Antiarrhythmic drug history was noted. Patients were followed for a period of one year for their clinical outcome and their response to different modalities of treatment was noted. clinical Events defined as death, hospitalizations, DC shocks and recurrence of disease and time to event was also noted. Results: Among the total 50 patients, 27(54%) were males and 23(46%) were females. The mean age of presentation was 31 to 40 years.Most common presenting symptom was syncope (75%). Most common etiology was found to be idiopathic dilated cardiomyopathy with severe LV dysfunction (26%) followed by inflammatory cardiomyopathy (10%). post valvular replacement surgery for rheumatic heart disease , hypertrophic cardiomyopathy , idiopathic right ventricular outflow tract tachycardia were found in 6 percent of patients in each category. LBBB and RBBB morphology of VT in ECG seen in 37 and 44% of patients respectively. Immediate mortality rate was 12%, mainly seen in patients with electrolyte imbalance secondary to systemic infections and myocarditis related to covid 19 infection. Mean survival time in our study is 39.16 weeks with 95% confidence interval. Events have occurred in 30% of our patients most commonly in patients with idiopathic DCMP. Recurrent episodes of VT are more common in patients with DCMP ejection fraction less than 35 percent and also in ARVD patients after LV involvement. Conclusion: NIVT requires aggressive management to prevent mortality and morbidity.Recurrent episodes of VT can occur after disease progression in DCMP and these patients have poor prognosis. Aggressive management like cervical sympathetic denervation may be required in these patients when presented with VT storm. A comprehensive evaluation of patients with NIVT will allow recognition of underlying etiology and selection of appropriate treatment strategies like cervical sympathetic denervation ,radiofrequency ablation and AICD implantation apart from drug therapy for effective control of VT.

Keywords: Dilated cardiomyopathy with ventricular tachycardia, long QT syndrome, nonischemic ventricular tachycardia


How to cite this article:
Mani Krishna S V, Satish OS. Etiology, clinical profile, and 1-year outcome of patients presenting with nonischemic ventricular tachycardia: An observational study. J Indian coll cardiol 2022;12:168-72

How to cite this URL:
Mani Krishna S V, Satish OS. Etiology, clinical profile, and 1-year outcome of patients presenting with nonischemic ventricular tachycardia: An observational study. J Indian coll cardiol [serial online] 2022 [cited 2023 Feb 8];12:168-72. Available from: https://www.joicc.org/text.asp?2022/12/4/168/364217




  Introduction Top


Ventricular tachycardia (VT) is defined as three or more consecutive ventricular complexes that usually occur at the rate of 100–250 beats/min. Ischemic heart disease and nonischemic cardiomyopathies (NICMs) are among the most frequent causes of VT.[1] The overall incidence of sustained VT following myocardial infarction (MI) has been found to have declined in recent years due to major advances in MI management, resulting in smaller infarct scars.[2]

The etiology of nonischemic VT (NIVT) is diverse. It includes structural diseases like idiopathic cardiomyopathy, hypertrophic cardiomyopathy (ARVC), post myocarditis, cardiac sarcoidosis, in patients years after surgery for valvular heart disease and tetralogy of Fallot. Other channelopathies include catecholaminergic polymorphic VT, long QT syndrome, short QT syndrome, J wave syndromes like brugada and early repolarization syndrome. Outflow tract , annular and fascicular tachycardias are also important etiological substrates for NIVT. Acquired causes include electrolyte abnormalities such as hypokalemia, hypomagnesemia, hypocalcemia, antiarrhythmic drugs (AADs), antibiotics, antipsychotics, endocrine, intracranial, and nutritional disorders.

Information on clinical characteristics and outcomes of patients with NIVT in our patient population is limited. This prospective observational study was aimed at patients presenting with NIVT to our tertiary care center and to analyze their clinical features, electrocardiogram (ECG) characteristics, underlying disease, management, and clinical outcome at 1 year of follow-up.


  Material and Methods Top


This is a prospective observational study consisting of 50 consecutive patients of all ages presented to our center with a history of NIVT. Patients who fulfilled the below criteria were included in the study.

  1. Patients with ECG evidence of VT with no evidence of ischemia
  2. Patients with exercise-induced VT on the exercise stress test
  3. Patients presenting with VT with normal coronaries on coronary angiography.


History, physical examination, chest X-ray, ECG, and echocardiography were done in all patients who met the above inclusion criteria. Holter recordings and graded treadmill exercise stress test by Bruce protocol were done if required. Coronary angiogram was done to rule out the ischemic etiology of VT. Details of electrophysiological studies and radiofrequency ablation were collected. AAD history was noted. Patients were followed for 1 year and their clinical outcome and response to different modalities of treatment were noted. Events such as death, hospitalizations, and direct current (DC) shocks were recorded, and time to event was also noted. The data were entered and analyzed using the SPSS 19.0 (Chicago, IL, USA). All descriptive variables were expressed as mean value + standard deviation (SD). All categorical variables were presented as percentages and absolute values.


  Results Top


Among 50 patients, 27 (54%) were male and 23 (46%) were female. The mean age of presentation was 31–40 years.

The most common presenting symptom was syncope (75%), followed by palpitations (56%), followed by breathlessness (42%) [Table 1]. The most common etiology was found to be idiopathic dilated cardiomyopathy (DCMP) with severe left ventricular (LV) dysfunction (26%), followed by inflammatory cardiomyopathy (10%). Post valvular replacement surgery for rheumatic heart disease, HCM, and idiopathic RV outflow tract tachycardia was found in 6% of patients in each category. Peripartum cardiomyopathy (PPCMP), ARVC, posterior fascicular VT, and idiopathic RV cardiomyopathy as the cause of NIVT were also detected in 6% each [Figure 1]. In patients with long QT syndrome, exercise is the most common precipitating factor and they underwent successful cervical sympathetic denervation.
Table 1: Baseline characteristics of the study population

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Figure 1: Pie diagram showing etiology of nonischemic VT. VT: Ventricular tachycardia, RV: Right ventricular

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Left bundle branch block (LBBB) and right bundle branch block (RBBB) morphology VT ECG was seen in 37 and 44% of our patients, respectively [Figure 2]. Forty-four percent of patients underwent successful automatic implantable cardioverter defibrillator (AICD) implantation. Fourteen percent of patients underwent radiofrequency ablation of VT focus [Figure 3]. Sympathetic denervation through bilateral stellate ganglionectomy was done in one patient who presented with VT storm. During 1-year follow-up, recurrent episodes of VT with the need for additional AAD were required in 10% of patients. The immediate mortality rate was 12%, mainly seen in patients with electrolyte imbalance secondary to systemic infections and myocarditis related to COVID-19 infection. The mean survival time in our study is 39.16 weeks with a 95% confidence interval [Figure 4]. Events have occurred in 30% of our patients, most commonly in patients with idiopathic DCMP.
Figure 2: Kaplan–Meier curve showing 1-year event-free survival in nonischemic ventricular tachycardia patients

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Figure 3: Bar diagram showing various VT treatment modalities in our study

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Figure 4: Kaplen mayer curve showing one year event free survival in NIVT patients

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  Discussion Top


VT and ventricular fibrillation were more common in adults with coronary artery disease but also can occur in young people because of various other etiologies. In this study, we analyzed etiology, clinical features, precipitating factors, prognosis in different types of NIVT, and 1-year outcome of these patients.

The most common presenting symptom was syncope (75%), followed by palpitations (56%) and breathlessness (42%). In our study, about half of the patients with sustained VT did not have palpitations during the tachycardia. This observation has important implications regarding the evaluation of patients with unexplained syncope or near syncope. The lack of palpitations in association with these symptoms does not exclude the possibility that the symptoms were due to VT.

The most common etiology for VT in our study was found to be idiopathic DCMP with severe LV dysfunction (26%), followed by inflammatory cardiomyopathy (10%), followed by other etiologies such as valve replacement surgery for rheumatic heart disease, HCM, ARVC, posterior fascicular VT, and idiopathic RV cardiomyopathy (6%).

Idiopathic DCMP was among the known and frequent causes of VT.[3] Among all the patients of DCMP, idiopathic variety was found in 17 patients. History of viral myocarditis was present in two idiopathic DCMP patients. Two patients had alcoholic cardiomyopathy. Five patients with DCMP had evidence of inflammatory infiltrates by positron-emission tomography scan were classified as inflammatory cardiomyopathies. These patients also had late gadolinium enhancement (LGE) in cardiac magnetic resonance imaging (MRI) in noncoronary distribution, especially in the midventricular region similar to sarcoidosis. However, genetic testing for sarcoidosis and lymph node biopsy for giant cells was negative. The exact cause of inflammation could not be identified. Hypercalcemia and serum angiotensin-converting enzyme levels were also normal. Sustained VTs can occur any time after undergoing a valve surgery. In our study, VT was observed after mitral valve replacement in two patients after 3 years of surgery and 5 years after aortic valve replacement in one patient. Eckart et al.[4] reported that periannular scars were frequently observed in patients with VT developed after the valvular repair.

Idiopathic RV cardiomyopathy and idiopathic RV outflow tract tachycardia were found in 6% each. Patients having abnormalities in RV myocardium in cardiac MRI or echocardiogram not fulfilling the criteria for diagnosis of ARVD were classified as idiopathic RV cardiomyopathy in our study. HCM was the etiology in 6% of NIVT in our study. Two patients underwent AICD implantation. None had LV outflow tract obstruction. LGE on cardiac MRI was detected in both patients. ARVC and posterior fascicular VT were also seen in 6% of patients each. Of all the patients with ARVC, none of the patients had classical ECG features of ARVC. One ARVC patient developed LV dysfunction with recurrent implantable cardioverter-defibrillator (ICD) shocks during follow-up, and MRI showed LV involvement in the same patient.

Among three patients with PPCMP, two patients presented with incessant VT which was unresponsive to multiple DC shocks and intravenous antiarrhythmics and died within 10 h of their presentation. Vascular insult caused by antivascular or hormonal effects of late pregnancy and early postpartum period induces cardiomyopathy in women with an underlying predisposition. Three percent of the deaths occurred within the first 30 days of diagnosis in PPCM.[5]

Prolonged QT interval (QTc) >450 ms is seen in 14% of patients in our study. Long QT syndrome was found in two of our patients with exercise as the precipitating factor. Both were female children <15 years of age who presented with exertional syncope. Their resting ECG showed QTc of 580 ms. Exercise-induced QTc prolongation was also observed. They were treated with beta-blockers and left cardiac sympathetic denervation (LCSD). LCSD shortens the QTc, reduces catecholamines, and increases ventricular refractoriness and the VT threshold, which are proposed mechanisms for its efficacy in VT control. Bilateral cardiac sympathetic denervation is considered when LCSD is ineffective. Bradfield et al. reported the success of neuromodulatory interventions in controlling VT storm.[6]

Acquired electrolyte imbalance secondary to systemic infections and myocarditis related to COVID-19 as the cause of NIVT was noted in two patients each. Hypokalemia was the most common electrolyte abnormality in patients with systemic infections. One patient presented with VT following 5 years after the complete repair of tetralogy of Fallot. Sustained VT has occurred in patients with repaired tetralogy of Fallot, where it was seen as a manifestation of hemodynamic problems (usually severe pulmonary regurgitation) requiring repair; as a reflection of RV dilation and dysfunction; and in relation to ventricular scarring.[7] Our patient had no pulmonary regurgitation but had mild RV dysfunction. Another child presented with bradycardia-induced VT because of congenital complete heart block and was treated with permanent pacemaker. It is well-known fact that bradycardia causes QT prolongation that, in turn, is linked to transmural dispersion of repolarization, which acts as a substrate for initiation and perpetuation of phase 2 reentry in torsade de pointes.[8]

One patient presented with VT secondary to takotsubo cardiomyopathy developed because of prolonged abdominal surgery in our study. The above patient died 1 day after surgery.

Malignant ventricular arrhythmia, particularly torsade de pointes associated with takotsubo-related QT prolongation, may occur in these patients.[9] VT secondary to drugs was found in three patients. Tricyclic antidepressant drugs poisoning was the most common etiology, followed by anesthetic drugs. Two young girls presented with hypotension following amitriptyline self-poisoning. ECG showed long QT interval with polymorphic VT stabilized by DC shock and sodium bicarbonate infusion.

VT presenting with LBBB morphology was seen in 37% of patients. In 41% of patients, VT morphology has not shown any specific morphology as either LBBB or RBBB. The preprocedural analysis of the VT morphology is an indispensable tool for planning the ablation and increasing the probability of success.[10] There is a correlation between VT morphology and scar area in NICM patients. VT morphology can be an important clue to identify which patients are likely to benefit from an epicardial approach.[11]

Signal-averaged ECG (SAECG) abnormalities in the form of late potentials were observed in all three patients with ARVC, one patient with long QT syndrome, and four patients with idiopathic DCMP. SAECG may be useful to identify patients at low risk for SCD, but its routine use to identify patients at high risk for SCD is not yet adequately supported by the current American Heart Association Guidelines.[12]

Forty-four percent of patients underwent successful AICD implantation. ICD is the mainstay of VT therapy in those patients who are at risk of sudden cardiac death. However, while the benefit of ICDs in patients with ischemic cardiomyopathies (ICMs) has been well described,[13] no randomized trials have yet clarified their beneficial role in NICM.[14] The recent DANISH trial has raised questions about whether ICD therapy in patients with NICM results in the reduction of total mortality. A recent meta-analysis suggests that there is indeed a significant risk reduction in total mortality with ICDs in NICM patients without concomitant cardiac resynchronization therapy (CRT), especially in those with less advanced heart failure.[15]

Fourteen percent of patients underwent radiofrequency ablation of VT focus in our study. Many studies have reported more mixed or inferior outcomes after the ablation in patients with NICM as compared to in those with ICM likely because of the heterogeneous VT substrates and different VT ablation strategies.[16]

Bilateral stellate ganglionectomy was done in two patients in NICM who presented with VT storm. Clinical reports of bilateral cardiac sympathetic denervation to treat severe ventricular arrhythmias date back to 1961 when successfully utilized by Estes and Izlar.[17] BCSD is favored if the monomorphic VT originated from an RV scar, a structurally normal heart, NICM without scar, or if the VT is polymorphic.[17]

The VANISH trial showed a 34% reduction in the relative risk of recurrent VT storms with radiofrequency ablation compared to the addition of AADs.[18] Nademanee et al. showed sympathetic blockade is superior to AAD in managing VT storm and suggested that left sympathetic ganglion block effectively controls VT because left-sided cardiac sympathetic nerves have high arrhythmogenic potential.[19] During 1-year follow-up, recurrent episodes of VT with the need for additional AAD were required in 10% of our study patients. Recurrence of VT episodes was most commonly noted in idiopathic DCMP and ARVD patients.


  Conclusions Top


  • NIVT requires aggressive management to prevent mortality and morbidity
  • Patients with NIVT require a comprehensive strategy of management, including metabolic correction and AADs, radiofrequency ablation, sympathetic denervation, and AICD for effective control of VT.


Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Aronow WS, Ahn C, Mercando AD, Epstein S, Kronzon I. Prevalence and association of ventricular tachycardia and complex ventricular arrhythmias with new coronary events in older men and women with and without cardiovascular disease. J Gerontol A Biol Sci Med Sci 2002;57:M178-80.  Back to cited text no. 1
    
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3.
Sudan R, Yaqoob I, Aslam K, Bhat IA, Beig JR, Alai S, et al. Profile of patients presenting with sustained ventricular tachycardia in a tertiary care center. Indian Heart J 2018;70:699-703.  Back to cited text no. 3
    
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Eckart RE, Hruczkowski TW, Tedrow UB, Koplan BA, Epstein LM, Stevenson WG. Sustained ventricular tachycardia associated with corrective valve surgery. Circulation 2007;116:2005-11.  Back to cited text no. 4
    
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Sliwa K, Petrie MC, VSan der Meer P, Mebazaa A, Hilfiker-Kleiner D, Jackson AM, et al. Clinical presentation, management, and 6-month outcomes in women with peripartum cardiomyopathy: An ESC EORP Registry. Eur Heart J 2020;25:112-4.  Back to cited text no. 5
    
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Bradfield JS, Ajijola OA, Vaseghi M, Shivkumar K. Mechanisms and management of refractory ventricular arrhythmias in the age of autonomic modulation. Heart Rhythm 2018;15:1252-60.  Back to cited text no. 6
    
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Kamiya CA, Iwamiya T, Neki R, Katsuragi S, Kawasaki K, Miyoshi T, et al. Outcome of pregnancy and effects on the right heart in women with repaired tetralogy of fallot. Circ J 2012;76:957-63.  Back to cited text no. 7
    
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Engle MA, Ebert PA, Redo SF. Recurrent ventricular tachycardia due to resectable cardiac tumor. Report of two cases in two-years-olds in heart failure. Circulation 1974;50:1052-7.  Back to cited text no. 8
    
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Syed FF, Asirvatham SJ, Francis J. Arrhythmia occurrence with takotsubo cardiomyopathy: A literature review. Europace 2011;13:780-8.  Back to cited text no. 9
    
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Miller JM, Jain R, Dandamudi G, Kambur TR. Electrocardiographic localization of ventricular tachycardia in patients with structural heart disease. Card Electrophysiol Clin 2017;9:1-10.  Back to cited text no. 10
    
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Oloriz T, Silberbauer J, Maccabelli G, Mizuno H, Baratto F, Kirubakaran S, et al. Catheter ablation of ventricular arrhythmia in nonischemic cardiomyopathy: Anteroseptal versus inferolateral scar sub-types. Circ Arrhythm Electrophysiol 2014;7:414-23.  Back to cited text no. 11
    
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Goldberger JJ, Cain ME, Hohnloser SH, Kadish AH, Knight BP, Lauer MS, et al. American Heart Association/American College of Cardiology Foundation/Heart Rhythm Society scientific statement on noninvasive risk stratification techniques for identifying patients at risk for sudden cardiac death. A scientific statement from the American Heart Association Council on Clinical Cardiology Committee on Electrocardiography and Arrhythmias and Council on Epidemiology and Prevention. J Am Coll Cardiol 2008;52:1179-99.  Back to cited text no. 12
    
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Kadish A, Dyer A, Daubert JP, Quigg R, Estes NA, Anderson KP, et al. Prophylactic defibrillator implantation in patients with nonischemic dilated cardiomyopathy. N Engl J Med 2004;350:2151-8.  Back to cited text no. 14
    
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Anantha Narayanan M, Vakil K, Reddy YN, Baskaran J, Deshmukh A, Benditt DG, et al. Efficacy of implantable cardioverter-defibrillator therapy in patients with nonischemic cardiomyopathy: A systematic review and meta-analysis of randomized controlled trials. JACC Clin Electrophysiol 2017;3:962-70.  Back to cited text no. 15
    
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Gökoğlan Y, Mohanty S, Gianni C, Santangeli P, Trivedi C, Güneş MF, et al. Scar homogenization versus limited-substrate ablation in patients with nonischemic cardiomyopathy and ventricular tachycardia. J Am Coll Cardiol 2016;68:1990-8.  Back to cited text no. 16
    
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Liang JJ, Santangeli P, Callans DJ. Long-term outcomes of ventricular tachycardia ablation in different types of structural heart disease. Arrhythm Electrophysiol Rev 2015;4:177-83.  Back to cited text no. 17
    
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Sapp JL, Wells GA, Parkash R, Stevenson WG, Blier L, Sarrazin JF, et al. Ventricular tachycardia ablation versus escalation of antiarrhythmic drugs. N Engl J Med 2016;375:111-21.  Back to cited text no. 18
    
19.
Nademanee K, Taylor R, Bailey WE, Rieders DE, Kosar EM. Treating electrical storm: Sympathetic blockade versus advanced cardiac life support-guided therapy. Circulation 2000;102:742-7.  Back to cited text no. 19
    


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