Tag Archives: electrophysiology

Ventricular Tachycardia – Classification

Ventricular Tachycardia – Classification

Ventricular tachycardia is a common arrhythmia. The manifestations include mild symptoms of palpitation to sudden death. In next few blog posts, we will try to understand the basics of ventricular tachycardia/fibrillation and we will discuss management of these arrhythmias.

Definition:

Ventricular arrhythmias are defined as arrhythmias that originate below the bifurcation of His bundle, in the specialized conduction system, the ventricular muscle, or in combination of both tissues.

electrocardiogram_of_ventricular_tachycardia

Ventricular Tachycardia ECG

(Image created by Karthik Sheka, M.D. [CC BY-SA 2.5 (http://creativecommons.org/licenses/by-sa/2.5)], via Wikimedia Commons)

There are different classifications of ventricular arrhythmias, according to their duration, morphology of QRS complexes, and clinical characteristics.

Classification According to Duration

(1) Premature ventricular complexes (PVC): isolated complexes originating from the His-Purkinje system or ventricular myocardium.
(2) VT: 3 or more consecutive QRS complexes at a rate greater than 100 beats per minute.
(3) Nonsustained VT: VT that terminates spontaneously within 30 seconds.
(4) Sustained VT: continuous VT lasting for ≥30 seconds or that requires an intervention for termination (such as cardioversion).

Classification According to Morphology of QRS Complexes

(1) Monomorphic VT: VT that has a similar QRS configuration from beat to beat. Some variability in QRS morphology at initiation is not uncommon.
(2) Multiple monomorphic VT: more than one morphologically distinct monomorphic VT, occurring as different episodes or induced at different times.
(3) Polymorphic VT: VT that has a continuously changing QRS configuration indicating a changing ventricular activation sequence.
(4) Pleomorphic VT: VT that has more than one morphologically distinct QRS complex occurring during the same episode of VT, but the QRS is not continuously changing.
(5) Ventricular flutter: rapid VT that has a sinusoidal QRS configuration that prevents identification of the QRS morphology.
(6) VF: ventricular tachyarrhythmia that has a totally chaotic
morphology.

Classification According to Clinical Characteristics

(1) Clinical VT: VT that has occurred spontaneously based on analysis of 12-lead ECG QRS morphology and rate.
(2) Hemodynamically unstable VT: VT that causes hemodynamic compromise requiring prompt termination.
(3) Incessant VT: continuous sustained VT that recurs immediately despite repeated spontaneous or therapeutic termination.
(4) Repetitive monomorphic VT: continuously repeating episodes of self-terminating nonsustained VT.
(5) VT storm: 3 or more separate episodes of sustained VT within 24 hours, each requiring termination by an intervention.
(6) Unmappable VT: VT that does not allow interrogation of multiple sites to define the activation sequence or perform entrainment mapping. It may be due to hemodynamic
intolerance that necessitates immediate VT termination, spontaneous, or pacing-induced transition to other morphologies of VT, or repeated termination during mapping.

In the next post, we will discuss clinical features and ECG features.

DR. ANUPAM JENA
CONSULTANT INTERVENTIONAL CARDIOLOGIST & ELECTROPHYSIOLOGIST
KALINGA INSTITUTE OF MEDICAL SCIENCES
BHUBANESWAR, ODISHA
INDIA
EMAIL: drjena@live.com

Primary prevention ICD in Nonischemic cardiomyopathy

There is a recent online first article in NEJM  ( Defibrillator Implantation in Patients with Nonischemic Systolic Heart Failure – DANISH Study). The study is summarized below:

Summary:

The benefit of an implantable cardioverter–defibrillator (ICD) in patients with symptomatic systolic heart failure caused by coronary artery disease has been well documented. However, the evidence for a benefit of prophylactic ICDs in patients with systolic heart failure that is not due to coronary artery disease has been based primarily on subgroup analyses. The management of heart failure has improved since the landmark ICD trials, and many patients now receive cardiac resynchronization therapy (CRT).

Methods

In a randomized, controlled trial, 556 patients with symptomatic systolic heart failure (left ventricular ejection fraction, ≤35%) not caused by coronary artery disease were assigned to receive an ICD, and 560 patients were assigned to receive usual clinical care (control group). In both groups, 58% of the patients received CRT. The primary outcome of the trial was death from any cause. The secondary outcomes were sudden cardiac death and cardiovascular death.

Results

After a median follow-up period of 67.6 months, the primary outcome had occurred in 120 patients (21.6%) in the ICD group and in 131 patients (23.4%) in the control group (hazard ratio, 0.87; 95% confidence interval [CI], 0.68 to 1.12; P=0.28). Sudden cardiac death occurred in 24 patients (4.3%) in the ICD group and in 46 patients (8.2%) in the control group (hazard ratio, 0.50; 95% CI, 0.31 to 0.82; P=0.005). Device infection occurred in 27 patients (4.9%) in the ICD group and in 20 patients (3.6%) in the control group (P=0.29).

Conclusions

In this trial, prophylactic ICD implantation in patients with symptomatic systolic heart failure not caused by coronary artery disease was not associated with a significantly lower long-term rate of death from any cause than was usual clinical care.

This is the summary of the study. This study proves the point that primary prevention ICD doesn’t reduce the all cause mortality. But there are few points to consider in this very well designed study:

  1. SCD was the cause of death in 24 out of 120 (20%) total deaths in the ICD group. SCD was the cause of death in 46 out of 131 (35%) total deaths in the non-ICD (usual care group). So that means majority of mortality even in the non-ICD usual care group are due to non arrhythmic causes.
  2. The number of non-arrhythmic mortality in the ICD group is 96 out of total of 120 (80%) and in the non-ICD group is 65%.
  3. The question still remains that – How is a device (i.e. ICD) which prevents arrhythmic deaths, is expected to reduce the All Cause Mortality (the primary end point of this study) when the majority of deaths are due to non-arrhythmic causes.
  4. When considering the sudden cardiac deaths, ICD definitely reduced the mortality [Sudden cardiac death occurred in 24 patients (4.3%) in the ICD group and in 46 patients (8.2%) in the control group (hazard ratio, 0.50; 95% CI, 0.31 to 0.82; P=0.005)].

This study is a landmark study. It shows that the present indications for primary prevention ICD in non-ischemic cardiomyopathy are likely  include patients who may not after all benefit from a primary prevention ICD. It further shows that ICD is effective in preventing SCD in non-ischemic cardiomyopathy.

So to conclude this important study shows that we need to find markers of SCD in non-ischemic cardiomyopathy so that ICD implantation can be more effectively done in patients who are at high risk of SCD.

(Disclaimer: The views expressed are entirely personal of the author of this blog and are aimed towards an educational discussion on the study. These opinions are not meant for application in medical practice and are for the purpose of discussion only)

Keywords: Electrophysiology, Cardiomyopathy, Implantable cardioverter defibrillator, Sudden cardiac death

Cardiology MCQ – 14.05.2016


What is the most probable site of origin of the tachycardia in a patient with structurally normal heart ?

MA VT epicardial1. Right ventricular outflow tract

2. Mitral annular VT

3. Tricuspid annulus

4. Idiopathic left fascicular VT

Cardiology MCQ 18.5.15

Q. All of the following are effective in the management of reflex syncope except

A. Life style modifications like avoiding triggers

B. Physical counterpressure maneuvers

C. Beta blockers

D. Cardiac pacing in patients with cardioinhibitory reflex syncope

Explanation:

According to ESC guideline 2009, beta blockers are no longer recommended and have been given class III recommendation for the treatment of reflex syncope. The first step in the management of reflex syncope is life style modifications like – avoiding triggers such as crowded places, prolonged standing etc.

-Physical counterpressure maneuvers are emerging as nonpharmacologic treatments for
syncope. These maneuvers include tensing of crossed legs, handgrip and arm tensing, abdominal binders, and support stockings.

-Class IIa recommendations include cardiac pacing for patients with dominant cardioinhibitory, carotid sinus sensitivity, and frequently recurrent reflex syncope after 40 years of age with documented cardioinhibitory responses during monitoring.

-Remember that pacemaker implantation in patients with reflex syncope and no evidence of cardioinhibitory reflexes is not indicated and can be harmful (class III).

Reference:

1. Guidelines for the diagnosis and management of syncope (version 2009) The Task Force for the Diagnosis and Management of Syncope of the European Society of Cardiology (ESC). European Heart Journal (2009) 30, 2631–2671

Answer: C

Keywords: Cardiology review, Cardiology, Multiple choice questions, medical tudents, Electrophysiology,  Syncope

Cardiology MCQ 26.4.15

All of the following statements about Arrhythmogenic Right Ventricular
Dysplasia/Cardiomyopathy are correct except

A. Pathogenic mutations can be identified in 50% of patients

B. The clinical presentation is between 2nd to 5th decade of life

C. Left dominant arrhythmogenic cardiomyopathy most commonly involves apical septal segment of left ventricle

D.  Left-dominant disease is more commonly seen in patients with desmoplakin mutations

Explanation:

-Arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) is an inherited cardiomyopathy. Although structural involvement of the right ventricle predominates, a left dominant form of ARVD/C has been described

-Ventricular arrhythmias, increased risk of sudden cardiac death, and abnormalities of right ventricular structure and function characterize this disease
-The pathognomonic features are right ventricular myocyte loss with fibrofatty replacement.
-Because a pathogenic mutation can be identified in approximately 50% of affected individuals

-Patients usually present during the second to fifth decades of life with palpitations, light-headedness, syncope, or sudden death. Patients younger than 12 years and those older than 60 years rarely manifest clinical signs or symptoms of ARVD/C

-Cardiac MRI can be to detect involvement of left ventricle in patients with ARVD/C, especially those with advanced disease

-Left-dominant arrhythmogenic cardiomyopathy also occurs in and is defined by early disease of the LV, often affecting the posterolateral wall, in the absence of significant right ventricle (RV) systolic dysfunction. Left-dominant disease is more commonly seen in patients with desmoplakin mutations.

References:

1. Marcus F, Fontaine G, Guiraudon G, et al: Right ventricular dysplasia: A report of 24 adult cases. Circulation 65:384–398, 1982.
2. Corrado D, Basso C, Thiene G, et al: Spectrum of clinicopathologic manifestations of arrhythmogenic right ventricular cardiomyopathy/dysplasia: A multicenter study. J Am Coll Cardiol 30:1512–1520, 1997.
3. Dalal D, Nasir K, Bomma C, et al: Arrhythmogenic right ventricular dysplasia: A United
States experience. Circulation 112:3823–3832,2005.
4. Marcus F, Zareba W, Calkins H, et al: Arrhythmogenic right ventricular cardiomyopathy/dysplasia clinical presentation and diagnostic evaluation: Results from the North American Multidisciplinary Study. Heart Rhythm 6:984–989, 2009.
5. Sen-Chowdhry S, Syrris P, Prasad SK, et al: Leftdominant arrhythmogenic cardiomyopathy: An under-recognized clinical entity. J Am Coll Cardiol 52:2175–2187, 2008.
6. Dalal D, Tandri H, Judge DP, et al: Morphologic variants of familial arrhythmogenic right ventricular dysplasia/cardiomyopathy: A genetics-magnetic resonance imaging correlation study. J Am Coll Cardiol 53:1289–1299, 2009.
7. den Haan A, Tan B, Zikusoka M, et al: Comprehensive desmosome mutation analysis in North Americans with arrhythmogenic right ventricular dysplasia/cardiomyopathy. Circ Cardiovasc Genet 2:428–435, 2009.

Answer: C

Keywords: Cardiology review, Cardiology, Multiple choice questions, medical tudents, Electrophysiology,  Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy, ARVD/C

Cardiology MCQ 22.4.15

 CARDIOLOGY MCQ & REVIEW

Q. All of the following statements about accessory pathways (AP) are correct except

A. Majority of APs conduct both antegradely and retrogradely

B. Around 50% of patients with preexcitation have bypass tracts that conduct only antegradely.

C. Retrograde only conduction is more common than antegrade only conduction via APs

D. In around 10% of patients spontaneous disappearance of preexcitation may be seen

Explanation:

 -The vast majority of A-V bypass tracts conduct both antegradely and retrogradely.

-Less than 5% of patients with preexcitation have bypass tracts that conduct only antegradely (1). This is much less common than the converse situation of retrogradely conducting bypass tracts in the absence of antegrade preexcitation (i.e., so-called concealed bypass tracts).
-In patients who manifest only antegrade conduction over their bypass tract, spontaneous circus movement tachycardia, either antidromic or orthodromic, is not usually observed, but when it is, it is antidromic. The primary rhythm disturbance they manifest is atrial fibrillation 

-Over time antegrade conduction over an A-V bypass tract may disappear. Chen et al. (2) noted a loss of preexcitation in one fifth of symptomatic patients with WPW. Only 7.8% lost retrograde conduction. Spontaneous loss of preexcitation has been observed in one fifth to one half of children with WPW.
References:
1. Hammill SC, Pritchett EL, Klein GJ, et al. Accessory atrioventricular pathways that conduct only in the antegrade direction. Circulation 1980;62:1335–1340.
2. Chen SA, Chiang CE, Tai CT, et al. Longitudinal clinical and electrophysiological assessment of patients with symptomatic Wolff-Parkinson-White syndrome and atrioventricular node reentrant tachycardia. Circulation 1996;93:2023–2032.
Answer: B
Keywords: Cardiology review, Cardiology, Multiple choice questions, medical students, Electrophysiology, Atrial fibrillation, WPW syndrome

Cardiology MCQ 21.4.15

CARDIOLOGY MCQ & REVIEW

Q. All of the following statements about atrial flutter – fibrillation in WPW syndrome are correct except

A. Atrial fibrillation can precipitate ventricular fibrillation in patients with accessory pathways

B. The incidence of atrial flutter and/or fibrillation appears to be higher in patients with A-V bypass tracts than in the normal population

C. Prevalence of atrial fibrillation is same in patients with manifest preexcitation and those with concealed preexcitation

D. Atrial flutter-fibrillation may be the presenting arrhythmia in 5% to 10% of patients with A-V bypass tracts

Explanation:

-In patients with WPW syndrome atrial flutter and fibrillation are less common presenting arrhythmias, but they are potentially more life threatening, because they can result in extremely rapid ventricular rates that precipitate ventricular tachycardia and/or fibrillation

-Atrial flutter-fibrillation may be the presenting arrhythmia in 5% to 10% of patients with A-V bypass tracts and occurs even more commonly when orthodromic or antidromic tachycardia also is present

-As many as 50% of patients with symptomatic arrhythmias will have atrial fibrillation of variable duration at some time.

-The incidence of atrial flutter and/or fibrillation appears to be higher in patients with A-V bypass tracts than in the normal population

-Atrial fibrillation appears to be five times more common when overt preexcitation (i.e., WPW) is present than in patients with concealed bypass tracts at similar locations and similar rates of tachycardias

-Patients with atrial fibrillation have a higher incidence of inducible atrial fibrillation than those without the arrhythmia

1. Klein GJ, Bashore TM, Sellers TD, et al. Ventricular fibrillation in the Wolff-Parkinson-White syndrome. N Engl J Med 1979;301:1080–1085.
2. Cosio FG, Benson DW Jr, Anderson RW, et al. Onset of atrial fibrillation during antidromic tachycardia: association with sudden cardiac arrest and ventricular fibrillation in a patient with Wolff-Parkinson-White syndrome. Am J Cardiol 1982;50:353–359.
Answer: C
Keywords: Cardiology review, Cardiology, Multiple choice questions, medical students, Electrophysiology, Atrial fibrillation, WPW syndrome

 

Cardiology MCQ 20.4.15

Cardiology MCQ & Review

Q. Which of the following drugs is found to be useful in idiopathic ventricular fibrillation ?

A. Quinidine

B. Bisoprolol

C. Verapamil

D. Sotalol

 

Explanation:

Idiopathic ventricular fibrillation has a high recurrence rate.

The recommended therapy is implantation of implantable cardioverter defibrillator. Currently, recommendations for a specific drug therapy are not available.

Antiarrhythmic agents had no effect on the recurrence rate in the patients from the Unexplained Cardiac Arrest Registry of Europe

In a study by Belhassen et al.,patients with IVF have received oral quinidine guided by serial electrophysiological studies. In patients receiving continuous quinidine treatment, no recurrences of VF were reported during a mean follow-up period of 9.1 ± 5.6 years. In a subset of patients, these promising results were confirmed during longterm follow-up.

Currently pharmacologic therapy serves as an adjunct to ICD therapy in patients with multiple ICD discharges.

 

References:

1.Belhassen B, Viskin S, Fish R, et al: Effects of electrophysiologic-guided therapy with Class IA antiarrhythmic drugs on the long-term outcome of patients with idiopathic ventricular fibrillation with or without the Brugada syndrome. J Cardiovasc Electrophysiol 10:1301–1312, 1999.
2. Belhassen B, Glick A, Viskin S: Excellent longterm reproducibility of the electrophysiologic efficacy of quinidine in patients with idiopathic ventricular fibrillation and Brugada syndrome. Pacing Clin Electrophysiol 32:294–301, 2009.

Answer: A (Quinidine)

Keywords: Cardiology review, Cardiology, Multiple choice questions, medical students, Electrophysiology, Ventricular fibrillation

Cardiology MCQ 18.4.15

Cardiology MCQ & Review

All of the following statements about fascicular reentry ventricular tachycardia are true except

A. Fascicular VTs  account for around 10% of idiopathic VTs

B. Left posterior fascicular VT is the most common, with a narrow right bundle, left inferior axis QRS morphology.

C. Left anterior fascicular VT is less common and has right bundle, right inferior axis QRS morphology.

D.  These tachycardias are also referred to as verapamil-sensitive fascicular tachycardias, given their tendency to slow or terminate with intravenous verapamil.

Explanation:

-Most patients with VT have structural heart disease, 10% have idiopathic VT, occurring in the setting of a structurally normal heart

-Among idiopathic VTs, those arising from the right or left ventricular outflow tract are most common, followed by fascicular VT, which accounts for between 7% and 12% of idiopathic VTs

-Left posterior fascicular VT is the most common, with a narrow right bundle left superior axis QRS morphology.
-Left anterior fascicular VT is less common and has right bundle right inferior axis QRS morphology

-These tachycardias are also referred to as verapamil-sensitive fascicular tachycardias, given their tendency to slow or terminate with intravenous verapamil
-Fascicular VT typically manifests in young adulthood with a slight male preponderance

-Presentation consists of palpitations, presyncope and, rarely syncope, but not sudden cardiac death

-Incessant, fascicular VT has been reported to cause tachycardia-mediated cardiomyopathy

-In some patients, the arrhythmia may manifest only during exercise.

References:

1. Tada H, Ito S, Naito S, et al: Idiopathic ventricular arrhythmia arising from the mitral annulus: A distinct subgroup of idiopathic ventricular arrhythmias. J Am Coll Cardiol 45:877–886, 2005.
2. Lin D, Hsia HH, Gerstenfeld EP, et al: Idiopathic fascicular left ventricular tachycardia: Linear ablation lesion strategy for noninducible or nonsustained tachycardia. Heart Rhythm 2:934–939, 2005.
3. Belhassen B, Rotmensch HH, Laniado S: Response of recurrent sustained ventricular tachycardia to verapamil. Br Heart J 46:679–682, 1981.
4. Bennett DH: Experience with radiofrequency catheter ablation of fascicular tachycardia. Heart 77:104–107, 1997.
5. Nakagawa H, Beckman KJ, McClelland JH, et al: Radiofrequency catheter ablation of idiopathic left ventricular tachycardia guided by a purkinje potential. Circulation 88:2607–2617, 1993.
6. Lee HW, Kim JB, Joung B, et al: Successful catheter ablation of focal automatic left ventricular tachycardia presented with tachycardia-mediated cardiomyopathy. Yonsei Med J 52:1022–1024, 2011.

Answer: B (Left posterior fascicular VT has right bundle branch and left superior axis )

Keywords: Cardiology review, Cardiology, Multiple choice questions, medical students, Electrophysiology, Ventricular tachycardia