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

MCQ 17.04.2015

All of the following statements about ventricular fibrillation are true except

1.Ninety to ninety-five percent of individuals with ventricular fibrillation reveal underlying structural heart disease.

2. No structural heart disease can be identified in 55% to 60% of patients.

3.According to the results of the Cardiac Arrest Survivors With Preserved Ejection Fraction Registry (CASPER) among patients with normal left ventricular function, idiopathic ventricular fibrillation (IVF) was diagnosed in 44% of patients with ventricular fibrillation without structural heart disease.

4.The diagnosis of idiopathic ventricular fibrillation (IVF) is based on the exclusion of currently known structural and primary electrical heart diseases following a complete noninvasive, invasive, and genetic workup.

Explanation:

-Ventricular fibrillation in patients without structural heart disease is rare. 90-95% of individuals with ventricular fibrillation reveal underlying structural heart disease

-No structural heart disease can be identified in only 5% to 10% of patients

-According to the results of the Cardiac Arrest Survivors With Preserved Ejection Fraction Registry (CASPER) among patients with normal left ventricular function, a causal diagnosis
for ventricular fibrillation can be found in 56%. Most diagnoses were primary electrical diseases (catecholaminergic polymorphic ventricular tachycardia [CPVT], long QT syndrome, early repolarization syndrome, and Brugada syndrome [69%]). In 31% of patients, a subtle structural heart disease (i.e., coronary spasm, subclinical arrhythmogenic right ventricular cardiomyopathy and myocarditis) was identified. In addition, idiopathic ventricular fibrillation (IVF) was diagnosed in 44% of patients with ventricular fibrillation without structural heart disease.

-The diagnosis of IVF is based on the exclusion of currently known structural and primary electrical heart diseases following a complete noninvasive, invasive, and genetic workup.

Ref:
1.Krahn AD, Healey JS, Chauhan V, et al: Systematic assessment of patients with unexplained cardiac arrest: Cardiac Arrest Survivors With Preserved Ejection Fraction Registry (CASPER). Circulation 120:278–285, 2009.

2. Rosso R, Kogan E, Belhassen B, et al: J-point elevation in survivors of primary ventricular fibrillation and matched control subjects: incidence and clinical significance. J Am Coll Cardiol 52:1231–1238, 2008.

3. Napolitano C, Bloise R, Monteforte N, et al. Sudden cardiac death and genetic ion channelopathies: long QT, Brugada, short QT, catecholaminergic polymorphic ventricular tachycardia, and idiopathic  ventricular fibrillation. Circulation 125:2027–2034, 2012.

Answer : B

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

MCQ 16.04.2015

All of the following arrhythmias are usually seen in structurally normal heart except

A. Right ventricular outflow tract ventricular tachycardia

B. Fascicular reentry ventricular tachycardia

C. Bundle branch reentry ventricular tachycardia

D. Catecholaminergic polymorphic ventricular tachycardia

 

Explanation:

Bundle branch reentry (BBR) ventricular tachycardia (VT) is a unique, fast (200 to 300 beats/min), monomorphic tachycardia associated with hemodynamic collapse, syncope, and/or cardiac arrest.

It is caused by a macroreentry circuit involving the right and left bundle branches, an upper common pathway, and septal ventricular muscle.

BBRoccurs in patients who have dilated cardiomyopathy and in those with coronary artery disease, valvular heart disease, myotonic dystrophy, or even no heart disease with associated His-Purkinje system disease.

The incidence is reported to be 3.5% and 6% of ventricular tachycardias

Classification of ventricular arrhythmias in the absence of structural heart disease

I. Non–life-threatening (typically monomorphic)
A. Outflow tract
Right ventricular outflow
Left ventricular outflow
Aortic sinus of Valsalva
Peri His bundle
B. Idiopathic left ventricular tachycardia
Left posterior fascicle
Left anterior fascicle
High septal fascicle
C. Other
Mitral annulus
Tricuspid annulus
Papillary muscle
Perivascular epicardial
II. Life-threatening (typically polymorphic)
A. Genetic syndromes
Long QT
Brugada
Catecholaminergic polymorphic ventricular tachycardia
Short QT
B. Idiopathic ventricular fibrillation

Answer: C

Ref:

1. Blanck Z, Dhala A, Deshpande S, et al: Bundle branch reentrant ventricular tachycardia: Cumulative experience in 48 patients. J Cardiovasc Electrophysiol 4:253–262, 1993.

2 . Blanck Z, Jazayeri M, Dhala A, et al: Bundle branch reentry: A mechanism of ventricular tachycardia in the absence of myocardial or valvular dysfunction. J Am Coll Cardiol 22:1718–1722, 1993.

3. Eric N. Prystowsky, Benzy J. Padanilam, Sandeep Joshi,  Richard I. Fogel. Ventricular Arrhythmias in the Absence of Structural Heart Disease. J Am Coll Cardiol 2012;59:1733–44

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

One MCQ a day- 15.04.2015

MCQ 15.04.2015

Which of the following statements describes the ECG findings of Intramural septal premature ventricular contractions ?

A. RBBB morphology with inferior axis

B. RBBB morphology with superior axis

C. LBBB morphology with inferior axis

D. LBBB morphology with superior axis

 

Explanation:

Intramural septal PVCs arise from the interventricular septum. They have been described recently.  In one series seven of 93 consecutive patients (8%) referred for ablation of idiopathic ventricular arrhythmias (mean age, 4914 years; 52 men; ejection fraction, 5212%) were found to have a site of origin in the interventricular septum.Five of 7 patients had symptomatic frequent premature ventricular complexes (PVCs) and 2 had frequent asymptomatic PVCs. The left ventricular ejection fraction was reduced in 2 of 7 patients who had ejection fractions of 30% and 42% before the ablation. The mean ejection fraction of the 7 patients was 55.9%. There was no evidence of structural heart disease in these patients, based on echocardiography, stress testing, and cardiac MRI.

-All 7 patients with an intramural focus had PVCs with a left bundle-branch block, inferior-axis morphology

-The differential diagnosis of a intramural septal PVC includes origin from

1. RVOT

2. Aortic cusp

3. Para-Hisian area

There are no definite ECG findings to differential these sites of origin and final localization needs mapping.

The mapping is done through advancing a catheter through a septal perforator vein

Answer : C

 

One MCQ a day- 14.04.2015

Answer to the question on 13.04.2015:

Answer : A (Right ventricular outflow tract)

Explanation:

12-lead electrocardiographic (ECG) morphology helps in identifying the PVC origin

Left bundle branch block morphology with an inferior axis indicates an outflow tract origin of the PVCs, with a late precordial transition (>V3) pointing to an origin in the right ventricular outflow tract, and an early transition (V3) suggesting an origin from the aortic cusps, the left ventricular outflow tract, or the basal left ventricular epicardium.

Right bundle branch block PVC morphologies indicate a left ventricular origin, with positive concordance indicating a basal origin and a precordial transition to an R/S complex suggesting origin in the papillary muscle.

Intramural arrhythmias are more difficult to localize, and a specific pattern has not yet been described.

Ref:

1. Baman TS, Ilg KJ, Gupta SK, et al: Mapping and ablation of epicardial idiopathic ventricular arrhythmias from within the coronary venous system.Circ Arrhythm Electrophysiol 3:274–279,2010.

2. Good E, Desjardins B, Jongnarangsin K, et al: Ventricular arrhythmias originating from a papillary muscle in patients without prior infarction: A comparison with fascicular arrhythmias. Heart Rhythm 5:1530–1537, 2008.
3. Yokokawa M, Good E, Chugh A, et al: Intramural idiopathic ventricular arrhythmias originating in the intraventricular septum: Mapping and ablation. Circ Arrhythm Electrophysiol 5:258–263, 2012.

MCQ 14.04.2015

Treatment to decrease or eliminate frequency of premature ventricular contractions (PVC) is indicated in all of the following cases except

A. PVC triggering VT/VF

B. Frequent PVC causing nonresponse to cardiac resynchronization therapy

C. Asymptomatic occasional PVC

D. Very frequent PVC (>24% of QRS complexes on holter monitoring)

See below for answers

 

Explanation:

Treatment to decrease or eliminate PVCs should be considered in patients when an expected benefit in terms of symptoms or cardiac function exists. The categories of patients who should undergo treatment that targets PVCs can be summarized as follows:
• Patients with PVCs believed to be causing or contributing to LV dysfunction or dilatation
• Patients with symptomatically limiting PVCs • Patients with VT or VF for which a PVC trigger can be identified
• Patients in whom response to cardiac resynchronization therapy is limited by frequent PVCs
• Patients in whom deterioration of LV function may be expected, such as those with very frequent PVCs (>24%), may also be considered for therapy to reduce PVCs

Although clinical data regarding the last category are not yet definitive, PVC frequency in this range has been shown to often result in LV dysfunction, and a decision must be made on an individual basis between close follow-up of cardiac function versus prophylactic treatment to eliminate the PVCs.

Answer : C

(Ref: Cardiac Electrophysiology: From Cell to Bedside: 6th edition. Page 810)

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

One MCQ a day: 13.04.2015

Answer to the question on 12.04.2015:

Answer : A

Explanation:

The ECG is showing atrial fibrillation with fast ventricular rate. The important issue in this ECG is that the ventricular rate is extremely fast, reaching up to 300 bpm. AF with very fast ventricular rate is suggestive of conduction over bypass tracts. Patients with preexcited atrial fibrillation who are hemodynamically stable are to be treated with intravenous procainamide or ibutilide. Patients who present with hemodynamic instability should undergo urgent direct current cardioversion. So the right answer is intravenous procainamide. after management of the acute episode the patient should be advised to undergo electrophysiological study with ablation of the accessory pathway as definitive therapy.

Ref: Blomstrom-Lundqvist C, Scheinman MM, Aliot EM, et al: ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias—executive summary: A report of the American College of Cardiology/American Heart Association task force on practice guidelines and the European Society of Cardiology committee for practice guidelines (writing committee to develop guidelines for the management of patients with
supraventricular arrhythmias). Circulation 108:1871–1909, 2003.

MCQ 13.04.2015:

What is the site of origin of the premature ventricular contractions :

VPC-RVOT

A. Right ventricular outflow tract

B. Left ventricular outflow tract

C. Papillary muscle

D. Left ventricular basal epicardium

Answers please

I will put the explanation and answer tomorrow

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