Approach to the management of Venous thromboembolism

Step 1 :Confirm PTE or DVT diagnosis

Step 2: Look for contraindications for full dose anticoagulation. If contraindications exist then insert IVC filter.

Step 3 : If no contraindication then look for impending venous gangrene (in case of DVT) or cardiopulmonary collapse (cardiogenic shock/ RV dysfunction in case of PTE). If yes then start thrombolysis

Thrombolysis for DVT:

Indications : Impending venous gangrene, symptom duration < 14 days and low risk of bleeding

Mode : a)Catheter directed thrombolysis (CDT) : Fluroscopy guided placement of multiside holed catheter (pigtail) into the thrombus segment and infusing alteplase for 1-3 days at a rate of 0.5 mg to 3 mg/hour (50 mg diluted in 50 ml of NS). CDT is superior to systemic anticoagulation alone because of reduced post thrombotic syndrome and reduced bleeding complications

b)Pharmacomechanical Catheter directed thrombolysis (PCDT)

PCDT uses either the “Power Pulse” or “isolated thrombolysis” techniques. Power Pulse employs the AngioJet rheolytic thrombectomy system (Bayer, Warrendale, PA) to deliver and disperse the thrombolytic agent by a powerful pulse-spray injection. After bathing the clot in the thrombolytic agent, the AngioJet catheter aspirates the softened thrombus fragments. Isolated thrombolysis uses the Trellis peripheral infusion system (Covidien, Mansfield, MA) to deliver the thrombolytic agent directly into the clot. The agent is then circulated within the clot by an oscillating wire.

Advantage of PCDT over CDT : Reduced dose and infusion duration of alteplase thereby reducing bleeding complications and better efficacy

Thrombolysis for PTE :

For PTE there is insufficient evidence to recommend thrombolysis via a pulmonary artery catheter rather than systemic thrombolysis

Systemic thrombolysis dose: Alteplase 100 mg (10 mg as iv bolus over 10 min f/b 90 mg in 100 ml of NS infused over 2 hours)

Step 4

If there is no evidence of impending gangrene or cardiopulmonary collapse then initiate systemic anticoagulation

Phases of anticoagulation treatment:

Initial phase0 to 10 days:

IV or SC unfractionated heparin/LMWH/Fondaparinux/Rivaroxaban/Apixaban

Long term phase- 10 days to 3 months

Vitamin K antagonist – warfarin/acitrom (target INR: 2-3.5)

Rivaroxaban/Apixaban/Edoxaban/Dabigatran/LMWH

Extended phase-3 months to indefinite 

Indictions for extended therapy- 1.unprovoked/recurrent VTE    2. Malignancy related VTE

Drugs :

Vitamin K antagonist – warfarin/acitrom (target INR: 2-3.5)

Rivaroxaban/Apixaban/Edoxaban/Dabigatran/LMWH

Newer agents : Rivaroxaban(15 mg bd)/Apixaban(10 mg bd)/Edoxaban/Dabigatran(110 or 150 mg bd)

Pros- No need for INR monitoring, non-inferior or slightly efficacious then warfarin/acitrom, lesser major bleeding rates

cons- costlier, lesser availability especially in developing countries and no specific reversal agents

Myocardial Infarction- Third Universal definition and classification

Definition of myocardial infarction

Criteria for acute myocardial infarction :

The term acute myocardial infarction (MI) should be used when there is evidence of myocardial necrosis in a clinical setting consistent with acute myocardial ischaemia. Under these conditions any one of the following criteria meets the diagnosis for MI:

Detection of a rise and/or fall of cardiac biomarker values [preferably cardiac troponin (cTn)] with at least one value above the 99th percentile upper reference limit (URL) and with at least one of the following:

  1. Symptoms of ischaemia.
  2. New or presumed new significant ST-segment–T wave (ST–T) changes or new left bundle branch block (LBBB).
  3. Development of pathological Q waves in the ECG.
  4. Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality.
  5. Identification of an intracoronary thrombus by angiography or autopsy.

•Cardiac death with symptoms suggestive of myocardial ischaemia and presumed new ischaemic ECG changes or new LBBB, but death occurred before cardiac biomarkers were obtained,or before cardiac biomarker values would be increased.

• Percutaneous coronary intervention (PCI) related MI is arbitrarily defined by elevation of cTn values (>5 x 99th percentile URL) in patients with normal baseline values (≤99th percentileURL) or a rise of cTnvalues >20% if the baseline values are elevated and are stable or falling. Inaddition,either(i)symptoms suggestiveof myocardialischaemia or (ii) new ischaemic ECG changes or (iii) angiographicfindings consistent with a proceduralcomplication or (iv) imaging demonstration of new loss of viable myocardium or new regional wall motion abnormality are required.

• Stent thrombosis associated with MI when detected by coronary angiography or autopsy in the setting of myocardial ischaemia and with a rise and/or fall of cardiac biomarker values with at least one value above the 99th percentile URL.

• Coronary artery bypass grafting (CABG) related MI is arbitrarily defined by elevation of cardiac biomarker values (>10 x 99th percentile URL) in patients with normal baseline cTn values (≤99th percentile URL). In addition, either (i) new pathological Q waves or new LBBB,or (ii) angiographic documented new graft or new native coronary artery occlusion, or (iii) imaging evidence of new loss of viable myocardium or new regional wall motion abnormality.

Criteria for prior myocardial infarction

Any one of the following criteria meets the diagnosis for prior MI:

• Pathological Q waves with or without symptoms in the absence of non-ischaemic causes. • Imaging evidence of a region of loss of viable myocardium that is thinned and fails to contract,in the absence of a non-ischaemic cause.

• Pathological findings of a prior MI

 UNIVERSAL CLASSIFICATION OF MYOCARDIAL INFARCTION

Type 1: Spontaneous myocardial infarction

Spontaneous myocardial infarction related to atherosclerotic plaque rupture, ulceration, fissuring, erosion, or dissection with resulting intraluminal thrombus in one or more of the coronary arteries leading to decreased myocardial blood flow or distal platelet emboli with ensuing myocyte necrosis. The patient may have underlying severe CAD but on occasion non-obstructive or no CAD.

Type 2: Myocardial infarction secondary to an ischaemic imbalance

In instances of myocardial injury with necrosis where a condition other than CAD contributes to an imbalance between myocardial oxygen supply and/or demand, e.g.coronary endothelial dysfunction, coronary artery spasm, coronary embolism, tachy-/brady-arrhythmias, anaemia, respiratory failure, hypotension, and hypertension with or without LVH.

Type 3: Myocardial infarction resulting in death when biomarker values are unavailable

Cardiac death with symptoms suggestive of myocardial ischaemia and presumed new ischaemic ECG changes or new LBBB, but death occurring before blood samples could be obtained, before cardiac biomarker could rise, or in rare cases cardiac biomarkers were not collected.

Type 4a: Myocardial infarction related to percutaneous coronary intervention (PCI)

Myocardial infarction associated with PCI is arbitrarily defined by elevation of cTn values >5 x 99th percentile URL in patients with normal baseline values (£99th percentile URL) or a rise of cTn values >20% if the baseline values are elevated and are stable or falling. In addition, either (i) symptoms suggestive of myocardial chaemia, or (ii) new ischaemic ECG changes or new LBBB, or (iii) angiographic loss of patency of a major coronary artery or a side branch or persistent slow- or no-flow or embolization, or (iv) imaging demonstration of new loss of viable myocardium or new regional wall motion abnormality are required.

Type 4b: Myocardial infarction related to stent thrombosis

Myocardial infarction associated with stent thrombosis is detected by coronary angiography or autopsy in the setting of myocardial ischaemia and with a rise and/ or fall of cardiac biomarkers values with at least one value above the 99th percentile URL.

Type 5: Myocardial infarction related to coronary artery bypass grafting (CABG)

Myocardial infarction associated with CABG is arbitrarily defined by elevation of cardiac biomarker values >10 x 99th percentile URL in patients with normal baseline cTn values (£99th percentile URL).In addition,either (i) new pathological Q waves or new LBBB,  or (ii) angiographic documented new graft or new native coronary artery occlusion, or (iii) imaging evidence of new loss of viable myocardium or new regional wall motion abnormality

AMBITION: Initial Use of Ambrisentan plus Tadalafil in Pulmonary Arterial Hypertension

Data on the effect of initial combination therapy with ambrisentan and tadalafil on
long-term outcomes in patients with pulmonary arterial hypertension are scarce.

METHODS
In this event-driven, double-blind study, patients were randomly assigned, in a 2:1:1 ratio,
participants with World Health Organization functional class II or III symptoms of pulmonary arterial hypertension who had not previously received treatment to receive
initial combination therapy with 10 mg of ambrisentan plus 40 mg of tadalafil (combination-therapy group), 10 mg of ambrisentan plus placebo (ambrisentanmonotherapy group), or 40 mg of tadalafil plus placebo (tadalafil-monotherapy group), all administered once daily.

The primary end point in a time-to-event analysis was the first event of clinical failure, which was defined as the first occurrence of a composite of death, hospitalization for worsening pulmonary arterial hypertension, disease progression, or unsatisfactory long-term clinical response.

RESULTS
The primary analysis included 500 participants; 253 were assigned to the combination-
therapy group, 126 to the ambrisentan-monotherapy group, and 121 to the tadalafil-monotherapy group. A primary end-point event occurred in 18%, 34%, and 28% of the participants in these groups, respectively, and in 31% of the pooled monotherapy group (the two monotherapy groups combined). The hazard ratio for the primary end point in the combination-therapy group versus the pooled-monotherapy group was 0.50 (95% confidence interval [CI], 0.35 to 0.72; P<0.001). At week 24, the combination-therapy group had greater reductions from baseline in N-terminal pro–brain natriuretic peptide levels than did the pooled-monotherapy group (mean change, −67.2% vs. −50.4%; P<0.001), as well as a higher percentage of patients with a satisfactory clinical response (39% vs. 29%; odds ratio, 1.56 [95% CI, 1.05 to 2.32]; P = 0.03) and a greater improvement in the 6-minute walk distance (median change from baseline, 48.98 m vs. 23.80 m; P<0.001). The adverse events that occurred more frequently in the combination-therapy group than in either monotherapy group included peripheral edema, headache, nasal congestion, and anemia.

CONCLUSIONS
Among participants with pulmonary arterial hypertension who had not received
previous treatment, initial combination therapy with ambrisentan and tadalafil
resulted in a significantly lower risk of clinical-failure events than the risk with
ambrisentan or tadalafil monotherapy.

Source : http://www.nejm.org/doi/full/10.1056/NEJMoa1413687?query=featured_home

Approach to Arrhythmia part 1: Bradycardia

Approach to Arrhythmia part 1: Bradycardia

Bradycardia is defined as heart rate <60/min. To understand the cause of bradycardia we have to understand the structures involved in the production and conduction of cardiac impulse.

The normal cardiac structures involved in electrical activity of the heart are
1. SA node- It is the pacemaker of the heart, because it fires at the highest rate hence predominates over other pacemakers of the heart.
2.AV node – In normal hearts its function is to conduct impulses generated in the SA node to the ventricles through the Bundle of His and bundle branches.It can act as a slow pacemeker when the SA node is diseased
3. Bundle of His and bundle branches- Normally their function is conduction of cardiac impulses. They can act as a slow pacemeker when the proximal structures (SA node & AV node) are diseased.
4. Purkinje fibres
5. Ventricular myocardium- In complete heart block the ventricular myocardium produces escape rhythm at a slow rate of 20-40/min

Disease in any of the structures can lead to bradycardia.

The diagnosis is made from ECG in most of the cases.
Now we will discuss how to systematically analyze an ECG for diagnosing a bradycardia.

Step 1: Calculate the rate first. Bradycardia by definition heart rate <60/min
Step 2: Analysis of rhythm begins with search for P-wave. Normally P-waves are produced by SA node, so absence of P-waves indicate disease of SA node. Which is called as sick sinus syndrome
Step 3: Absent P-waves can be due to
1. Sick sinus syndrome with escape rhythm. (R-R intervals fixed)
2. Atrial fibrillation with slow ventricular rate. (R-R intervals variable)

Sick sinus syndrome: no visible P waves, fixed R-R intervals.

Sick sinus syndrome: no visible P waves, fixed R-R intervals.

 

Step 4: P-waves present
If P-waves are present look for P-P interval, PR-interval and relation between P and R waves.

Step 5: P-P interval variable
Nonconducted APCs
Step 6: P-P interval fixed
The next stepis evaluation of PR-interval and relation between P and R waves

Step 7: PR interval normal and fixed: Sinus bradycardia

Sinus bradycardia

Sinus bradycardia

PR interval prolonged but fixed and each QRS complex is preceeded by P wave: First degree AV block

1st degree AV block: Prolonged fixed PR interval

1st degree AV block: Prolonged fixed PR interval

(ECG courtesy of www.lifeinthefastlane.com)
PR interval lengthens then dropped beat and return with short PR interrval: Mobitz type 1 second degree AV block

Wenckebach block

Wenckebach block

(ECG courtesy of www.lifeinthefastlane.com)
PR interval fixed then dropped beat : Mobitz type 2 second degree AV block
No PR relationship : Third degee AV block

Complete heart block

Complete heart block

(ECG courtesy of www.lifeinthefastlane.com)

 

The flow chart below summarizes the whole approach

ECG  approach to bradycardia

ECG approach to bradycardia

 

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

Revised Jones Criteria for Acute Rheumatic Fever – 2015 guideline

Acute rheumatic fever remains a serious healthcare concern for the majority of the world’s population despite its decline in incidence in Europe and North America. This statement reviews the historic Jones criteria used to diagnose acute rheumatic fever in the context of the current epidemiology of the disease and updates those criteria to also taking into account the use of Doppler echocardiography in the diagnosis of carditis as a major manifestation of acute rheumatic fever.

1. Epidemiology:

1. It is reasonable to consider individuals to be at low risk for ARF if they come from a setting or population known to experience low rates of ARF or RHD (Class IIa; Level of Evidence C).
2. It is reasonable that where reliable epidemiological data are available, low risk should be defined as having an ARF incidence <2 per 100 000 school-aged children (usually 5–14 years old) per year or an allage prevalence of RHD of ≤1 per 1000 population per year (Class IIa; Level of Evidence C).
3. Children not clearly from a low-risk population are at moderate to high risk depending on their reference population (Class I; Level of Evidence C).

2. Clinical Manifestations of ARF:

Generally, the clinical profile of ARF in low- and middle-income countries closely resembles that of high-income countries. Universally, the most common major manifestations during the first episode of ARF (the “major criteria” for diagnosis) remain
carditis (50%–70%) and arthritis (35%–66%). These are followed in frequency by chorea (10%–30%), which has been demonstrated to have a female predominance, and then
subcutaneous nodules (0%–10%) and erythema marginatum (<6%), which remain much less common but highly specific manifestations of ARF.

3.Carditis: Diagnosis in the Era of Widely Available Echocardiography:

Classically, as discussed in the 1992 AHA revised Jones criteria statement, carditis as a major manifestation of ARF has been a clinical diagnosis based on the auscultation of typical murmurs that indicate mitral or aortic valve regurgitation, at either valve or both valves. Numerous studies over the past 20 years have addressed the role of echocardiography (compared with purely clinical assessment) in the diagnosis of ARF. More than 25 studies have reported echocardiography/Doppler evidence of mitral or aortic valve regurgitation in patients with ARF despite the absence of classic auscultatory findings. This writing group concludes the following:

1. Echocardiography with Doppler should be performed in all cases of confirmed and suspected ARF (Class I; Level of Evidence B).
2. It is reasonable to consider performing serial echocardiography/ Doppler studies in any patient with diagnosed or suspected ARF even if documented carditis is not present on diagnosis (Class IIa; Level of Evidence C).
3. Echocardiography/Doppler testing should be performed to assess whether carditis is present in the absence of auscultatory findings, particularly in moderate- to high-risk populations and when ARF is considered likely (Class I; Level of Evidence B).
4. Echocardiography/Doppler findings not consistent with carditis should exclude that diagnosis in patients with a heart murmur otherwise thought to indicate rheumatic carditis (Class I; Level of Evidence B).

Evolving role of echogardiography in acute rheumatic fever

Evolving role of echogardiography in acute rheumatic fever

4.Specific doppler criteria for diagnosis of rheumatic valvulitis

Pathological mitral regurgitation (all 4 criteria met)
1.Seen in at least 2 views
2.Jet length ≥2 cm in at least 1 view
3.Peak velocity >3 m/s
4.Pansystolic jet in at least 1 envelope

Pathological aortic regurgitation (all 4 criteria met)
1.Seen in at least 2 views
2.Jet length ≥1 cm in at least 1 view
3.Peak velocity >3 m/s
4.Pan diastolic jet in at least 1 envelope

Morphological Findings on Echocardiogram in Rheumatic Valvulitis

Acute mitral valve changes
Annular dilation
Chordal elongation
Chordal rupture resulting in flail leaflet with severe mitral regurgitation
Anterior (or less commonly posterior) leaflet tip prolapse
Beading/nodularity of leaflet tips

Chronic mitral valve changes: not seen in acute carditis
Leaflet thickening
Chordal thickening and fusion
Restricted leaflet motion
Calcification

Aortic valve changes in either acute or chronic carditis
Irregular or focal leaflet thickening
Coaptation defect
Restricted leaflet motion
Leaflet prolapse

5.Evidence of preceding Streptococcal infection:

Because other illnesses may closely resemble ARF, laboratory evidence of antecedent group A streptococcal infection is needed whenever possible, and the diagnosis is in doubt when such evidence is not available.

Any one of the following can serve as evidence of preceding infection:
Increased or rising anti-streptolysin O titer or other streptococcal antibodies (anti-DNASE B) (Class I, Level of Evidence B). A rise in titer is better evidence than a single titer result.
A positive throat culture for group A β-hemolytic streptococci (Class I, Level of Evidence B).
A positive rapid group A streptococcal carbohydrate antigen test in a child whose clinical presentation suggests a high pretest probability of streptococcal pharyngitis (Class I, Level of Evidence B).

6. Diagnosis of Acute rheumatic fever:

For all patient populations with evidence of preceding GAS infection

Diagnosis: initial ARF: 2 Major manifestations or 1 major plus 2 minor manifestations
Diagnosis: recurrent ARF: 2 Major or 1 major and 2 minor or 3 minor

Major and minor criteria for diagnosis of Acute rheumatic fever

Major and minor criteria for diagnosis of Acute rheumatic fever


Flow charts for diagnosis of rheumatic fever

Flow charts for diagnosis of rheumatic fever

 

7.Rheumatic Fever Recurrences

As stated in the 1992 guidelines, patients who have a history of ARF or RHD are at high risk for “recurrent” attacks if reinfected with group A streptococci. Such an attack is considered
a new episode of ARF, but one in which the complete set of Jones criteria, even as revised, may not be completely fulfilled.

The guideline recommendations for diagnosing rheumatic fever recurrences are:
1. With a reliable past history of ARF or established RHD, and in the face of documented group A streptococcal infection, 2 major or 1 major and 2 minor or 3 minor manifestations may be sufficient for a presumptive diagnosis (Class IIb; Level of Evidence C).
2. When minor manifestations alone are present, the exclusion of other more likely causes of the clinical presentation is recommended before a diagnosis of an ARF recurrence is made (Class I; Level of Evidence C).

8.“Possible” Rheumatic Fever

In some circumstances, a given clinical presentation may not fulfill these updated Jones criteria, but the clinician may still have good reason to suspect that ARF is the diagnosis.
This may occur in high-incidence settings. In such situations the clinicians should use their discretion and clinical acumen to make the diagnosis that they consider most likely and manage the patient accordingly.

1. Where there is genuine uncertainty, it is reasonable to consider offering 12 months of secondary prophylaxis followed by reevaluation to include a careful history and physical examination in addition to a repeat echocardiogram (Class IIa; Level of Evidence C).
2. In a patient with recurrent symptoms (particularly involving the joints) who has been adherent to prophylaxis recommendations but lacks serological evidence of group A streptococcal infection and lacks echocardiographic evidence of valvulitis, it is reasonable
to conclude that the recurrent symptoms are not likely related to ARF, and discontinuation of antibiotic prophylaxis may be appropriate (Class IIa; Level of Evidence C).

Summary:

Jones criteria needed revision to meet current technological advances and clinical needs. Strict application of echocardiography/Doppler findings may be used to fulfill the major criterion of carditis, even in the absence of classic auscultatory findings, providing that ambient loading conditions are taken into consideration. In addition, monoarthritis or polyarthralgia could be accepted as fulfilling the major criterion of arthritis, but only in moderate- to high-risk populations. For low-risk populations, monoarthritis is not included, and polyarthralgia remains a minor criterion. Similarly, the requirement for the presence of fever can be fulfilled with oral, tympanic, or rectal temperature documented at 38°C in moderate- to high-risk populations, but only at ≥38.5°C in others.

Refernce:

1. http://circ.ahajournals.org/content/early/2015/04/23/CIR.0000000000000205.abstract

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