supraventricular tachycardias

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Suprav ent ricular Tachycard ias Dr.Nagula Praveen 10-08- 2011

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Page 1: Supraventricular tachycardias

Supraven

tricular

Tachycard

iasDr.Nagula Praveen

10-08-2011

Page 2: Supraventricular tachycardias

Introduction Paroxysmal SVT is a common arrhythmia in the emergency

room, outpatient clinic and EP laboratory. Quality of life of patients suffering from PSVT is frequently poor. Non paroxysmal SVT is less frequent. Tachy cardiomyopathy with LVSD results from incessant SVT –

usually reversible after permanently abolishing the arrhythmia. AVNRT – young,no heart disease,AT – structural or pulmonary. Patients >55yrs can have spontaneous cure or death due to HF. Can be usually cured by catheterablation techniques. Surgery has no role today in treatment of SVT . Incidence is 35 cases /1,00,000 person/year. Prevalence is 2.25/1000 …

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ELECTRICAL CONDUCTION SYSTEM OF THE HEART

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Cardiac Action potential, Pacemaker potential

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REENTRY circuit

Reentry occurs when a propagating impulse fails to die after normal activation of the heart and persists to excite the heart after expiration of the refractory period.

The circuitous propagation of an impulse around an anatomic or functional obstacle leading to the reexcitation of the heart describes a circus movement reentry.

Continous circulating excitation.

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CRITERIA for REENTRANT CIRCUIT to occur( MINES and GARREY )

An area of unidirectional block must exist. The excitatory wave progresses along a distant

pathway ,returning to its point of origin and the following the same path again.

Interruption of the reentrant circuit at any point along its path should terminate the circus movement.

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TYPES OF REENTRANT CIRCUIT

Four distinct models of reentry have been described: 1.The ring model 2.The leading circle model 3.The figure of eight model 4.The spiral wave model. Ring model -- an anatomical obstacle is required. Others --- functional obstacle Functional – VF due to MI,brugada syndrome.LQTS.

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ENHANCED AUTOMATICITY

It is due to the subsidiary pacemakers taking the role of giving impulses when the SAnode is inactive or degenerated.

Pacing does not provoke.

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TRIGGERED ACTIVITY

It is due to EAD of the phase 3,LAD of phase 4 of action potential.

Attributed to an increase in intracellular calcium accumulation It is due to the increased catecholamines,adrenergic drive. Seen in postoperative cases.. Subsides on removal of the stimulus or cause. EAD –TDP LAD – atrial,junctional,fasicular ,catecholamine

sensitive VT Can be provoked by pacing

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SUPRAVENTRICULAR ARRHYTHMIAS

ATRIALAV JUNCTIONAL EXTRASYSTOLES

SINUS NODE DISORDERSWANDERING PACEMAKER

SUPRAVENTRICULAR TACHYARRHYTHMIAS

SUPRAVENTRICULA

R TACHYCAR

DIA

AT,AFL,AVJT

AVNRT,AVRT,NPJT,PJR

T

ATRIAL FIBRILLAT

ION

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SUPRAVENTRICULAR TACHYCARDIA

Supraventricular tachycardia is any tachycardia that originates in the atria or that uses the atrium or AVjunction and that requires the participation of the tissue above the bifurcation of the bundle of HIS for propagation as a critical component of the tachycardia circuit….CRAWFORD

SVT – include all tachyarrhythmias that either originate from or incorporate supraventricular tissue in a reentrant circuit…HURST

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AV NODE dependent junctional tachycardias

AVNRT Typical common

Atypical uncommon

AVRT Concealed accessory pathway

WPWsyndrome

JUNCTIONALJunctional ectopic

tachycardia

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TERMS

PAROXYSMAL – one with sudden onset and termination and which is recurrent.

PERSISTENT – the one which exists and terminates with treatment. INCESSANT – the one that continues without stopping on itself. PERMANENT –which persists despite treatment –refractory,chronic PREEXCITATION – activation of the part of ventricle by an anomalous

connection before it is depolarised by the normal AV conducting system.

RECIPROCATING – same time existant one being active other being refractory during conduction of an impulse.

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TACHYCARDIAS due to reentry circuits are usually paroxysmal,rarely incessant.they occur in normal hearts.

Those due to automaticity,triggered activity are persistent and have phenomenon of warm up .

They occur in the background of structural heart disease.

Physiological sinus tachycardia has gradual onset and termination

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APPROACH TO A PATIENT

WITH NARROW

QRS COMPLEX

TACHYCARDIA

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CASE scenario

A 28 yr old woman has rapid palpitations accompanied by chest pain and dizziness while playing her cello.she is brought to an ED.she has a faint regular pulse of 180 bpm.her blood pressure is 100/70 mm Hg.cardiovascular signs reveals no signs of heart failure.an ECG show a regular tachycardia with a narrow QRS complex and no apparent Pwaves ..how should her case be managed?

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Clinically

Patient complains of recurrent palpitations,chest fullness,light headedness,presyncope,syncope.

Ppt factors may be present – exercise,caffeine,cigarette smoking,alcohol.

h/o heart disease,pulmonary disease,post AFablation. CAUTION :H/O DIGOXIN USE On examination– neck pounding –cannon waves “frog’s sign “

– practically pathognomic of AVNRT. HR is a non specific feature in differentiating SVTs.

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STEP wise

Look for QRS duration. QRS complex regular/irregular. Then look for presence of p waves. P waves morphology P waves and QRSrelationship 1:1 AVblock present. QRS alternation Termination initiation of tachycardia. Effect of BBBon tachycardia cycle length.

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Decision tree schema by BAR and colleagues STEP 1 –FOR ANY FAILURE OF AV CONDUCTION –AV block present ectopic atrial tachycardia.

STEP 2 – QRS alternation –each QRS is different from subsequent one by 5 mm –AVRT ,other tachycardia also

STEP 4 – p wave morphology in frontal plane –negative in lead I LEFT SIDE BYPASS TRACT.

STEP 5 –P WAVE in horizontal plane .left side,right side ..

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In brief from the diagram clues

Response to carotid sinus massage or adenosine –with termination of arrhythmia with Pwave –AVNRT with atrial premature beat .

Termination with QRS complex –ventricular reciprocating rhythm.

Tachycardia persists with AV block –AT,AFL,SANRT Pseudo r ‘ wave in V1 –AVNRT SHORT RP interval – AVNRT,AVRT Long RP interval – AT,SANRT,AVNRT atypical

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NARROW COMPLEX QRS TACHYCARDIA

SHORT RP INTERVAL

TYPICAL AVNRT

AVRT

LONG RP INTERVAL

ATYPICA

L AVNRT

AVRT

slow retrograde

conduction

Permanent Form

junctional

tachycardia

ATRIAL TACHYCARDIA

SANRTINAPPROPRIATE ST

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Ecg findings

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Main Mechanisms and Typical Electrocardiographic Recordings of Supraventricular Tachycardia.

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Pwaves

no

Irregular R-R

intervalATRIAL

FIBRILLATIO

N

Regular

R-R interv

al

AVNRT

yes

NORMAL MORPHOLOGY

SINUS TACHYCARDIASINUS NODE REENTRY

INAPPROPRIATE SINUS TACHYCARDIA

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Differentiation of AVNRT from AVRT

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P wave present but not of same morphology as sinus rhythm

Pseudo r’ wave in

V1

AVNRT

Pseudo S wave on lead II

AVNRT

Pwave ST-T

changesPositive in

inferior

leads

AVRT

Right

posterosepta

lAccessor

y pathway

Negative

in lead

I

AVRT

Left side

d accessory pathwa

y

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AVNRT

Presence of a narrow complex tachycardia with regular R-R intervals and no visible p waves.

P waves are retrograde and are inverted in leads II,III,avf.

P waves are buried in the QRS complexes –simultaneous activation of atria and ventricles – most common presentation of AVNRT –66%.

If not synchronous –pseudo s wave in inferior leads ,pseudo r’ wave in lead V1---30% cases .

P wave may be farther away from QRS complex distorting the ST segment ---AVNRT ,mostly AVRT.

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AV NODAL REENTRANT TACHYCARDIA

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AFTER ADENOSINE

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AV-nodal-re-entry-tachycardia-(AVNRT)-on-an-ECG-heart-monitor[www.savevid.com].flv

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AVRT

Typical – RP interval < PR interval RP interval > 80 milli sec Atypical –RP interval > PR interval Concealed bypass tract – only retrograde conduction Manifest bypass tract– both anterograde and

retrograde. Electrical alternans –the amplitude of QRS complexes

varies by 5 mm alternatively. Rate related BBB occuring and the rate of tachycardia

is decreasing –then the bypass tract is on the same side of the block.

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AV REENTRANT TACHYCARDIA

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PRinterv

al RP

interval

PR interval

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WPW syndrome

Two types Orthodromic Antidromic Antidromic is wide complex tachycardia In NSR detected by delta wave. Can ppt into AF and VF on use of AV nodal blockers MEMBRANE ACTIVE ANTIARRHTYHMIC DRUGS are safe. CONCEALED WPW syndrome – no delta wave .less risk of

AF

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Orthodromic AVRT

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LOWN GANONG LEVINE syndrome Short PR interval Normal QRS complex PSVT

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Sinus Tachycardia

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Focal Atrial Tachycardia P wave morphology changes. PR interval > 0.12 sec . Second,third degree AV block can occur. Tachycardia terminates with a qrs complex .. Right atrial origin– p wave inverted in V1. If biphasic in V1—initially positive then negative. Upright in lead AVL Opposite if of left atrial origin Superior origin –upright p waves in inferior leads Inferior origin –p waves are inverted in inferior leads.

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Focal atrial tachycardia (LA focus)

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Multifocal Atrial Tachycardia

At least three consequtive p waves with different morphologies with a rate > 100 bpm to be present.

Isoelectric baseline between p waves. Also called as choatic atrial tachycardia Mostly seen in COPD ,electrolyte abn,theophylline Rate usually does not exceed 130-140 bpm.

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Multifocal Atrial Tachycardia

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SANRT

Microreentrant tachycardia Usually precipitated and terminated by

premature atrial complexes. Atrial rate is usually 120-150 bpm. IART - Large or small reentrant circuit. AV block can occur.

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Junctional tachycardias Non paroxysmal – accelerated junctional rhythm Rate < 100 bpm Usually junctional node 40-60 bpm Paroxysmal or focal junctional tachycardia is rare –automaticity. 110-250bpm. P waves may be before or after QRS complex Infrequent and nonsustained episodes –no treatment Acute termination of SVT and establish the mechanism of SVT

in case of acute setting. Long term goal is abolishing the arryhthmia substrate. Precipitating factors – electrolyte

imbalance,hypoxia,ischemia,hyperthyroidism to be sought out.

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Acute Treatment

Of SVT

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A 12 lead ECG during tachycardia and NSR.

No delay in therapy if the mechanism of SVT is not known.

Perform CAROTID SINUS MASSAGE,or give 6mg bolus adenosine.

In case of severe hemodynamic compromise a synchronised cardioversion to be given.

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Carotid sinus massage

Check for carotid bruit before massage. At the level of cricoid cartilage,at the angle of

mandible the carotid sinus is situated. Gentle pressure is applied over the carotid sinus

for 5 -10 seconds. ECG recording to be present. In case of no response – try on the other side. Simultaneous pressure not to be applied both sides. Alternative manuevres are valsalva,gag reflex,ice

water pouring over the face.

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If SVT is suspected to be AVNode dependent – drug of choice is adenosine and CCBs verapamil and diltiazem.

Useful for sustained cases of AV node independent tachycardias.

But digoxin,BBs,CCBs better control of ventricular response in atrial tachycardias

Class I agents to be combined with AV nodal blocking drugs – to eliminate 1:1 conduction of atrial to ventricles.

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HEMODYNAMIC STATUS

STABLE BP >90/60 mmHg

Narrow QRSand regular

R-RVagal

maneuveresIV

adenosineIV

verapamil,diltiazemIV sotalol

refractory

Wide QRScomplex

Vagal

manuevresIV

adenosine

procainamid

e

Digoxin

Verapam

il Are contraindicated

UNSTABLEBP< 90/60 mmHg

Direct cardioversion

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DRUG DOSE SIDE EFFECTS

AV NODAL BLOCKERS

ADENOSINE 6-12 mg bolus Flushing ,dyspneaChest pain

VERAPAMIL 0.15 mg/kg over 2 min

Hypotension bradycardia

DILTIAZEM 0.25-0.35 mg/kg -2 min

same

DIGOXIN 0.5-1.0 mg --- 2-10 min

Digoxin toxicity

PROPANOLOL 1-3mg over I min Hypotension bradycardia

CLASS I AAD

QUINIDINE 6-10MG/KG at 10 mg/min

hypotension

PROCAINAMIDE 10-15mg/kg at 50 mg/min

hypotension

DISOPYRAMIDE 1-2 mg/kg at 10 mg/min

hypotension

PROPAFENONE 1-2mg/min at 10 mg/min

Bradycardia,GI disturbance

FLECAINIDE 2 mg/kg at 10 mg/min

Bradycardia,dizziness

CLASS III SOTALOL 1-1.5mg/kg at 10 mg/min

Hypotension,proarrythmic

AMIODARONE 1.5 mg/kg during 15 min

Hypotension,bradycardia

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Pharmacologic Agents for Short-Term Treatment of Supraventricular Tachycardia (SVT).

Delacrétaz E. N Engl J Med 2006;354:1039-1051.

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AFTER ADENOSINE

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Algorithm for Short term management

of SVT

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Algorithm for long term

Management of SVT

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Refractory cases

Narrow QRS complexesIV adenosine

IV procainamide

IV amiodaroneAtrial pacing

Direct cardioversion

Wide QRS Complexes

Atrial pacingDirect

cardioversion

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Pill in the pocket approach In whom recurrences are infrequent. But sustained.well tolerated hemodynamically. Patients who have had only a single episode of SVT.. 100-200mg of flecainide at the onset of SVT is a reasonable

approach…until he reaches the hospital. 40-160 mg verapamil –without preexcitation, Betablockers Propafenone 150-450 mg. 80% cases interrupted with a combination of CCBand BB in 2

hrs…

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Long term control of SVT Frequency and severity of episodes. LVF Cost benefits of radiofrequency ablation

over the pharmacotherapy . Pharmacotherapy is considered in patients

who defer catheter ablation,whom in which ablation failed,or carries a risk of AV block.

Multifocal atrial tachycardia Trial and error Accessory pathway – class Ia,Ic,III AV node blocking drugs Young patients – Ia drugs Class I agents LVD < 35% not used.

Long term treatment

Membrane active

AAD

Catheter

ablation

Curative surgery

Antitachycardia pacing

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Catheter guided Radiofrequency Ablation

Several multipolar catheters are introduced High right atrium ,bundle of

his ,RVapex,Coronary sinus. Radiofrequency is delivered at the site of earlier

activation Success is defined by elimination of the

tachycardia or loss of pre excitation. 90-98% success in AV node dependent 60-80% in case of AV node independent. Cryoablation more useful…

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Catheter Ablation of Cardiac Arrhythmias.

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Pacemakers

Temporary role in case of digoxin toxicity. Permanent in case of long term control To terminate the tachycardia Revert into sinus rhythm Prevent the occurrence. Overdrive suppression RF induced atrial pacing are used

No role of surgery presently in PSVT rx .

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ACUTE LONG TERM

PHYSIOLOGICAL rest ,sedation valsalva

Valsalva maneuvre Carotid sinus massage

Carotid sinus massage

PHARAMACOLOGICAL

vagomimmetic Suppress triggering arrhythmias

Direct effect on AV node

Change properties of reentrant pathways

Slow VR Control VR

CATHETER ABLATION SURGERY

Ablation or sectioning of reentrant pathway

ELECTRONIC DEVICES

Temp .pacing cardioversion

Permanent pacemakerAntitachycardia pacing

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Some important points

Rxof PSVT given for patient comfort except in IHD,MS

When the QRS complex is wide and VT is mistaken as SVT with ABERRANT conduction IV verapamil – not recommended decreases BP.

If DC cardioversion to be avoided because of possible adverse response to digitalis adm …pacing Rt atrium and ventricle via temp pacing.

In WPW syndrome avoid VERAPAMIL,LIDOCAINE . Avoid digoxin. In SANRT ,IART –class IA,IC ,BB SANRT –digoxin.

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Cont…

Rx of ectopic atrial tachycardia – consider digitalis toxicity,chronic lung disease,metabolic abn,electrolyte abnormalities,acute MI ----temporary pacing.

Unsuccessful is EC Removal or reversal of inciting factor Surgical excision of focus. Rx of MAT –chronic lung disease,metabolic,rare

is digitlais toxicity ---CCBS,BBs ..no role of cardioversion,devices ,surgery.

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In case of WPW syndrome symptomatic concealed or manifested ..and evidence of preexcitation on NSR …send the patient for catheter ablation…

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Our case

1. carotid sinus pressure 2.IV adenosine. 3.long term treatment depends upon episodes. 4.any underlying abnormality to be checked for. 5.definitive etiology only knon by EP study. 6.95% cases respond to RF ablation. 7.much less complications with cryoablation. 8.in case if SVT recurrs after ablation –opt for

pacemaker..

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SUPRAVENTRICULAR TACHYCARDIAS“You only get so many heart beats – you should save some for later in life” Dr. Samuel Levine

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Special problems 1.Coexisting Double Tachycardias May not be identified during noninvasive

testing ..needs EP study. Ex—typical AVNRT and AT. Concentric –eccentric –concentric. AVNRT –both APC,VPC AT only APC 2.Pseudo AF- infrequent presentation of PSVT. Occurs during onset and termination of tahcycardia. Multiple accessory AV pathways. In young who have AF without other risk factors. 5% of AVNRT. Group beating is seen

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REFERENCES CARDIOLOGY third edition –Michael. H.Crawford HURST’S THE HEART – 12 th edition. BRAUNWALD’S HEART DISEASE –A TEXTBOOK OF CARDIOVASCULAR

MEDICINE – 7 th ED HARRISON’S PRINICPLES OF INTERNAL MEDICINE -17 th ED SUPRAVENTRICULAR TACHYCARDIA –NEJM 2006 CARDIOVASCULAR MEDICINE – SVT – JERONIMO FERRE’ BASIC AND BEDSIDE ELECTROCARDIOGRAPHY –ROMULO.F.BALTAZAR SCHAMROTH –ELECTROCARDIOGRAPHY www.medscape.com www.ecglibrary.com www.googleimages.com www.acc.org. www.clinicaltrials.gov www.nejm.org

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Aim for any case of cardiology

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Than

k youSagittari

an