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Archive for the ‘Tutorial in clinical cardiology’ Category

Ebstein anomaly :An illustration with pressure tracing

Posted in cardiology -congenital heart disease, Hemodynamics, tagged , , , , , , , , , , , , on April 7, 2009| Leave a Comment »

ebstein-anomaly

Down load high resolution PDF file

ebstein-anomaly

Ref:

An excellent article from H.Watson in british heart journal

HERNANDEZ FA  The intracavitary electrocardiogram in the diagnosis
of Ebstein’s anomaly. Amer J Cardiol 1: 181,  1958

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The Aortic dissection : What you wanted to know about true and false lumen !

Posted in cardiac surgery, Cardiology - Clinical, Cardiology -Interventional -PCI, Tutorial in clinical cardiology, tagged , , , , , , , , , , , , , , , , , on March 24, 2009| 4 Comments »

Why is identifying false and true lumen important ?

This helps the interventional cardiologist to plan the specific therapeutic procedure .

aortic-dissection-table

Is it really difficult to differentiate the two ?

One may wonder , why is that  difficult  to identify  the true aortic lumen by echo, after  all  , the LV empties the blood into true aortic lumen ! Yes  , in aortic root dissections  identifying the true from false lumen is rarely an issue.

aortic-dissection-4

The issue becomes  important and complicated as the propagation of dissection goes in a random and erratic way into the ascending aorta and arch and downwards.The situation could further get  complicated  by the fact there could  be multiple communication between the two lumens .Some of these communication are  hemodyanically patent others form  a simple anatomical continuity.The size and the configuration of true and false lumen are not uniform it is highly  variable.In the aortic root the size of the true lumen is usually  large and when it reach the descending aorta  as in type3 the whole thing could be reversed.

The enigma  of  these lumonomics , is that some of the native branches of aorta , would  either be, subtended by false or true lumen. This is a real tricky issue for the surgeons . If a aortic vessel branch (Say bronchial artery . . .) is perfused successfully by the  hemodynamically active false lumen should we meddle  that  at all ?


circumferential-dissection1 What are the types of false lumen ?

Usually single septae divide the aorta into two , one false lumen and true lumen.There can  be other types.

Triple lumen aorta :This is usually seen in the aortic root following dissection .Usually there is two false lumen and and one true lumen in the centre

Double barreled aorta: A circumferential   aortic dissection with a central true lumen surrounded by a  circumferential false lumen  mimicking a double barrel on within the other.

aortic-dissection

What determines blood flow within false lumen ?

  • Site of  intimal tear
  • Length of tear
  • Plane of cleavage  . Superficial  subinitmal tear with minimal  medial thickness is likey to give in easily  as the blood  dissects the plane  so it more often manifest as a flap  rather than sustained  dissection
  • Number  of exit points (It is often assumed  aortic dissection  there is typically one entrance and one exit point .

but  more  often  multiple exit points can occur. Some points can have both two and fro flow as it may act as both as entry or exit points

What  is the importance of identifying  point, exit point , true  lumen false lumen etc ?

  • This is vital for planning   repair  of  the segment
  • optimising side branch blood flow
  • some time one may require to create an exit point  for providing useful thermodynamics   of false lumen that could give branch to a vital area.

Why false lumen is  prone for thrombosis ?

  • Sluggish flow within false lumen
  • Plane of cleavage of intima  and media  create an  irregular surface that  trigger  tissue factor mediated thrombus.
  • Free floating cob webs   intimal  remnants may accelerate thrombus formation

What is the clinical significance of  finding  a thrombosed false lumen ?

Large thrombus can occur within false lumen.The presence of which , sometimes an advantage as

it limits further progression of false lumen (An organised thrombus is sort  of  natural  stent graft !)

many of these patients do well with medical management.

Ref : Clotted false lumen: reappraisal of indications for medical management of acute aortic dissection.

C J Sanderso Thorax 1981;36:194-199;

Can thrombus occur in true lumen also ? How common it is ? If so what is the mechanism ?

Yes , but it is rare  as the velocity  is  more .But it can occur in following situations.

  1. Preexisting atherosclerosis can be  a milieu for  insitu thrombus
  2. Thrombus in true lumen  can occur at the entry point where there is intimal tear ,  which  projects  into true lumen. that can  deccelerate the  flow(Rare)
  3. Thrombus in the false lumen may project into true  lumen  through another tear.
  4. Migration of false lumen thrombus may occur distally and reenter the  true lumen.

What is a cobweb ?

Cob web are the residual ribbons of dissected internal elastic lamina of aorta .
They are variably called as aortic bands, strands ,  septae, flaps etc.

What is the significance of the junction between false and rue lumen ?

The classic false lumen is crescent shaped. True lumen is either round or oval(Gibbous moon)
Tunction between false and true lumen has some characteristic feature.It mimics  the letter Y. The mainstem of Y correspond to main(  Normal full thickness)aortic  wall of the true lumen.The  oblique lines represent the outer wall of the false lumen and the septae dividing true (Fig 3)

dissection-41

What is the natural history of false lumen after surgical correction ?

Surgeons often leave the false lumen insitu , especially beyond the arch in type A dissection.

If false lumen is large  >70% of aorta , secondary dissections may occur in the long term.

Which is the best imaging modality  for  assessing dissection of aorta  ?

Even though MR angiogram and CT scans are shown to be good imaging tools in the evaluation of  dissection of aortamany practical issues creep in doing MR or CT angiogram.Many of these patients are too ill and will be on multiple arterial and venous lines Doing an MRI is  too dificult a task .Further these imaging modalities require a another arterial access .Requires contrast injection and  CT has in addition , radiation hazard.

TEE is a simple investigation can be done even in unstable patients in the bedside .Further also help us  us evaluate the aortic valve function and associated complications of dissection. TEE will be very useful peroperative also in assessing the repair.

*But MRI  and CT can give a long axis , saggital cuts of aortic dissection depicting the entry and exit points in a single image

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What is the incidence of insignificant left main disese ? How will you manage it ?

Posted in Cardiology -Interventional -PCI, cardiology- coronary care, Cardiology-Coronary artery disese, Hemodynamics, Uncategorized, tagged , , , , , , , , , , , , , , , , , , , , , on March 6, 2009| Leave a Comment »

Left main coronary artery disease (LMCAD) often evokes  a panic reaction  among cardiologists .Not every LMD deserve that re. To  label  it as  significant, we have a criteria ,  that is 50% diameter stenosis.  So what you do , for a tapering  or narrowed left main with 40% stenosis. Isolated insignificant left main is rare *, but real incidence is not known.  LMCAD  is  most often due to  , atherosclerosis of left main coronary artery without limiting the flow.

What are the options ?

  • Leave it alone, with intensive medical management assisted by high dose statin(80mg)
  • Elective PCI with stenting , even though the lesion is not significant.

*If associated LAD  or LCX is there decision making is easier .

How  significant is a coronary stenosis ?

The significance of a coronary lesion with reference to “lumen diameter obstruction” is basically flawed. The significance of a coronary stenosis, by tradition is  based on it’s hemodynamic impact ,right from the  CASS days in early seventies.Unfortunately our mind set has not changed even after realising    non obstructive – sub critical lesion is more prone for acute coronary syndrome.  Is it not ironical to call a  40% lesion a non significant one !

So, the  significance of coronary stenosis is two fold.

  1. Hemodynamic  significance
  2. Clinical and  pathologic significance

The former predisposes to often chronic stable angina, later likely to result in ACS.

How will you approach a apparently insignificant left main disease ?

A 40 % lesion in left main is hemodynamically not significant , but pathologically very significant.It needs intensive treatment. Plaque passification with medical approach is first choice.If the lesion morphology is eccentric,  has irregular margins or involves  LAD  or LCX ostium doing a PCI or even a CABG is to be considered in spite of the lesion is  hemodynamically insignificant .

Why , PCI is   considered  “not appropriate”  for   less tighter lesions , even though these lesions  have great clinical significance ?

The answer is simple, The risks  and the  potential cost are more than the benefit !

And further ,  stents are  not innocuous devices  either  , they  always carry a risk of sudden occlusion as like  a sub critical lesion  !

Answer to the title question

True incidence is not known . Our experince (Class 1 c evidence) would suggest Left main disease constitutes up to 10 % of CAD.Among this one third would be hemodynamically insignificant

Suggested reading

Handbook of Left Main Stem Disease


edited by Seung-Jung Park

hbleftmn

//

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How to localise focal atrial tachycardia with P wave morphology in ECG ?

Posted in cardiology -ECG, Cardiology-Arrhythmias, Cardiology-Land mark studies, Tutorial in clinical cardiology, tagged , , , , on March 3, 2009| Leave a Comment »

What is the simplest and accurate way to predict  the   origin of Right atrial tachycardia(RAT)  from left atrial tachycardia(LAT) ?

Look at the P waves in V 1 ( Don’t look further ! )

  • A  negative  or  a biphasic (+/- ) P wave in V 1  is 100% specific  for a right atrial tachycardia
  • A positive P in V1 or  a biphasic ( –/+ ) P-wave in lead V1  has 100%  sensitivity  for a left atrial tachycardia

What are the incidence of left and right atrial tachycardia ?

RA- 75%

LA -25%

What are the common focus of right atrial tachycardia ?

  1. Crista terminalis (60% of all RAT)
  2. Tricuspid annulus
  3. Coronary sinus ostium
  4. Perinodal tissue
  5. Right side of IAS
  6. Right atrial appedage

What are the left atrial focus in Left atrial tachycardia ?

  1. Right & left pulmonary vein (50% of all LAT)
  2. Superior mitral annulus
  3. LAA
  4. CS body
  5. Left septum

(Please note  this rule is not applicable for re-entrant tachycardias, atrial flutter, AV nodal tachycardias)

Source :

P-Wave Morphology in Focal Atrial Tachycardia

Development of an Algorithm to Predict the Anatomic Site of Origin

peter M. Kistler  et all. 

This paper  from  Melburne, Australia is a rare gem of  an article for understanding  atrial tachycardia .This  paper won the  the Eric and Bonny Prystowsky Heart Rhythm  society Fellows Clinical Research Award, New Orleans, Louisiana, 2005.

Click on the Link  to reach the article

http://content.onlinejacc.org/cgi/content/full/48/5/1010

 
 
 
 
 
 
 
 
 
 
 
 
 
 

 

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Top ten inventions and concepts in cardiology

Posted in Cardiology - Clinical, Cardiology - Electrophysiology -Pacemaker, cardiology-ethics, Hemodynamics, Top ten in cardiology, tagged , , , , , , , , , , , , , , , on December 24, 2008| 1 Comment »

 Selected on the basis of ,  impact  on survival , relief of  human suffering index and also innovation

10.Percuateneous interventions

9.  Electrocardiography

8 . Hemodynamics of cardiovascular system

7.Fruesemide

6.Thrombolysis

5.Pacemakers

4.Defibrillation

3.Heparin

2.Prosthetic valves

1.Coronary care units

 

Waiting list

Concept of vascular biology

Statins

RF ablation

Nitric oxide

Total Artifitial heart

Echocardiography

 

Ten least important concepts and  inventions in cardiology

Selected based on duplication of research, futile scientific concepts and   of course impact on survival

10.Low molecular weight heparins

9.Cardiac resynchronisation

8.Rotablator

7.Multi  chamber pacing

6.Newer ARBs

5.C reactive protein

4.Three dimensional echocardiography

3.

Comments welcome  and please contibute

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Cardinal symptoms in cardiology : Palpitation , some observations

Posted in Cardiology - Clinical, Tutorial in clinical cardiology, tagged , , , , , , , , , , , on October 2, 2008| Leave a Comment »

                        Palpitation is one of the common symptoms for which cardiac patients are referred. Like dyspnea , palpitation can either be a physiological expression of normally beating heart or a  dangerous pathological state of the heart. This makes this symptom unique and warrants careful evaluation.                                                                                                                                                         By definition palpitation  is abnormal  awareness  of ones own heart beat. Heart is a mechanical organ with multiple mobile anatomical structures. There is  constant  blood  flow in multiple directions . Apart from this the heart   has  it’s unique translational, rotational movement . These intrinsic movements combined with proximity to chest wall  generate vibratory  motion  signals .These signals are generally dampened by the encircling pericardial space .The neural signals responsible for  perception  of palpitation is not clear. If the heart hits against the chest wall it is the  somatic nerves from the chest wall that carries the signal. Vibrations generated within the heart chambers, and  and the  valves  are  carried  by the  myocardial and intravascular  sensors.( Autonomic) 

What are causes of palpitation?

       Cardiac

  • All hyperdynamic circulatory states. It may be generated from either  right or left ventricle or both.
  • Regurgitant lesions ( Mainly Mitral and aortic regurgitation)
  • MVPS*
  • Congenital heart disese ( Mainly left to right shunts-ASD/VSD/etc)
  • Apart from this patients  with prosthetic heart valve, and pacemaker patients can feel their heart beats.
  •  Cardiac arrhythmia .Both tachycardia, and bradycardia . Ventricular ectopic beats are the very common cause .( It is often described as missed beat)

* Mitral valve prolapse, a very benign condition, over diagnosed in the last few decades raised considerable anxiety and palpitations for the patients (mainly after the diagnosis ! ).Now the cardiology community has sought to underplay this entity with strict diagnostic criteria.( Thickened mitral leaflet ,presence of MR both must be present to label a patient  as MVPS)

       Non cardiac

  • Physiological
  • Anxiety state
  • Anemia 

What is the relationship between ejection fraction and palpitation?

                                        Generally palpitation indicate a  hyper kinetic state of heart .The commonest cause of palpitation is  anxiety  state .This also happens in hyper dynamic circulations like anemia , fever, thyrotoxicosis, pregnancy etc . In all these situations palpitation indicate increased force of contraction which   generates high dp/dt(Rate of rise of ventricular pressure)  . So  the left ventricularejection fraction is normal or more than normal . So  presence of  palpitation could be an  indirect evidence  of reasonably good LV function.

    “Patients  with dilated cardiomyopathy or CHF rarely feel their heart beat during exertion , instead they have dyspnea  as the LV force of contraction is less”

What is the significance of palpitation that occur during rest ?

                              Palpitation occurring at rest indicate more often a  pathology.It is invariably due to an cardiac arrhytmia  either tachycardia or bradycardia. Intelligent patients can give accurate information about the  regularity of rhythm , any  extra beats or missed beats . Atrial fibrillation, VPDs  could be  diagnosed by history alone in them !

If palpitation  is associated with visible chest pulsation what is the likely diagnosis ?

    If  significant visible pulsation over chest wall  pulsations are seen   in young adults it could simply mean a hyper dynamic circulation and thin chest wall. Pulmonary arterial pulsations is not normally felt in left 2nd inter costal space.If felt one has to rule out shunt lesions like ASD or pulmonary hypertension.
                    “ASD is the commonest cause  of right ventricular  palpitation “  

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How does squatting help relieve exertional dyspnea in patients with tetrology of Fallot ?

Posted in Cardiology - Clinical, Infrequently asked questions in cardiology (iFAQs), Tutorial in clinical cardiology, tagged , , , , , , , , , , , on October 1, 2008| 2 Comments »

.

It is a well known fact squatting is a simple compensatory posture adapted by children with cyanotic heart disease during exertion to get relief from breathlessness. The children with tetrology of Fallot and related conditions have baseline hypoxia due to right to left shunting .This gets aggravated during exertion. Squatting promptly relieves this exercise-induced worsening of dyspnea. The oxygen saturation improves immediately after assumption of squatting posture. The exact mechanism by which squatting relives the dyspnea is not clear.

Apart from squat induced po2 raise there is a fall in the concentration of pco2 and raise in blood Ph that pacify the sensitive respiratory centers,thereby bringing down the tachypnea

Hemodynamics of squatting has two phases

  • Immediately ( First 15 seconds) after squatting there is a sudden drop in venous return.
  • Sustained squatting for 1-2 minutes result in steady increase in venous return, raised systemic vascular resistance.

Both these effects help the children with TOF. The initial trapping of highly desaturated blood in the lower extremity gives a quick relief as soon as the child assumes this posture. In the next 15 seconds or so the systemic vascular resistance increases and bring the aortic after load sufficiently high to divert the blood into the pulmonary artery.

The net effect of squatting is there is a transient or sustained (as long as child squats) increase in pulmonary blood flow and this is made possible by the relative reduction of right to left shunt as the aortic and systemic resistance is raised by this posture.

Other explanations

There is one more possible effect of squatting. By, compressing abdomen (Knee chest) cause a mechanical push on the splanchnic blood pool into the aorta which has high o2 saturation. This is thought to provide immediate relief to brain hypoxia and avoid the vicious respiratory/ hemodynamic cycle

What is the clinical inference from squatting in cyanotic heart disease?

Squatting implies there should be a large VSD, associated with a delicate right to left shunting very much dependent on the degree of pulmonary stenosis or ( any RVOT obstruction) and the systemic vascular resistance.

How common is squatting history in pulmonary atresia with VSD ?

It can occur with collaterals are sparse.The mechanism of relief is slightly different.

The likely mechanism of relief with squatting in Pulmonary Atresia, VSD is two fold.

1. The Initial relief is due to trapping of deoxygenated venous blood in squat posture, which is similar to TOF

2.The sustained benefit is due to raised systemic vascular resistance which favors more flow across MAPCAs from Aorta.

The second one has no authentic reference , but its a hemodynamic plausiblity as there is zero RVOT flow in PA with VSD.

What are the other cyanotic heart diseases in which squatting is reported ?

  • Tricuspid atresia
  • Double outlet right ventricle with pulmonary stenosis
  • Any combination of large VSD and RVOT obstruction
  • Rarely in Eisenmenger syndrome*10%)

*Mechanism of squatting episodes in Eisenmenger is tough to explain. But, it does give relief. The most plausible mechanism is the raise in SVR with squatting tilts temporarily a favorable QP/QS as PVR -SVR ratio falls .(Venous return component doesn’t operate here as in squatting of TOF) It should be noted squatting is mainly reported only in VSD Eisenmenger.. ASD/PDA -Eisenmenger is extremely rare or doesn’t occur. This is understandable as Interventricular communication has to be present to shift in QP/QS with a response to a rise in SVR.

Squat equivalents

Assuming a squat position has cultural issues. Grown-up children may avoid these public places. Standing with legs crosse is a common posture. In fact, the mother holding a crying baby in a chest with knees folded promptly prevents a spell . This can be called “squatting by proxy”

*Though squat equivalents do give relief from dyspnea they are given less significance in terms of diagnostic value of TOF

Reference

1.Paul R. Lurie ,Postural effects in tetralogy of Fallot The American Journal of Medicine Volume 15, Issue 3, September 1953, Pages 297-306

2. Warren G. Guntheroth. M.D.Beverly C. Mortan. m.Venous return with knee-chest position and squatting in tetralogy of Fallot American Heart Journal Volume Volume 75, Issue 3, March 1968, Pages 313-318

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What is the mechanism of pericardial rub ?

Posted in Cardiology - Clinical, Tutorial in clinical cardiology, tagged , , , , , , , , , , , , , on September 28, 2008| 6 Comments »

Heart is externally covered by two layers of pericardium .  Pericardial space is formed between parietal and visceral layers of pericardium . It is a narrow space which is normally lubricated with pericardial fluid up to 25ml. When these two tissue surfaces  come into contact ,  pathological  rub takes place.It is heard  whenever the pericardium is inflammed . Pericardial rub is a distinctive but uncommon  clinical sign .

Common clinical conditions

  • Acute pericarditis
  • Uremic pericarditis.
  • Rheumatic pericarditis
  • Post myocardial infarction

Pericardium has two layers .

There are four  possibilities for pericardial rub to take place.

The rub can occur

1.Between the two layers of pericardium

2.Between the visceral pericardium and the epicardial layer of  heart*.

3.Between parietal pericardium and the  chest wall

4.Pericardium can rub with the adjacent pleura( Pleuro pericardial rub )

The second and third mechanisms are very rare.

An update

We have realized one more possibility . Diaphragm forms the floor of the heart on which the hanging heart  rests . Rubbing of pericardium over diaphragmatic surface is a beat to beat affair that lasts the entire life !. In inflammatory states of  diaphragm especially  the contagious  ones from abdomen  , can result in pericardio- diaphragmatic rubs .These rubs are almost impossible to hear clinically.

pericardial effusion rub plural pleuro pericadial

*The anatomic mystery : Is epicardium same as visceral layer of pericardium ?

Some anatomist feel that both are same entities. If that is the case myocardium can never split its relationship with visceral pericardium.But it is also a anatomical fact visceral pericardium engulfs the coronary artery and  are located sub epicardially.

How many components of pericardial rub are clincally heard ?

Pericardial rub  classically has three components. Systolic, mid diastolic, and pressytolic atrial components. Pericardial rubs are typically described as to and fro rub. Systolic component is most consistent. In atrial fibrillation mono component pericardial rub is heard.

Quality

Superficial , scratchy, high pitched ( Can also be low pitched)

Location

Left sternal border , left 2nd or 3rd space  .Best heard in  sitting , leaning forward in inspiration. Many times the rubs are transient and evanescent . Since it has multiple components it may be mistaken for added heart sound like S 3 or S 4.

What is the mechanism of pericardial rub in the immediate post MI phase ?

Presence of pericardial rub post MI indicate a transmural involvement or atleast significant epicardial involvement . Recognition of this is important as presence of pericardial rub increases the risk of rupture  and hemorrhagic effusion if anticoagulants are used.

What is the  relationship between  pericardial effusion and  pericardial rub ?

Generally it is said with the onset of effusion pericardial rub disappear.But this is not necessarily true.

Rubs after contusion chest and fracture ribs can be with the chest wall and may have  no relationship with effusion.

Is pericardial rub a painful condition ?

Pericardial  rub associated with acute inflammatory pathology is severely painful (like a pleuritis).But pericarditis associated with chronic inflammatory conditions are less often generate pain.The exact reason is not known.

What is pleuro pericardial rub ?

This  clinical entity is poorly defined , often taught by veteran professors  in clinical auscultation classes.It can be heard in the mid segment  or diaphragmatic pleuritis with or without pericardial effusion in patients with  atypical pneumonias.

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What is the difference between left ventricular pressure curve and right ventricular pressure curve ?

Posted in Hemodynamics, Tutorial in clinical cardiology, tagged , , , , , , , , , , on September 18, 2008| 2 Comments »

The pressure tracing between two chambers of the heart are distinctly different .

 Apart from the magnitude of the  pressure ,(LV at systemic pressure ) The morphology also changes.

  •  RV pressure curve is triangular in shape,
  •  Upstroke is not rapid , (Low dp/dt)
  •  There is no sustained peak ,
  •  There is an early fall and
  •  The pressure falls to zero which  never happens in LV.

Contary to this LV pressure curve is bullet shaped,  with a rapid upstroke, sustained peak, fall later, and does not touch zero.

RV/LV pressure curves in normal persons .Adapted from , Curtiss 1975 Circulation

Note : The shapes of RV curve will change in pathological states.Example in TOF, large VSD there will be left ventricularisation of RV pressure wave forms. Also  in pulmonary hypertension RV pressure may mimic a LV curve.

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How is LAD angina differnt from RCA angina ? Can we localise the “Angina related artery ” from the the type of chest pain ?

Posted in Cardiology - Clinical, Infrequently asked questions in cardiology (iFAQs), Tutorial in clinical cardiology, tagged , , , , , , , , , on July 2, 2008| 1 Comment »

How is LAD angina differnt from RCA angina ?

Can we localise the “Angina related artery ”  from the  the type of chest pain ?

Patients with stable  angia  many times have  multivessel CAD. There has been some correlation with radiation of anginal pain and the culprit artery.If the angina spreads to jaw or neck it is possibleit might indicate RCA(RIGHT coronary angina) but rarely it indicates LAD/LCX lesions. if the angina radiates to left shoulder it virtually ruels out a RCA disease

Source .Braunwald 1992 Edition

Dr.S.Venkatesan ., Madras medical college. Chennai.

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