Archive for March, 2009

CABG is the most common cardiovascular surgery  done world wide .

When the ventricle is dilated it is a common practice to do a ventricular  reduction surgery.

It was a logical to expect benefit when we correct the adverse remodelling of heart  that aoccur following an MI.

The STICH trial compared  plain CABG with ventricular  reconstruction and reduction .

Unfortunately , in medicine , the logics often fail  as this study  found no  mortality advantage .

Click here to read the land mark article from NEJM

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Coronary collateral circulation is the most poorly understood, and often neglected concept among the cardiology community.There is a general perception , in obstructive CAD ,  coronary collaterals are an inferior modality of  back up blood supply than artificial collateral (Also called CABG ) ! One of the reasons,  it is   been ridiculed by many  mainstream cardiologists is   because  , it comes by nature , and also free of cost !

The often quoted statement* ,collateral blood flow can not sustain blood flow during exercise ,  is not based on solid scientific data. In the real world , there are thousands of patients actively pursuing life with chronic total occlusion and good collaterals.

It is surprising , there is no  physiologically valid ,  controlled study available to compare CABG with natural collaterals

*When repeatedly told , a  statement becomes a fact !

It can be assumed (Unscientifically ofcourse ! )   the  remarkable  success  of medical therapy  in COURAGE  and the OAT * study  can be attributable to the naturally occurring coronary collateral circulation.

* Summary of COURAGE & OAT : A   block  in the coronary artery  need not be opened  to prolong human survival !

You draw your own conclusions from the  following case study

A 40 year old women , with stable angina and good physical activity

Her angiogram shows.


RCA injection


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Coronary artery  perforation is a dreaded complication of PCI. Perforations are the Interventional cardiologists ultimate worry   as they need to  manipulate their  hardware for  long periods in many complex lesions.  Especially  it is a  real threat in chronic total occlusions.

Still , an important fact is ,  many of the coronary perforations are not life threatening ?

How is this possible ?  (Type 1 Ellis has zero mortality Read below)

As the guide wire injures and perforates the cor0nary vessel,  it results in  small puffs of dye extravasating  into peri coronary space .

The coronary artery , which is located   within the  atrioventricular groove  (LAD), or AV groove (LCX, RCA) have  two distinct anatomical relationship with reference to epicardium and pericardial space.

50 % 0f circumference of the coronary artery is  hugged  by the myocardium  another 50% or so is related directly to the pericardial aspect.

Guide wires hitting on the myocardial aspects face a stiff resistance than the pericardial aspect. So , generally the risk of perforating pericardial aspect is more than myocardial aspect

Even if , the coronary artery is punctured on myocardial aspect , no great danger occur as there is no potential space for the blood to drain and further,  the  elastic nature of myocardial muscle plane effectively seals the leak. At the most , mild myocardial staining is noted .


While ,  perforations  into  the pericardial space  , often threaten with a tamponade. The fact that pericardial space has negative pressure and  the mean  coronary arterial pressure around 40mmhg ,  it is  , all the more likely blood is sucked into the pericardial  space. Of course , very minute  perforations  even into the pericardial space ,  could  be self limited and  benign.


What is unrecognised coronary perforation?

Many times , the guidewire goes in a false track in the tissue plane.This is  nothing,  but perforation without hemodynamic implication. Most often , these are the instances of guide wire entering the epicardium.They mimic , false lumen entry , dissections, etc. There are occasion , where false lumen of the  coronary artery were  stented.

What are the  factors which increase risk of perforation ?


 How do you classify coronary perforations ?


*Ellis SG, Ajluni S, Arnold AZ,  Increased coronary perforation in the new device era. Incidence, classification, management, and outcomeCirculation. 1994;90:2725–2730


How do you manage coronary perforation?

Simple guide wire induced perforations are less trouble some unless we have crossed it with balloon without realising the fact the wire has entered the pericardial space. So, caution is required and always watch for guide wire tip movement which is often funny looking wihtin false lumens or very freely moving within pericardial space. Anticipate the complication especially so when you do CTOs and venous graft PCI.  Keep one cath lab  tamponade crash  bin  in ready mode before embarking upon a complex PCI

  • Neutralise the heparin action with protamine is the first step
  • Most are self limited, no intervention is required  but requires close observation for next 24 hours.
  • Temporary balloon occlusion may be suffice in many cases
  • Tamponade requires immediate tapping. Small collection without fall in BP can be observed.
  • keep doing the echocardiogram liberally to assess the leak and watch for any new collection.
  • PTFE covered stents if prolonged leak.
  • Emergency surgery may required in few.

2018 update 

This is  nearly 10 years old article. Now, we have gained much experience and hardware utilisation have rapidly expanded. While expertise has minimised this complication , more PCIs in complex lesion subset tend to keep the incidence static , if not higher.(Its around .5% )

Tips to use balloon occlusion during perforation

Perforations which are active and flowing should be immediately occluded with a balloon either at the site of leak or just proximal to it. Doing a proximal occlusion is easier in emergency , as often times its technically difficult to reach the site of leak especially in CTOs where the leaky site is not defined clearly or forward looking (Local balloon inflation across the leaky site is not feasible )


How long to occlude , Intermittent /complete, proximal ? or at the site of perforation ? These queries are answered in Ref 4


1.Largest report (1762 cases) of perforation from British Cardiovascular Intervention  Society Database Circ Cardiovasc Interv. 2016;9:e003449.

2.Al-Lamee R, Ielasi A, Latib A,. Incidence, predictors, management, immediate and long-term outcomes following grade III coronary perforation. JACC Cardiovasc Interv. 2011;4:87–95.

3Xiangfei Wang and Junbo Ge Balloon Occlusion Types in the Treatment of Coronary Perforation during Percutaneous Coronary Intervention   Cardiology Research and Practice Volume 2014, Article ID 784018,

4.A very good review comes from Royal Hospital, Muscat, Sultanate of Oman


iFAQs in coronary perforations

1.Does the plane of the coronary artery (Sub epicardial within the fat layers)  determine the likely hood of tamponade ?

While myocardial tissue can resist flow we are not sure about sub-epicardial fat on the pericardial aspect.

2.How common is Intra-cavitory perforation ?

Perforations into chamber is invariably associated with septal branches (PCI to septal branch itself is less common )

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  • CAD is the major cardiovascular disease of our population.
  • CABG is the most common cardiac surgery done world over.
  • LIMA to LAD graft is the most common by pass done.

The purpose is to short circuit some of the blood meant for the hand to the heart.

But ,  is it always a helping hand ?

May not be . . . at times  of crises  the  hand  sucks  blood  from the heart .This is called coronary-subclavia steal phenomenon

Is it not dangerous ?

How to anticipate or prevent this complication in patients who are posted for CABG-LIMA graft ?

Click on the link for the reveiw article from Annlas of  thoracic   surgery


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Biochemical diagnosis for PHT and Eisenmenger syndrome

Identifying reversibility of pulmonary arterial  hypertension remains a difficult clinical problem.Heath edwards grading of pulmonary hypertension is based on lung pathology .Grade 4 and 5 constitute severe obstructive vascular pathology including pulmonary vascular necrosis.

Lung biopsy is an invasive procedure and has a  huge risk in patients with elevated pulmonary artery pressure.

Do we have an alternative ?

Does the pulmonary artery  sheds  necrosed  endothelial cells  into the circulation  ?

Yes it seems so , This month’s Nature cardiology  reveals a breakthrough concept

The CEC (Circulating endothelial cells count )  can be used as marker  and  may be considered a non invasive equivalent of lung biopsy




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Left main coronary artery disease is  a  major form of CAD .

left-main-41A long left main by virtue of  it’s surface area   statistically ,  are  more prone for atherosclerosis as it preferentially affect the proximal vessel.A long and tubular leftmain generally give  the LCX branch at right angles(In the above pateint it is 90*).This makes  interventions in Lcx difficult.

A short leftmain or absent leftmain could be a blessing for the simple reason these people have the unique freedom from developing left main disese the dreaded form of  CAD !

Have a look at this angiogram


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Beta blocker use in cardiac failure has come a full circle from a “contraindication to indication”

You don’t need gimmicks of statistics for science to progress. What you require is meticulous observation.

F .Waagstein of    Sweden just did this  with a  study population of seven  patients .

This land mark study , was least significant statistically , but most significant clinically

Today , as on 2009 , if any one submits a manuscript of a study  to a journal  ,  done with seven patients   he or she   will be called as a  fool  !  BMJ  , in 1975 had a courage in not  doing  so  and thus a break through concept was born.

So young scientists , should not  get bothered about sophisticated statistical method.

Science is not about number gimmicks it is about truth and nothing but truth  ! Truths  may  come out from  single digit study or even a single patient study


To read & download  this land mark article click here

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Dopamine and dobutamine are  the most commonly used inotropic agents in clinical cardiology.

The following table represents a simple comparison of the two drugs.


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Why is identifying false and true lumen important ?

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


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.


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.


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.

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)


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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First and foremost is

Avoid the procedure if  not really indicated.A lesion which  has more thrombus load  than a plaque and it is ,  subcritical and not limiting the flow  , PCI may be inappropriate  especially if the ACS is stabilised.

  • Adequate anticoagulation  along with  2b 3a blockers should be used
  • Predilatation should be minimally used or to avoided.Direct stenting preferred.
  • In primary PCI suction devices (Export etc may be useful)
  • Distal protective devices  are  “hyped up devices” rarely useful in an occasional patient with good distal vessel diameter.
  • Pseudo stent approximati(fig 1) may occur. A Layer of thrombus may get plastered between stent and the vessel wall.In the post PCI  phase , with intense anticoagulation and antiplatelet regimen this layer may get dissolved and stent  may lose it’s grip and may dislodge or migrate.Another possibility is the dead space  beneath the stent  becomes a potential site for future  thrombus and ACS.


Fig 1

  • To prevent this complication , high pressure inflations and Post procedure IVUS (Intra vascualr ultraound may be done to ascertain lack of thromus between stent/vessel wal  interface)
  • Drug eluting stent evoked a special concern , when used in thrombotic milleu.This , has now been  proven to be  safe

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