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One may recall some stunningly simple facts from our high school biology classes that every living cell needs energy on a moment to moment basis.

Blood vessels which take care of the vital organ’s energy supply also need the same blood (Nutrients /Oxygen) for its own survival.

Coronary arteries carry about 250 ml of blood every minute , 24/7 supplying ATP enriched fuel to the heart.

Who is feeding these delicate vessels which carry on this life-sustaining work ?

It is easier to assume the three layers of the blood vessels which are bathed with blood would never suffer from Ischemia. Reality is different .Blood vessels do suffer from Ischemia.We do have evidence medial necrosis, plaque instablity , fibrous cap disruptions may be due to a vascular insult or vessel wall energy deficit.

The much debated entities like endothelial erosion and dysfunction are often atributed to mechanical stress , sympathetic spike , or smoke . This may be a virtual guess as no one knows what causes these. It could well be a patchy Ischemia due to endothelial perfusion defect from within or a vasavasoral dysfunction from outside. Coronary ulcers some times mimic gastric ones and guess the cause ! yes it is mucosal ischemia !) *Ischemic ulcers in GI tracts can be common (Schweiz Rundsch Med Prax. 1993 Jun 15;82(24):709-13)

How does coronary artery gets it blood supply ?

Busy cardiologists have no time to worry about nourishment of the coronary arteries . . . even as they play inside with unlimited arms and ammunition.We leave it to our basic scientists.

So , how does coronary artery gets its blood supply ?

The easiest answer is, blood supply to coronary artery is taken care by a vast network of micro vessels called vasa vasorum(VV) . Of course, the inner layers of Intima and media do get some nourishment by the flowing blood as mentioned earlier.No one really knows the quantum of blood flow that perfuse within the planes of coronary artery.

*By the way , does the vasa -vasorum comes from extra-coronary source or from the same parent vessel ? (I think the answer is both ! will try to find out!)

It should be noted Vasa vasorum is well developed only in large arteries. VV has one more important function ie to drain the metabolic excreta from the walls of blood vessels. This function could never be taken lightly as failure to do so will result in vascular wall edema in acute setting or thickening In chronic setting.

Does coronary arterial tree goes for necrosis in STEMI ?

There is some evidence , when acute total occlusion happens in an epicardial vessel , not only the myocardium is ischemic , the entire distal coronary vascular tree becomes vulnerable. The ischemic time and resistance of coronary macro vs micro vasculature is currently not known. It is expected to show significant variation . We know ,one of the important mechanism of no re-flow following PCI is due to microvascular damage(Non thrombotic)

Many times we fail to realise myocardial viablity and micro-vasculature integirty are two different things. ! This questions the concept of reperfusion based on the status of viable myocardium alone.This we have experienced in many patients as myocardial viability doesn’t guarantee you full recovery from LV dysfunction as microvasculature may recovery may lag behind or never restored (Permanent vasa-vasoral damage ?)

What is our knowledge base about exclusive pathology of coronary vasa vasorum ?

Do you know, ectasia, arteritis, aneurysms and external band like compression of coronary artery all are related to some sort of vasa vasoral dysfunction ? We are not yet clear whether atherosclerosis really involves the vasa vasorum.(Takayasu does it for sure ! )

What is the relationship between vasa vasorum and coronary collaterals ?

It seems to me , many of bridging collaterals are nothing but extension of vasa vasorum and ultimately arise from epicardial coronary collaterals. (Some youngster’s take up this topics for research)

Why is high pressure post dilatation a double-edged sword ?

It’s often thought , larger the lumen its better. Need not be. These are all some questions which we don’t have an answer.

What is the radial pressure exerted by coronary stents on coronary trans -arterial perfusion ?

Does coronary artery go for Ischemic necrosis with high pressure Inflations ? As such there is no published evidence . By the time we wait for published evidence enough number of coronary arteries might get damaged. So try to use common sense .

Relationship between delayed Mal-apposition & vasa vasoral damage

It is very likely ,the so-called endo-leak which is quiet prevalent in aortic interventions is could be seen in coronary arteries. We are not recognising it. It could be same as Intramural hematoma in certain subsets.

Meanwhile, self expanding stents with good radial strength has made a come back .While it may prevent a mal-apposition ,has a potential to stress the vessel wall (Radially) and in the process interfering with perfusion.

 

Does Vasa vasorum promotes Atherosclerosis or negates it ?

hehttps://www.hindawi.com/journals/bmri/2014/701571

 

The irony is, while de-novo vasa vasorum is the life line for coronary arterial nutrition, neo-vascularisation is problematic .Then how to selectively promote good vasa vasoral growth and avoid the pathological network that promotes adventitial nodular degeneration ? This is were the curious basic scientists and casual cath lab guys need to interact.What is positive remodelling ? (Often referred to the famous concept of Glagov ) How can we promote it to maintain good luminal diameter inspite of large burden of atherosclerosis by manipulating the vasavasorum.

 

Final message

Cardiologists are ahead of others in many cutting edge technology. There is no two opinions about it. Who can repair a live beating heart without stoping it for a moment ? Still, there is a whole lot of coronary Ignorance waiting to be explored. Blood supply to coronary artery is one such area to be decoded.This will have larger implications as Vascular healing , plaque survival and growth depends upon vasa vasoral integrity as well as neo vascularisation.

While , metallic management of CAD seems to be the order of the day as it tends to give an instant fix .My guess would be medical sense would ultimately prevail one day with controlled vascular aging and natural ,pharmacological ,biological repair of cells will prevail over temporary patch work in cath labs.

Reference

What is the role of newer Imaging and OCT in visualising Vasa vasorum ?

It is going to open up new avenues in our coronary vision.

Vasavasorum review article

(Kensuke Nishimiya European Cardiology Review 2017;12(2):121–3)

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There is a tough ongoing rivalry between drugs and catheters to conquer the commonest electrical chaos in human heart, namely Atrial fibrillation (AF). Mind you,the confusion about the importance of this arrhythmia is huge and real.Bulk of these episodes are transient , paroxysmal and do not require rigorous management.While stroke prevention seems to be the major aim and target , the real world scenario seems to tell  a different story.

The nomenclature conundrum 

AF may be classified as many ways a learned cardiologists can think . Often it’s done with reference to etiology, duration , rate, neural (sympathetic or parasympathetic)  humoral , cardiac or non cardiac , reversible or irreversible ( Endocrine, Electrolytic, hypoxia etc).

Unlike VT , bifurcating  AF with reference to the  presence or absence of structural heart disease is rarely meaningful.Subclinical atrial interstitial fibrosis in elderly is so common especially so in hypertensive individuals making all lone atrial fibrillation as true structural disease.

Classifying AF with reference to atrial enlargement again is problematic as any sustained AF can dilate these thin atrial chambers in few weeks time making  it a sequel to AF rather than a cause to it.

Adding further fuel to the confusion is the  recent man-made (read cardiac scientists!)  problem .Linking the etiology of AF with the presence or absence of valves pathology is definitely not helping us. In the process , we forget a casual fact that valvular AF needs aggressive valvular Intervention and not arrhythmia Intervention !*A patient with dilated cardiomyopathy with mitral regurgitation and LA enlargement with AF is considered non valvular AF in spite of clear pathology in mitral valve apparatus.(Is there myocardial AF by the way ?)

What is the current role for catheter ablation in AF ?

The question of advanced catheter based management boils down to a minority of refractory, fast , troublesome AF which has failed by most available drugs. More Importantly the long-term success of ablation is lowly 20% ( PV reconnection, geographical miss, atrial focus etc) and follow-up medication  is  absolute must even after successful ablation. Its well-known , severe the underlying heart disease more likely is the recurrence .Ironically these are same ones that attract the catheters.

The previous debate of rate control vs rhythm control gave sufficient lessons  that complex modalities to restore sinus rhythm is unwarranted . As scientific  cardiologists we continue to be adamant and don’t learn from our mistakes and blindly adore and adopt technological excessess.

Now, thanks to CABANA* the ablation for AF has proven to be a fruitless  process considering the time ,effort and potential (& real )complications.

*The Catheter Ablation Versus Anti-arrhythmic Drug Therapy for Atrial Fibrillation . Just presented in HRS annual meet at Boston MAy 2018.

The bright spot is even in these commercial medical world the study like CABANA is a silver lining. Mind you it’s partly sponsored by Industry , still went against them. Three cheers to the genuine medical research team of CABANA for bringing out a truth. Now, I am optimistic more such trials in cardiology will be proposed

A companion to CABANA from UK

A 2018 landmark paper from  published in BMJ reveals a dramatic truth that the risk of stroke continues to persist even after resolved Atrial fibrillation,  largely concurring with CABANA.(Nicola J Adderley, Risk of stroke and transient ischaemic attack in patients with a diagnosis of resolved atrial fibrillation: retrospective cohort   studies   BMJ 2018;361:k1717)

So, how to get out of these AF conundrum ?

Practically , an extreme simplification of AF classification is warranted . It should answer these couple of  questions !

1. Will the  AF in a given patient require long-term oral anticoagulants  or not ? (or ok with antiplatelet drug !)

2. Should I make any meaningful attempt to convert the AF to sinus rhythm at all* ?

* You can also redefine the second question , does this AF deserve a EP consult or not ?

Final message

AF is largely a benign arrhythmia in global perspective . However, In those patients were  its troublesome , safe and effective drugs are available to tackle it.We shouldn’t Insist to make it complicated.

Meanwhile . . .the anxious pulmonary veins seems  to enjoy the  moment as they escape from the fire .No wonder they will thank and celebrate the CABANA.

Reference

http://www.acc.org/latest-in-cardiology/clinical-trials/2018/05/10/15/57/cabana

Post-ample and counter point

The RF ablation is a high risk procedure , as we develop less injurious cryo balloons the results of Invasive ablation procedures may score over drugs.Let us wait and don’t prematurely ditch the catheters.

 

https://1drv.ms/v/s!Ahm_xjThT-nXgY5EtHnqjxFkb_PWtQ

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Yes, Medicine is a funny science ( some don’t agree , Isn’t Art ?) Many of the noble professionals  are silently pursuing their job of saving lives and removing human suffering .Meanwhile, people like this author are needlessly bothered about some Imaginary Issues and write stuff like this one , . . that you are reading now !

Yes, there is an invisible  tectonic shift taking place in the name of  science.The way we practice  medicine currently, it fits in with any of the following descriptions . Divine, Godly,dramatic,miraculous , comical ,cruel or  even outright  brutal ! (I dare not quantify the weightage of each adjectives used above !)

The field of cardiology as I know personally for the past three decades is challenged by  uncontrolled growth (How about proposing 1000 dollar PCSK blocker Evolocumab for a meaningless reduction of few mg of LDL over and above Statin ) Further,the technology goes on to Implode at every corners of wall street ,(Mitra clip for mild MR of DCM ! TAVR for aged Aortic valve )  hijacking  commonsense and cost (where is the effectiveness ?) of every stake holder .

In the process ,the critical  healing power that resides within every biological system is ignored and ridiculed upon .(You become a fool if you say endothelial tissue plasminogen activator and lytic system will take care of a  bulk of the intravascular vascular thrombus if we wait, and  we shall permanently defer an Intervention! Current space aged physicians want to invade every existing (or non existing ) problem with multi pronged military strategy and guess what will happen to the humble  body which becomes the  battle ground.

Coming to the content proper

Sometimes I feel God throws some random truths at an unexpected  time through some extraordinary men ! Here is a most unusual study of its kind from the  Sanctum sanctorum of Medical science , namely  Harvard medical school and Massachusetts  General hospital .I think it was  presented  in ACC Scientific sessions 2018 , Orlando and published in Journal of American heart Association.

Cheers and congratulations to the lead author Dr.Anupam  B Jena* , Physician and professor , Department of health care policy , and Health economist

* A video profile of author is in the reference

There is no surprise a paper with such a title had a huge  media backlash. USA today reacts  . . .

My observations and final message 

The paper from MGH,  Boston  dwells a sensitive area ,of course it has come with a gross conclusion (However,  I feel it has hit the bull’s eye.) Still, for the critics, I want to tell one thing , who can deny the fact ?  the massive evidence base with 100s and thousands of research papers created by cardiology scientific Industry over the decades is largely a damn squib.

(The problem with acquiring this sort of  ready to synthesise knowledge stuff  is, It sits right inside our brain and bonds irreversibly , refuse to leave even if these dubious practices are proven dangerous ultimately !)

It might appear , the only option  to tackle fake science would be through some dramatic ,less than ideal or mediocre research papers (Or even another fake!) As long as final outcome is good for the public don’t bother about methodology  of such studies.(Does it sound in any way I am a supporter of Donald Trump ,! No I am not !)

Reference 

Now have a look at this (a long post ) which I wrote some time  back. Find out whether  these  scribblings of mine seem to have grown some scientific backing now .

A brief Info about  the author of this unusual paper that has put the field of Interventional cardiology into tail spin and fluttering in cross winds !

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One car company  recalls 100s of  thousands of cars for faulty equipment  issues in recent years . It goes on to add , beware , it’s potentially dangerous  . . . please fix it and bring your car at the earliest !

Toyota-Gra

Mean while , scientific medical literature is flooded with dangerous articles, papers and guidelines . . . and  pose serious threat to your patients !

Please search for the junk knowledge and then go on to expose, erase and  ,  . . . and throw it to dustbin ! After all , research is searching for truth , again and again !

Let us welcome a new era , where we shall get alerts about wrong knowledge  withdrawals and reversal ! Let it challenge  the self proclaimed sancto-scientific medical world  and a new medical literature cleansing movement (MLCM) begin in every sub specialty.

One such paper from Yale is linked below .

medical reversal

Finally  . . . the forbidden message !

venkat quotes 2

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Answer 

Though PTMC in the presence of LA clot is an option in low risk clots , my strategy would be the last one ,whenever feasible. Intensive, monitored Heparin /Oral anticoagulants ( Heparin 5000 units tds or qid  or Low molecular weight heparin Enoxaparin  40-60mg twice a day , Tablet Warfarin /Acitrom with an INR of 3 ) will dissolve  LA clot in  30-50% of times.(Our experience).

The percutaneous clot retrieval system is not available as on 2018.Aortic filters are FDA approved during TAVR. (Why not use the same in PTMC ?)  LA Catheter based regional lysis through PFO is can be an option if patient agrees to the risk.

How long to wait for clot dissolution with Heparin /OAC?

Most small clots or intermediate sized clots ((Up to 2 CM ?)  have been dissolved by 3  months. Even large clots gets dissolved at least in few Instances.Please note, this strategy is applicable only with valves that is fit for PTMC. All others are referred for surgery.

How does heparin lyse a clot  ?

Its a miracle to see it happen, though heparin / OAC are  never considered as thrombolytic agents .It happens because  both heparin and OAC tilts the local   endogenous fibrinolytic forces and thrombus melts , dissolves or disappear altogether. (I am waiting for the day , the scientific community to re-label heparin as a thrombolytic agent, Indirectly though !)

Is there a risk of dislodgement of LA clot during heparin /OAC therapy ?

This question shall be addressed to  God ! It all happens if bad luck strikes you and your patient.

Be wise  . . .  and call your surgeon Immediately when you encounter something like this !

Even if the valve is perfectly eligible for PTMC , high risk  mobile clots, history of  embolic episodes , probing and hyper-googling patients , its better to refer for surgery Immediately. Wait and watch game has a definite risk of stroke and it is especially bound to happen if your patient or their family is anxious !

Reference

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In the modern era of cardiology,  PCI has become the single therapeutic modality  that determines the survival of both cardiologists and possibly their patients! The procedure is all about launching  a metal coil inside the coronary artery of a live beating heart.

Post dilatation vs pre dilatation

Millions of diseased and (not much) diseased coronary arteries are serviced (either re/deconstructed ) world-wide on a day-to-day basis.The benefits of the modality is  directly related to the wisdom of treating cardiologist and patient’s luck than the original severity of the disease. However, with greatly improved coronary  metallurgy , well assisted by drug coating technology and antiplatelet Industry , cardiac physicians believe they have reached the zenith of this procedure.

But the truth is , PCI still has many lingering issues regarding safety , efficacy and cost effectiveness.Early hazard in the form of acute stent thrombosis and sudden death is  a  reality. Blaming it on patients and their lesions ( condition of blood , gene included) , metal behavior is easy , but, wrong selection (Ignoring the option of CABG) and technical inadequacy of the procedure in the setting of complex  vessel wall disease (Hard calcium , deep tunnels , fissures , dead spaces ) is a major cause for concern.

Some personal thoughts about Post dilatation 

Lesion preparation , pre/per-dilatation /POTS , etc by itself  a big topic (which is not discussed here) Post dilatation after direct stenting is much more vital concept that determines not only the immediate but also the , Intermediate and long-term outcome.

Is routine post dilatation harmful ? or beneficial ?

This is the most tough question to answer . The answer is both Yes and No !  While it was thought useful and mandatory by some , the oppositeis also being adviced few  (CCL 2003 POSTIT trial)

What balloon pressure one should post dilate ? At what compliance ?  What is the Inflation time ? 

It’s akin to asking a musician  how to play a piano with fingers or guitar with various strings !

The effect of balloon pressures in the long term outcome. note both low and high pressure dilatation ( blue and orange worms ) hike the risk of restenosis. Too gentle is as dangerous as too harsh making post dilatation a secret and unique art.

 

Physics of post-dilatation  . . . again more questions !

  • Is there a role for compliant balloons ?
  • Does the compliance of balloon gets altered with hard lesions?
  • Is regional compliance matters ?
  • Can balloon exert same radial pressure all 360 degrees ?

It’s very likely, the moment balloon encounters an area of resistance it tends to avoid that area and would love to drag on to the area of least resistance and this is often diagonally opposite  zone of hard lesions ( if that segment  is free from hardness).Then , it  will face more stress and likely to bear the brunt of the force risking endothelial disruption . In other words , concentric hard lesions are more amenable for dilatation than patchy hard segments. While the physical forces vary in a stented vs non stented segment , the principle of dynamic forces on static tissue masses  with Intervening metal is too complex. (Mind you , we are not discussing  entirely different  issue , ie  thrombus laded ACS lesion , where displacement and pinching of of inter-strut thrombus into distal circualtion would cause no reflow!)

Impact of newer hardware

*Ablation catheters either rotational or Orbital can help , but must be done prior to stenting .Unfortunately , the hardness of a lesion is often realised  only after stenting

Is selective high pressure inflations over a particular struts possible ?

As of now , it would be challenging ,( if not outright impossible) .

Let us realise with all our intellect, complex PCI as a whole is taking an uncalculated risk  and leave the rest to GOD and DAPT !

Reference article 

In an elegant study of more than 90000 PCIs from Sweden and  Holland (Ref : Fröbert O, PLoS ONE. 2013 ) found routine post-dilatation pushes the harm curve little more than benefit.  The was more with both low and very high pressures .

The outcome of post-dilatation  in 900,00 PCIs 

 

Estimated cumulative event rates of stent thrombosis (Panel A) Restenosis (Panel B ) Cumulative death (Panel C) in relation to post-dilatation .Note the height of coronary Irony, Post dilatation Increase stent thrombosis and restenosis but saves life too !

 

The stunning truth revealed in this study was , early deaths were more common if  post dilatation was not done ! (Panel C in above figure) 

Role of Imaging in the decision-making prior to  Post dilatation

IVUS, OCT has been extensively used in recent times to diagnose suboptimal deployment and to asses lesion morphology.Though they are expected to improve the quality of angioplasty and hence the  outcome , the real world scenario is not really confirming our expectations.

This is because , eagle-eyed HD  imaging throws  more questions than answers in many and it converts coronary artery into a confused Pandora’s box . In fact these Imaging modalities has created fresh confusions , definitions and guidelines for malapposition under and over expansion , strut fracture, plaque prolapse, internal elastic laminar stress.( Still , I am not able eo understand  whats malapposition  vs  under deployed stent from a practical , pateint point of view !)

Is the Self expanding  stent is the answer ?

The conundrum of post dilatation might be cracked if the built-in radial force of self expanding stents is optimally utilised .This could be useful in some  tricky lesions when the vessel goes for progressive Glagovian  remodeling post PCI. The self expanding stent because of the stored potential energy keep hugging the vessel wall as it expands centrifugally.

Final Message

Post dilatation is neither a mandatory nor a sacred  protocol in cath lab. However , it would seem bulk of PCI’s still will require it . Its done judiciously with reference to   clinical setting, (ACS vs CCS) , type and location of lesion , stent characteristics etc .Most Importantly , the experience of the cardiologists counts ,and he or she will decide when, where, how much of post dilatation is required (or not required) .

Please remember , PCI as a whole (more so the Pre/ Post dilatation !)  is an art by itself. It’s never learnt in text books or even  watching  live work shops. Every young Cardiologists are enouraged to master the art of PCI ,  with a huge caveat . Always ensure  patient’s  Interest are placed first in every step forward. If you are not clear in comphrehending  “What is meant by true  patient’s Interest ? never Indulge in the procedure or call your mentor , if you have one !

Reference

1.Brodie BR1, Cooper C, Jones MCatheter Cardiovasc Interv. 2003 Jun;59(2):184-92. Is adjunctive balloon postdilatation necessary after coronary stent deployment? Final results from the POSTIT trial. Postdilatation Clinical Compartative Study (POSTIT) Investigators.

2.Fröbert O, Sarno G, James SK, Saleh N, Lagerqvist B. Effect of Stent Inflation Pressure and Post-Dilatation on the Outcome of Coronary Artery Intervention. A Report of More than 90 000 Stent Implantations. Agostoni P, ed. PLoS ONE. 2013;8(2):e56348. doi:10.1371/journal.pone.005634

3.Zhang Z-J, Marroquin OC, Stone RA, et al. Differential effects of post-dilation after stent deployment in patients presenting with and without acute myocardial infarction. American heart journal. 2010;160(5):979-986.e1. doi:10.1016/j.ahj.2010.07.007.

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Cardiologists at confused cross roads !

Perils of  limited Intellect & Infinite greed  

When not so appropriately trained cardiologists  do Inappropriate things “use becomes misuse” . . . then, it won’t take much time for science to become total abuse. That’s what happened with the murky world of coronary stents .No surprise, it’s time to firefight the healers instead of the disease !

Now ,Comes the ORBITA study . Yes , it looks like a God sent path breaking trial that spits some harsh truths not only in cardiology, but also in behavioral ethics .Let us not work over time and hunt for any non-existing loop holes in ORBITA. Even if it has few, it can be condoned for sure as we have essentially lived out of flawed science  for too long  Injuring many Innocent hearts !

ORBITA pci vs medical mangement drsvenkatesan courage bari2d ethics in stenting auc criteria inappropriate coronary stenting placebo effect of stenting acc aha esc guidelines chronic st

Yes , its enforced premature funeral  times for a wonderful technology !

GIF Image courtesy http://www.tenor.com

Meanwhile, let us pray for a selective resurrection of  stenting in chronic coronary syndromes  and stop behaving like lesser professionals !

Postample

Extremely  sorry . . . to  all those discerning academic folks , who are looking for a true scientific review of ORBITA , please look elsewhere !

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