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100% occlusion of a coronary artery result in STEMI.This includes both thrombus and mechanical component .We are very much blinded till we touch , feel and see the lesion with a wire or IVUS to quantify the mechanical component’s  contribution in the genesis of  STEMI.It is generally believed (True as well ) thrombus is the chief culprit .It can even be 100 % thrombotic STEMI with  just a residual endothelial  erosion and hence
zero mechanical component .However , the point of contention that non flow limiting lesion is more likely to cause a thrombotic STEMI than a flow liming
lesion  seems to be biased and misunderstood scientific fact .

What happens once 100 % occlusion take place ?

Sudden occlusion , is expected to evoke a strong fire fighting response within the coronary artery.The immediate reaction is the activation of  tissue plasminogen system. In this aftermath  few succumb . ( Re-perfusion arrhythmia  generated as VF ) .The TPA system activates and tries to lyse the clot.The volume , morphology, attachment, content of thrombus ,  and the elasticity of fibrin mesh , location of  platelet core would determine the life and dissolvablity of thrombus. Even a trickle flow can keep the distal vessel patent .(Please note a timely TIMI 2 flow can be a greater achievement than a delayed TIMI 3  flow !)

thrombus propgation
What happens to the natural history of thrombus in STEMI ?
Thrombus formed over the culprit lesion can follow any of the following course

  •  Can remain static
  •  Get lysed by natural or pharmacological means
  •  Progress distally (By fragmentation or by moving en-mass )
  •  Grow proximal and and involve more serious proximal side branch obstruction
  • Organise and become a CTO

Factors determining thrombus migration

The interaction between the hemodynamic  forces that push a thrombus distally and hemo-rheological factors that promote fresh proximal thrombus formation are poorly understood. The altered intra-coronary milieu with a fissured plaque covered by  platelet vs RBC / fibrin core,  totally of obstruction,  reperfusing forces , re-exposure of raw areas and  the distal vessel integrity all matters.

While, logic would tell us,  thrombus more often migrates  distally  assisted by the direction of blood flow, an  opposite concept also seeks attention , ie since the blood flow is sluggish  in the proximal (to obstruction site )more thrombus forms in segments proximal to obstruction.

(In fact, its presumed  in any acute massive proximal LAD STEMI , it takes hardly few minutes for the thrombus to  queue up proximaly and  clog the bifurcation and spill over to LCX or even reach left main and result in instant mechanical death.)

What is the significance of length and longitudinal resistance of the thrombotic segment in STEMI ?

If thrombus is the culprit let us get rid of it , this concept looks nice on paper , but still  we don’t  know why thrombus aspiration in STEMI is not consistently useful. We also know little about  the length of the thrombotic  segment .When a guide wire is passed over a STEMI ATO it may cross smoothly like  “cutting a slice of  butter” in some , while in few we struggle and  end up with severe no-reflow inspite of great efforts .Why ?

What is the Impact of distal collateral flow in flushing fresh thrombus ?

The efficacy of collateral flow in salvaging myocardium is underestimated. Distal vessel flow if perfused partially by acute collaterals the thrombus load is not only less it’s soft and fail to get organised early that would help cross the lesion easily.

Mohandas Karam Chand Gandhi ,  father of my country , India , made these observations in year 1925  about the  fundamental constituents of  violence in society . These words of monumental wisdom came when he was  addressing young Indians in a country- side rally .

mahatma gandhi quotes medical science humanity

Note, his finger points to , what  exactly is relevant to our profession ! He emphasized this  nearly  100 years ago, when medical science was at its infancy .One can only guess what would be Mahatma’s comment about our profession in it’s  current form !

Should we include moral, behavioral and ethical classes  right from the first year of medical  school along with Anatomy , physiology and bio chemistry.Medical council of India obviously need to burn more mid night oil , I wish it happens in my life time. !

Here is a  video recipe  !

Please click here to  see more videos from my you tube site

Prosthetic valve implantation has revolutionized the management of  valvular heart disease . The original concept valve  was a ball in a cage valve  , still considered as a  fascinating discovery.  It was conceived by the young Dr Starr and made by Engineer Edwards  .This was followed   by long hours of arguments,  debates and  experiments that ran into many months . The  silent corridors of  Oregon hospital Portland USA remain the only witness  to their hard work and motivation.  At last,  it happened , the first human valve was implanted in the year 1960. Since then . . . for nearly  50 years these valves  have done a seminal  job for the mankind.

With the advent of  disc valve and bi-leaflet valve in the  later decades of 20th century , we had to say a reluctant good-bye to this valve.

There is a  lingering question among many of the current generation cardiologists and surgeons why this valve became extinct ?

Starr and Edwards with their child !

We in India , are witnessing these old warrior inside the heart functioning for more than 30 years.From my institute of Madras medical college  which probably has inserted more Starr Edwards valve than any other  during the 1970s and 80s by Prof . Sadasivan , Solomon victor , and Vasudevan and others .

It is still a mystery why this valve lost its popularity and ultimately died a premature death.The modern hemodynamic  men  working from a theoretical labs thought  this valve was  hemodynamically  inferior. These Inferior valves worked  like a  power horse  inside the hearts  the poor Indian laborers  for over 30 years.

A Starr Edwards valve rocking inside the heart in mitral position

The cage which gives  a radial support* mimic  sub valvular apparatus, which none of the other valves can provide.

* Mitral  apparatus has 5 major  components. Annulus, leaflets, chordae, pap muscle, LV free wall.None of the artificial valves has all these components.  Though , we would love to have all of them technically it is simply not possible.  The metal cage of Starr Edwards  valve partially satisfies this  , as  it acts as a virtual sub valvular apparatus.Even though the cage has no contact with LV free wall, the mechano hydrolic  transduction of  LV forces to the annulus  is possible .

Further , the good hemodyanmics of this valve indicate , the cage ensures co axial blood  flow  across the mitral inflow throughout diastole. .Unlike the bi-leaflet valve ,  where the direction of  blood flow is determined by the quantum of leaflet excursion  in every beat . In bileaflet valves  each leaflet has independent determinants of valve  motion . In Starr Edwards valve the ball is the leaflet . In contrast to bi-leaflet valve , the contact area  of the  ball and the blood in Starr Edwards  is a smooth affair  and  ball makes sure  the LV forces are equally transmitted to it’s surface .

The superiority of bi-leaflet valves and disc valves  (Over ball and cage ) were  never proven convincingly in a randomized fashion . The other factor which pulled down this valve’s popularity was the supposedly high profile nature of this valve. LVOT tend to get narrowed in few undersized hearts.  This  can not be an  excuse , as no consistent  efforts were made to miniaturize this valve which is  distinctly possible.

Sudden deaths from  Starr Edwards valve  .

  • Almost unheard in our population.
  • The major reason  for the long durability of this valve is due to the  lack of  any metallic moving points .
  • Absence of hinge  in this  valve  confers  a huge mechanical  advantage with  no stress points.
  • A globe / or a ball  has  the universal hemodynamic advantage. This shape makes it difficult for thrombotic focus to stick and grow.

Final message

Science is considered as sacred as our religion Patients believe in us. We believe in science. A  good  durable valve  was  dumped from this world  for no good reason. If commerce is the  the main issue ( as many still believe it to be ! )  history will never  forgive those people who were  behind the murder of this innocent device.

Cardiologists and Cardio thoracic surgeons are equally culpable  for the pre- mature exit of this valve from human domain.  Why didn’t they protest ?  We  can get some solace  ,  if  only we can impress upon  the current valve manufacturers  to  give a fresh lease of life to this valve .

http://www.heartlungcirc.org/article/S1443-9506%2810%2900076-4/abstract

It is often said life is a cycle , time machine rolls without rest and reach  the same  point  again and again . This is  applicable for the  knowledge cycle as well .

We  live a life ,  which is infact a  “fraction of a time”(<100years) when we consider the evolution of life in our planet for over 4 million years.

Man has survived and succumbed to various natural and  self inflicted diseases &  disasters. Currently,  in this  brief phase of life  , CAD is the major epidemic , that confronts  modern  man.It determines the ultimate  life expectancy . The fact that ,  CAD is a new age  disease   and  it was  not  this rampant ,   in our ancestors  is well known .The disease has evolved with man’s pursuit for knowledge and wealth.

A simple example of how the management of CAD over 50 years will  help assess the importance of  “Time in medical therapeutics”

  • 1960s: Life style modification and Medical therapy  is  the standard of care in all stable chronic  CAD The fact is medical and lifestyle management remained the only choice in this period as   other options were not available. (Absence of choice was  a blessing as we subsequently realised  ! read further )
  • The medical  world started looking for options to manage CAD.
  • 1970s : CABG was  a major innovation for limiting angina .
  • 1980s: Plain balloon angioplasty a revolution in the management of CAD.
  • 1990s: Stent scaffolding of    the coronaries  was  a great add on .Stent  was too  dangerous  for routine use  was to be used only in bail out situations
  • Mid 1990s : Stents  reduced restenosis. Stents are  the greatest revolution for CAD management.Avoiding stent in a PCI  is unethical , stents  should be liberally used. Every PCI should be followed by stent.
  • Stents have potential complication so a good luminal dilatation with stent like result (SLR)  was  preferred so that we can avoid stent related complications.
  • 2000s: Simple  bare metal stents are not enough .It also has significant restenosis.
  • 2002: BMS are too notorius for restenosis and may be dangerous to use
  • 2004 : Drug eluting stents are god’s gift to mankind.It eliminates restenosis by 100% .
  • 2006:  Drug eluting stents not only eliminates restenosis it eliminates many patients suddenly by subacute stent thrombosis
  • 2007 : The drug is not  the culprit in DES it is the non bio erodable polymer that causes stent thrombosis. Polymer free DES  or   biodegradable stent , for temporary scaffolding  of the coronary artery  (Poly lactic acid )  are likely to  be the standard of care .
  • All stents  are  potentially dangerous for the simple reason any metal within the coronary artery  has a potential for acute occlusion.In chronic CAD it is not at all necessary to open the occluded coronary arteries , unless  CAD is severely symptomatic in spite of best  medical therapy.
  • 2007: Medical management is superior to PCI  in most of the situations in chronic CAD  .(COURAGE study ) .Avoid PCI whenever possible.
  • 2009 :The fundamental principle of CAD management  remain unaltered. Life style modification,  regular  exercise ,  risk factor reduction, optimal doses of anti anginal drug, statins and aspirin  is the time tested recipe for effective management of CAD .

So the CAD  therapeutic  journey  found  it’s  true  destination  ,  where it started in 1960s.

Final message

Every new option of therapy must be tested  against every past option .There are other reverse cycles  in cardiology  that includes the  role of diuretics  in SHT , beta blockers in CHF etc. It is ironical , we are in the era  of rediscovering common sense with sophisticated research methodology .What our ancestors know centuries ago , is perceived to be great scientific breakthroughs . It takes  a  pan continental , triple  blinded  randomised trial   to prove physical activity is good  for the heart .(INTERHEART , MONICA  studies etc) .

Medical profession is bound to experience hard times in the decades to come ,  unless we  look back in time and “constantly scrutinize”  the so called  scientific breakthroughs and  look  for genuine treasures for a great future !

Common sense protects more humans than modern science and  it comes free of cost  too . . .

NSTEMI  constitutes a  very heterogeneous population .The cardiac   risk   can vary  between very low to very high .  In contrast ,  STEMI patients  carry  a high risk for  electro mechanical complication including   sudden death .They all need immediate treatment  either with  thrombolysis or PCI to open up the blood vessel  and salvage the myocardium.

The above concept , may  be true in   many situations  ,  but what we fail to recognize   is  that ,   STEMI   also  is  a heterogeneous clinico pathological  with varying risks and outcome !

Let us see briefly ,  why this  is very important  in the management of STEMI

Management of STEMI  has undergone great  change  over the past 50 years and  it is the standing example of evidence based coronary care in the modern era ! The mortality  ,  in the early era was around 30-40% . The advent of coronary care units, defibrillators, reduced the mortality to around 10-15%  in 1960 /70s . Early use of heparin , aspirin   further improved the outcome .The inhospital mortality  was greatly  reduced to a level of  7-8% in the thrombolytic  era. And ,  then  came the interventional approach, namely primary PCI ,  which is now considered the best form of reperfusion when done early by an experienced team.

Inspite of this wealth of evidence   for the   superiority  of PCI  , it is only a fraction of  STEMI patients get  primary PCI   even in some  of the  well equipped centers ( Could be as low as  15 %)

Why ? this paradox

Primary PCI   has   struggled  to establish itself  as a global  therapeutic concept  for STEMI ,   even after   20 years of it’s introduction (PAMI trial)  .  If we  attribute ,  lack of   infrastructure  , expertise are  responsible for this low utility of primary PCI , we are mistaken ! There are so many institutions , at least in developing world ,   reluctant to do primary PCI  for varied reasons.( Affordability , support system , odd hours ,and finally perceived fear of untoward complication !)

Primary PCI may be a great treatment modality , but it comes with a inherent risk related to the procedure.

In fact the early hazard could exceed the potential benefit in many of the low risk STEMI  patients !

All STEMI’s are not  same , so all does not require same treatment !

Common sense and logic would   tell us any medical condition should be risk stratified before applying the management protocol. This will enable  us to avoid applying “high risk  – high benefit”  treatments in low risk patients . It is a great surprise,  the cardiology community has extensively researched to risk stratify NSTEMI/UA   ,  it has  rarely  considered risk stratification of STEMI before  starting the treatment.

In this context , it should  be emphasized  most of the clinical trails on   primary PCI  do not address  the clinical  relevance and the  differential outcomes   in various  subsets of  STEMI .

Consider the following two cases.

Two young men with STEMI  , both present within  3  hours   after  onset of symptoms

  1. ST elevation in V1 -V6 , 1 , AVL   ,  Low blood pressure , with severe  chest pain.
  2. ST elevation in 2 ,3, AVF , hemodynamically stable , with minimal  or no  discomfort .

In the above example,   a  small inferior  MI by a distal RCA occlusion  ,  and a proximal LAD lesion jeopardising entire anterior wall , both  are  categorized as STEMI !

Do you want to advocate same treatment  for both ?  or Will you  risk stratify the STEMI and treat individually ?  (As we do in NSTEMI !)

Current guidelines , would  suggest PCI for both situations. But , logistic ,  and real world experience would clearly favor thrombolysis for the second patient .

Does that mean,  the second patient is getting an inferior modality of treatment ?

Not at all . In fact there is a strong case for PCI being inferior in these patients as the risk of the procedure may far outweigh the benefit especially if it is done on a  random basis  by  not so well experienced cath lab team.

(Note : Streptokinase  or TPA does not  vary it’s action ,  whether given by  an ambulance drive or a staff nurse or even a  cardiologist !  .In contrast ,  the infrastructure and expertise have the  greatest impact on the success and failure  of PCI )

Final message

So , it is argued the world cardiology societies(ACC/ESC etc)  need to risk stratify STEMI (Like we do in NSTEMI ) into low risk, intermediate risk and high risk categories and advice primary PCI only for high risk patients.

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)

This seems to be good side branch sir, … a resident was mumbling as he was reviewing the RAO caudal test shot .Forget that diagonal man , focus your mind on main vessel , If you keep pitying these small twigs , you can never become a glorified Interventionist .I heard one of the senior consultant  was telling (rather yelling) at his assistant !

I used to wonder ,why should the fate of side branches be decided by the mercy of semi cardiac Intellectuals ?

What determines the hemodynamics after side branch jailing ?

  • Size
  • Territory
  • Myocardial viability
  • Alternate source
  • Collaterals

How do you classify side branch jailing ?

Okamura et all (Ref 3)offered a new OCT based classification based on the shape of the jail grills.

TakayukiOkamura classification of side branch jailing

JACC Cardiovascualr Interventions 2010 : Okamura  types V, T , and H jails. Implications are many both during short term as you cross , recross /rewire etc.Long term implications are largely unknown.

Does Jailing Implies flow is Interrupted  ?

This is the most critical question, We got the answer from University of Southampton in 2007 a rare and vital contribution to the knowledge base of coronary physiology. It said the struts won’t block the flow, it simply bumps on the path of blood.

You know , if the side branch ostial diameter is 2.5 mm the luminal area will be around 6sqmm. At least 1 or two struts is likely  occupy and criss cross the ostium. The issue is more than  simple compromise of side branch flow .The major concern is  the ostial jail should not be a nidus for future thrombosis that can spill over to main branch.Unfortunately there is no single meaningful study that addresses this issue of long-term patency of main vessel  in which  small side branches were jailed.(We in our department  have just started to analyse this aspect of coronary Intelligence )

Markers of significant side branch compromise.

For most of us it is not a big deal .I think there is none .There are little discussion  on new onset angina or troponin elevation after side branch jailing.

Can we Jail LCX ostium (or even LAD ostium ) during Left main PCI ?

  • Jailing a side branch can be casual or even a fashionable act , but can you do the same for left main bifurcation ?
  • It’s all about what you mean by side branch ? and the reaction time , and the useful muscle mass the branch would supply etc.
  • In emergency situations , there has been occasions one even put a stent across left main to LCX.Tackle the jailed LAD later if required.

FFR analysis of side branch jailing

Image courtesy from Bellenger 2007 Heart

Doing a FFR to assess the significance of side branch is simply a obsessive academic exercise .It is not warranted in most clinical situations. This study has taught us most side branches retain good FFR give us more confidence to sacrifice the sibling branches of main stem arteries.

Final message

Practicing cardiology in a truly professional way in cath lab can be tricky.We need to disrespect most of the side branches .Believe in your gut feeling (or your consultant’s.) If you are a sensitive scientific cardiologist do FFR pre / post procedure to the side branch .If compromised physiologically try probing the jailed struts and dilate one of them in absolute blindness , of course with a strong conviction of doing good for the science’s  sake.

A Research concept  

Long term sequelae of side branch jailing on the main branch ostia  (Please acknowledge  if some one take up this study )

References

1.

2. Bon-KwonKooMD, Hyun-JaiKang,Tae-JinYoun Physiologic Assessment of Jailed Side Branch Lesions Using Fractional Flow Reserve Journal of the American College of Cardiology Volume 46, Issue 4, 16 August 2005, Pages 633-637

3. Okamura T1, Onuma Y, García-García HM, Regar E3-Dimensional optical coherence tomography assessment of jailed side branches by bioresorbable vascular scaffolds: a proposal for classification. JACC Cardiovasc Interv. 2010 Aug;3(8):836-44

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

It was 1912 , Titanic had just sank off the Atlantic . When the world attention was elsewhere , An unassuming young Dr.Herrick J.B silently working in his Michigan lab inquisitively proposed thrombus occluding the coronary artery is the chief culprit in acute myocardial Infarction.It took seven more decades when Davis et all from Glasgow .UK. proved it by doing dramatic angiographic studies soon after STEMI in year 1979.

Now, even after 100 years , we, the confused cardiologists debate endlessly in glamorous global conclaves in exotic locales whether to aspirate these humble looking thrombus, threatening to damage the myocardium with every passing moment !

Why is this controversy ?

My answer

I am failing to understand the concept and the answer is elusive .While every one agrees that thrombus is true culprit, in bulk of the STEMI , still we are not authorised (In an assertive fashion ) either to lyse as first choice or to aspirate as second choice.

It seems vital, thrombus must be tackled vigorously by any means. Drugs,lytics,(Intravenous or Intra-coronary.) by micro and rheolytic catheters .Only documented, flow limiting complex mechanical lesions must be stented. If we are convinced tackling thrombus by mechanical means is problematic (As studies would suggest ) lysis should prevail over aspiration as a routine measure by default isn’t ?

*It’s a been quite a while , the world cardiology community has made it appear thrombolysing a patient who is otherwise eligible for primary PCI ! a “coronary crime*” Ofcourse , I must say , I proudly commit that crime with rewarding results in many MI patients.

*In fact , I would think not promoting or delaying prompt lysis should qualify for the definition.

In the management of STEMI, prehospital lysis followed by a Intensive care in a good coronary care center is best modality.

This doesn’t mean in-hospital lysis is banished. Yes, STEMI is a cardiac emergency , but triaging STEMI patients must be done by scientific means (STEMI risk score) as well with accumulated wisdom .Rush only true emergencies into cath lab. (A best estimate is about 20 % of all STEMI) If we are not able to decide which STEMI will require prompt PCI , it would Imply we need to go back and do once more the basics postings in coronary care of resident days !

An angry counter from a young Interventionist

Only God can tell whether a given patient with STEMI will (or will not) derive maximum benefit from pPCI. We are not yet trained to make that decision by looking at patient and his ECG.So my logic is all STEMIs are equal. I will continue to do emergency angioplasty in all STEMI patients . I expect them blindly to accept all the potential complications arising out of poking the thrombotic milieu in those low risk patients who might have done well with thrombolysis.

Never afraid of challenges. It is like going to war. Casualties are bound to happen.We have enough technology , Imaging , expertise, to tackle all those complex lesions we encounter during primary PCI especially in elderly comorbid patients. We can even do a triple vessel angioplasty , left main etc. Only Yesterday I posted in my nonstop whatsapp group , where I did a dramatic acute angled bifurcation angioplasty for a stable STEMI patient that required a iFR guided jailed side branch assessment and 3d OCT transmitting stunning snaps of fresh thrombus, ending with a semi culotte procedure.The patient is doing well with a Impella 2.5 device and a high frequency ventilator support and my anesthetist has promised me to wean him soon ! I must actually thank his Glo-Health plus Insurance company for clearing the procedure.

An Important tip for complex lesions during STEMI

We need to know there is always a saving grace , if for some reason we couldn’t accomplish PCI due to complexities of the lesion with multiple IRA mimickers. We can always sheepishly thrombolyse these patients inside cath lab . . . a modality just few minutes ago would have been ridiculed with all our vigor to convince the anxious family for a costly Invasive procedure !

Reference

3. Herrick Original paper . https://jamanetwork.com/

Hyperlipidimia is one of the well-known coronary  risk factor.Serum cholesterol ( Various fractions ) levels are measured to represent that risk. Epidemiologically ,it does a perfect job , however , the fact is , circulating lipids has little correlation with the lipids that’s deposited in the vessel wall.

Time and again , we have proven this as severity of CAD has little  to do with the absolute levels of lipid levels.The number  volume of plaques , the thickness of lipid core, and degree of vulnerability  show  poor correlation with circulating lipid levels than  what we would expect.It tempts us to make a statement , that serum lipid is a poor surrogate marker for CAD. (Still, it may predict the risk of developing it !)

Why this paradox ? What are the  missing links and hidden secrets ?

If you plot a simple graph with serum lipids with  plaque mass, volume and content in CAD population , we might get an  answer .I don’t know whether such a study exist. (Those who find one , please share)

A new concept called cholesterol crystalisation 

It’s not the lipids alone that are responsible for CAD . There is a whole lot of factors , circulating  pro inflammatory  mediators, altered blood coagulation system  , various  inflammatory molecules, , heightened  intra-coronary pressures, genetic vulnerabilities .

Most importantly ,the format  of lipid molecule in side  the plaque seems to matter more  rather the  absolute content.(Small dense LDL, oxidised lipids,Lipid fed macrophages etc )

There is lesser reported phenomenon  called cholesterol crystalisation , with sharp edges (Lipid knife ?) that are responsible random episodes  plaque fissure and rupture.

It was reported in  one of the  rare research paper that came from  (Abela Am J Cardiol.2009)  Factors that crysalise cholesterol include local saturation,  PH, temperature , hydration and plaque RBC contact.

If you argue lipid levels are not  correlating with CAD , how is that reducing it with statins dramatically reduce  CAD and the events ?

Like blood pressure the normality of serum lipids itself is not defined.One insightful definition was proposed , that the level at which a person develops CAD is high for that patient however low it may be..A person who develops extensive CAD  say at a level of  90mgLDL what to infer ? We do not know exact  answer.

That’s why the  concept of satin for all with clinical CAD looked attractive. Still , statin’s action doesn’t help  answer the original query about the relationship between blood lipids and plaque lipids.

Statins beneficial effect is not by reduction of serum cholesterol.It primary acts by  regressing intra-plaque lipids by blocking synthesis of lipids in every cell.The anti inflammatory,plaque stabilisation action of  statin may be  independent of lipid reduction.How much it contributes to overall benefits is not known.

The mystery will deepen

Not every LDL is bad.(I will be slapped if I call them Good LDL !) Small dense LDL , LDL P (Particle) ApoB (The real culprit on which LDL piggybacks ) lipoprotein little a and so many other lipid sub particles are being studied.

Final message

The purpose of this post is not to confuse our understanding about coronary  lipidology but to widen our vision . Serum lipids remain a poor surrogate marker for plaque lipids. This is because , It’s rather a small fraction of sample volume we catch in the  circulating blood , while loads of lipids gets deposited elsewhere in the body ! This also make it clear,no single risk factor in isolation is really CAD risky.It is the combination of risks , genetic susceptibility , LDL subfractions, few unknown risk/protective factors and finally a mandatory trigger(Hemodynamic, Emotional ?) that determine the outcome of  CAD.

So ladies and gentle men , just don’t over react to mildly abnormal lipid levels you often find in  master health checks .There is much more untold stories behind the true CAD risk than the glossy lab printouts would suggest !

Reference

2.

3.The Role of Lipids and Lipoproteins in Atherosclerosis MacRae F Linton, MD, Patricia G Yancey, 

Indian subcontinent has a grand old history with a great civilization that began even before the ancient Greek and possibly Egyptian pharaohs .Post renaissance Europe made the British monarchy enter the country in early 1600s .This could be perceived as a new journey of modern India.In the early days of British colonization through East India company , the province in southern Indian Coramandal coast called Madras (Currently named Chennai) was a key economic and power center. Since the hospitals were the prime requirement to take care the Incoming officers ,Govt general hospital is the first major health care center to appear in India more than 300 years ago (In which the author of this blog is currently associated for over two decades) !

history of madras medical college government general hospital elihu yales

Though we currently call it as GGH , the original name was MGH* Madras General Hospital .

Originally built for the sick soldiers of east India company which functioned in the present St George fort premises.Then president of Madras fort Elihu Yale allotted the adjoining land and was instrumental in building the Govt general hospital in the year 1664 .The academic limb of the hospital the Madras medical college came more than a century later in 1835 .

elihu yale madras medical college

Few decades later in 1718 a Governor of New heaven Connecticut , Cotton Mather from far way North America wanted to start a small hospital who was short of money.He requested through his American contacts of British east India company for a donation from a successful British businessman Yale from Wales who making a fortune in the Indian county of Madras . Since, Yale had an American connection by birth in Boston, was willing to donate the money through Indian gifts worth of 560 pounds which was good enough to build the legendary hospital in New Haven which was named later after his name.

*It should mentioned the first seed of this hospital was planted by another British Sir Edward winter (1622-1686) , the Madras agent for the East India Company .

An article which appeared in Yale journal recently recalled the link between these two institutes.

history of madras medical college yale university drsvenkatesan dr s venkatesan cardiologist

Yale, of course carried a tag of being a controversial leader of British empire for misusing his power, still has his name permanently etched in the history of two great medical institution located far across the globe.

His life ended in 1721 , was laid to rest inside the quiet compound of church of Wales .The dark black concrete letters telling to the occasional visitors about the extraordinary life he lived over 300 years ago.

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Elihu Yales 1641 -1721.Born in Boston , Lived in Madras died in London. This memorial is found just outside St.Giles Church Wrexham , Wales .UK

st giles church elihu yales memorial Wrexham 2 wales

St.Giles Church Wrexham , Wales .UK

Click here : How to reach Wrexham ?

Another MGH . . .

The MGH as we know today is Massachusetts General hospital which was stated 150 years later than MGH senior in 1811 in Boston. It some times pains me to compare the growth of two . In terms of science , technology and research they are poles apart But in terms of equitable service , care , and social impact I think the senior MGH would still prevail over. !

Postamble

It is fascinating to know origins of college that taught us medicine.I wonder how many of the current students and the alumni know the grand old history of their Alma mater.I wish they pay a visit to St Giles church Wrexham , Wales once in life time. As we stand in-front of the Yale’s memorial one will definitely get that unique feel of travelling to the vintage past when Chennai GH was born with a baby cry !

Reference

1.http://en.wikipedia.org/wiki/Elihu_Yale

2.http://en.wikipedia.org/wiki/Yale_University

Reading X -ray chest can be as blind as a bat flying in the dark . It needs lots of Imagination . (Many times the blindness continues to cath lab as well  during structural interventions is a different story !)

Yes ,its true  any one can recognise a cardiomegaly in X-ray  . . . but  Which chamber is responsible for cardiomegaly ? and quantifying each ones contribution to the increased CTR is the critical question. 

We know the 4 chambers in the heart are arranged in a complex pre-specified  (Antero -superior and right to left orientation ) still , the CT ratio in X-RAY chest is based on the diameter formed by two chambers only ie right atrium and left ventricle.

However, any of the 4  chamber enlargement can increase  CT ratio in pathological conditions.

  • LV enlargement is the most common cause for cardiomegaly as it is the normally  border forming.(DCM, Aortic valve, HT diseases)
  • RV can do it when it enlarger grossly forming the left heart border(COPD, Severe pulmonary hypertension of any cause)
  • RA can enlarge to both pressure and volume overload.(CHF, with RVF)
  • LA is least likely to be border forming as it is midline structure .Since It tends to enlarge posteriorly and superiorly it rarely enlarges sideways. Occasionally In severe mitral stenosis it can enlarge to the right and cross the right heart border causing the classical shadow in shadow.

Since I have struggled with X ray orientation of heart chambers in my early days (Still i do sometimes!) Just thought , why we are not fusing a X-ray with a given patients echocardiogram that will help understand the chamber anatomy .

Fusion Image of X ray chest PA view with apical 4 chamber in ECHO. (Rotated to specified angle to match heart border)

Note : The Left atrium is not only left of RA , its also posterior and superior to RA.This makes the IAS  not actually  pure right left to relationship but also a slight  infero to superior and antero posterior  orientation.(This can be realised when we puncture the IAS from RA side the needle goes more of superior)

X ray chest left lateral view is  fused with para- sternal long axis view. Please note this is not true anatomical correlates. The RV shown in echo is actually RVOT but in X-ray its more of RV body .

* A note of caution : The fused Images are rough attempt to co-register x-ray with echo. There is sophisticated software in some new generation cath labs to mix fluro images with live TEE data that aid in Interventions.

Postample
A bedside Instant point of care echo is becoming a norm in clinical cardiology practice. Why bother about  X-ray then ? Agreed to that point to a certain extent. But, I used to tell my (amused ) students that technology based lazy learning doesn’t help build a strong scientific  foundation which would ultimately threaten the patient care one day !