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Prosthetic valve obstruction is becoming a common clinical issue .It can be either acute, sub-acute or chronic . The pathology is usually thrombus formation , scar tissue growth (Pannus) or rarely a mechanical defect. Echocardiographic differentiation of thrombus from  pannus can be difficult .Generally , pannus is smaller , linear (less round) ,encroach from the periphery to central , mean gradients are consistently lower  than thrombus mediated obstruction. Clinically  pannus related obstruction present less acutely and occur in-spite of good compliance of anticoagulant medication and a well maintained  INR .

Trans thoracic (TTE)  , Trans-esophagel (TEE ) echocardiography , and real time 3D TEE are useful imaging modalities .The value of cine fluroscopy should be never underestimated and it is probably still the the best way assess the struck metallic leaflet.

Though the pathogenesis of pannus and thrombus are considered different there  is no reason they can’t  occur in a given patient at the same time.We know at least  one patient who had been referred to surgeon for mitral valve obstruction due to failed thrombolysis  had showed heavy load of thrombus  attached over a well formed pannus originating in medial sewing ring.

FInal message

However intelligent one may be , human brain often  tends to get skewed when confronted with a sudden query like  “What is your diagnosis , This or that  ?  Pannus or thrombus ? .Most will  go with  any one of it ! However, cardiac physicians must be aware  both pannus and thrombus can occur overlaid simultaneously in a given patient .The exact incidence  of such “combined thrombo-pannus”  is not known  but bound to be higher as we look for it. In fact , many of the residual gradients after lysis is attributable to undiagnosed pannus.  There is also a  suggestion scarred  , injured  ,  rough surface of the pannus could be the initial trigger for thrombus formation .

Reference

1.Differentiating thrombus from pannus formation in obstructed mechanical prosthetic valves: an evaluation of clinical, transthoracic and transesophageal echocardiographic parameters  John Barbetseas,  Sherif F Nagueh,  Christos Pitsavos, ;J Am Coll Cardiol. 1998;32(5):1410-1417. 

We know right from our pathology days in medical school , Atherosclerosis , the killer human vascular disease has a predilection for branch points. It’s no surprise around 30-40% of coronary stenosis has some degree of involvement of branch points .

PCI essentially involves palliative metal bracketing of this inflammatory cum degenerative process of the vessel wall.Tackling bifurcation lesions (BFL) requires special expertise , hardware and technique as carina and two ostia (In fact three !) are exposed to complex hemo-rheological stress de-nova and more so after the metal invasion.

The complication rate as well as long- term patency are considerably more  in BFL than regular lesions. This is why a “4S strategy “ (simple single stent strategy ) is the preferred default strategy in most BFL.

There are about dozen strategies  to tame  the BFL with  stents.One such modality is dedicated BFL stent.Various designs have been proposed in both balloon and self expansion platform.

The ACCSEES is a prototype dedicated BFL stent with DES and  a self expanding system

Reference

Degenerative Aortic stenosis occur with either normal  or congenitally malformed/ bicuspid valve.This contributes to the major chunk of  aortic valve surgeries and interventions (TAVR) in elderly population  . The optimal  timing of aortic valve replacement in patients with AS is debatable inspite of  well formed guidelines.

Three factors determine it .Symptoms , severity of aortic valve narrowing  and the tactness of LV function .The last parameter is a tricky one .We used to think in the past , severe LV dysfunction is a contraindication to aortic valve surgery. Now we realise ,however severe the LV dysfunction may be , relieving the obstruction will benefit  the patient and  the LV function is  also  likely to improve.

Cardiac physicians  face a dilemma when confronted with a patient  with low gradient and severe LV dysfunction .In this situation they are advised to do doubtamine stress Echo and watch for the gradient .If the gradient  increases that would  imply true fixed stenosis . (In pseudo aortic stenosis increased contractility opens the aortic valve and gradient will fall )

While this concept appears simple .There  are few  important issues that goes unaddressed  as we have not yet fully understood the  mechanism of LV dysfunction in aortic stenosis .(Link to mechansim of LV dysfunction in Aortic stenosis.)

At what degree of aortic stenosis LV goes down fighting and fail to generate the required  gradient ?

Myocardial function  and behaviour at times of hemodynamic stress can be highly  variable and most of us believe it is determined primarily by the genetic switches of myosin and other contractile elements .This is naturally proven at times of hypertensive left ventricular failure (Only in a fraction of the hypertensive population  LV is set to fail  when BP acutely raises.)

Proposed concept

Considering the complexities in cardiac mechanics , hemodynamics (and not to forget the vast control exhibited by genetic imprints over the hemodynamic behavior of LV) , it seems highly plausible even mild degrees of Aortic stenosis can inflict significant myocardial dysfunction in certain patients . Hence the phenomenon of pseudo aortic stenosis needs further critical analysis If this is proven to be true there could be a realistic indication for aortic valve intervention even in patient with low gradient / true Mild AS with LV dysfunction.
A word of caution is required .Relying too much (Which we often do ) on gradients in the assessment of aortic stenosis has skewed our common sense. Its wiser to have a  meaningful look at the valve morphology . A normal appearing  valve in 2D can never cause significant stenosis. Pressure recovery phenomenon also is to be given due respect as it over estimates gradient .This will effectively avoid surprises and guilt on table when we find a relatively good looking valve posted for AVR /TAVI

An attempt is made to look for individual components of cell viability .See the table below. It is a generalized statement for understanding purpose only. Various imaging modalities assess the overall physiology of myocyte function (however  they test  an individual component of a cell more than the other) We may believe an unit of cell would die in “one-go” at times of ischemic injury.Reality is much complex.There is considerable variation in intracellular survival mechanisms . A cell can die in a regional fashion with residual signs of life scattered across among the different organelles. The quantum of damage to Nucleus /mitochondria may appear determine the recovery . The reverse can also happen .What is the purpose of mitochondria respiring if contractile element is totally damaged ? It becomes a “vegetative cell”. The gross discrepancy we are witnessing in myocyte cell function recovery with reference to both acute and chronic reperfusion is attributable to this gap in our knowledge.

myocyte viability demri spect thallium dobutamine contrast echo 2

It is believed  (assumed ?), medical science is propelled by constant quest for knowledge and improvement in basic and clinical science that eventually would transform into better patient care and favorably impact  global health standards. We know the field of medicine is growing in an unimaginable pace.It’s obvious  any growth if uncontrolled or not properly guided is at risk of deviation from the main goal and ultimately  turn malignant and destroy the system which it’s supposed to guard.

How many times we realise the current treatment we administer would soon become obsolete and  even become dangerous ? What is the point in replacing treatment A by B , and  then  B is pulled over by C or D   and suddenly finding A is better than either C or D (and still we hesitate to fall back on A because its an oldie!)

Still ,this is what we call  as practicing ” State of the art medicine” How about a person who defies state of the art ,  and able to fore- see the futility which is threatening to be the  norm in modern medicine. Then,who is really Ignorant ?

I stumbled upon this  wonderful writing on this issue by ex BMJ editor by Richard Smith. Mind you , this was published way back in 1992, when the boom of  futile  ” Human  Health shopping”  was just about to explode !

medical  ethics ignorance based mediicine

Link to The ethics  of  Ignorance

Post-amble

Don’t get confused .Noble professionals are  licensed to  practice  with whatever is published as science as long as their intentions are deemed to be genuine .Harm arising out of  practicing what’s considered best as on today is acceptable in the court of law.

Meanwhile , its a tragic truth, If you do not follow the herd , you are at risk of being punished even for goodness committed by you. Wisdom and conscience  can never win a legal battle ! If you have the courage try practice them !

Heart and kidney work in tandem and share a close functional relationship  during health and disease.Progressive cardiac failure causes kidney function to deteriorate,what we call it as cardio -renal syndrome.Similarly, progressive renal disease inflicts either a reversible /irreversible LV dysfunction .The mechanism of  LV dysfunction has not been fully decoded. It is primarily biochemical mediated but at later stages it can be irreversible and structural damage can occur.

We believe uremic  micro molecules leaking from plasma  into cardiac Interstitium  (Myocardial proteinuria ?)  are somehow responsible for the progressive LV dysfunction. Now ,  we have new evidence for albumin – carbon interaction  possibly at myocardial level due to formation of carbamino albumin (C-alb) .

This paper from  Kidney International (2015) 87, 1201–1208;  highlights this new finding .

C-Albumin carbamylationElevated C-albumin is a new  marker for this unique , still not fully understood  entity  “Uremic cardiomyopathy”.

Further reading

Radial coronary interventions has become a global norm .Even complex procedures are being accomplished with ease adding on to the patient comfort and low risk for access site complications.However !occasionally we need to have multiple access sites to know the detailed real time  contra lateral coronary  anatomy is desirable .This becomes  vital in the retrograde approach for CTO.

Want to  have a quick glimpse of  RCA flow while one is attempting LAD PCI without additional puncture ?

How about doing a contra-lateral  angiogram with the same guiding catheter and wire in-situ within the ipsilateral ostia ? Here is an Innovation.

Of course ,the same concept can be used in femoral angiogram as well.It could reduce procedural time, adds more  efficiency of the hardware system handling.  One can’t ignore the idea as well as the comment of the  author, who says the trick is only for an advanced Interventional cardiologist.

Reference

STEMI occurs due to acute occlusion of a coronary artery  (ATO) which needs emergency opening at the earliest, ideally within  3 hours , or up to 12h . The opening shall be either by pharmacological / catheter means  or both. After 24 hours opening  a ATO has questionable benefit unless the patient is hemodynamically unstable or symptomatic.

What is a CTO ?

Traditionally we believe 3 months is the period to call a coronary occlusion as chronic.(Previously it was 6 months) This time frame was considered appropriate based on our understanding of the infarct process , that may take up to 3 -6months for complete healing of infarct  .This 3 month period is arbitrary as the chronology of intra-coronary lesion organisation  is different from myocardial infarct healing. Its worthwhile to note the chronicity of  a coronary lesion and its morphology is nothing to do with the quantum of myocardial damage it inflicts .This is because in many patients with STEMI who present late , the ATO progresses to CTO silently without any clinical demarcation or progressive myocardial damage.

chronic total occlusion acute total coronary bridging collateral

If 24 h is the cut off point for opening the ATOs to accrue any meaningful benefit , can we call  all ATO’s beyond 24 h as  physiological  CTO equivalents ?It doesn’t make sense  isn’t ? But , consider this , how do you call an occluded coronary artery between 24 h t0 say  2 weeks or 2 weeks to  to 3 months ? Sub acute total occlusion (STO) ? .Some  experts have argued to remove CTO as an entity from acute coronary setting .This can’t be done as chronicity has to set in  for ACS lesion as well. Obviously , we have a nomenclature issue here. We require a  new terminology to differentiate CTO related to ACS and CTO related to chronic coronary syndromes.

Therapeutic implication

The moment we  diagnose  a true chronic total occlusion , not only the urgency of intervention but also the indication to open becomes  questionable in an otherwise asymptomatic population.

An ironical situation often arises , when we can’t technically open a ATO in a one week old STEMI .However , the same lesion one may  open after 3 months as it has acquired a new name by now as CTO , which is perceived  a lesser guilty act of violating the sacred PCI guidelines !

effect of inspiration on jvp and bp pulsus paradoxus bernhiem effect ventricular interdependence

Image  modified  from  http://www.anatomygallery.info

That’s  normal . . . what happens during pathological states ?

There are important diseases  that  restricts entry of blood into right heart chambers. They can occur either in an acute  (Tamponade) or in chronic  fashion like constrictive pericarditis  and restrictive cardiomyopathy.These entities  show distinctive impact on JVP and systemic pulse.

The two pathognomonic signs are Kussmaul sign and pulsus paradoxus* that go hand in hand in most  situations.Inappropriate elevation of JVP with inspiration is termed as Kussmaul sign , while exaggerated fall in systemic BP with inspiration is called Pulsus paradoxus.The later is the  arterial counter part of  Kussmaul sign in JVP .However, there can be dissociation between these two signs occasionally.

* Pulsus paradoxus is a term originally  used by Kussmaul when he noted heart sounds were  retained while pulse dissappeared  in  patients with cardiac  tamponade .Later we realised the loss of pulse was linked to inspiratory cycle  of respiration. To make  this sign objective  sphygmomanometery  criteria was formulated which measured the difference between inspiratory  and expiratory korotkoff’s  sounds .

Coming up next 

Why Kussmaul sign  is often absent in Tamponade while  its arterial counterpart pulsus  paradoxus may still be conspicuous ?

Right ventricle,being a venous chamber has distinct anatomical and physiological features to carry out this function.RV has a complex shape, its triangular in long axis and  crescent like in short axis , thin (<5mm)  more distendable  .Contraction of RV begins slightly early but ends later than LV  (30ms )

RV receives blood from RA and ejects in to PA in a sequential manner .The inflow, body and outflow contract somewhat like  intestinal peristalsis. This is facilitated  by the incremental  delay in the electrical depolarization of right ventricle.In physiological conditions, the later half of QRS  is  responsible for RV activity and RVOT is the last to contract. (This intrinsic electrical and mechanical  delay in RV contraction is a physiological inter ventricular  desynchrony . One  should be aware of this when planning cardiac resynchronisation therapy in cardiac failure.  )

Click over the image for an animation of RV contraction.

wpid-wp-1430586787404.gif

Image courtesey Oxford spcialist hand book in cardiology :Echocardiography Paul Leeson , Second edition ,.Oxford university press 2012 Multi media .

Note:LV is  a fairly   elliptical and strongly  muscular pump and contracts in a  single go with maximum force.(dp/dt).

Final message

Though both right and  left ventricle originate from same  straight heart tube , developmentally the right ventricle evolves for a different form and function . Now,we realise there are lots of sharing of parental muscle fibers that engulfs and bonds both chambers.(Mind you ,This is the fundamental mechanism of ventricular interdependence.Of course ,IVS is a common wall shared lifelong by both chambers  without any (sibling related?)  hemo-dynamic dispute !

3D echocardiography and MR imaging has helped us to understand the RV morphology better and exciting articles written by pioneers are available  free for those who are interested.

Reference