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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

These two quotes  on practice of medicine are close to my heart , one from Voltaire , a non medical man (a French poet )  and  the other from ,one of the greatest medical professional of our times, William  Osler .

gretest medical quotes william osler voltaire

It is amazing ,how the thinking pattern of a  philosopher  and a true scientific professional living  centuries apart are almost in sync with a great medical reality !

J point is a critical point in the  ECG  when the ventricles hand over the baton in  the  electrical relay race from depolarization to repolarization .This the time the sodium  channels extinguish itself  and the potassium current begins its activity  from Phase 0 to 1 .

If the  potassium channels  activate little early and snatch the baton prematurely from sodium , we get early repolarization pattern .When this happens , the J point of ECG show a conspicuous wave  called J wave , originally  denoting  Junctional wave between QRS/ST segment  (Now  perceived as  Jitter waves ?) The other implication of premature K+ activity is , lifting up of  ST segment , making it the most common cause of non ischemic ST elevation.

* J wave in hypothermia is referred to as Osborne wave and  may not be  not related to ERS(Ref.4)

J wave and J point early repolarisation syndrome

Image source.www.cardiology.org

The Ito current is responsible for the phase  1 of action potential (AP), where a rapid outward k + ion flux take place and draws the dome of AP . The dynamics of Ito is complex .It depends  upon the density of epicardial K + channels , which are  clustered in a heterogeneous manner .There seems to be a concentration gradient   along the epicardium and endocardium , making the wave appear prominent in some. This is especially true in healthy, athletic  male population  where we have some evidence for androgen  to  play a role on how  these channels will behave.Here comes the overlap between Brugada  syndrome and ERS as well.

The subset of patients with J wave pattern were recently shown to have increased risk of primary VF due to phase 2 reentry ,  when they develop ACS. (Rather J wave pattern was more common in patients who had primary VF following STEMI(Ref 1).This resulted in a spate of worrying articles .Now we know , the  fear is  largely unfounded ,the risk is far less.

Current thinking is,  persons who have asymptomatic ERS pattern with prominent J waves should not be investigated electro-physiologically . (Please remember , every human  heart can be induced  to VF in EP lab  if appropriately  stimulated ! )

In fact , I used to tell the  young men  who  harbor  prominent J wave , as a marker of healthy heart  rather. Let us not  fear them with a remote risk  that could be as  negligible as risk of  intercontinental flight crashing into the ocean  !

References

1.Haissaguerre M, Derval N, Sacher F, et al. Sudden cardiac arrest associated with early repolarization. N Engl J Med. 2008;358:2016–2023.

2.Idiopathic Ventricular Fibrillation “Le Syndrome d’Haïssaguerre” and the Fear of J Waves , Sami Viskin, J Am Coll Cardiol. 2009;53(7):620-622. 11

Have you felt like this query any time in your office ?

If “Yes” is your answer, then you are not alone .There was a unique  conference  that  took place  in 2010 to answer the same query in Rome , Italy on behalf of Italian cardiology society  , where this entity is researched more than any other place.Its worth going through this.

Reference