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It is just past midnight: This is a gloomy conversation between a patient’s son and a cardiologist in the silent waiting room, just outside the dim-lit ICU of a popular 4-star hospital in Chennai.

“I am sorry to say, Mr. B., your father didn’t make it. Has succumbed to the heart attack. We have been trying to resuscitate him for the past one hour. We have done everything. We have managed to open up IRA, and 2 more critical blocks still it couldn’t help. It was a massive one. Sorry again.

“Doctor, I feel very bad. What went wrong, I want to know. Doc, did you try ECMO ?,” the elder son queried

“No, we didn’t”

Do you have it in your hospital doctor?

“No,we don’t have it”

The son in distress couldn’t take it lightly. “How can you say that doctor? such a big hospital doesn’t have ECMO, “What a mistake we have done, we should have gone elsewhere” he quipped 

The visibly exhausted cardiologist was taken aback and struggled to retain his composure. He took some time and tried to explain the bereaved family with a semi-scientific explanation.

Please understand the reality. Do you know, how likely an emergency ECMO will resuscitate a patient with cardiogenic shock and arrest” 

  • ECMO is not a magic machine  that will bring back your heart to life
  • It is a temporary circulatory support device ideally used prophylactically in high-risk situations
  • It takes a minimum of 20 to 30 mts (If it’s in ready mode) to insert the AV ECMO , Further, there must be some cardiac activity till the ECMO takes over.
  • It is almost impossible to resuscitate with ECMO after cardiac arrest and circulatory standstill.
  • In fact, prolonged CPR with an absent pulse is a contraindication for ECMO.
  •  

“Let me go little deeper into the hemodynamics of ECMO, even if it is inserted on time, ECMO doesn’t support coronary circulation much, (the one that matters most in the failing heart) ECMO circuit that brings oxygenated blood from below upwards in descending aorta. This stream may not reach the aortic root as it has to competes with ventricular contractions however feeble it may be” (Ref 1)

“Don’t mistake me, In my opinion, all these macines like ECMO Is more like a fancy customary add on machine in a high profile patients”.  

“So, you are saying, my dad is destined to die, that’s not at all fair doctor”.

“I can’t say that openly, it could be the fact. A series of miracles could have saved your dad’s life. A tandem heart as a bridge to an emergency heart transplant is a dream thought. Of course, for a heart transplant to happen someone else should have lost their lives in time, just to save your father’s life. That’s in God’s domain”.

The son gradually got back to his quieter sense. “Sorry doctor, I misunderstood  ECMO I was told it was like a lifeboat that will bring back life from a dying heart. Thanks for all your efforts doctor. “No worries, even, many of us haven’t come to real terms with this ECMO stuff. Thanks to misplaced mainstream media coverage concerning celebrity lives”

The much-relieved cardiologist left for home in peace of mind.

Reference

1.Junji Kato, Takahiko Seo ,Hisami Ando et al  Coronary arterial perfusion during venoarterial extracorporeal membrane oxygenation,  The Journal of Thoracic  and Cardiovascular Surgery, Volume 111, Issue 3, 1996, Pages 630-636,

 

Postamble

Final message

We must realize ECMO is not a new breakthrough technology. It’s  a 50-year old concept, that was used primarily in infants with respiratory failure. (VV ECMO) In the complex high-risk interventional cardiology field, it has a different purpose. It gives the aggressive players a little more time to try their luck of reperusing a failing heart. 

All these circulatory assist devices Like ECMO, Impella, IABP help to support the heart before a cardiac standstill. Ideally, we may use them prophylactically ( in situ and ready to fire)  It has helped save  lives especially in pre and post-transplant hearts However, it’s too complex a procedure to be relied upon after unanticipated Ischemic cardiac arrest. We can expect, It might get miniaturized and user friendly soon.

 

Few individual’s works mattered more than others in the field of cardiology. Here was a man born 1914 in Utah, studied at Rush university trained in Mayo, settled in Seattle as a pediatrician. But his passion drove him to become a specialist cardiac physiologist with an urge to find the answers to all those lingering queries that arise as a practicing clinical cardiologist.  He built an exclusive animal lab to study the mechanics and physics of circulation and cardiac pumps in the 1950s 

 

                          1914-2001

He can be called the new age, Harvey of the 20th century. He seemed to always bother, how is it that the 6 liters of blood traverse from heart to the periphery and comes back going through vast lengthy circulation with variable pressure and little energy loss.? He also made the very pertinent discovery in neural control, the effect of gravity on circulation. His interest in how venous return would have to match cardiac output was phenomenal. 

His grasp of cardiovascular physiologic concepts was so powerful and his book on cardiovascular dynamics was so popular. probably the first scientific textbook on circulation. I am sure he had shaped the thought process of so many physicians (I will vouch for myself) and helped create hundreds of cardiologists all over the globe. Dr.Rushmer also did pioneering work on diagnostic ultrasound and doppler. I can recall a video on cardiac embryology edited by him in the 1960s in pre-computer era that probably can not be beaten even today in terms of clarity of content and production value.

Through his thoughts like an engineer and mathematician still, he was able to blend the knowledge together and pass it on to the generation next clinician. No wonder, he was the founder and headed the department of biomedical engineering in the UW. The University of Washington holds an annual Rushmer lecture. 

If one person deserves an award for excellence in cardiovascular science for the 20th century, Dr.Rushmer’s name should definitely, come on top. Though he won several accolades, I feel scientific societies have missed an opportunity to felicitate him with the more worthy award. If the Noble prize in medicine is given for a lifetime contribution to cardiovascular physiology wonder why he can’t be considered for it posthumously.  

It is heartening to note, at the fag end of his career he moved from core science to philosophical and ethical truths of science and technology. He once said, “We’re confronted with the ethical, political, and technological consequences of our medical triumphs. We have to learn quickly how to deal with these profound problems by looking ahead to recognize and avoid complications of our technical breakthroughs’ How true his observation has turned out to be!

 

Reference

https://www.washington.edu/news/2001/07/16/dr-robert-rushmer-diagnostic-ultrasound-pioneer-dies-at-age-86/

Heart is a dynamic organ, so any auscultation by default becomes dynamic. Still, what we mean by dynamic auscultation is, to look(hear) carefully at what happens to the sounds and murmurs during different phases of respiration*, posture and induced hemodynamic stress by altering preload, and afterload, etc. (* Some of us may not consider respiratory changes as part of dynamic auscultation, But, it is to be noted even spontaneous respiration is subtle dynamism and is reflected in JVP as well as second sound mobility. While forceful breath-holding or exhalation can dramatically shut down & release venous return from entering the thorax.This is the basis of the most popular maneuver of Valsalva.

I know, dynamic auscultation is a lost art. For fellows, the only issue that seems to bother is to understand the dynamic auscultation in various types of LVOT obstruction, MVPS , and to differentiate  aortic from pulmonary regurgitation murmurs, with or without VSD, RVOT/LVOT vascular /Valvular clicks etc

Here is an old presentation (2010) of mine from the archive.

One of the great resources on this topic is from Dr Delman. Hope this book is available. There is one more exclusive atlas by Delman & Stein dynamic auscultation with phonocardiographic and pulse correlation 

.

The commonest cause* for repeated entry of right radial catheter to descending aorta is not due to any anomaly. Most times,it is just a skewed angle between right brachio-cephalic artery with Aortic arch, that deflects the catheter to the descending aorta . Just make sure, aortic root is entered with a deeply held inspiration.

*Anomalies of the aortic arch, aberrant right subclavian, Kommerell’s diverticulum, vascular ring must be kept in mind.

 

Postamble: A true abnormal course

Though, It might appear prudent to avoid the radial route when encountering anomalous subclavian arteries, the reality is different and adventurous. We have acquired great expertise and successful PTCAs have been done through these tortuous vascular highways.

This is a case report from Dr H.S. Isser, Gunjan Garg, from Safdarjung hospital New Delhi. 

A successful PTCA through arteria lusoria : The right subclavian connect to the descending aorta, distal to the left subclavian at the level of ductus arteriosus. and pass retrotracheal and retroesophageal before reaching right arm. Image source and courtesy: H.S. Isser, Gunjan Garg, Arteria lusoria: A challenge for transradial coronary interventionist, IHJ Cardiovascular Case Reports (CVCR), Volume 4, Issue 1, 2020,

 

One of the topics rarely discussed in heart failure is  CAD as a contributory factor in HFpEF.

This is a copy of the presentation done at the ECHO India Annual scientific meet  2019 at Kolkatta. India.

 

Will try to find out the recorded version with audio. Here is a GIF run through.

PDF version Download here

Embryology

Sinus venosus ASD (also referred to as SVC ASD)  is a defect in the failure of the sinoatrial orifice to lateralize completely to the right side during atrial septation.Left venous valve, as well as the septum secundum, fails to fuse with the roof of the atria creating interatrial communication. During this process, the developing pulmonary vein overshoot to the right side making PAPVD a mandatory add-on defect. (Harley ,Thorax 1958 ) It can be referred to as embryonal venous migration defect at the level of RA. In the same sense, it is not a true defect in IAS but a defect in septation between SVC/PV. It may also be referred to as unroofing of RUPV. The so-called Inter atrial communication actually is the confluence point of RUPV/SVC/RA.(See TEE images below) 

We know, in SVC ASD-commonest associated anomaly is PAPVC . It is not an ideal term to use though, instead, it is encouraged to use the term PAPVD (drainage) . Technically true PAPVC can not be connected to RA cavity as PV can connect either to cardinal or vitelline vein only. This distinction is helpful when we search for additional PAPVCs cranial to SVC. Sometimes we might recognize this error only after closure of SVC ASD. 

Should we close SVC ASD ? How do we close?

Age, natural history, symptoms, the quantum of shunt will answer an occasional troubling query , “should we close it at all? Surgery is the standard approach till now. What makes device closure popular? Two reasons 1.Patient /or parent’s fear of surgery  2.Cardiologist’s urge for innovative Interventional procedures. (The fact that a simple covered stent will do the job is too tempting to make an attempt) However,please note, the procedure is not at all simple as one would Imagine.

Anatomical prerequisite for device closure 

The defect must fulfill some critical anatomical essentials.  

  • It should be an isolated defect.
  • RA should not be grossly enlarged
  • Re-routing of RUPV to LA should be possible 
  • A significant circumference of RUPV should be committed to LA.
  • There should not be downward extension involving septum secundum making it an SVC + OS ASD 

Technical issues

  • Self-expanding vs balloon expanding stent (Anyone may be chosen)
  • Stent flare-up SVC RA junction crucial
  • Must ensure  RUPV doesn’t get compressed with device.

  • Forces that hold the SVC end of the stent is very important. Sometimes It may require a second proximal stent just to prevent migration of the first stent.
  • Live LA pressure and RUPV monitoring may be critical to recognize PV ostial compromise. For this, a transeptal puncture may be required (Ironically creating another mini ASD !)

 

Finally, and most importantly follow-up is mandatory with device closure since the stent is on the venous circuit as RA, SVC thrombosis expected. (Anticoagulation protocol not clearly  defined as of now )

Final message 

Device closure for SVC ASD is a good Innovation. A perfectly delivered covered stent at the RA/SVC junction will do the trick. However, In my  opinion, surgeons do a neat(More complete)  job It is time-tested. Single or double patch or warden procedure may be done.(Ref 2)

Reference 

1.Hinnerk Hansen, Phuoc Duong, Salim .M. Jivanji, A. Qureshi, Eric Rosenthal Transcatheter Correction of Superior Sinus Venosus Atrial Septal Defects as an Alternative to Surgical Treatment J Am Coll Cardiol. 2020 Mar, 75 (11) 1266-1278.

2.Warden HE, Gustafson RA, Tarnay TJ, Neal WA. An alternative method for repair of partial anomalous pulmonary venous connection to the superior vena cava. Ann Thorac Surg 1984;38:601-5. 

 

https://doi.org/10.1016/j.pedneo.2019.06.013

 

https://doi.org/10.1016/j.athoracsur.2020.03.113

Mitra clip is a small metal device that is delivered percutaneously, to clip the incompletely coapting (closing) mitral valve. It was first introduced to treat degenerative mitral regurgitation. It is an interventional imitation of the famous edge to edge Alfieri stitch repair.This procedure in fact converts the single mitral valve orifice into two. In the process, curtails the regurgitation jet orifice significantly. Though the technique looks nice and simple to hear, lots of per and post-procedure issues need refinement. Conceptually it is ideal in primary disorders of the mitral valve. (Read EVEREST 2 criteria for optimal patient selection)  There have been more than 60000 Mitra clips implanted worldwide wide. Thanks to Abbot.

In secondary MR (due to LV dysfunction) Mitra clip has shown mixed results( MITRA-FR not much benefit, COAPT -Did show benefits)

Now, what about Mitra clip as a remedy for rheumatic mitral regurgitation?

This is the question everyone likes to ask. Now we have some interesting breakthroughs. Dr. Ningyan Wong from the National University of Singapore reports probably the first case (Ref 1) . The videos are reproduced with the creative commons license.

 

Note the classical thickened AML in rheumatic mitral regurgitation.

 

 

TEE showing severe MR

 

Post Mitra clip : A real surprise to note near-total abolition of regurgitation. (This really is good news for the rheumatic mitral valves )

Technical issues

  • Should be isolated MR
  • P2/A2 scallop clipping is the key to success. 
  • The thickness of the leaflet limits the success (Grasping the leaflet will be difficult)
  • Clip Induced mitral stenosis is a distinct risk.

Potential role and future

RHD forms 90 % of valvular heart disease in a country like India. The incidence of Isolated MR in both acute rheumatic fever and chronic  RHD are substantial. If only we refine the hardware and technique to suit these thickened rheumatic valves, Mitra clip is expected to make an impact in this unique group of patients where surgery can be avoided or at least postponed

Though we would very much like to do such a trial in our place, logistics has effectively precluded it. I wish some large centers like AIIMS New Delhi or PGIMER Chandigarh and others can take this concept to the next level.  

 

Reference

1.Ningyan Wong, Peilin Cheryl Marise Tan, Zee Pin Ding, Khung Keong Yeo, Successful MitraClip for severe rheumatic mitral regurgitation: a case report, European Heart Journal – Case Reports, Volume 3, Issue 3, September 2019

Two queries that linger in the medical profession for a long. I am afraid they aren’t addressed specifically by the stakeholders.

Question 1 

Foe a moment, let us assume there is no option to answer all three are equally important. Medical colleges are supposedly Godly places where high-quality noble professionals would germinate, let into the community thereupon, to heal the ill and suffering. The teaching faculty has a huge responsibility. They must ensure that students are transformed into responsible caregivers in the first place. They should be made to understand that the knowledge they acquire has a short half-life and medical education is all about continuous learning and unlearning. Unless teaching and research are morally genuine and scientifically perfect, the things we do in the name of patient care is going to be redundant. Hope you got the answer right!

 

Question 2

Now that, we got the answer to the question 1, here is a more difficult question. 

Out of the four, only one addresses the skill and expertise. The rest of the three generally happen away from the bedside. The answer is strikingly clear I guess.

 

Postamble

I agree the answers to these queries can be extremely sensitive, and contentious for many of us. Little deeper lies the truth. Hope, the quote from the much-stigmatized father of modern medicine  “Primum non-nocere” will help find the answer.