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Archive for September, 2020

Heart failure has been classified in many ways, with prevailing levels of our knowledge and ignorance. It is based on a variety of factors like rapidity of onset, etiology, chambers involved, hemodynamics, etc. 

  • Forward vs backward failure
  • Acute vs chronic failure
  • RV/LV or Biventicular failure 
  • Systolic vs diastolic heart failure
  • High output vs low out failure
  • Ischemic vs non-ischemic failure 
  • Reversible vs Refractory HF 

None of them have really helped at the bedside though it helped us understand the condition. Now, in the last decade, we have crash-landed on our favorite obsession to classify HF ie based on Ejection fraction. We believe we have found an exciting new classification. (HFrEF/HFpEF/HFmrEF).We embraced it, even after recognizing EF as a battered LV functional parameter due to its high load-dependence with a dubious reproducibility.  

If we rely too much on echo, there can be a few more classifications for HF 

  1. HF failure with preserved diastolic function(25% of all DCMs with HFrEF )
  2. HF with preserved mitral valve function
  3. HF with preserved Global longitudinal strain(Still normal EF%)
  4. HF with preserved RV function
  5. HF with preserved Torsion and Twist.
  6. Finally, HF with normal Heart (Anemia/CKD etc)  In anemia heart never fails in true sense. In fact, it works at peak capacity.(More of a Success than failure). Similarly isn’t odd to put primary CKD/CRF in the CHF basket.

Probably the most important and practical classification  could be

  1. Primary vs secondary HF (Primary means all muscle diseases under MOGES system ) 
  2. Valvular vs non-valvular failure (Surgically correctable MVR/DVR/Mitral valve repair)
  3. Revascularisable  or Non-revascularisable HF (STICH study responders)
  4. ICD/CRT eligible HF vs Non-eligible HF ( Rule out DANISH study non-responders)
  5. Refractory failure -Novel drugs/ Assist device/TAH/ Transplant suited 

Final message

 Dr Thomas Lewis said over 100 years ago, the essence of the practice of cardiology is to recognize HF early. Looking back at the literature, there will be no dearth of classification for HF. It will come and go according to academic and Imaging whims. Of course, that may aid in ruling out primary cardiac conditions. But, we must always emphasize to the next-generation that HF is often due to systemic*(reversible too) conditions in substantial numbers. Here the heart is just a bystander watching helplessly, trying to adapt to a remote systemic comorbid problem. Such hearts don’t require cowboy aggression but gentle care by concerned physicians.(One study reveals weight reduction and systematic exercise program adds more life to HF than drugs and devices. Will link the reference/ or try google)

*Eg: Anemia is the commonest cause of HFpEF on a global scale. .CKD, undiagnosed autoimmune disorders, malignancy, are other classical examples. Let us be first a physician then a cardiologist, that will ensure our we don’t miss important treatable conditions with our short-sighted definition of heart failure based on EF%.

 Reference 

1.Y. Juilliere, J.N. Trochu, P. de Groote, et al.Heart failure with preserved systolic function: a diagnostic algorithm for a pragmatic definition  Arch Mal Coeur Vaiss, 99 (2006), pp. 279-286  View Record in ScopusGoogle Scholar
 

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Is sudden, unaccustomed, physical exertion a trigger for plaque rupture and an ACS ?

Yes, it is, but don’t get apprehensive. The underlying risk factors, plaque burden, and its morphology matter much to result in a coronary event.

What is the mechanism?

Plaque morphology,  the lipid core, the shoulder region’s eccentricity, the crystallization of cholesterol lay the foundation. The Isometric component of stress surges Intra-coronary pressures and facilitate vascular injury.  Endothelial dysfunction leading to erosion and subsequent acute total thrombotic occlusion is a well-known response to stress. Currently, spontaneous coronary dissection secondary to unaccustomed stress is increasingly recognized to be a culprit.

 

plaque fissure and exertion physical and mental exertion and plaque

Which is more dangerous? Mental or physical stress* ?

No one can answer this query with certainty. The combination of both can prove deadly in vulnerable patients. The final common pathway for both physical and mental stress seems to be the same. Adrenergic toxicity at the cellular level.

* Mental stress-induced primary electrical events (CPVT/ Inherited channelopathy ) are unrelated to plaque destabilization that is often confused with ACS in many SCDs.

What are the natural protective factors to stress?

Coronary autoregulation,stress-busting hormones like endorphins , natural anti-fibrinolytic systems do play a role. Human beings experience infinite episodes of mental stress in their lifetime. Only a fraction (of a fraction ) result in ACS. It is obvious , there must be some major invisible protective factors. One may call this as metaphysical force ( scientific equivalent to fate ?) operating on a particular plaque to destabilize it.

 

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History is rarely kind to the original heroes in the scientific world.The classical Blalock-Taussig shunt,(BT shunt) the term we heard for the first time in the early clinical years of MBBS .We know, it as a dramatic surgery (Palliative though) connecting subclavian artery to the pulmonary artery for the commonest congenital cyanotic heart disease -Tetralogy of Fallot.

Now, half a century later, came to know, there is a gripping story of an oppressed black hero behind this famous cardiac surgery. This post is all about the fascinating life of Vivien Thomas, a humble carpenter’s son from Nashville. While he dreamed to become a doctor, circumstances and fate had some thing different to offer .He could join only as helper in the wards of John Hopkins, Baltimore . His extraordinary hand skills were recognised by then surgeon Alfred Blalock and made him as an assistant in the Hopkins animal lab.He was working on a project to resuscitate traumatic shock victims then. Dr Helen Taussig who was a pediatric cardiologist was wondering whether Dr Blalock could offer some surgical cure for the sick blue babies under her care.

When Dr Blalock was brainstorming the problem , it was Thomas ,who created dog models of hypoxic circulation and helped create the concept and methodology of diverting blood from subclavian artery to pulmonary artery .He single handedly operated on nearly 200 dogs. He literally taught the chief surgeon Blalock the delicate vascular suture tricks .

Come October 24th 1944 , the first blue baby was operated , with Blalock Insisting Thomas to stand beside. History was created -first heart surgery in USA. Which later on became the most famous concept that gave a fresh lease of life to thousands of children with TOF.

Vivien thomas blalock tausig BTT shunt baltimore jhon hopkins gross. 2 jpg

It’s painfully emotional to watch the Vivien Thomas standing right behind Dr Blalock,guiding his boss anxiously,with his hands tied just because he is not a qualified doctor. The others in the team included Dr Denton Cooley and Helen Taussig.

No surprise, when this famous work was reported in the media, the entire cardiology community rejoiced as the news broke out over the globe .It was published in JAMA in 1945 (Blalock1945.pdf ) . Did you guess it , yes, the name Thomas was not to be found anywhere though. How can you expect it ? , after all , he is a black lab supervisor working with dogs !

wp-16005739262243523194074888226565.jpg

Thomas’ , work was never recognized for the next 30 years until a grand occasion (Lord made?) that happened in the Baltimore in 1971. His dream of becoming doctor became a moment of truth. Baltimore school,of medicine finally recognised his work and conferred a honorary doctor . Unfortunately Dr Blalock was no more by then to attend to his famous pupil.
Its 2020 , 80 years after the monumental surgery , the BT shunt has since been renamed as Blalock, Thomas ,Taussig shunt . A new exclusive center for congenital heart surgery in Baltimore has come up in their name. What a great end to this black man’s journey in troubled racial times.

Thanks to Hollywood minds who thought this story deserved to be made as movie. “Something Lord made” directed by Joseph Sargent. It was a gripping scientific roller coaster .No surprise it got so many awards including three Emmys.

Every physician,especially the cardiologists should watch this movie. I can vouch, the one and a half hours  you are going to spend will enrich  professionally  and Intellectually. Lucky to find this movie free on you tube.

The Remarkable Story of Vivien Thomas, the Black Man Who Helped Invent Heart Surgery

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It was April 15th 1912, Titanic, the Invincible, had just sunk into the dark waters of the Atlantic coast off Newfoundland. Exactly same time around, Dr. James Herrick, In Chicago, Illinois was busy documenting the first diagnosed case of acute coronary thrombosis. A new disease was born ie Myocardial Infarction. This was also the era of the Noble Prize-winning  Invention of the ECG machine by Waller, Einthoven, and Thomas Lewis & co that sow the seeds for the specialty of electro-cardiology.

Though much was studied about MI with pathological specimens in the subsequent decades, there was a lull in the efforts to define the entity of myocardial Infarction till WHO  defined in the early 1970s. It was dogmatic, still fair enough. (Clinical, Enzymes, ECG criteria, with  any two feature, must be present to diagnose )

Since then, the field of cardiology has seen unprecedented development in both the diagnosis and treatment of ACS. We now have a universal definition( EHJ 2019 Thygesen K ) that asks us to triage based on high sensitive troponin followed by clinical and other parameters. STEMI usually doesn’t have much diagnostic confusion.

Nomenclature Issues in NSTEMI/UA

The definition of NSTEMI  refuses to settle, though we have come a long way since the times  UA/NSTEMI were clubbed together as siblings. The term unstable angina was coined by one of the most revered cardiologists of our times  Dr. Noble O Fowler in 1978. They are the same one hitherto referred to as Intermediate coronary syndrome/Pre Infarction angina. Later, if enzymes were raised it was labeled as non-transmural/Non-Q  MI. This became the classical NSTEMI later changed to NSTEACS (Still it is valid)

The semantics surrounding the NSTEMI  is unlikely to end as long as we depend largely on ECG to diagnose and treat complex coronary obstructive syndromes. This, by no means, undermine the importance of ECG in this setting. It will remain the gold standard as far as, I can look into the future.

Some observation about the new ESC 2020 NSTEMI guidelines

Anyway, ESC 2020 has addressed this issue. It suggests a new term “ACS without persistent ST elevation” for NSTEMI (Ideally they should have used this abbreviation  NP-STEACS)

(*I guess, the current ESC 2020 guidelines really wanted to get rid of both NSTEMI/NSTEACS for a very valid reason but still it was worried about the confusion it might create so retained the old term NSTEMI/NSTEACS  )

The categories included in the current NSTEMI scheme are

1.Transient ST elevation (How transient ? Prinzmetal/ Non Prinzmetal ?)

2.Persistent ST depression

3.T inversion

4.Flat (Absent ) T wave

5.Pseudo normalization of T

It may include the following as well (Not in official ESC 20220 guidelines)

6*.Hyperacute T (Very early STEMI ? or NSTEMI?

7*.Wellen/Dewinter or its variants

I think ESC is to be appreciated for recognizing an off ignored observation that UA may have a transient ST elevation and end up later as NSTEMI/NSTACS. This group of ACS still poses a challenge for us to understand the overlap between total and subtotal coronary occlusion (Non-Prinzmetal ST elevation)

Final message 

Does this nomenclature issue create problems in management? 

  • Yes, it does. The major implication is in the diagnosis ACS with dynamic ST segments ( ST-elevation / /depression or any combination)
  • If a probable STEMI after spontaneous lysis presents as NSTEMI, Is it the baby STEMI or neo NSTEMI ? One may not rush such NSTEMI patients to cath labs.
  • Of course, many of us are conditioned to follow a “single point agenda “ that dictates all ACS shall reach the cath lab and managed thereafter based on coronary anatomy. If that is the case, I am sure the bulk of this 79-page new NSTEMI guideline appears redundant.(Ref 1)

Reference

1.Jean-Philippe Collet,  ESC Scientific Document Group, 2020 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: The Task Force for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation of the European Society of Cardiology (ESC), European Heart Journal, , ehaa575https://doi.org/10.1093/eurheartj/ehaa575

2 Fourth Universal Definition of Myocardial Infarction (2018). Eur Heart J 2019;40:237-269. 

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The incidence of stroke during TAVI up to 5 % (minimum ). Stroke risk reduction during TAVI is a critical requirement that can be a deterrent against this wonderful Intervention.

Many devices are being considered

  1. EmbolX (Edwards life science)
  2. Emrella
  3. Sentinel (Claret medical)
  4. TriGaurd (Keystone)

1-s2.0-S1050173818300112-gr2

 

TriGaurd 3just got the approval from CE and appear promising. (REFLECT trial) It is inserted through the transfemoral route , deflects embolic material to descending aorta since it covers all the three branches of Arch.What happens to these deflected particles? Any bodys guess.

So , in my understanding it converts potential brain embolisation to peripheral microemboli , wh

This image has an empty alt attribute; its file name is triguard-3tavi-tavr.jpg

A nice descriptive animation .https://player.vimeo.com/video/232995629

While, these innovative aortic arch filters reduce the risk of periprocedural embolic stroke, please mind, TAVR patients continue to be at significant risk for stroke over a long period. This is due to other late causes like TAVR leaflet thrombosis, atrial fibrillation, arch atheromas, and bleeding due antiplatelet agents.

Reference

1.WienekeVlastra, JeroenVendrik,  Karel T.Koch et al Cerebral protection devices during transcatheter aortic valve implantation  Trends in Cardiovascular Medicine  Volume 28, Issue 6, August 2018, Pages 412-418

2.(REFLECT trial) 

 

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           Practice of cardiology is simple as long we don’t dwell deep into coronary physiology.

One of my patients asked, why he was told his total occlusion in LAD appears safer now, which was subtotal a few months ago.I told him, it is indeed true. It is the fear of subtotal disease that’s prone to a fresh coronary event. In total occlusion, chances of that happening are less or nil.

 

How can you say 100% block is safe?  Is that always true?

No, it’s not always true. He was surprised when I said it is not 100 %, even 90% lesion can be safe if it’s not causing significant angina and responding to OMT. Of course, It is the morphology and stability of the lesion that will dictate* the outcome in the subtotal occlusion. If the lesion is stable, FFR is good >.8 (TMT is poor man’s FFR equivalent )  you can leave it as it is. Doing OCT /Virtual histology /NIR spectroscopy to define the vulnerability of plaque is neither practical nor desirable (Extreme academics is injurious to health) 

So it is not the degree of the block that’s going to matter, but the effects of that block on distal circulation that will decide the rules of the myocardial revascularisation game. But unfortunately, both you, (the patients) we (the cardiologist) are finding it so difficult to come to terms with this basic truth in spite of multiple guidelines. 

 

Meanwhile, CTO however makes it much easier to make a decision. One need not bother the content of CTO unless you plan an Intervention. I guess there is no FFR for CTO. Are we aware of any studies that have quantified antegrade flow across a 10% patent LAD and compare it with the Collateral flow in LAD in 100% CTO?

We have long glorified a concept of the open artery hypothesis. (Mainly in Post STEMI though) No one has dared to test and compare a hypothesis that a closed artery might still score over the open in at least some of the subsets of stable CAD. Such a study can never be ethically forbidden after all its a well-observed truth in the real world. 

Reference 

Trials on CTO  revascularisation DECISION CT (Not useful )   EURO-CTO  (May be useful) 

 

 

 

EURO CTO https://academic.oup.com/eurheartj/advance-article-abstract/doi/10.1093/eurheartj/ehy220/4990878?redirectedFrom=fulltext

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