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“Dialysable LV dysfunction In CKD ” : Myocardial edema clearance plays a role.

October 11, 2020 by dr s venkatesan

In CKD, LVH is a near-constant feature with echo showing thick, bright echoes from IVS. The LV mass increases, partly due to physiological hypertrophy ,also contributed by deposits of uremic middle molecules and fluid collection in the interstitium as myocardial edema.This, is recognised as T 2 weighted MRI signals. Chronic fluid stasis may progress to myocardial fibrosis. (Kidney Blood Press Res 2018;43:134–142 )  

Effect of Frusemide on myocardial edema 

We know, loop diuretics cause aggressive depletion of ECF volume and to a lesser extent Interstitial fluid. The effect of diuretic on myocardial water content is a poorly studied parameter.(Still more visible to a shrewd echocardiographer)

Effect of dialysis

While the effect of diuretics on myocardial edema is not consistent, however, we have observed definite regression of myocardial thickness, mass, and rigidity following dialysis. This transforms into a better LV systolic and diastolic function. At least in one patient, we have observed  the E velocity shrunk more than 50% the next day following dialysis pushing them to lower grades of HFpEF( A potential study topic.)

Final message 

The Improvement of the functional class of CKD patients immediately after dialysis is not only attributable to the removal of excess fluid and toxic uremic molecules, regression of myocardial edema plays an important role.

Further reading

Trinh E, Chan C, T: Intensive Home Hemodialysis Results in Regression of Left Ventricular Hypertrophy and Better Clinical Outcomes. Am J Nephrol 2016;44:300-307.

Posted in cardiology research topics for fellows, cardiology thesis topics, Uncategorized | Tagged , , , , |

Amiodarone in Ischemic VT : Doesn’t work always,.. IRA patency could be the missing link.

October 10, 2020 by dr s venkatesan

Curiously, the management of VT is simple if the patient is unstable. Just, we need to shock. Cardiologists are troubled only with a hemodynamically stable patient with VT. Some of us still think Amiodarone is a universal antidote for any VT. Though It is effective in both ischemic and non -Ischemic VT, the success rate is not uniform.

The mechanism of action of the Initial IV bolus is not a class 3 K + blocking action, instead, it is thought to be its beta-blocking action. If amiodarone fails, we may try Lignocaine,  magnesium, Flecainide. .Many times it is the cumulative dose of amiodarone that reverts the VT. In some patients, it may reduce the ventricular rate instead of reverting to sinus rhythm. This is due to the prolongation of re-entrant circuit time. The question of amiodarone worsening polymorphic VT with a deleterious effect on the QT interval is still not clear yet.

Why Amiodarone fails to revert VT in some ?(Up to 40 % ?)

One of the factors we looked at some 15 years back was the relationship between IRA patency and amiodarone efficacy. Presented in CSI meet 2004.

It was a simple conclusion. For Amiodarone to be effective IRA must be at least partially patent to enable the drug to reach the target tissue. I am not aware of any study on this issue. Request anyone to expand this study and publish it as a full paper. (Royalty-free research topic!) Please acknowledge the concept if you think it’s original.

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Newer frontiers in cardiac pacing : Wireless dual-chamber pacing

October 9, 2020 by dr s venkatesan

The field of cardiology is always at the forefront of any technological breakthrough. Cardiac pacing stands tall among all Innovations. While remote monitoring and pacemaker telemetry are well-known concepts. One would have wondered why Intracardiac leads couldn’t communicate with each other wirelessly. Yes, It was just a matter of time, for that to happen. 

The leadless pacemaker Micra/Nanostim was Introduced recently but lacked the much needed physiological pacing as they were single chamber based pacing. Though mechanical sensing of atrial activity was possible with Micra TPS software patch  (A  VDD like mode) it wasn’t providing perfect AV synchrony.  (https://drsvenkatesan.com/2020/04/03/av-synchrony-in-lead-less-micra-av-pacemaker-how-does-it-sense-atria/)

 

Now, technology has made it possible for dual-chamber leadless pacer. Here atrial and ventricular channels communicate in a wireless fashion, making it a truly wireless dual-chamber pacing. Interestingly the communication between them is not Bluetooth or NFC based but a concept called low-frequency Galvanic coupled intrabody communication. (Currently Implanted  pig models.)

Final message 

We have crossed new frontiers in the management of electrical cardiac disorders. While inadvertent cross-talk between atrial and ventricular lead was an issue in the past, now we are mastering the art of appropriate talk between these leads in a wireless fashion and use it for synchronized pacing. 

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Medical distillery : How to eliminate evidence based falsehoods in medical literature ?

October 5, 2020 by dr s venkatesan

If science is considered as a journey towards truth,.. knowledge, data, and statistics are the key companions in this infinite voyage to an unknown destination. While hundreds & thousands of scientists do travel in this turbulent road daily, pursuing their mundane work, there are very few researchers worried about the true purpose of their journey, the quality of the road they travel, the dangerous fault lines they create.

It has become a taboo topic to criticize medical science even after realizing the fact that we are compelled to follow and glorify some of the best nonsense.

Dr. Jhon Loannidhis Professor of statistics and public health from Stanford University is of a different genre. He became so popular after his landmark paper

Loannidis JPA (2005) Why Most Published Research Findings Are False. PLoS Med 2(8): e124.

His lectures are so important to us. Physicians need to listen to his talks, infested with absolute truths, unpalatable though.

Final message 

It is my wish there is a need for a new specialty called quality assessment of published medical literature and knowledge distillery. 

 

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Role of RT-PCR in the diagnosis of Rheumatic fever/RHD

October 1, 2020 by dr s venkatesan

RT-PCR: Real-time polymerase chain reaction, a sophisticated gene sequence-based biochemical test. Thanks to corona, this complex medical investigation has become a household name.

Jones proposed his criteria to diagnose acute rheumatic fever  in 1944, we still use it to diagnose with many modifications . Currently, AHA position statement – 2015 by Gewitz et all is  being followed. (Circulation 2015)

From Braunwald textbook of cardiology. Apart from this, there is one catch . Even if the child fulfills Jone criteria, there needs to be evidence for preceding streptococcal sore throat, either by culture or antibody. Now, can we include an RT-PCR as a new parameter to diagnose streptococcal infection is the question?

Why we Insist on evidence for preceding GAS?

It is for a the simple reason, many entities other than rheumatic fever may fulfill Jones’s criteria. (Still disease, HS purpura OR even simple viral arthritis etc) Some may even call it an essential criterion in the past. Practically it is not done is a  different story.

Tests for preceding streptococcal sore throat are ASO titer and anti-DNAase B. How about the now  glamorous RT-pCR for streptococcus ?  Though it was suggested as a useful test in the past ,the cost and logistics were  prohibitive so it was never considered to be included in the Jones scheme of things.

There could be three roles for RT-PCR testing in Rheumatic fever /RHD

1.RT-PCR as evidence for recent streptococcal sore throat.(GAS organism) Which still not practically used often but has big scope.(Ref 1)

2.To rule out co-viral (influenza-like) infections as a cause for fever and Joint pain (Used in population-based screening in a high endemic area (Ref 2)

3.There could be one more indication (experimental though) Micro-RNA detection by RT-PCR to identify children who are prone for progression to RHD. (Ref 3)

Final message

Now, we must introspect. While billions of dollars are going down the drain on  RT-PCR for diagnosing  a common cold pandemic which has no specific treatment. Will WHO and other cardiovascular preventive authorities  consider to include RT-PCR as screening  test for GAS in children. This will enable  early start of primary prophylaxis and prevent  RF/RHD  a century-long scourge of the third world.

Reference

1.

2 .Emmy Okello et all J Am Heart Assoc. 2020;9:e016053. DOI: 10.1161/JAHA.120.016053

3.Lu, Q., Sun, Y., Duan, Y. et al. Comprehensive microRNA profiling reveals potential augmentation of the IL1 pathway in rheumatic heart valve disease. BMC Cardiovasc Disord 18, 53 (2018).

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If EF% is a most flawed LV functional parameter,.. why we Insist HF to be classified based on it ?

September 25, 2020 by dr s venkatesan

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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“Meta physical” effect of “Physical exertion” on coronary plaque

September 20, 2020 by dr s venkatesan

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 of cardiology : A soulful story of “Dr.Thomas”and his BT shunt

September 17, 2020 by dr s venkatesan

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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NSTEMI : Is it the baby of STEMI or a Neo NSTEMI ?

September 14, 2020 by dr s venkatesan

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, , ehaa575, https://doi.org/10.1093/eurheartj/ehaa575

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

Posted in acute coronary syndrome | Tagged , , , , , , |

Peer reviewed perils: Medical science is still far away from true democracy !

September 12, 2020 by dr s venkatesan

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