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The branching pattern of the human cardio-vascular tree is as unique as one’s fingerprint. One such hugely variable anatomy is the SA nodal blood supply.

Certain salient features

  • Variation can be seen in origin, course, and termination.
  • Now it is estimated to arise from RCA in 70% (Moved up from 55% in old studies )
  • From LCX (25%)
  • Dual SA node supply(5%)
  • Direct from Aorta

It is heartening to find this good anatomical review on this topic.

A) From the Right Coronary Artery; (B) From the Left Circumflex Artery (proximal); (C) From the Left Circumflex Artery (distal); (D) From the Left Coronary Artery; (E) From the Aorta; (F) Dual origin from the Right Coronary Artery and the Left Circumflex Artery. Image source : Vikse J, PLoS ONE 11(2): e0148331

Implication for the surgeon

The whereabouts of this tiny, yet important artery is critical to the surgeons’ as they incise and explore the atrial roof. (A gateway, that gives access to so many cardiac surgeries) The SA nodal artery mostly goes retro caval but it can be peri-caval or even anterior to SVC.

This image shows (a,b,c) the course in relation to SVC, Developmentally as the venous pole go posteriorly to fix the SA artery behind it.Image source : Vikse J, PLoS ONE 11(2): e0148331

For the Interventional cardiologist

A rare but distinct mechanical compression of SA node artery is reported with large ASD closure device. The plane of compression is usually occurring in the superior aspect of IAS when the SA node artery cross over the RA to reach the SA node. Should be suspected whenever unusual bradycardia occurs during the manipulation of the device or just after deployment. Always mind the delicate gap  between the antero superior rim and disc where SA nodal artery is likely to trespass.

AV node Ischemia with ASD device

With precise imaging modalities, new secrets are emerging. Additional AV node arteries from proximal RCA is documented.This is a surprising learning point for us. This artery is referred to as the right superior descending artery, which provides an alternative blood supply to the AV node from the proximal right coronary artery. The transient compromise of this hitherto unknown AV nodal twigs by the ASD device cause AV blocks. With this new info, we also got an answer to one more lingering question, why would disproportionate bradycardias are observed in inferior MI even when distal RCA is flowing well. We can’t blame high vagal tone always.

SA node compression by ASD device amplatzer

A CT angiogram showing how the ASD device encroaches the SA node artery. Image Source:Tsunehisa Yamamoto JACC 2016 (Linkedbelow)

The original article has an excellent video clipping of how an ASD device hugs the SA node at the superior edge of ASD.

Final message

Human anatomy is not the subject meant to be read in the first-year medical school cadavers, & forget thereafter. Surprisingly. the field of anatomy is also evolving with new mysteries exposed by modern imaging.SA nodal arterial blood supply is one such interesting aspect of cardiac anatomy. Young fellows in cardiology shall pursue further anatomical dark spaces in the heart (One such topic is how cardiac lymphatics compete with the venous system in draining cardiac interstitium)

Reference

Vikse J, Henry BM, Roy J, RamakrishnanPK, Hsieh WC, Walocha JA, et al. (2016) AnatomicalVariations in the Sinoatrial Nodal Artery: A Meta-Analysis and Clinical Considerations. PLoS ONE 11(2): e0148331

It’s gratifying a unique and committed group exclusively doing research in Anatomy. It Department of Anatomy, Jagiellonian University Medical College, Krakow Poland.

http://www.eba.cm.uj.edu.pl/

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Corona has triggered the scare of the century, even among the scientifically savvy brave men & women. The scale of the panic was unprecedented. However, one positive outcome of this pandemic was, this 20 nm RNA particle forced many of us, to ponder over the true purpose of life. It demanded a course correction in those who found one. Now, after 9 months Corona, in its second wave seems to be somewhat kind to humanity. The case fatality rate is dropping to nearly one-tenth of its peak in the first wave. 

 

 

 

 

Where is the evidence coming from?

Apart from our own personal experience from 1500 bedded corona hospital, this paper reports data from 53 countries.

 

Note, the red covid mortality curves are not matching the black positive waves (Both Europe and Asia)

Link to the original article https://doi.org/10.1111/tbed.13819

The possible reasons for the low case fatality rate.(Personal observation)

  1. Viral apologetic  behavior*
  2. Second wave affecting more healthy younger who fight it better.
  3. Less panic in the health care delivery system
  4. Though there is no specific therapy, at least some basic treatment strategies are in place.(Timely steroids & mindful oxygen did the trick)
  5. Initial aggression out of Ignorance (ie ventilator deaths) has largely ceased.
  6.  RT-PCR(which helped In diagnosing /isolating ), CT scans,(helped in grading) the Remdesvirs(gave peace of mind ) the Tocilizumab(did nothing great ) has at best played a minuscule role at a huge cost.

Among all these factors, which do you think is the most important contributor to a declining fatality?

The single important factor could be, “The virus has decided unilaterally to forgive the frightened human beings, and become less virile“.(At least in those people who sincerely respected the viral might by wearing masks and other paraphernalia) Sorry, for uttering this forbidden stuff in science, still it could well be the truth. 

If corona is losing its sting & steam what would be the realistic role of the vaccine? What is the likelihood of vaccine getting false credit*?If we are allowed to be optimistic, Corona in all likelihood is waiting to say goodbye after a feeble third or fourth wave. All these are speculative, still, one thing looks positive. Unlike the much-quoted fact about the Spanish flu of 1920, which resulted in more damage in the second wave, which is unlikely to happen with corona.

Disclaimer

* This article never intends to undermine the importance of preventive measures and vaccines for this worst pandemic in recent human history.

Counterpoint 

The decline in case fatality is may not be uniform as fresh data from Europe suggest. It’s hyperbole to expect corona’s second wave to bring good news. It is largely left to the people’s behavior to contain the pandemic than to get a pardon from the virus. 

 

 

 

 

 

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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.

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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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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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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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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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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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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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