Dr.S.Venkatesan MD

ASD device closure: “Mind the gap” to avoid SA nodal artery compression.

November 20, 2020 by dr s venkatesan

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.

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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Posted in Cardiology research topics, cardiology research topics for fellows, Uncategorized | Tagged ASD device closure, cardaic lymphatics, cardiology reserach topic, sa nodal compression during asd device closure |

Corona second wave might bring some good news !

November 17, 2020 by dr s venkatesan

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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Posted in Uncategorized | Tagged corona second third wave, corona second wave, corona vaccine, what is the case fatality rate in corona |

Arrhythmia basics: How often we need to know the mechanism of arrhythmia ?

November 2, 2020 by dr s venkatesan

How many times you have treated cardiac arrhythmia in both emergency & non-emergency situations?

Infinite times.

How many times did you really bother to know the mechanism of a given arrhythmia before ordering medication or shocking?

Hmm,.. let me think. (Except for AVNRT/ AVRT, and few VTs, very rarely I have worried about the mechanism  !)

Why is it so? because treatment takes priority and we are able to tame the arrhythmia even without knowing the real mechanism.

The following slide is a gross summary of the cardiac arrhythmia mechanism

Understanding cardiac arrhythmia is vitally important for a few reasons in a few settings.

• In acute settings, we need to know automatic tachycardias will not respond to shocks. Reentry tachycardias will respond more promptly. (Of course, we may not know it till we shock ) Calcium blockers like verapamil might block triggered activity in MAT. Overdrive pacing is the answer for many automatic tachycardias and some refractory reentrant tachycardias (ATP protocols in ICD has taught us this ) 
• In the chronic setting when you contemplate mapping, locating, and ablating arrhythmias, mechanisms are important. The task here is locating slow conduction paths and decoding the diastolic circuit around the scar  (If you plan ICD, knowledge about mechanism  becomes redundant again)

• Finally, knowing the mechanism of arrhythmia is a fascination by itself to help understand the great subject called cardiac electrophysiology, where 100s of ion channels work nonstop drawing the action potential on a moment to moment basis sustaining our life.

A challenge

Can you localize a VT and find the mechanism in a patient who is Ischemic /hypoxic and acidotic? You can never do it. Please note, most polymorphic VTs can’t be localized. The mechanism is either automaticity, trigger activity, or even micro-reentry. You need to shock and look for the causes.(Link to How does the treatment of monomorphic VT differ from Polymorphic VT? )

Final message

Should we need to know about the mechanism of arrhythmia we treat?  Definitely yes, if you have that passion to know the truth, or else just order Amiodarone or shock and check out of CCU. (Of course, we have a very good option of calling EP consult the next day.)

 A review article on mechannism of cardiac arrhymias

Rev Esp Cardiol. 2012;65(2):174–185

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Posted in Basic science -Physiology, Brugada syndrome, cardiac electrophysiology, cardiology -Therapeutics, Cardiology-Arrhythmias | Tagged brady dependent vt, brugada syndrome, eads dads, early and late after depolarisation, enhanced automaticity vs triggerred activity vs reentry, mechanism of cardiac arrhythmais, phase 2 reentry, phase dependent vt |

Acute Aortic syndrome : Please mind the length of “Ascending Aorta” as well.

November 1, 2020 by dr s venkatesan

 Aorta probably is the most critical structure in the entire circulatory system. (apart from the heart of course !) It is a 1.5 to 2.5 mm thick tube, with a diameter of 2.5 cm/length of 30 -35 cm from the aortic valve to the iliac bifurcation.(Eric Borsero 2011) It handles about 7500 liters of blood every day. Understanding the Aortic pathology has vastly improved at the molecular level with deep gene sequencing that defines fibrillin phenotypes.  Meanwhile, CT ,  4D MRI and 3D prototyping have landed us in a new era where we can feel the exact models of a patient’s virtual aAorta for monitoring and treatment purposes.

Image source https://doi.org/10.1002/jmrs.212

 

While acute Aortic syndromes is the one that bothers us most, even chronic aortic enlargements are equally risky as at any time it can become acute. Though the risk of aneurysm and rupture is related to the histology and molecular disruption at the level of aortic media, we can only rely easily on is its dimension. Traditionally we bother about the diameter since it is the aortic radius that Influences the stress through to Laplace law.(Wall stress equals twice the radius /Thickness of wall)

Click over the Image for ESC Aortic disease guidelines

The annulus is the narrowest part, it gains about 50% width (10mm) at the level of the sinus of Valsalva to reach about a maximum of 35 mm and again narrows at ST to a junction (almost to the same diameter of the annulus) It continues further as ascending, arch and descending aortas with gradual tapering. 

Risk of rupture

Katherine H.Chau et all https://doi.org/10.1016/j.pcad.2013.05.007

Are you aware aorta keeps growing with age?

Unlike many other organs, growth of which gets arrested by adulthood, aorta appears to grow well into middle and elderly age.The aorta grows by 6cm in total length between age 20 to 80 (Ref 1)   The average growth of the ascending aorta is .18mm /year

This fact was reported 70 years ago Dotters famous study Circulation 1950  https://www.ahajournals.org/doi/pdf/10.1161/01.CIR.2.6.915

I used to wonder in many elderly why chest x-ray shows wide superior mediastinum still echocardiogram didn’t show any dilatation.This we call it as aortic unfolding. The term unfolding of aorta may represent the elongation of both ascending and descending aorta. The mechanism is due to multiple factors, like lax ligamentous of aortic attachment, dilatation, and longitudinal elongation.

Unfolding of the aorta . (How to measure unfolding Lee JW, (2014) Aortic Unfolding Determined Using Non-Contrast Cardiac Computed Tomography: Correlations with Age and Coronary Artery Calcium Score. PLoS ONE 9(4): e95887. )

How Important is the length of the aorta?

Risk of Aortic aneurysm is usually attributable to the diameter (Accepted normal 2.1cm/m2) . However, in IRAD registry, 50 % of aortic dissection happened in aortas less than 5 cm. So there is something more than the diameter that confers the risk of an aortic event. Is it the length and elongation?  After years of observation, we now realize it is indeed true. It is a surprise we didn’t realize  elongation of aorta also confers the same aortic wall weakness like that of Increased diameter (Longitudinal deformation/Stretch )

How to measure the length of Aorta?

It is best measured by CT scan or MRI. There is a new parameter called  Wu Index, which is based on both length and width of the aorta , which predicts the risk of aortic event. 

 

 

Jinlin Wu, Mohammad  Zafar, Yupeng Li,  J Am Coll Cardiol. 2019 Oct, 74 (15) 1883-1894.

Final message 

Aneurysm of the aorta is traditionally defined based on the degree of dilatation. It’s time, Aortic length should also be included in defining aortic aneurysm. We need to monitor it periodically as well in the population at risk. 

Reference 

1.Adriaans BP, Heuts S, Gerretsen S, et al. Aortic elongation part I: the normal aortic aging process. Heart 2018;104:1772–7.

2.Ascending Aortic Length and Risk of Aortic Adverse Events  Jinlin Wu, Mohammad  Zafar, Yupeng Li, 

J Am Coll Cardiol. 2019 Oct, 74 (15) 1883-1894.

3.Pape LA, Tsai TT, Isselbacher EM,  Aortic diameter > or = 5.5 cm is not a good predictor of type A aortic dissection: observations from the International Registry of Acute Aortic Dissection (IRAD). Circulation 2007;116:1120-1127

 

The comprehensive reference 

4.Hiratzka LF, Bakris GL, Beckman JA,  2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM Guidelines for the diagnosis and management of patients with thoracic aortic disease. A Report of the American College of Cardiology Foundation/American Heart  J Am Coll Cardiol 2010;55:e27-e129.

 

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Posted in aortic aneurysm | Tagged marfan aortic dissection aorta size, new coconcepts in aortic dimension, normal aorta size, normal aortic root size, what is normal length of ascending aorta |

All time best quote on “Principles of learning and education “

October 26, 2020 by dr s venkatesan

Today is one of the most auspicious days in Indian traditional festive time. Saraswathi pooja, a celebration of the Goddess of knowledge and education. I would like to share one of the all-time great quotes on learning from Thiruvalluvar a sage poet who lived in the southern Indian state of (mine), Tamil Nadu in 4th -5th century BC  2500 years ago.

 This Thirukural number 391 in the chapter of education goes on like this. (In the Tamil Language)

In English

Karka, Kasadara, Karpavai , Katrapin,

Nirka , Atharkku Thaga !

It says

Karka : Learn

Kasadara: Here comes the punch. Kasadara means pure.  He says simple learning is not at all-sufficient. One has to learn from good sources, learn deep that should be devoid of errors, contaminations, and falsehoods.

Karpavai  : Thus you learn all lessons in life meticulously.

Katrapin:  So, after this hard and enlightened learning, what we should do?  He answers next.

Nirka Atharkku Thaga: This means , don’t just stop with learning, follow it with action in a righteous way. Unless we do that he warns to conclude ( in another poem in the same chapter) there is no purpose of learning itself and we are again at risk of becoming illiterates.

So, what does this Thirukural teach the Nobel professionals who follow cutting edge medical research?

I think I need not elaborate . . . Acquiring knowledge and true learning has become two different processes.

It’s just a sample of one kural (Quote) among 1330 poetic quotes written in 133 chapters by this great philosopher of Tamil Nadu who shared the same timeline with Aristotle and Socrates of ancient Greece 5000 miles west of India. For those ,If you are interested in his monumental work on literature which can be referred to as the manual for effective living  (I wish to call it as “Standard operating protocol”  for human life)  please follow the link.

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Posted in bio ethics, medical quotes, Quotes | Tagged bioethics, medical education, principles of practice of medicine, princniples of learning, quotes on education, Thirukuraal |

DAPT blues in ACS : Does Prasugrel really bother to know about the coronary anatomy before it acts ?

October 19, 2020 by dr s venkatesan

It appears,antiplatelet agents are waging a turf war on the CAD battlefield. It is no secret either, the fight often goes beyond academic reasons. Though NSTEMI connotes a true cardiac emergency, it consists of a highly heterogeneous population. A patient with UA can be treated even at home (Low-grade angina with little ECG changes, when it’s due to Increase demand situation). While, in the other extreme of NSTEMI, a patient with a GRACE score >200, in Ischemic  LVF, might need an emergency multivessel angioplasty along with Mitra clip ±  ECMO support. 

Antiplatelet agents along with heparin will remain the cornerstone* in the management of NSTEMI/NSTEACS, irrespective of our fine catheter skills within index lesion. They are administered right from the pre-hospital phase/ In ER, CCU/ or on way to the cath lab(upstream)/or within the cath lab/or after CAG /PCI.  It is the right balance between the prevention of stent-related coronary thrombus vs systemic bleed we are worried about. Definitely, DAPT is warranted. (See the chart below) Prasugrel has been reinvented as the most powerful P2/Y12 blocking antiplatelet agent. It squarely beats its other colleague drugs like Aspirin, Clopidogrel, and Ticagrelor in terms of potency as well as its risk of a bleed. This is the current antiplatelet protocol in NSTEMI in a patient planned for PCI after visualizing the coronary anatomy. Note, Aspirin plus Prasugrel combination occupies the top slot among various options. The principle of DAPT strategy is all about Initial escalation to match the heightened risk of thrombosis/ cardiac events and later de-escalate once the risk period is over (Which can vary between 1 month to 12 months or even 2 years)* The popular concept of attributing NSTEMI to platelet clot and STEMI to fibrin clot is no longer valid. The contribution of the individual component(white vs red)  in a given load of coronary thrombus was never quantified accurately. That’s why antiplatelet agents alone are grossly inadequate in NSTEMI. This will be vouched by this NSTEMI algorithm, which begins with red clot busters heparin. 

So, how to handle sharp-edged drug-like Prasugrel?

A powerful drug-like Prasugrel is at high risk of being misused. It has taught us some harsh lessons in stroke. So, we have to be wiser to extract the maximum out of this drug in the presence of a high thrombotic milieu (or at risk of developing it after a PCI.)

Since ECG and clinical features are not sufficient to predict the coronary thrombus. It is suggested to have a look at coronary anatomy and decide only if a PCI is contemplated.Some of the situations where Prasugrel is likely to be Indicated  

• Any PCI with a stent in the culprit artery.
• High  thrombus load

• Prolonged procedure time

   

  When to Avoid Prasugrel?

  Just looking at coronary anatomy is not sufficient.  Estimating the risk of bleeding is required. Attempting to use various scoring systems during a cardiac emergency is a self-inflicted mathematical burden. In my opinion, none of these scoring systems(CRUSADE , ACUITY,  ARC-HBR) truly discriminate patients in a useful way. Mindfulness with an eye on co-morbid conditions is required.This has to be matched with coronary lesion /PCI complexity. Realistically, the confidence in our technical adequacy of stent deployment shall decide the need for aggressive post PCI  DAPT or anticoagulation

Final message

Just because we know the coronary anatomy, don’t expect prasugrel to be kind enough to lower the risk of stroke. The risk is the same whether we know anatomy or not. It is the funny evidence base we have created that makes us believe it so. Routine DAPT for all patients with ACS is not warranted without assessing the bleeding risk. Meanwhile, there can be an important subset of patients who can really benefit from prasugrel even within coronary care units who are unplanned for PCI. (Which the current guidelines seem to forbid without any valid reason)

Postamble

We know, stents love to befriend thrombus instantly, that demands aggressive antiplatelet/anticoagulants) which beget bleeding. So, should we stent all lesions in a given patient with NSTEMI ? is a very valid question (rarely asked though) needs to be answered by the custodians of patients’ heart. When dealing with a complex PCI case scenario, simple mindfulness with an eye on comorbid conditions and downgrading ourselves to a good general physician mindset is welcome.

Reference

1.The DUBIUS trial downstream vs upstream use of antiplatelet agents in NSTEACS- No difference

https://www.acc.org/latest-in-cardiology/clinical-trials/2020/08/31/21/44/dubius

 

 

 2.

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Posted in acute coronary syndrome, oral anticoagulants warfarin acitrom, prasugrel | Tagged 2b3a vs prasugrel, coronary anatomy in nsteacs dapt mapt, NSTEMI guidelines esc acc 2020, prasugrel vs aspirin vs ticagrelor, reopro vs prasugrel, themis twilight study |

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/)

 

Leadless Dual-Chamber Pacemaker Leadless pacemakers are implanted in the right atrium and the right ventricle. To synchronize, the devices communicate wirelessly with each other. Bereuter et al. JACC:  2018:813 – 2 3

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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Posted in Uncategorized | Tagged av micra tps, ddd vs dddr pacemaker, dual chamber wirless lead less pacemaker, micra nanostim paceaker, naspe cardiac rhythm society |

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