Archive for April, 2020


If you think coronary artery ostia are exclusively related to LVOT, and they nowhere come closer to RVOT, we are seriously wrong for some hidden anatomical reasons. Though, Its a well recognised anatomical reality , we had to learn it from EP labs during the ablation of RVOT VT. The left main ostium is at equal (If not more ) at risk as we ablate across RVOT.The reason being the complex twist God conferred on the outflow tracts of heart.

The LVOT goes beneath and posteriorly travels from left to right, while the opposite happens for RVOT. This results in the net anatomical conundrum of RVOT and LVOT sharing common wall at some part.

Here is an excellent article that specifically looked into this issue of the relationship between RVOT and the coronary artery.

(VASEGHI, M., CESARIO, D.A., MAHAJAN, A., WIENER, I., BOYLE, N.G., FISHBEIN, M.C., HOROWITZ, B.N. and SHIVKUMAR, K. (2006), Catheter Ablation of Right Ventricular Outflow Tract Tachycardia: Value of Defining Coronary Anatomy. Journal of Cardiovascular Electrophysiology, 17: 632-637. doi:10.1111/j.1540-8167.2006.00483.x)

The following illustration from this paper reinforces this . The left main is just 4mm away from RVOT.(While, the distance from LVOT to left main ostium is much wider)

Final message

Never underestimate the risk of injuring the left coronary ostia when you manipulate catheters and devices across RVOT. This is especially true with RVOT ablations. There has been so many instances of injuring coronary arteries and precipitating ACS. Working within the right heart tends to give a false sense of safety, as if you are away from systemic coronary circulation. After all, both outflow tracts originate from the same embryological source (bulbus cordis) still, intertwined in adult life, not willing to leave its innate anatomical Intimacy that began and ended between 4 th and 8th week of fetal life.

  1. D. Biermann, J. Schonebeck, M. Rebel et al., “Left coronary artery occlusion after percutaneous pulmonary valve implantation,” The Annals of Thoracic Surgery, vol. 94, pp. e7–e9, 2012.View at: Google Scholar

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Found a wonderful anatomy teaching resource. A succinct yet comprehensive lecture on Aortic valve .A must-read for anyone who deals with valvular Interventions. For the cardiology fellows , I can tell you can’t find anything better than this. Thanks to Prof Gregory M Scalia and the structural heart disease Australia. It starts with this one master diagram of Aorta in the center with all surrounding structures and goes on to ensure we watch this 25-minute lecture nonstop.

At the end of the lecture, you should be able to learn about.

  • The complex fusion points of LVOT with Aorta. Understanding them is critical as we deploy Aortic valve percutaneously.
  • Understand the illusion of Aortic annulus.
  • When it is an advantage to keep the aortic valve supra annularly.
  • The Implication of sharing of myocardial cells into the aortic cusp zone, and Aortic tissue into the myocardium.
  • How closely the conduction tissues located beneath the non-coronary cusp making it vulnerable with calcific spur Injury.
  • How pathology of Aortic root with its central location reaches the surrounding tissue.

These are just a few . . . It is a treasure out there.

Over to Prof Gregory Scalia

Please note ,the talk on Aortic valve begins after a brief conference Introduction.If you are not patient enough begin at 2.45mts.

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The resting coronary blood flow (CBF) is about 5 % of cardiac output. It amounts to 250 ml /min (0.8 ml /mt/gram of myocardium ) It is estimated, blood flow across LAD is 50% . LCX and RCA share 25% each, depending upon the dominance. No need to say , the net return to coronary sinus  should match the CBF at rest or exertion.(Minus a small fraction contributed by  thebesain and vene cardia minimi flow, into the right heart chambers)

Great cardiac vein (GCV) is the venous cousin of LAD. It must receive and empty 125ml of deoxygenated blood every minute into the coronary sinus, if LAD flow is normal. When LAD microcirculation is obstructed as in severe obstruction , GCV will fill and empty  sluggishly. 

Let us move on from physiology to bedside.

Primary PCI & No -reflow in LAD 

We have painfully realized, no-reflow is almost a hemodynamic death sentence to the concerned coronary artery during  primary PCI. For practical purposes, no-reflow is common in left coronary circulation, that too in LAD.  Decades of research and experience haven’t really helped us to either overcome or treat this complication effectively. 

So, it’s worth considering experimental mechanical options.

  1.  The first option is, to forcibly open the closed microvasculature by pushing the debris across arterioles, venous capillaries and subsequently to the coronary sinus. This appears tricky as the high-pressure injection can be hazardous. This can be done either hand or even controlled pressure Injection. (It is believed few centers do this unofficially and found some success. I am not sure)


  2. The second option is again mechanical but uses negative pressure to suck from the far end of microcirculation. We can pull the debris into the coronary venous circuit by using vacuum suction deep inside the main stem of the coronary sinus or even the great cardiac vein, the venous counterpart of LAD. This appears to be more comforting to the coronaries at least theoretically. (Never under-estimate the power of vacuum as a biological Intervention.I recall tender newborns pulled out with massive vacuum pressure without any issues during my O&G days)



We have proposed this idea to scientific committee. It was rejected promptly as expected even prior to applying for ethical clearance. In fact, we were eager to try our hands on this, as a life saving modality in desperate situations. Now, It is an appeal to all those scientificaly  liberal centers to try this concept that can be made legal as a part of an official trial.

Antegrade vs retrograde aspiration

It is wiser to introspect, why most antegrade thrombus aspiration strategies in epicardial coronaries failed in STEMI .Still, what is the possiblity  it might work retrogradely? Let us hope this concept becomes a success and doesn’t add on to the long list of failed attempts to this ubiquitous hemodynamic entity.

Potential risk

Since the mechanism of MVO and no=reflo  is multifactorial, mechanical suction might help only in the clearance of thrombotic debris. Further risk of microvascular endothelial injury is real.

Final message

Many fellows write to me,  asking for some research ideas. Please acknowledge if anyone proceeds with this one (If you really believe no one has thought about this Intervention before)

Reference  for Interventions within Coronary sinus 

  1. EP guys do it , in a regular fashion with CRT.They also specifically enter the Anterior cardiac and great vein during ablation in VTs originating from LV summit .
  2. Coronary sinus aspiration done for contrast removal after angiogram to prevent AKI in renal compromised patients.(Ref Osama Ali Diab Circulation: Cardiovascular Interventions. 2017)
  3. Stem cell delivery has been done through coronary sinus (Wouter A. Gathier J Cardiovasc Transl Res. 2018)
  4. Coronary  sinus retrograde perfusion  has been tried for refractory angina (David P. Faxon Circ Cardiovasc Interv. 2015)



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The Medtronic leadless Micra TPS pacemaker

In 2016, EP world saw a major breakthrough when Medtronic introduced leadless Micra TPS pacemaker. This device that looked like a small bullet, was implanted in the RV apex without the need for lead insertion and surgical pocket. It was real innovation but was not able to take off even after 4 years of marketing. The reason was simple. Though it was a smart device, it was a journey backward in time, as Micra TPS provided only non-physiological VVI pacing. (In the current era of multi-site and His bundle pacing)

Physiological pacing requires two are more leads.(Except single lead VDD, now obsolete AAI ) . Atria must be sensed for AV synchrony to happen. Atrial sensing is accomplished by

  1. A dedicated atrial lead as in AAI or DDD
  2. A floating atrial lead as in VDD mode

How does the leadless pacemaker attached to RV apex bring in AV synchrony without any add on leads ?

Medtronic, has come out with new add on to TPS ie “Micra AV” .The same gadget has been upgraded with a software to do atrial sensing. The accelerometer in the pacemaker senses the motion of the blood in early diastole followed by atrial contraction mediated S4 . This is sensed, and ventricular lead is set to fire after a programmed Interval.

Medtronic micr AV pacing 2

The initial experience appears promising. The results of the MARVEL study is published (Ref 1) However, there are important limitations. The atrial sensing function is not fully tested in real-life exertion. Further, It’s actually a form of mechanical sensing. The atrial electromechanical association has been taken for granted. The absence of electrical atrial sensing can mislead the ventricle. Currently, I guess it is a software patch that converts Micra TPS to AV . One more issue is, the soft ware consumes more energy and cut shorts the life of the pacemaker.


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The Country of mine with 140 crore population, is under complete lockdown mode. We are anxiously tense in one aspect, but enjoying the free time due to the peculiar “Corona effect” on cardiac emergencies.

Unable to understand you . . . please go away

What happened to our 24/7 busy CCU ? Does it happen only in my hospital? Can’t be. Let me check it right now. I called my fellow, who has since become a leading cardiologist in the nearby town.


I have since called many of my close contacts. In both Government and private hospitals. The pooled data were analyzed in a virtual cloud memory. I am fairly convinced, our observation was indeed true.

The following can be considered as near facts.

  • There have been at least 50% minimum dip of Overall ACS cases. It even went down to 80%reduction in a few places
  • Even UA/NSTEMI showed a significant drop.
  • There was general hesitancy to do primary PCI even if it’s technically Indicated.
  • All most all STEMI were lysed. Heparin was liberally used.
  • Many patients preferred telephonic consultations.ECGs were reported over mobile platforms
  • None of the back pains & gastric pains were admitted as atypical chest pain.
  • Most cardiologists closed down their regular OPD
  • For the first time, Govt institutions were considered worthy to refer.

Why ACS Incidence nose dived?

  1. Under recognition?
  2. Under-reported ?
  3. Low Incidence?
  4. Low rate of referral?

STEMI that goes under-recognized and unreported? The consensus was, it’s less important factor as currently, very few are unaware of the Importance of chest pain and widespread availability of emergency services 108/911

Does that mean real incidence has Indeed come down?

The global atherosclerotic burden,(the substrate for STEMI) in the society is nearly constant. Still, the incidence of ACS has declined dramatically in the lockdown period. This conveys an important message and compels a search (research)

The plaques that are waiting to rupture in the population somehow getting a reprieve. Mind you, the presence of a risky plaque in LAD alone won’t cause a STEMI. It needs a trigger. The day to day physical stress, spikes of catecholamine, emotional swings, traffic pollution etc. The only plausible explanation appears to be the vulnerable patients along with their plaques are also locked up inside its Intimo-medial home. (Armchairs and bed rests can not only treat STEMI , they can prevent it too !)

Why the incidence of NSTEMI /UA has also come down?

Again, the same factors might operate. But, more likely self-stabilizing pseudo / Low-risk ACS is a distinct possibility.

A significant chunk of UA /?CSA/suspected NSTEMI patients come from referrals by GPs.The biggest pool of cases for cath labs comes from this group of noncardiac/Atypical chest pain syndromes*. Which shows some Incidental (In)significant lesions that subsequently becomes a cardiac emergency.

Since they have reduced their consultations the numbers have quite significantly reduced.

*Chronic CAD masquerading as ACS is not a forbidden concept

Final message

We are taught some important lifetime lessons in cardiac practice by this 20 nm, lifeless RNA particles.

1. The bulk of the ACS in the society is triggered by the day to day stress of the fast and furious “Just do it” world. The mitigating effect of social lockdown on physical and emotional stress on plaque dynamics on the incidence of ACS will be a big research subject in the coming months.

2. More importantly, It has exposed the existence of one more hidden epidemic in the community “manufactured coronary emergencies” propagated by a resistant cardio tropic virus that has disseminated deep into evidence-based cardiology. Let us cleanse this virus too after finishing off the Corona.


It’s just a crazy opinion from a scribbling, blogger. However, I am sure, It’s only a matter of time, great journals like NEJM, JAMA, and Lancet will be screaming the same truths in a more palatable evidence-based manner.

Meanwhile, I can see early signs of restlessness(withdrawal) among us waiting for early release from the lock-up and resume the customary mode of evidence-based cardiology practice.

As I complete this write up . . . .surprised to find this report from TCT MD. Similarities if found, could only be coincidental.

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