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Archive for April, 2024

Atrial dilatation in Atrial fibrillation : A query with multiple twists!

Posted in Uncategorized, tagged , , , , , , , , , , , on April 28, 2024|

(This is supposed to be a poll. Sorry, readers, you can’t select the answer. WordPress is not kind enough and suddenly made the poll service payable extra. I am already paying nearly a $100 fee to maintain this site. I can’t afford any more.)

We have been taught Bi-Atrial enlargement is the rule in AF .It is still true in most situations. But, we rarely dispute it , & ask which atrium dilates more in AF ?

Let us see few factors.

  • Both atria develop from a combination of the primitive atrium, sinus venous, and pulmonary veins.It is logical to presume there must be a hidden morpho-electrical continuity.
  • The baseline RA dimension is a few mm more than LA. Further, it is thin-walled, more compliant and can distend depending on volemic status.
  • When atrial fibrillation (AF) begins, it can start with a single focus, degenerating to multiple wavelets, and it spreads throughout the entire surface area of both atria. A fibrillatory wave that occurs at a rate of more than 600 beats per minute can cause fatigue in the long run, leading to atrial dilation.
  • In all probability, this dilation is a form of atrial tachycardia and atrial cardiomyopathy. However, underlying lesions such as hypertension, mitral valve disease, COPD, ASD, and TR greatly influence the degree of atrial enlargement.
Spatial relationship of sites for atrial fibrillation drivers and atrial tachycardia in patients with both arrhythmias July 2017 International Journal of Cardiology 248(3)
  • AF begets AF. This is similar to MR begets MR. Atrial functional MR occurs when the lower part of the atria stretches the mitral annulus. It is important to recall that a small area of the posterior aspect of the LA is a part of the mitral valve apparatus. Therefore, AF begetting MR and MR begetting AF should not be considered a funny rhyme, but rather a realistic possibility.
  • Histopathological specimens of atrial tissue in chronic AF can present with surprising results. The atrial muscle can be entirely normal, or the interstitium can be infiltrated with lipids, fibroblasts, amyloid, etc.
  • Regarding the issue at hand, it is widely known that in cases of mitral stenosis with AF, the left atrium (LA) is larger than the right atrium (RA) due to the obvious reason that the baseline LA was larger at the onset of AF. However, in cases of lone AF, AF in hypertension, or chronic AF, both atria tend to dilate equally..

Implications for electrophysiologists.

In contrast to other tachycardias, with atrial fibrillation (AF), the focus is often speculative, and ablation attempts are made accordingly. Pulmonary veins have been the primary target for ablation for many years, yet the success rates remain inconsistent. To determine if the AF focus is non-pulmonary venous, such as right atrial, septal, or involving the inferior vena cava (IVC) or superior vena cava (SVC), several techniques are employed to provoke and localize these non-pulmonary vein triggers

Localized atrial fibrosis and interatrial blocks can result in differential fibrillatory counts across the atria. (RA fib-rate can be more than LA, and vice versa.) Is there proof for this, or just an academic gossip? We know atrial flutters can be confined to one atrium. (Pierre Jaïs Circulation 2000) When such flutters transform into fibrillation, how does the spillover of signals occur to the contralateral atrium? On a personal note, we have recorded good E & A Doppler signals across the tricuspid valve, in RHD mitral stenosis, and AF. No published proof as such. I strongly suspect the right atrium can resist the tsunami of approaching fibrillatory waves from engulfing its chamber in at least some patients. An appeal to the new generation EPs who have special flair in AF should look into this and either prove or disprove it.

Final message

My answer to the question is either D or E. Atrial size in AF is not a trivial thing to ignore. This question pushes a simple idea. In primary or lone AF, just by having a look at the RA to LA size ratio, one might get a reasonable guess,about the Initial focus, trigger & pathology of the AF.

A request to all the high profile stake holders involved in the science of PV ablation (either with Ice or fire). Think about all the possible right-sided or septal focuses, before going overzealously for the jugulars of Pulmonary veins, especially if the RA significantly larger than LA . This will save time, effort & of course our reputation.

References

Nil

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Over-diagnosing MI is not* as negligent as missing it !

Posted in Uncategorized, tagged , , , , , , , , , on April 25, 2024|

As the medical literature expands exponentially, the quality and intent of the research questions sound awry. There are only a handful of journals like JAMA that are bold enough to ask some tough and pragmatic questions in this glitzy world of medical extravaganza.

The current issue wants to set the pace for an important debate, on a topic that is rarely discussed.

The question is

Link to the article

Check whether your answers concur with this crucial query from Harvard Medical School and Massachusetts General Hospital. Three questions this article wishes to address.

1.What is the reason it is happening?

2. What are the implications?

3. What can be done for it?

My thoughts

“It is indeed over diagnosed. Once labeled, a chain reaction is set in. The cost, and resource consumption that follow a misdiagnosis are nearly identical to that of a true MI. More than that, the adversities of the tense investigative protocol can convert a misdiagnosis into a real one because that sadly includes even an overzealous poking right at the mouth of the coronary artery just o exclude a non existing MI . and ICU-related anxiety stand apart in this scientific comical game of ruling out a cardiac emergency.

The paper seems to blame mostly on the powerful screening test high sensitivity Troponin, Everyone will agree it has a major role in this. But, the more important reason is the cardiology community’s vigorous adoption of a universal definition of MI criteria (which is never intended to apply at the bedside) .Next factor is probably more important. The fear of missing a potential MI and legal consequences thereafter. I wish, the experts who sit on medical juries need to learn few extra lessons in the art of medical uncertainties.

Medical jurists, need to take some Intellectual cues from their criminal courts. How is it that, even well-planned criminal murders are successfully allowed to be argued and won in courts,…while inadvertent events such as missing an inconsequential MI by doctors are rarely pardoned?

How to avoid over diagnosis of MI ?

In this scenario, It is sad, that only very few cardiologists have the guts to ignore this omnipotent molecular sub-fraction of cardiac muscle Troponin, with their clinical skills. What we can do, at our level is to incorporate a new term “benign or micro myocardial Infarction” – akin to lacunar infarcts or TIA equivalents of the brain in the heart. We need to de-list the vast majority of chronic ischemic,non-ischemic, or systemic causes of Troponin leaks from the myocardial infarction chart. Physicians must realize, that protocol violation should not be deemed a crime always, rather it has a sure potential to benefit your patient if it is done properly and intelligently.

Final message

Recently one cardiologist in a sub-urban center was thrashed both physically and in social media ,for missing an ACS , which was subsequently recognised and treated well and good.

“Doctors should be legally allowed,* (rather forgiven) to make permissible levels of errors in the medical decision-making process ” like any other profession .However, we must ensure our constant pursuit towards zero error, which may not be possible always. This should include overlooking apparently positive lab results if they have reasonably applied their clinical acumen. *Until this happens, the unquantifiable suffering of our patients* due to over-diagnosis and inappropriate interventions can not be reigned in.

*Maybe, this sounds more controversial statement in my 15 years of writing. Beloved patients shall note, it is a rare for me to make what probably, look like an anti-patient statement. Till now, I have been blamed my many of our colleagues, as self slandering my own profession for too many errors in many of the posts. Nothing can be done for this. When you search for truths , you need to tolerate all these.

Reference

1.McCarthy CP, Wasfy JH, Januzzi JL. Is Myocardial Infarction Overdiagnosed? JAMA. Published online April 24, 2024. doi:10.1001/jama.2024.5235

2.Shah  ASV, Sandoval  Y, Noaman  A,  et al.  Patient selection for high sensitivity cardiac troponin testing and diagnosis of myocardial infarction: prospective cohort study.   BMJ. 2017;359:

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A Pacemaker quiz and a new concept.

Posted in Uncategorized, tagged , , , , , , , on April 22, 2024|

This image comes with courtesy of the Journal of SCAI Jai Parekh, Vikram Sharma, Jared Robl,et al Journal of the Society for Cardiovascular Angiography & Interventions 3 (2024) 101310

What is your diagnosis ?

I thought, it was pacemaker extrusion. It was indeed a close answer, still terribly wrong. It is an intentional exterior placement of a permanent pacemaker generator mimicking an extrusion due to pocket infection. Here is a patient, where a permanent pacemaker was kept temporarily for a few weeks or a month in high-risk reversible complete heart block situations. This typically occurs after an inferior posterior myocardial infarction, drug-induced CHB.

Currently, with the arrrival of TAVR, CHB has beceome a glamorous complication and is getting wider attention. This happens due to the anatomical uncertainties where the inferior landing zone of TAVI is pre-destained and is beyond our control. This is more true in the self expanding Core valve platform . When the lower edge treaspass the non-coronary cusp- membranous septal junction, it hits perfectly the compact post-penetrating bundle of His, confering a high risk of CHB.

Still, the good thing is some of them recover as the pressure edema regress .Putting a PPM in all such patients was considered mandatory or even a vanity in the past. Now we realise it is an additional metallic luggage in an already strained heart, Temporary-PPM the oxymoronic innovation is perfect option in this setting.

Final message

A typical external temporary pacemaker can be kept for up to 2 weeks maximum. (We have kept it for a month or so) It’s done via the jugular, subclavian, or even femoral. If the underlying condition demands more time for recovery of CHB, many do a regular permanent pacemaker.

Now , we have this unique option of using PPM as TPM. This is not a new concept though. It was used few decades ago .Has come back in more centers .Thanks to TAVI and its specific complications.

Reference

1.Rodés-Cabau J. Ellenbogen K.A. Krahn A.D. et al. Management of conduction disturbances associated with transcatheter aortic valve replacement: JACC Scientific Expert Panel. J Am Coll Cardiol. 2019; 74: 1086-1106.

2. Leong D, Sovari AA, Ehdaie A, Chakravarty T, Liu Q, Jilaihawi H, Makkar R, Wang X, Cingolani E, Shehata M. Permanent-temporary pacemakers in the management of patients with conduction abnormalities after transcatheter aortic valve replacement. J Interv Card Electrophysiol. 2018 Jun;52(1):111-116. doi: 10.1007/s10840-018-0345-z. Epub 2018 Mar 12. PMID: 29532275.

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Forbidden quotes in medicine

Posted in Uncategorized, tagged , , , , , , , , , , , , on April 22, 2024|

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Corvia atrial shunt system: Mean LA pressure reduction device in HFpEF

Posted in Uncategorized, tagged , , , , , on April 18, 2024|

Lowering the raised LA mean pressure is a major therapeutic goal in any severely symptomatic left heart disease, whether it is valvular or myocardial disease. It is prudent to understand, that even in systolic LV failure; it is the raised LVEDP that causes the symptoms and marks the limits of exercise capacity. Drugs like inotropes, pre-load , afterload modulators like diuretics and vasodilators can take care to a certain extent.

When symptoms are refractory and the underlying condition has no primary correction , we need to intervene with some extreme procedures. We know a small ASD decompresses mitral stenosis, and the combination of ASD and MS, Lutembacher, is a well-known syndrome called Lutembacher. The concept of LA flow regulator or decompressor came from this .

When the left ventricle is stiffened and restrictive, and LA mean pressure is prohibitively high,we have a viable option now. This is to create a small regulatory orifice in the IAS ( A complicated term for a small ASD) to decompress the LA and reduce pulmonary congestive symptoms. Curious minds might ask, can’t we decompress LV it self by creating a small VSD. Probably in the thin membranous area. May be, it will come soon in the innovative lanes of cardiology.

As of now, we have an important human study REDUCE LAP-HF II , from Chicago with a 2-year follow-up up .The device used here was Corvia atrial shunt system.

The study finds the device can be beneficial without compromising much on RV side function.

Animation Courtesy: Corvia website; The procedure looks simple when compared with other procedures inside the LA .The device looks like an octopus, and sits on either side of IAS, like a stapler and maintains the orifice.

Here is an audio podcast from the primary author published in JAMA network.

Interview with Sanjiv J. Shah, author of Atrial Shunt Device Effects on Cardiac Structure and Function in Heart Failure With Preserved Ejection Fraction: The REDUCE LAP-HF II Randomized Clinical Trial. Hosted by James E. Udelson,

Final message

This device’s core concept lies in requesting the right ventricle to help its bigger brother LV at its difficult times. You can call this an artificially created interventricular dependence. Though it might help, we need to watch the right heart’s dynamics closely. Maybe, if RV is experiencing difficulty, we can have external control over the IAS orifice and flow as and when required. (This is not new, a remote-controlled switch regulation was done for pulmonary banding in children with congenital heart disease who needed regulation of pulmonary flow by a device FloWatch-R-PAB  (Ref 2)

It is logical to expect the same device would be useful to decompress RA at high pressures as in severe primary pulmonary hypertension. If you think backwards, it looks the same as a life-saving, reverse Rashkind procedure variant in adult

Reference

1.Patel RB, Silvestry FE, Komtebedde J, et al. Atrial Shunt Device Effects on Cardiac Structure and Function in Heart Failure With Preserved Ejection Fraction: The REDUCE LAP-HF II Randomized Clinical Trial. JAMA Cardiol. 

2.Antonio F Corno, et al JTVS 2003 Remote controlled pulmonary artery banding

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Does the “Non -IRA” lesion status confuse you often ?..Try a blind primary PCI !

Posted in Uncategorized on April 13, 2024|

Primary PCI of IRA , continues to be a clinically popular & statistically validated  (In spite of some critical ifs & buts) coronary reperfusion strategy.

What to do, if  we happen to detect, a significant or borderline lesion in the Non- IRA territory during pPCI ?

There are too many guidelines scattered across cardiology literature to “help or confuse” us on this issue. They argue for either immediate intervention or defer transiently, postpone or just ignore , based on clinical ,hemodynamic*, Individual, institutional , or some other non academic factors. (Permanently deferred PCI is other wise called medical management, is practiced by some inferior cardiologists or GPs who never refer such patients to higher centers after a stand alone thrombolysis)

* The FFR, iFR RFR, related stuff

What if if we are completely blinded to the status of Non IRA vessel ?

What do you mean ?

I mean , can we be, “not- aware” of contra-lateral lesion status ?

Yes, “Simply don’t do a non IRA angiogram , that’s it. If its RCA PCI , don’t shoot Left main, and vice versa for LAD. Do a PCI without doing a completed CAG. I mean IRA PCI alone, by guessing it by ECG .

What a crazy Idea ?

This week’s JAMA has something* relatable to this idea. The aim was to do PCI before complete CAG , to document any advantage. (It is important to note, CAG was done in all patients)

Click to access levi_2024_oi_240163_1711065732.05999.pdf

Did this study really happen ? Seem to have many ethical issues . That too, published in JAMA net work. Yes, it was done, I guess , with a legal protection . Apparently, It was done without an informed consent even.

Was there any advantage of proceeding directly to IRA PCI ?

Yes. Reperfusion times were significantly shorter as expected.

Any other advantage ?

I think there are definitely few more, that can’t be reported by many of us, for either unscientific or ethical reasons.

Any disadvantage?

Proceeding to do PCI without knowing contralateral coronary status is unprofessional act and potential to end up in low quality reperfusion.

Final message

Incidentally, this study raises lots of interesting possibilities. Why should we know , the status of non IRA at all, if IRA is opened and flowing well ?( Missing a critical lesion in non IRA is a crime , is it not ?) I agree. but, don’t use big words. Wish some one does a study with totally blinded about non IRA status, however unethical and unscientific it may be. After all, globally 90% of all successful myocardial reperfusion is done by the humble streptokinase or the more glamorous TNK -TPA . Both these agents never bother to know, which coronary arterial thrombosis its going to work .

As a learnt cardiologist, we must realize most of the STEMIs can be managed successfully* without even knowing which is the IRA, forget about the non-IRA. Tackling non IRA lesion is never considered as an emergency procedure , in fact it carries a fair chance of precipitating one.

*Post-amble

Beware, the conclusions of this study, and the core suggestion in this post may-not be related , if any one finds , it is at their own cost of “whims or wisdom“

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Ballooning an obstructed prosthetic Aortic valve : Can be a real tense procedure!

Posted in Mitral prosthetic valve-Surgical tips and techniques, prosthetic valve dysfunction, prosthetic valves, prosthetic valves -Technical issues, Uncategorized, tagged , , , , , , on April 10, 2024|

A 76-year-old woman with a history of double valve replacement (Aortic and mitral valves) for rheumatic heart disease, presented with acute dyspnea after a switch from Warfarin to LMWH before a planned bone marrow biopsy.

The investigations revealed a stuck aortic prosthetic valve ,that showed a prohibitive gradient of more than 50 mmhg. Since, she refused further surgery, a rare and risky effort was made to balloon dilate the prosthetic valve leaflet, though it is not a standard approved modality. It was decided to dilate the supero-lateral orifice and the central orifices by simultaneous kissing balloon. The results were dramatic.

The images and video are reproduced with courtesy of Dr. David Smith, Dr. Ayush Khurana, Department of Cardiology & Cardiac Surgery, Morriston Cardiac Centre, Swansea Bay University Health Board, Swansea, United Kingdom

The stuck valve

Twin balloon dilatation of bi-leaflet valve in between the superior and central orifice

There are few important lessons from this rare case report.

  1. The innovative double balloon catheter Inflation across the the mechanical prosthetic valve is possible. This technique is likely to emerge more useful in the post TAVI population as well.(JSCCAI 2023)
  2. Some times, a simple maneuvers like tapping , pushing or releasing stuck leaflet will solve the issue in few lucky patients. The reason is a clot less than 2mm can strategically sit on the hinge point and interfere with its motion. Dislodging a 2mm clot in all likely hood cause a benign TIA , or just vanish in the aortic stream down the hill,
  3. However , the risk of thromboembolism is genuine in those a clear thrombus is visualised. Hence distal protection by an Aortic sentinel device or its equivalent (FilterWire EZ, Tri-guard) is a must. If Aortic protection device is not available, proceeding with patient & family consent is not forbidden if circumstances demand.(In India ,we do PTMC with mini LA clots without any protection) A video on Sentinel aortic filter

4.It is to be noted if the obstruction is due to pannus , risk of thrombosis is almost nil and safety of prosthetic balloon valvuloplasty is almost ensured.(Of course with risk of device leaflet damage )

5.As on today, differentiating pannus from thrombus remains continues to be a learnt clinical guess game. CT and MRI can give more crucial inputs. To make things more difficult , a raw area over pannus could be the nidus for the thrombus.

6.Probably , the major learning point (rather a sort of mistake) is the decision to switch over to LMWH in lieu of OAC. Time and again we have seen LMWH is a weak anticoagulant, with erratic correlation of Anti X-a activity and efficacy.

7.I believe, in the above case. this complication might not have occurred if she had continued on OAC , if that was not possible , a switch to regular un-fractioned Heparin as a bridge during the surgery could have been the right choice. Generally, overestimation risk of bleeding viz a viz with life threatening thrombosis is quiet common especially in patients with prosthetic valve.

Current approach for prosthetic valve obstruction

A comprehensive review and surprise inclusion of leaflet release as an option.(Ref3)

Reference

1.David Smith, Ayush Khurana, Aprim Youhana, Adrian Ionescu, Kissing Balloon “Valvuloplasty” of Obstructed Mechanical Aortic Valve: When You Are Running Out of Options, JACC: Case Reports,Volume 4, Issue 13, 2022, Pages 799-801,

2.Kandzari DE, Carlson H, Gott JP, Kaul P, Brown WM. Balloon “Valvuloplasty” for Mechanical Valve Dysfunction. JACC Cardiovasc Interv. 2017 Mar 13;10(5):e47-e49. doi: 10.1016/j.jcin.2016.12.025. Epub 2017 Feb 15. PMID: 28216222.

3. A review on management of mechanical prosthetic valve

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