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Atrial DCM : A new entity in the making

November 4, 2023 by dr s venkatesan

A brief learning session with cardiology fellow about a possible new concept in Left heart failure.

What is the commmest cause for acute pulmonary edema?

“Left sided heart failure”

“Can you be more specific , Left sided means ?

“I meant LV failure , typically DCM of any cause or Severe un-controlled HT”

“Ok .good. Does Left Heart failure include mitral valve dysfunction also ?

“Yes sir, very much. Classical mitral stenosis and Isolated MR can cause pulmonary edema. In fact, acute AR Iis also part of left heart disease”

So far, so good, now coming to the complex part of left heart

Can LA fail in isolation independent of LV , ie I mean with normal Left ventricle ?

I am not sure. Can we call new onset atrial fibrillation as a primary atrial failure that can result in pulmonary edema?

Excellent. You are absolutely right. But I am talking about mechanical atrial failure, not electrical. Are you aware that most of the time AF is a well tolerated arrhythmia , it can even be silent in many cases. This is because the pumping function of the atria contributes only 20-25% to LV filling. This can easily be compensated by augmented LV suction force , provided the baseline LV function is normal.

Have you heard about ACM. Atial cardiomyopathy?

“No sir”,

“You will hear more about it soon” (Ref 1) Scientists, especially Echo guys are closing in on this concept. We know, the atria has three functional components, namely conduit, reservoir, and pumping. Curiously, we have realized that the pumping function of LA may not be that critical from indirect observations from some land mark studies . (Rate control vs rhythm control studies in AF are a powerful proof on the atrial pumping function .(AFFIRM/RACE etc ) I don’t know, whether I am right in saying the above statement.

LA volume assessment : A critical parameter with a time trouble !

It is tempting to conclude , only if all the three functional components of atria gets affected , then only primary atrial dysfunction can be diagnosed. The concept is more complex than we realise. In diastole , pulmonary vein, LA , LV all work as single functional unit. Only in systole, we see them as different things.

Atrial DCM

Like LV systolic function, which is coupled with RV in parallel , LA function is closely knitted to LV in series during diastole. The key to suspect or diagnose this entity is to demonstrate dissociation of LVEDP with LA mean pressure & PCWP. This is not an easy job in bedside. Isolated Increase in LA volume without any reason , is one clue. LA ejection fraction is possible marker. (Kanagala P, . Int J Cardiovasc Imaging. 2020)

Final message

We are in the early days of understanding primary atrial mechanical failure, Atrial cardiomyopathy (ACM) or atrial DCM is being proposed as separate entity. It is very likely, some subsets of HFpEF might turn out to be primary atrial disease, depending on the level of investigation we do.

Reference

1.Li M, Ning Y, Tse G, Saguner AM, Wei M, Day JD, Luo G, Li G. Atrial cardiomyopathy: from cell to bedside. ESC Heart Fail. 2022 Dec;9(6):3768-3784. doi: 10.1002/ehf2.14089.

2.Patel, R.B., Lam, C.S.P., Svedlund, S. et al. Disproportionate left atrial myopathy in heart failure with preserved ejection fraction among participants of the PROMIS-HFpEF study. Sci Rep 11, 4885 (2021). https://doi.org/10.1038/s41598-021-84133-9

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Empty myocardial syndrome : A risk marker of mechanical rupture during STEMI

November 1, 2023 by dr s venkatesan

Myocardial development is a complex process that begins in the precardiac mesoderm, and is regulated by number of genes.

Duelen R, Sampaolesi M. Stem Cell Technology in Cardiac Regeneration: A Pluripotent Stem Cell Promise. EBioMedicine. 2017 Feb;16:30-40.

After formation of tubular heart , the initial increase in ventricular mass is achieved by development of trabeculations. Trabecular compaction coincides with genesis of coronary circulation, and results in formation of ventricular chambers.The hallmark of sponge-like myocardium is delayed and poor compactive forces.

Time line of ventricular compaction

A deranged compaction process need not be macroscopic. It can be very localized, regional, or global. The timing and the quantum of compaction is important , that injects the contractile power to the ventricle . It is increasingly observed in echocardiography that a small percentage of the population has more echo-free zones in LV myocardium than others. They could represent potential weak spots, at times of mechanical stress.

A curious case of normal Echo

Would like to share few images from a routine echocardiography in a healthy young female.

The apparent absence of mid myocardial shadow was not entirely a surprise though .At the same time, it raises some curious thoughts as to why certain myocardial areas are not well visualized by the ultrasound.

Look at the IVS, why should mid myocardium is echo free (measured 5mm) and appear de-laminated.
Only endocardium and epicardium are echogenic .

How echo is able to pick up only endocardium and epicardium , making entire myocardium look like an empty shell .

Still, LV is contracting vigorously, implying muscle mass is just not visible to ultrasound eye.

Clinical implication

These echo free dark zones in IVS or LV is so common, one can safely ignore, but its worth recalling few entities, that can be related to this. Intramyocardial hematoma, dissection and ultimately rupture (A case report) when they happen to develop an ACS -STEMI. We know , free wall and IVS rupture and mechanical complication occur signiifcant population of STEMI. Though, we can easily blame it on fate, may be these are the ones , who harbor such silent echo free slits due to defects in compacting genes making the myocardium soft , spongy that gives way wihtout a fight at times of tissue necrosis.

Can non-compaction occur without LV contractile dysfunction ?

Unlikely , is the likely answer from most of us. But , routine TTE might miss subsclinical LV dysfunction . We know , now degree of LV fucntion is directly related to the imaging modal;ity we depende to define it.

Can a consistency or sponginess of a myocardium be detected by echo?“`

As of now, it is not possible. This might become a reality when the science of tactile haptics enters the ultrasound domain.

Final message

“The act of observing changes the observed”

Non compacted LV is casually used term nowadays. The title of this post was made Intentionally provocative to stress a point, that what appears as non- compaction can be observed in normal persons.. However, request the fellows to look little deeper into the myocardial architecture, especially when you witness large echo-free zones.

Mind you, this is different from the well-defined condition of classical non-compaction with excessive deep trabeculations. Don’t know how to name this. This is different. Maybe “Isolated Intra-mural partial non-compaction” is an ideal term.

Counterpoint

When I discussed this with an expert colleague, he said, “No, you’re imagining a non-existing entity.” The ultrasonic interface with myocardium and the interstitial echoes that define the echo texture is so variable.Let us see.time will tell .(See this video and case report )

Postamble

This post is meant to be looked up purely from an academic perspective. Reporting such entities, unless you are absolutely sure, should be avoided, as it ends up increasing the anxiety of our beloved patients.

Reference

1.Sedmera D, McQuinn T. Embryogenesis of the heart muscle. Heart Fail Clin. 2008 Jul;4(3):235-45. doi: 10.1016/j.hfc.2008.02.007. PMID: 18598977; PMCID: PMC2715960.

2.Kirby ML. Cardiac Development. New York: Oxford University Press; 2007. [Google Scholar] [Ref list]

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“Proportionate” vs “Disproportionate” Mitral regurgitation : A new concept in the making

October 25, 2023 by dr s venkatesan

Cardiologists have always struggled to classify, assess, and grade one important valve disease, which is Mitral regurgitation. While valve replacement is the ultimate treatment, the timing of MVR is still a big debate. Apart from valve replacement, valve repair is a strong contender in selected patients. In recent times, cardiologists have made great strides to grab MR patients from cardaic surgeons. MitraClip, a percutaneous edge stitching , is possible with a varying degree of success.

Mitral valve edge-to-edge repair (MEER) is an interventional clone of Alfieri surgery that has shown conflicting results in the MITRA-FR and COAPT studies. The reason for this discrepancy in the MITRA-FR population is that they had larger-sized ventricles, which continued to pose challenges for the clip, which is focused only on the leaflets.

A new subdivision of secondary MR

Now, some of the cardiologists want to classify SMR/FMR into Proportionate vs Disproportionate MR. It may not be a great innovation, but it sub-divides secondary MR for optimal therapy. It simply says if LV dilation is significant, clipping the leaflet alone will not be sufficient; it would rather need an annular restriction either at the time of the index clip procedure or in due course. While Disproportionate MR implies, it is more of a leaflet coaptation defect, dominating over annular contribution.

Who proposed this ? What is the implication?

It is an afterthought, I think, from the makers of annular restriction device makers. MEER is found to be less effective in proportional MR.The Carillon device is a new arrival to tackle secondary MR .It is actually a wire that forcibly tightens the AV annulus inserted through coronary sinus . This modality takes advaantage of the aantomical proximity of coronary sinus to mitral annulus. Coronary sinus encircles and from a virtual wall along significant circumference of mitral annulus.

Unlike mitraclip, the Carillon device is claimed to tackle secondary MR irrespective of whether it is proportional or disproportional. It also has the potential to reduce LV dimensions in the long run. We have another device called IRIS-Millipede (to compete with Carillon).

Front. Cardiovasc. Med., 20 November 2020
Sec. Structural Interventional Cardiology
Volume 7 – 2020 | https://doi.org/10.3389/fcvm.2020.576058

Final message

We are free to have as many classifications in MR (Primary, Secondary, Functional, Atrial MR, & now Proportionate Disproportionate.) It is not the aim to bring up a rivalry between leaflet vs annular intervention. Ultimately, the most powerful component of the mitral valve apparatus, i.e., the LV muscle that matters.

I would request the esteemed researchers in MR ,not to keep EROs, regurgitation fractions, or chamber dimensions as primary markers of success of a device. Having strong clinical outcomes as the endpoint should be made mandatory, i.e., prolonging good quality of life and survival (But, the reality can bite hard. Someone told me, walking 20 meters extra in a 6-minute walk test is enough to get device approval from the authorizing entities.)

Final message

1.Grayburn PA, Sannino A, Packer M. Distinguishing Proportionate and Disproportionate Subtypes in Functional Mitral Regurgitation and Left Ventricular Systolic Dysfunction. JACC Cardiovasc Imaging. 2021 Apr;14(4):726-729. doi: 10.1016/j.jcmg.2020.05.043. Epub 2020 Aug 26. PMID: 32861653.

Postamble : A surgeons perspetive

While we debate about devices, the true benefits may lie elsewhere. A good MVR done by a mitral heart surgeon is the need of the hour. Says this paper from a top heart surgeon in India. Yadava OP. Disseminating valve repairs – a clarion call. Indian J Thorac Cardiovasc Surg. 2020 Jan;36

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Extreme “Knowledge + Skill” is a powerful stress test for our Intelligence

October 22, 2023 by dr s venkatesan

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“Low quality” Interventions in “high quality” cath labs

October 20, 2023 by dr s venkatesan

Recently, I visited a seven-star cardiology center. It had a fascinating lab with a near-360-degree roaming arm and floor (even the roof, I think!). The lab also had provision for optional thoracotomy support by surgeons and a CT scan. What’s more, I was told that an adorable robot will soon be added to the cath lab workforce to assist in delivering and maneuvering catheters. It’s truly amazing to see the advancements in science!

I asked the chief staff nurse how many procedures are being performed per day. She pulled out an Excel chart from a gesture-controlled touch panel. It was clocking about 20 to 25 cases per day. The lab performed the best of all procedures in our country. Great, well done, and congratulations, even as my lips uttered, my mind was thinking the opposite. Do we require such labs when the majority of the population struggle to get even basic medical care in emergencies?

Quantity vs quality of procedures 

The said lab went on to achieve 2000 cases recently. It was crowned with glory in a stunning anniversary bash. We all take pride in numerical accomplishments. Quantity is easily measured. It’s simple mathematics. Assessing quality is a tricky one. Even professionally well-accomplished interventions may be of low quality.

Low quality and low impact may not be synonymous; still, it conveys the same meaning if we look at it from the patient’s perspective. The quality of the procedure shall be assessed with reference to the cost involved, clinical outcome, procedural as well as a perpetual chain of risk, finally, and most importantly the test of time.

Overall, the quality check of a cath lab is not only for the machines, it is also about the operators  &  what they do. 

Postamble

Whover wants join this cath lab award session. Welcome .

“Top 10 low-quality (Impact) cardiac Interventions” 

There were 10 nominees

  1. Distal bifurcation lesion
  2. LAA closure
  3. Delayed PCI in STEMI
  4. Valve in valve 
  5. VSR closure post-STEMI
  6. Septal ablation in HOCM
  7. His bundle pacings & CRTs 
  8. Poorly planned TAVRs
  9. Clumsy Paravalvular leak blockage
  10. Complex EVARS

 * The winner was selected without any difficulty: No 3 : Its delayed PCI beyond 24 hours after STEMI (This accounted for 30 % of all procedures put together)

Meanwhile following competes for “high-quality” intervention 

  1. PTMC
  2. Left the main/ proximal LAD stenting in UA/NSTEACS
  3. Permanent pacemakers in CHB (Not all in SND)
  4. ICD implantation for the truly deserving
  5. RF ablation for AVNRT/ Some VT
  6. Selected cases of Primary PCI
  7. Some life-saving palliation in the newborn(Ductal stenting/IAS septostomy)
  8. Diagnostic coronary angiogram in a strongly suspected ACS.

Choosing the winner was really tough, just leave it to the readers.

Final message

It’s worthwhile to go for such an analysis periodically to improve procedural quality & Impact. It’s wiser to allow our brains to prevail over hands. Global health is all about technology optimization, outcome analysis, comparative efficacy. The future sounds exciting though, with deep machine learning, data mining, skill transfer. However, there seems to be a definite risk. In the name of artificial intelligence, we might contaminate machines as well with humanness.

 Let us restrict funding and stop Insurance coverage for low impact procedures. Instead, may use the resources for a truly life-sustaining & healing process.

Reference & Further reading

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What is the normal Pericardial thickness ?

October 20, 2023 by dr s venkatesan

An unusal conversation with a flamboyant student fellow,

May I know , What is the normal Pericardial thickness, ?

Which pericardium you mean sir ? ,Parietal or visceral?

Would like to know both .

It is variable sheet of tissue .You want the thinnest part or thickest part ?

Don’t beat around the bush .Tell some answer.

You want, autopsy thickness, or real life thickness as surgeon sees it ?

I want it in practical Imaging modality

Do you want Echo, CT or MRI thickness ?

I should say , its too much for a first-year fellow in reverse questioning!

Ok relax sir, shall I tell the systolic or diastolic thickness?

So, you decided to spoil my day.

Ok, one final clarification sir,, you want thickenss over anterior RV aspect or over posterior atria ?

You are getting on my nerves. Thankyou, will you please leave the class .

Yes, pericardial anatomy ,can indeed make us crazy. Let us try to get some answer .

Whenever some one is asking about pericardial thickness, it generally mean the parietal,thicker fibrous outer layer. It’s about 1 to 4 mm*, never more than 3 -4 mm .As we can see, it is a highly variable sheet of folded tissue with different adherent surfaces. The visceral pericardium is very much less than 1 mm, in fact,it need to be measured in microns. It is called the epicardium and adheres seamlessly to the myocardium with intervening fat. (Sub epicardial fat)

Ref: Normal pericardium measures 0.4–1.0 mm thick in autopsy studies but normal pericardium measures 1.2 mm in diastole and 1.7 mm in systole on MRI studies [1].It is sort of surprising finding, to note pericardium also thickens in systole.

Mind you, echo over estimate the thickness, and its crudest form of measurement and should not be relied upon.Even CT over estimates.MRI is currently closer to true thickness.

In constrictive pericarditis, which pericardium compresses the heart?

In effusive constrictive pericarditis, organized fluid makes the two layers stick together and makes it thick, making it difficult to differentiate the two layers in any imaging modality. Hence, the answer is that both layers together compress the heart, but the fibrous layer is primarily responsible and exerts more pressure per inch.

Can epicardium per-se thicken with normal thickness of parietal pericardium?

We are not clear about it. The rarity of constriction in viral myo-pericardiits comparred to tuberculous suggest isolated epiicardial constriction is rare as epicardium is sngle sheet of cell .In wonder inflitrative pericarits might occur arsoing pure feom epeicardium following myo or epimyo caritis. . I dont know , may occur in some myopericardits.We need to ask Dr Renu virmani.

(*Answer to this question might alos explain why rheumtic pericardiits doesnt cause constriction as it doesnt involve fibrous pericardium )

Does sub-epicardial fat make epicardium appear thick ? How to differntiate it ?

This is a tough one to diffferentiate . There have been cases of constrictive physiology due to epicardial fat (Effusive-constrictive pericarditis with massive epicardial fat A Goto, M Lancet September 01, 2001)

One final question: Is it the thickness or the elastance /resistance of the pericardium that determines the likelihood of constriction?

Pericardial histology and elastance are more important. We know, that transient constriction with normal pericardial thickness is a very well recognized entity. (Haley JH,JACC 2004)

Final message

Never under-estimate the importance of pericardial anatomy. It can go as deep as its recesses and the tortuous sinuses. Try reading this wonderful review by Rodriguez.(Ref 1) I guess it might have taken tons of time to write such a great article. Don’t excuse yourself to waste 20 minutes in between your angioplasty times.

Rodriguez2017Download

Reference

1.Bogaert J, Francone M. Cardiovascular magnetic resonance in pericardial diseases. J Cardiovasc Magn Reson. 2009 May 4;11(1):14. doi: 10.1186/1532-429X-11-14. PMID: 19413898; PMCID: PMC2685792.

2.Haley JH, transient constrictive pericarditis: causes and natural history. J Am Coll Cardiol. 2004 Jan 21;43(2):271-5. 147

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How is forward cardiac output affected in MR & TR ?

October 18, 2023 by dr s venkatesan

AV valves exist to divert blood to the outflows when ventricles are contracting. If they leak significantly, obviously there are major consequences. What happens to the net cardiac output when these valves leak?

Clincally , we know ,fatigue is sign of reduced forward cardaic out put , that is more common in MR. But, edema , congestion, muscle fatigue is eqaully if not more common with TR. One importnat diference is MR jet is mainly a hemodynamic trouble in pulmonary circuit while TR jet , has one more component hits on liver function making it metabolic consequnce as well.

Can’t escape, tell us your answer for the question

*I am afraid, anyone has done a specific hemodynamic study on this. It should be clear for everyone, that RV stroke volume, is not only the preload of LV, and it is going to bcome LV stroke volume, a few seconds later. Hence TR equally reduce * (if not more ) the forward cardiac output as does MR. In fact, the compensatory mechanism of LV with its reserve work might maintain the forward output for a longer time. RV reserve functions are less.Fellows must analyze this. It is not a difficult one. Measure LV stroke volume by echo ( LVOT area X Aortic TVI) in patients with TR vs MR pre and post-correction.

Final message

RV & LV are like conjoined twins. One’s function can’t be decoupled from the other. Now we realize, TR plays a more central role in both symptom generation and the overall outcome in cardiac failure. Hence, aggressive interventions are being attempted to plug this leak. (We will come to know whether it is truly beneficial or not only later, as arresting TR puts more burden on RV, as TR has a pressure cooker release/relief effect on RV)

Reference

Unterhuber M, Kresoja KP, Besler C, Rommel KP, Orban M, von Roeder M, Braun D, Stolz L, Massberg S, Trebicka J, Zachäus M, Hausleiter J, Thiele H, Lurz P. Cardiac output states in patients with severe functional tricuspid regurgitation: impact on treatment success and prognosis. Eur J Heart Fail. 2021 Oct;23(10):1784-1794. doi: 10.1002/ejhf.2307. Epub 2021 Jul 28. PMID: 34272792.

Rebecca T Hahn, Luigi P Badano, Philipp E Bartko, Denisa Muraru, Francesco Maisano, Jose L Zamorano, Erwan Donal, Tricuspid regurgitation: recent advances in understanding pathophysiology, severity grading and outcome, European Heart Journal – Cardiovascular Imaging, Volume 23, Issue 7, July 2022, Pages 913–929, https://doi.org/10.1093/ehjci/jeac009

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STREAM -2, bats for “half dose” TNK-Tpa in elderly over pPCI

October 13, 2023 by dr s venkatesan

STREAM trial (New Engl J Med 2013) was a sort of paradigm-creating study, that made Pharamco-Invasive approach – PIA an authentic via-media strategy, trying to accure benefits from both lysis and PCI in the management of STEMI.

However, one question remained. Does PIA work safely in the elderly, where bleeding risks are higher? Do they tolerate the double whammy of P and I ? Both procedures keep the blood clotting process tentative for a prolonged period of time.

Emprical usage of half dose lysis is not new, is existingn, for more than 4 decades, right from streptokinase days.

Now the multi-center STREAM-2 trial , released from Belgium , Published in the current issue of Circulation, asked this specific query on the efficacy of half dose Tenecteplace in PIA.

Both strategies had almost similar outcome with 87 % TIMI flow, implying elderly people , are reciveing twice the dose of lytics without any true benefits, but enhancing other risk.

Final message

The conclusions are not surprising. Our empirical thoughts have now, become acceptable sort of evidence. So , let us go ahead with this renewed PIA strategy and proceed with half dose of Tenecteplase ln elderly ( A liberal cut off of >60 years) without any guilt.

Meanwhile, the STREAM team has one more important job to do. So far, no one has the guts to test “P” vs “PIA” in the current era, in a large scale ( ie proceed with “I” if and only if “P“has failed. After all , if P is successful, that has resulted in good TIMI 3, and normal LV function there is no need for I )

Hope, somebody or institution get that courage and funds to design a STREAM- -3 trial comparing three distinct strategies, ie stand-alone TNK vs PIA, & pPCI and make it a reality. I am sure, it will bring surprise and very likely a pleasant one for all stake holders.

Reference

ExpeVan de Werf F, Ristić AD, Averkov OV, STREAM-2 Investigators. STREAM-2: Half-Dose Tenecteplase or Primary Percutaneous Coronary Intervention in Older Patients With ST-Segment-Elevation Myocardial Infarction: A Randomized, Open-Label Trial. Circulation. 2023 Aug 29;148(9):753-764. doi: 10.1161/CIRCULATIONAHA.123.064521. Epub 2023 Jul 13.

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Chronic stable AF on warfarin: Don’t DOAC them just like that!

October 12, 2023 by dr s venkatesan

Are you still on warfarin? Come on, switch to DOAC./NOAC This seems to be a fashion statement among cardiologists and their patients with chronic AF. (By the way, NOAC has a new name, i.e., DOAC. NOAC stands for non-vitamin K anticoagulants. Now, N is replaced with D, direct-acting oral anticoagulants.)

NOAC does have some advantages. the major one is better patient compliance, and ease of administration as it doesn’t need routine monitoring. (One may wonder how this transforms into a real advantage? ) The drug acts in a dark invisible mode. Bleeding risks are either less, equivocal, or high. So we can’t conclude conclusively on true bleeding risk.

(We do have some cumbersome monitoring methods for NOACS)

(Rahmat NA Monitoring the Effects and Antidotes of the Non-vitamin K Oral Anticoagulants. Arrhythm Electrophysiol Rev. 2015 Aug;4(2):90-5. )

Switching games with DOAC

A detailed review of how and when to switch is in this article Adelakun BMJ open 2023

Switching to DOACs should be based on some solid scientific principles. (Of course, we have it !) But, getting rid of INR monitoring should not be the only reason. Still, the current thought process among us is to consider DOAC whenever possible or (if not make it possible somehow). In this context, this study from Circulation September 2023 (Ref 1)helps to choose which side of the OAC-DOAC debate one should fall, especially in the elderly.

Final message

Dad, are you still using that frail iPhone 11? I feel bad, will get you an iPhone 15 Pro. Its just out in Apple stores. You know, it has dynamic island technology. Wish to gift it to you this Diwali.

Oh, thanks, but I’m fine with the oldy. I can comfortably communicate with whoever I want to.Don’t enforce me, I will stick on with warfarin, my dear son.

Reference

1.Safety of Switching From a Vitamin K Antagonist to a Non-Vitamin K Antagonist Oral Anticoagulant in Frail Older Patients With Atrial Fibrillation: Results of the FRAIL-AF Randomized Controlled Trial. Circulation 2023;Aug 27:[Epub ahead of print].

2.Adelakun AR, Turgeon RD, De Vera MA, McGrail K, Loewen PS. Oral anticoagulant switching in patients with atrial fibrillation: a scoping review. BMJ Open. 2023 Apr 25;13(4):e071907. doi: 10.1136/bmjopen-2023-071907. PMID: 37185198; PMCID: PMC10151984.

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When does a fact become an opinion & vice versa?

October 11, 2023 by dr s venkatesan 

When we realise, even class 1-A indication often blinks at the bed side,while class III -C appear to pour more sense, practicing cardiology becomes "Tough and exhilarating” .

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