Dr.S.Venkatesan MD

Archive for the ‘Uncategorized’ Category

Why Oval shaped ASD device are not popular ?

Posted in Uncategorized, tagged amplatzer asd device, asd device, ASD device closure, asd device erosion, asd ostium secundum size, ivc rim vs aortic rim, oval asd, oval vs circular defects, ovoid asd device, size vs shape of asd on November 21, 2023|

ASDs are classically oval, but devices are typically circular.(Exact Incidence of ovoid ASD is not known. but it easily exceed 50 % .(Recall, the embryologically ill-fated hole expands around the fossa ovalis not circularis )

Do we have Oval devices ?

I think, we don’t have one . Please check from this list , a good document on ASD device implantation from Poland

Source : Grygier M, S. Percutaneous closure of atrial septal defect: a consensus document of the joint group of experts from the Association of Cardiovascular Interventions and the Grown-Up Congenital Heart Disease Section of the Polish Cardiac Society. Kardiol Pol. 2020 Oct 23;78(10):1066-1083.

Why do we accept this shape mismatch ? What are the potential issues because of that ?

When closing non-circular ASD, the size of device should be considered according to the multiple diameters of the defect. One diameter of the circular device could be too large for the shortest diameter causing a deformity in residual rims. The cardiac erosion after successful implantation as one of the most important complications due to a larger device in the oval defect compared to the circular defect (This text was taken from (Ref 1)

Why the idea ovoid device was never popular ?

Technical issues in sizing the exact oval defects ,device company’s lack of interest. However, designer devices with perfect fit with the help of 3D printing is very much possible.

Is it true ,an Oval device might hold good even in the setting of deficient IVC or posterior rim ?

May be. Some truth in it. I am not an expert to comment.

Do we really require a perfect fit devices ?

When I discussed with an expert , he said there is no need for oval device . A large circular device 2mm larger than the long axis diameter of the oval orifice is not an issue at all . Some how, find it difficult to accept that. What about you readers ? Please respond if you have any comments.

Any study on this issue ?

Yes. one study specifically looked into this. It compared the effect of circular device on oval defects. It concluded there no difference in any adverse outcome , but oversizing is unavoidable with oval defect.. This study , though addressed a vital query ,is never meant to find the truth we want, as it has no oval vs circular device to compare the outcome.

Final message

It is strange ,cardiologists look for perfection and precision in every cardiac intervention, … while in case of ASD device closure, size is sacrosanct, but shapes, we are allowed to shrug off. May be things will change.

Reference

1.Song J, Lee SY, Baek JS, Shim WS, Choi EY. Outcome of transcatheter closure of oval shaped atrial septal defect with amplatzer septal occluder. Yonsei Med J. 2013 Sep;54(5):1104-9.

2.Roberson DA, Cui W, Patel D, Tsang W, Sugeng L, Weinert L, et al. Three-dimensional transesophageal echocardiography of atrial septal defect: a qualitative and quantitative anatomic study. J Am Soc Echocardiogr. 2011;24:600–610. [PubMed] [Google Scholar] 

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Essential hematology for cardiologist

Posted in Uncategorized, tagged 4 factor prothrombin complex concentrate, 4F-PCC, : dilute thrombin time, andexanet alfa, anticoagulants, bleeding risk, Chromogenic anti-Xa assay, dabigatron, dapt, doacs, dTT: dilute thrombin time; ECA: ecarin chromogenic assay; 4F-PCC, hasbled, heparin, inr, lmwh, noac, protamine, prothrombin time, vitamin k antagonists on November 15, 2023| 1 Comment »

Forget NEJM, Circulation, JACC, for some time. Hope & wish every one of us is aware of a journal called Blood, bringing stunning and dramatic discoveries week after week ,about the most crucial fluid that sustains our life. The journal Blood is published by the American Society of Hematology since 1949. Its impact factor is currently 20.8, celebrating its 75th year of existence .

We know, heart disease consistently tops the global mortality and morbidity charts . Without blood, heart is just a purposeless organ with four empty chambers. More than ninety percent of the cardiac mortality happens due to freezing and interruption of blood flow to the vital organs. Can any one dispute, heart is an Innocent bystander, when ACS happens due to an unscheduled pitched battle between blood and the coronary arterial wall ?

It is no surprise ,cardiologists spend most of their practicing time, fighting blood from freezing and trying to restore the flow. It is hard to believe there is absolutely little interaction between Hematologists and cardiologists dealing with the same organ.

Meanwhile, the drugs we use , pose a constant threat of bleeding elsewhere.As a clinician and cardiologist, anxious queries from our fellows such as this one are not infrequent. Sir, that lady with a prosthetic valve in room 306, is bleeding in gums . Should I stop the OAC ? She is also getting clopidogrel for the recent PCI. What shall we do?

Want answers to such questions ? Need to spend time guys. In an excellent review article, the prestigious journal talks about tackling bleeding patients and how to counter various drugs that can cause bleeding.

Reversal strategies in a bleeding patient

This table is just a sample from the paper. Thankfully full text is free in its site.

BLood820746Download

Final message

It seems , there are about 30,000 medical journals listed in Pubmed . Cross-specialty reading for relevant, up-to-date knowledge is always welcome. This will help us come out of the undesirable tag of super specialist or individual organ specialist.

Looking forward to the days when hematologists and cardiologists sit together frequently to discuss the strategies in unexplained ACSs, DVTs, other procoagulant (as well as pro-bleeding conditions)

With more and more metallic foreign bodies ,making heart as their residence, this type of Interactions will become all the more important.

Reference

Piran S, Schulman S. Treatment of bleeding complications in patients on anticoagulant therapy. Blood. 2019 Jan 31;133(5):425-435. doi: 10.1182/blood-2018-06-820746.

Next thought

Trying to go deep into this journal, and find the truth behind Red and white clot , which I never understood right from the medical school days.

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Tampering Hippocratic oath,.. is not a blasphemy !

Posted in Uncategorized on November 13, 2023|

It is still a huge mystery, why the father of medicine stressed more about “not doing bad” than “doing good” .What made him to hold on to, such pessimistic thoughts , 2500 years ago . I am unable to think how he would react to this “tampered version” if he is alive ! My gut feeling is, he will find it hard to object .

Further reading (There is some debate , about the origin of this quote attributable to Hippocrates)

1.Origin and Uses of Primum Non Nocere—Above All, Do No Harm! by Cedric M. Smith

2.Relevance of the Hippocratic Oath in the 21st Century

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Rosuvastatin or Atorvastatin , Which is good and safe ?

Posted in Uncategorized, tagged acc, aha, atorvastatin vs rosuvastatin, avert study, bmj, esc, jamanetwork, lancet, lipid association, lodestar study, lodestar trial bmj, nejm, saturn trial, simvastatin, statins, which statin superior on November 10, 2023|

Statins belong to a group of drugs, stolen and reengineered from the blueprint of natural Chinese red yeast rice (Monocoline K) in the late 1980s. The rest is the remarkable history in the pharma industry.

Statins directly interrupt the cholesterol synthesis by blocking HMG-CoA within the hepatocytes. It significantly lowers the LDL, fights human vascular atherosclerosis. It makes the plaque either regress, prevent progress, make it harder and in the process make them less vulnerable . There are innumerable studies that document the evidence. Statin has become a must-prescribe drug in any one with clinically established CAD or even in concealed CAD. Guidelines are available to prescribe statins various intensity, depending on the risk profile.

Which statin ?

There has been a long list of statins. Many of them have retired from the ring .Currently, the fight is between Atorvastatin, a Rosuvastatin. Like Pepsi vs. Coke.

Note the graphic ,A meteoric rise of one drug since 2005 . (Can you guess the reason ?)

ATRORVA or ROSUVA Which one should I choose ?

There is very little “one to one” comparison study between Rosuvastatin and Atorvastatin .The gap in the pros and cons are narrow. Following points are observed, without much dispute.

1.Rosuvaststin is more powerful.

2.Plaque stabilisation effect is not different((Satrun, study NEJM 2011 based on IVUS)

3.New onset diabetic risk is more likely with Rosuvastatin

4.Worsening of cataract is also more with Rosuvastatin

5.Atrovastatin has some additional benefits in lowering triglycerides. (Bakker-Arkema RG, JAMA. 1996)

No one is dare enough to give strong verdict . Surprised to find one this month. BMJ has come out with a possible answer. It is called LODESTAR trial (Ref 1)

Mechanism of new onset diabetes with statins (REF 3)

It can be 7% with Rosuvastatin (less with Atorvastatin). We think, statins act primarily within the hepatocytes where cholesterol synthesis takes place, but they also have an eye on the pancreatic β-cells as well. It down-regulates GLUT-4 in adipocytes, and results in compromised insulin signalling. Furthermore, statins’ impact on epigenetics may also contribute to statin-induced T2DM via differential expression of microRNAs.

Mechanism of cataract with statins (Ref 2)

The cells lining that line the lens are dynamic and require cholesterol on a day-to-day basis. Statins inhibit proper epithelial cell development within the crystalline lens, where cholesterol biosynthesis is critical to maintain transparency and structure of the lens.

Final message

So, is it Atorvastatin or Rosuvastatin? It is left to you.

Mind you, “no statin at all” is the best option if circumstances and risk profile allows. Statins are never considered life-saving staple drugs in our fight with CAD and atherosclerosis. We, along with our scientists might may make you feel like that. Lipids can be controlled within desirable means exclusively with diet and exercise in most of the population* .

(*Forget about statins in the last 5000 years of known human existence, so many great people have lived a long and successful life in this world, without even knowing there is an organ called the heart that is responsible for the circulatory system)

Reference

1.Lee YJ, Hong SJ, Kang WC, Hong BK, Lee JY, Lee JB, Cho HJ, Yoon J, Lee SJ, Ahn CM, Kim JS, Kim BK, Ko YG, Choi D, Jang Y, Hong MK; LODESTAR investigators. Rosuvastatin versus atorvastatin treatment in adults with coronary artery disease: secondary analysis of the randomised LODESTAR trial. BMJ. 2023 Oct 18;383:e075837. doi: 10.1136/bmj-2023-075837. PMID: 37852649; PMCID: PMC10583134.

2.Leuschen J, et al Association of statin use with cataracts: a propensity score-matched analysis. JAMA Ophthalmol. 2013 Nov;131(11):1427-34.)

3.Carmena R, Betteridge DJ. Diabetogenic Action of Statins: Mechanisms. Curr Atheroscler Rep. 2019 Apr 30;21(6):23. doi: 10.1007/s11883-019-0780-z. PMID: 31037345.

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My EF is 45%, I am unable to walk to the mall, but …

Posted in Uncategorized, tagged eejection fraction, ef%, fallacies in ef% on November 8, 2023|

This a story from a middle aged IT professional who had recently suffered from a cardiac event. His concern is, he has an ejection fraction (EF) of 45%, finds difficult to walk to the nearby mall ,while his neighbour, also a heart patient, has only 32% EF , but goes for cycling and hiking ! He finds this very odd and totally unacceptable. .He desperately needed an answer from his cardiologist.

---

How is this possible, doctor? I am sort of depressed for two reasons. You are saying, I had only a mild heart attack and recovered well with no significant blocks in the angiogram, but, I still find it difficult to do routine activities. The latest EF is recorded as 45%. I am taking all your medications sincerely.

“Doctor, I feel awkward, but I can’t stop asking this question to you. More than my heart condition, it is my neighbour’s one that is bothering me. He was critically ill sometime back. Has undergone a bypass, after two early stent failures, I am seeing him daily now. So active he is, able to hike even the hill in our county. He told me his EF is just 32%. It sounds atrocious. What is the use of having more EF than him, doctor ? Do you think I need to be referred to any specialized cardiac centre ?”

“My dear patient, relax. If you want a straight-forward answer, “you are suffering from EF neurosis” Exercise capacity and overall well-being of an individual have little to do with the Ejection Fraction (EF) of the heart. Forget that number”.

“Sorry doctor, I am not clear , do you mean to say I have a mental health issue? ”

Ok , let me go little more deeper for the sake of your understanding. Hope you don’t mind. EF% can be sort of the daily weather report. It can change even beat to beat depending upon the loading conditions of the heart. We, the cardiologists are partly responsible for creating this anxiety at your level with this number .The prevailing literature and the confused google , has misled you guys, to believe that EF% is akin to “bank balance” of available heart function. Let me apologize on behalf of all of us.

There are many cardiac and non-cardiac parameters that determine one’s exercise capacity. Lung function is vital. Systemic factors like quality of your Hb%, renal function, lastly, the most important factor, the status of your skeletal muscle structure and function. If I can go technical, the degree of LV size, associated MR, the stress of LV filling, pulmonary vein compliance, the way your lung vasculature reacts, RV function, degree of PH, all that matters.

In your case, each of these parameters is good. So, I can reiterate that your heart is in fairly good condition. It is most likely that your skeletal muscles are hibernating and taking too much rest, and their mitochondria are suffering from disuse. Further, your thinking pattern also makes you easily fatigued. You must also understand dyspnoea is a cortical sensory perception defect. It depends upon the behaviour of your cerebral centres that are localized in the amygdala nuclei.

“Please doctor, I expected a practical solution from you”

“Ok, let me tell you a positive proposal which will definitely help. Trust your heart and believe in my words and the drugs you take. Ignore this EF stuff. Send a friend’s request immediately to your neighbour and join him on his daily hiking. If he can do it, you can also do it. I expect ,both the issues that is causing you depression will vanish soon. One caution, don’t overexert. Stop 10 to 20% short of your maximum possible capacity.”

“Thank you doctor , I think you’re right I am not taking enough efforts and lack confidence .Will meet you again with good news “

Final message

Unless, it is extremely low contractile function, EF% has no linear correlation with functional capacity. This is the message to all those heart failure patients. Don’t feel bad if you are labelled as LV dysfunction or ‘Heart failure’. You can steal a success story from with the help of skeletal muscle training and dyspnea sensitization program (This is not a great new discovery, it’s all there in the ancient Indian medicine, it was called pranayama, a controlled regular breathing exercise)

Reference

1.Lv J, Li Y, Shi S, Xu X, Wu H, Zhang B, Song Q. Skeletal muscle mitochondrial remodeling in heart failure: An update on mechanisms and therapeutic opportunities. Biomed Pharmacother. 2022 Nov;155:113833. doi: 10.1016/j.biopha.2022.113833. Epub 2022 Oct 7. PMID: 36271583.

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Atrial DCM : A new entity in the making

Posted in Uncategorized, tagged Atrail dcm, atrial cardiomyopathy, DCM, HFpEF, la pressure volume loop, primary atrial failure on November 4, 2023|

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

Posted in Uncategorized on November 1, 2023|

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.

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

Posted in Uncategorized, tagged acc aha esc, alfiery repair, annals of thoracic surgery, carillon device, functional MR, meer, millipede itis device, mitra clip, mitra fr cs coapt, mitral annulus, mitral regurtitation, mitral valve replacement, mitral vlave edge to edge repair, secondary mr, valvular heart disease on October 25, 2023|

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).

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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