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How to treat restrictive LV filling ? Will you Increase or decrease diuretic dose ?

February 20, 2025 by dr s venkatesan

Restrictive LV filling is an advanced form of diastolic dysfunction. The mean LA pressure is high, and LVEDP is also correspondingly elevated (need not be linear though, as LA reservoir/conduit dysfunction can independently hike the LA pressure). This clinical scenario of restrictive LV filling usually occurs as part of HFpEF, though it can occur in HFrEF as well. (25% of DCM have restrictive filling)

Image source and courtesey : Sean Haney, Denise Sur and Zijian Xu The Journal of the American Board of Family Practice May 2005, 18 (3) 189-198; DOI: https://doi.org/10.3122/jabfm.18.3.189

Pre-load reduction is the mainstay in relieving pulmonary congestion, but it has a trade-off at a particular point, as it impacts the stroke volume and forward cardiac output. Diuretic excess, ultimately worsens the symptoms, especially fatigue, though they keep the lungs dry.

So, dear fellows , remember prescription of diuretics in restrictive LV filling is a tight pharmacological rope walk.It requires continuous monitoring of symptoms and E/E” in echocardiography.

“Whether to push the LA blood with more preload or bring it down to redcue pulmonary congestion is the question“

Some physicians use the E-DT as a visual guide (Deceleration time of E velocity, which is inversely related to the degree of restriction). Normal is more than 150 ms. In most restrictive filling, it is 100 ms or less. Diuretic dose can be adjusted based on E-DT.

The usual daily dose of frusemide is 80 mg. There is a huge upper limit.It will be useful if the dose of frusemide is somehow indexed to the LV filling parameter.

I have tried a personal working formula for optimal diuretic dose. It can be titrated upwards ,twice the value of E-DT when it is less than 100 ms.(Eg if E-DT is 80ms Frusemide can be 160mg, but, note there is an U curve in this .If DT is too short, diuretics will worsen the hemodynamics .At 60 ms E-DT diuretics need to be reduced to 120 mg )

I keep tellling my fellows to do an authenticated study on this. Hope some one pursues(Mayo clinic guys are well equipped to do this , may be with the help Dr Jae.K OH or Sherif F Nagueh from Methodist, Houstan, the pioneers in the field )

Final message

We realise, treating restrictive LV filling is a delicate and often difficult task.There are no specific drugs to improve the lusiotropic property of LV. Further, since LV contractility is normal in HFpEF, there is no point in using LV inotropic agents. The only available parameter to manipulate is LV preload. However, It would be a stunning discovery , if some one discover a atria specific LA inotropic agent to overcome the LV restriction .

Meanwhile, it is critical to treat associated HT, CAD, or infiltrative disease like Amyloid*. We may soon have LA sensors , that can throw LAP to your iPhone . Till then, treating restrictive LV filling is essentially a hemodynamic/clinical pharmacological guess game. Ofcourse ,*We do have protein unfolders and declutters like Tafamidis & Patiseran to clear interstitial amyloidosis. Also, IAS flow regulators are new devices being tested to decompress the LA in HFpEF. (Paitazoglou et al Ther Adv Cardiovasc Dis. 2020 )

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What do you see in this ST segment?

February 5, 2025 by dr s venkatesan

How do you report this ST segment ?

A. Isolated ST depression

B. Isolated T Wave Inversion

C. Combination of both

D.Primarily T wave Inversion ,with secondary ST dragging

Answer: Response C, is logical, but applying some ionic sense to the various repolarisation currents in the left shoulder region of action potential , it is the clash between late phase 2 and the premature phase 3 activity, that deforms the initial limb (forward) of T waves , dragging and effacing the ST segment mimicking ST depression. This we have proposed to call it as ST drag effect by T waves. (ST drag is generally more benign , than ST segement depression that begins at J point.

Clinical significance of such ST segment

Without knowing the symptoms or the reason for which this ECG was taken, we shouldn’t interpret this ECG. In this case, it was taken in a 36-year-old woman, routine health check and who has no specific symptom. This almost rules out an ACS or even a CCS. Firther, the fact that the heart rate is normal rules out demand side ischemia as well. Very likely, it should be LVH or anemia or some other systemic medical conditions. (Rarely, neuro-adrenergic-emotional signals from brainstem can tilt the ST segment like this. (Tansient Tako-subo equivalents)

Next step

However, we can’t leave her alone. She needs an echocardiogram to rule out any subclinical myocardial disease. TMT would seem to be a necessity, but false positivity is very likely.( A flamboyant cardiologist would order a CT angiogram either striaghtaway or a day-care radial angiogram. Nothing wrong with that, as long as the patient insists on reaching the bottom of the truth)

What will you do?

Will sit with the patient for atleast 15 minutes, listen to her daily activity ,past history and look for any subtle symptoms, and then decide. It needs lots of courage (or Ignorance) to leave her without any further Investigation. Echocardiogram is a must. (Have seen a HCM variants like this ).TMT is redunant, if her excercise capacity is excellent.

Final message

One more concept on ST segment can be extrapolated by curious observation of some of the ECGs who present at ER. . It is the secondary ST sagging by primary T wave downward forces. (Pushing ST up is also possibe , as we already know it as ERS pattern )

Postamble.

We know, the S point (Technically J ) in ST segment is well defined , while the end of ST segment is hidden in deep mystery in many clinical situations.Mind you, a flattish ST segment, with absent T wave can be an aboslute normality. Here, you can’t measure either ST segment or even the QT interval.

Reference

1.D’Ascenzi F, Anselmi F, Adami PE, Pelliccia A. Interpretation of T-wave inversion in physiological and pathological conditions: Current state and future perspectives. Clin Cardiol. 2020 Aug;43(8):827-833. doi: 10.1002/clc.23365. Epub 2020 Apr 7. PMID: 32259342; PMCID: PMC7403675.

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“Non-superiority” trial of sub-optimal PCI vs OMT : A proposal for a study design

February 3, 2025 by dr s venkatesan

The therapeutics of coronary stenosis has become a technogical wonder, interwoven with statistical wordplay in the last few decades. PCI is sitting pretty at its peak glory.The term OMT or GDMT is a popular terminology, but realistically exist only in guidelines.

It is a strange academic habit among cardiologists, that they have subdivided medical management into optimal and suboptimal. Meanwhile, we haven’t seen any papers from cardiology forums that classify PCI according to its quality. How many of use a term like optimal PCI or guideline-directed PCI (O-PCI, GDPCI). Every PCI, by default, is perceived as good by our flawed coronary intellect.

A single patient experience

Let me share a patient consult from a remote town of north India. He is a STEMI patient (1 year old) with mild LV dysfunction and thinning of IVS and anterior wall. His CAG showed a significant looking, yet non-flow limiting LAD lesion without any troubling symptoms. I came to know he had consulted two institutions and was apparently not happy with their approach (In his own words, “They seem to be primarily interested in caging my LAD than listening to me”).

Somebody has suggested my name. He called me over the phone for a consult. I asked him remain there to follow his doctor’s advice. But, he flew some 2000 km to meet me. He was so knowledgeable and was aware of everything I wanted to tell. Like, viability, scars, futility, and benefits of revascularization, imaging-assisted PCI, impact of PCI on exercise capacity, importance of risk factor management, etc.

I told him, “In my opinion, you have technically a single vessel disease that can be managed well with drugs. But if PCI is to be done, it should be done in a proficient manner, as the lesion looked hard and was close to the LAD ostium, trespassing LCX as well.” I stressed the importance of a professionally done procedure with enough expertise and follow-up maintenance care.

He was not entirely satisfied with my response. He wanted a clear yes or no! . I told him, “If you have full trust, continue with the drugs at full intensity and do a stress test after 3 months. otherwise, if you keep getting even the slightest doubt and anxiety over the hidden blocks, go for a stent immediately at a good Institution. (My conscience said the latter half of my advice was unwarranted, but I had to; after all, me too need a protective mechanism)

He left my clinic profusley thanking me. I am not sure , how my consult was useful for him and what he is going to decide.

Academic lessons from this patient.

1.Patient fear factor over coronary blocks may be the ultimate game changer. Cardiologists should try to mitigate this fear and at the least should not be an amplifier to this emotion.

2.Leaving tricky profesionaly complex decisions to the patient, is an easy escape route for us, however it comes very close to professional incompetence. (Of course, we do this on a routine basis, approved by the modern medical guidelines, ethics, and legal system, in the name of patient empowerment)

3.Finally, we can grow a potential research hypothesis. A sub-optimal PCI is non-superior to OMT.It is curious there is no study available to compare sub-optimal PCI to OMT. We must also realize there is nothing called standalone PCI. Without concomitant OMT, PCI is a dud. Every young cardiology fellow need to etch this fact in their cortical cardiac memory. OMT often turns out to be the savior of stents, but the latter ruthlessly steals the credit.

Postamble

I could find one study analyzing suboptimal stenting (Ref 1), but it didn’t compare it with OMT. Suddenly, as I finish writing this, a big fact struck me hard, i.e., even a well-done PCI in sophisticated core labs with meticulous care struggled to beat OMT in a barrage of landmark trials (like COURAGE, ISCHEMIA, ORBITA). What is the big deal to analyze suboptimal PCI vs OMT?

Prati F, Romagnoli E, Gatto L, La Manna A, . Clinical Impact of Suboptimal Stenting and Residual Intrastent Plaque/Thrombus Protrusion in Patients With Acute Coronary Syndrome: The CLI-OPCI ACS Substudy Circ Cardiovasc Interv. 2016 Dec;9(12):e003726. .

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CTEPH : A presentation

January 30, 2025 by dr s venkatesan

This is a GIF run through of a recent presentation in PH seminar at Coimbatore, India.

Topic: Chronic thrombo embolic pulmonary hypertension.(CTEPH)

In this lecture, I have tried to highlight

1.Newer definitions, Incidence and prevalence of CTEPH

2.The pathologic transition phase between acute PE to CTEPH

3.Risk factors for this conversion

4.Potential errors in missing some systemic conditions

5.Importance of CT angiogram as a key to diagnose

6.Value of V/Q scan

7.The rare pulmonary veno occlusive disease mimicking CTEPH

8.Role of radiologists and pulmonologists in diagnosing the entity.

9.Value of dual energy CT scan

10.New age anti PH drugs and role of surgery in proximal CTEPH

A PDF presentation shall be sent on request.

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Right atrial origin of Atrial fibrillation : Why we Ignore IVC ,SVC focus?

January 28, 2025 by dr s venkatesan

For right or wrong reasons, the world of electrophysiology has pushed us into a belief system that, if it is AF, the culprit must be pulmonary veins. In fact, non-pulmonary vein origins can be a staggering 70% in some series. (See below) It can be in the free walls of the left atrium, LA appendage, IAS, IV, SVC junctions, coronary sinus, ligament of Marshall, crista terminalis, etc. (Ref 2)

For example , where will be the initial focal trigger for AF in a pateint with COPD ?

Can you ever think of ablating PVs in a patient with AF and COPD, where the right atrium is under stress and strain? It doesn’t require any extraordinary intelligence to conclude any chronic focal atrial tachycardia can get degenerated to AF in the long run. In that case, the famous atrial tachycardia localizing map from Peter Kistler et al from Australia JACC 2006 holds good for location AF focus too.

If we look at the above map,RA prevails over LA convincigly in termes of focal atrial tachycardia. Only 20% of focal AT arise from pulmonary veins. I guess, the same should be true for AF.

Focus-less Atrial fibrillation

Right from the days of James Mckenzie, when AF was refered to as delirium cordis or ataxia of pulse, AF was always considered as a chaotic, focus-less arrhythmia. It is still true in many cases. The recent pulmonary vein triggers are just a small revelation and need not be a revolutionary paradigm shift , as we are taught. There are innumerable patients who develop de-novo AF without any focus. Hypoxic or acidotic milleu of a single atrial myocyte can iniitiate an AF, alosan episode of atrial ischemia, diffuse inflammation as in atrial epi-myocardiits can trigger AF from any spot on the atrium.

Reference

1.Francis Marchlinski Cory M. Tschabrunn Pasquale Santangeli , Maciej Kubala J Am Coll Cardiol EP. 2019 Nov, 5 (11) 1328–1330

2.Yang, S.Y., Cha, MJ., Oh, H.J. et al. Role of non-pulmonary vein triggers in persistent atrial fibrillation. Int J Arrhythm 24, 7 (2023). https://doi.org/10.1186/s42444-023-00088-0

3.Aronson JK. One hundred years of atrial fibrillation. Br J Clin Pharmacol. 2005 Oct;60(4):345-6. doi: 10.1111/j.1365-2125.2005.02501.x. PMID: 16187965; PMCID: PMC1884824.

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Indian cardiology community, bids adieu to a great heart surgeon Dr. K.M. Cherian.

January 26, 2025 by dr s venkatesan

As India celebrates its 75th Republic day anniversary, we hear a silent news, of loss of its one of the great citizens , a doctor , a scientist and humanist par excellence. Dr Kotturathu Mammen Cherian

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CABG or PCI ? : Think beyond revascularisation guidelines & the evidence base

January 24, 2025 by dr s venkatesan

Wars and scientific debates do not end that easily. Parallel to the Vietnam war days of 1970s to the current Ukraine-Russia conflict of 2025, one silent academic war is going on, in the conflict-ridden corridors of cardiology and cardiac surgery. (The CASS study of 1970s to the ORBITA era of 2025) Any amount of scientific literature, debates, guidelines, failed to tick the right choice of revascularisation in chronic CAD. Ironically, as our knowledge increased the decision making process got more murky.(Largely due to non academic factors)

To find an answer to this, CTSNET, a hugely popular cardiac surgery forum orgainsed a seminar trying to create a globally unifying approach. This is an hour long seminar , I am sure will enlighten us further. Please make yourself free for 60 minutes. Better , not to go to the summary, without watching the video.

Link to the you tube video

Observation and brief summary

1.First and foremost, academic guidelines are created primarily, to make us understand the disease process fully, which would help us make a good decision. Interpretation of these guidelines can vary widely . As a professional physician , we are supposed to use the official guidlines judiously, at no time, we can be slaves to them.

2. It is possible ,the term myocardial revascularisation itself is largely misunderstood. What is being vascularised ? & What is the impact of that vascularisation are the right questions to be asked.I feel this seminar genuinely adds some sense to the flawed understanding of the prevailing concept of myocardial revascularization.

3.Think mechanistically and extrapolate the potential benefits and risks .Try to sort out the issue individually. Recall the classic truth that, revascularisation rarely improve contractility in chronic LV dysfunction to the desired levels.(Inspite of the patchy benefits shown by CABG-PATCH/ REVIVED BCIS-2 trials)

4. Realise, the confusion in choice of revascularisation is more in chronic coronary syndromes. PCI has an edge in acute situations if done in a timely fashion.

5. It is a open secret ,there is a big conflict of interest in the guideline writing committee. A huge transatlantic academic gap exists with American guidelines of 2021, 2023 favoring more PCI, while ESC recommends more CABG in complex lesions and left main. The big controversy ,that brewed was when Indication 2A was confered for both PCI and CABG in left main and multivessel CAD.

6.Global experts unanimously endoresed the European guidelines ,which favors for more liberal CABG . Still, they were hesitant to denounce the American guildelines.

7. Curiously, I believe the debate question itself is not fair.We should not be debating PCI vs. CABG at all ? This makes GDMT not a standalone option at all. In both hindsight and foresight, this may be the best option in the majority of patients, as indicated by many landmark studies of revascularization.(There is an Interesting comment made by the panelist relevant to the above point)

8.Every CAD patient should have an option finalising his decision with a heart team comprising of a clinical cardiologist, an Interventional cardiologist and the cardiac surgeon .

9.Quality and expertise of surgeons and PCI team is vitally important.We can’t bring the same trial outcomes in any neigbourhood hospitals, especailly in less well developed countries.

10. Finally, most importantly, it is agreed by more experts that CABG has more potential to prevent a future MI than PCI in most subsets of patients. This is because, CABG gives realtive immunity to potential the disease progression in the proximal segments which are the original high risk zones .

Final message

I have shared some key personal observations triggered by this extrodinary seminar. It can be called as a personlised version and a summary .Please listen to it completely and try to find whether these observations are good enough.

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Trust the coronaries : There are benign forms of ACS too !

January 22, 2025 by dr s venkatesan

ACS is one of the sinister diagnoses made at medical ER. The fear comes built in with the diagnosis often amplified by young felllows on call (& often times by senior consultants as well) It may appear real, from a clinical angle, but, please trust, when we deal with the whole gamut of ACS scenerios (other than STEMI), there is indeed a benign face, in many of them.

One big chunk of ACS-UA is secondary UA, where there is increased demand as in stable angina with tachycardia* . In these patients there is no plaque triggered ACS. For example, in a febrile patient who has associated HT, anemia, etc., we can witness menacingly deep resting ST depression with absolutely no thrombotic process going on in the coronary. (*Mind you, all stress-induced ST depression,, are not ACS, but a marker of chronic CAD.) I used to tell my fellows, a patient with hidden CAD, who develops fever for whatever reason, is acutually doing a tread mill test equivalent , and showing off the diagnosis. It is near- foolishness, if we rush them to cath lab.

How can biomarkers help us grade these ACSs?

The high sensitivity troponins not only help us to diagnose NSTEMI, it also tells us which one of them may be innocuous ACS or benign ? Strangely, we are also taught , “No ACS should be considered benign, until you see the coronary anatomy”. I wish patients realise, how difficult it is to practice cardiology, for that matter any field of emergency medicine. You can’t err at the same time , you are not supposed to treat inappropriate as well.

High sensitivity Troponin (hsTnT) do play a useful role in identifying low risk UA/NSTEMI , as seen in the following study. See how the Kaplans diverge dramatically depending upon the hsTnT levels. I don’t understand how the curve of non-cardiac chest pain trespasses in the middle of a Troponin race (False positives? Real concern then)

Final message

Clinical, biochemical, and overall risk profile assessments do help us risk stratify ACS. We have numerous predicting algorithms and scoring systems in UA/NSTEM led by GRACE, etc. Still, it can be a tricky game to make a call on ACS. Mind you, even a coronary angiogram will not bail you out in terms of decision-making and risk prediction. An incidental 80-90% lesion with a normal FFR is quite common.

Avoiding innocuous ACS patients getting admitted in CCUs is a real problem. Of course, getting trapped in a CCU for a few days is better than tampering with the coronaries in the cath lab. Some of the stakeholders may welcome both, but that is not science.

I recall some old guidelines saying not all UA need to be admitted. Many low-risk categories can be managed as outpatients; it is still true. I am not sure how many of us have the courage to do it. Courage alone is not sufficient; the fear of statistical misbehavior of ACS, compounded by potential ridicule from peers or even patients, always haunts.

Reference

1.Wiens EJ, Deviaene M, Shah AH. Clinical Applications of High-Sensitivity Troponin Testing: From Diagnosis to Prognosis. Can J Cardiol. 2022 Oct;38(10):1521-1524. doi: 10.1016/j.cjca.2022.05.008. Epub 2022 May 13. PMID: 35569799.

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Early TAVR trial : Too early to call

January 18, 2025 by dr s venkatesan

We know TAVI is in the striking distance , to literally take over most aortic valve interventions. From a humble beginning from very high surgical risk with prohibitive comorbidity, now it has almost touched the totally asymptomatic, relatively morbid-free patients. Thanks to the hardware, expertise, and motivation from multiple forces.

While the numbers increase, still the debate between SAVR and TAVR is riddled with speculation, skepticism, and absolute confidence. (Reason: TAVI is a passively fixed valve in a blind procedure at a self-selected annular plane, with no option to remove the crushed native leaflet debris and the resultant complications. Lastly, TAVI’s lifespan* is currently less than half of a mechanical valve. *Expected to improve with polymer valves)

The latest trial to join the litereture is EARLY TAVR in October 2024

Here is a brief, personal comment about the paper for non-academic consumption. Look carefully at the 15th second of the video. Pause it, look at the number over there on the bar of unplanned hospitalisation.

It is a staggering 41.7% in clinical surveillance group, twice more than TAVI group, pathologically tilting the conclusion of the study.

Video source and courtesy https://youtu.be/3wwQEEG4aWg

By the way, what is that unplanned hospital admission? Who is planning that admission in the asymptomatic control group? If 41% of people in the clinical surveillance group needed hospital admission, what does it mean? Does that mean clinical surveillance was so poor that they were rushed to the hospital despite being asymptomatic and stable in the surveillance period?

Why should totally asymptomatic patients get admitted in the control arm, in such huge numbers? You can presume what could be the reason. My guess is too sinister.

Another issue plaguing the RCTs for decades, is continuing even in 2025. That is putting together death, stroke, and unplanned hospital admission as a combined endpoint in the same basket. This is the familiar old cheat story i.e., used to intentionally torture the truth.

Final message

Any student with basic sense of statisitcs can interpret the result of this landmark trial from NEJM correctly. The question we need to ask is, what are the triggers for those unplanned hospital admissions?

Further, it is good for NEJM (and the medical community) not to accept any papers, if the studys’ endpoints are not appropriate or defined with the intention to manipulate, which happens in many sponsored trials.

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Carotid web : No longer a new kid in stroke risk

January 15, 2025 by dr s venkatesan

A carotid web is a shelf-like lesion along the posterior wall of the internal carotid artery bulb and an under-recognized cause of stroke in young individuals. Many studies suggest that patients with a carotid web have a high risk of recurrent stroke.

Various forms of carotid pathology

Image source : https://radiologyassistant.nl/neuroradiology/carotid-pathology/differentiating-carotid-pathology

In the famous Dutch study on ischemic stroke MR CLEAN, 30 patients had carotid web which is around 2% incidence. In this study 1 out of every 6 patients with a symptomatic carotid web had a recurrent stroke within 2 years, suggesting that medical management alone may not provide sufficient protection for patients with a carotid web.

Ref : Berkhemer OA, Fransen PSS, Beumer D, et al; MR CLEAN Investigators. A randomized trial for intraarterial treatment for acute ischemic stroke. N Engl J Med 2015;372:11–20

Histopathology & OCT

Choi PM AJNR Am J Neuroradiol. 2015 .Christopher R. Pasarikovski, Neurology: Clinical Practice 2019

How does it appear in carotid angiogram and in real time per-operative ?

Images : Chen H, Colasurdo M, Costa M, Nossek E, Kan P. Carotid webs: a review of pathophysiology, diagnostic findings, and treatment options. J Neurointerv Surg. 2024 Nov 22;16(12):1294-1298. doi: 10.1136/jnis-2023-021243. PMID: 38290814.

Management

The web can create a flow disturbance, potentiating local thrombus formation, which can embolize producing resulting in cerebral ischemia. Current treatment is with anti-thrombotics and/or anticoagulation .Lesser option is to alter the flow disturbance caused by the web (surgery or stent).

Final message

Cartoid web is no longer a diagnostic curiosity. Its worth looking forit an any young patients with cryptogenic stroke.

Reference

1.Rainer W.G., Cramer G.G., Newby J.P., et. al.: Fibromuscular hyperplasia of the carotid artery causing positional cerebral ischemia. Ann Surg 1968; 167: pp. 444-446.

2. Patel S.D., Otite F.O., Topiwala K., et. al.: Interventional compared with medical management of symptomatic carotid web: a systematic review. J Stroke Cerebrovasc Dis 2022; 31:

3.Gonzalez-Urquijo M, Vargas JF, Marchesini M, Marine L, Mertens R, Valdes F, Godoy-Santín J, Mellado P, Miranda H, Zoroquiaín JP, Sandoval P. Treatment of Symptomatic Carotid Webs. Ann Vasc Surg. 2025 Jan;110(Pt A):114-122. doi: 10.1016/j.avsg.2024.07.107. Epub 2024 Sep 27. PMID: 39343364.

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