Dr.S.Venkatesan MD

Knowledge check in Brugada syndrome : A rapid fire session

January 5, 2022 by dr s venkatesan

A 5-minute session: Answers are my own. Please cross-check.

1. Is Brugada syndrome clinical or ECG diagnosis?

Always clinical. Never get confused on this.

2. Spontaneous type 1 vs Induced Type 1 (from type 2) which carries more risk?

Both are risky since they are close cousins. But, spontaneous type 1 is the dreaded devil. 

3. Is Brugada primarily a defect of myocardial depolarization or repolarisation?

Not clear. Often in both. In fact a mismatch between them. (Don’t ask how Na+ Channel defect affects repolarisation !)

4. Is Brugada VT is monomorphic, polymorphic?

Both. What determines morphology is not clear though. (All de-nova monomorphic VT will degenerate to polymorphic en route to cardiac arrest)

5. Should  Fever induced Brugada pattern be investigated further?

Better, it is not to be reported in ECG. May not be important in the majority if there is no adverse family history. (If the patient is well educated and afflicted  by Dr.Google and cardiologists can’t escape from ordering sophisticated tests)     

6. What is the overlap between ERS and Brugada?

It is all about the Idiosyncrasy of the K+ channel phenotypes ( Transmural dispersion heterogeneity )  

7. Is a benign Brugada better than a malignant ERS?

Yes, it would seem so. (Inferior or Infero -lateral ERS prone for primary VF in case they develop ischemic / ? also non-ischemic stress)

8. How important is the link between Brugada and Long QT 3 syndrome?

A rare entity, but It is double jeopardy for VT risk. The entire action potential width is vulnerable right from phase 0 to 3 or 4 A case report Sandhu A Clin Case Rep. 2017;5(8):1315-1319.

9. Is Amiodarone really contraindicated in VT?

Not really. Though Amiodarone unmasks Brugada, it can still be used during episodes of VT in patients with manifest or unmanifest Brugada. Maybe in Long QT 3 overlap, it may perpetuate the VT.

10. How important is the structural myocardial defect in Brugada?

Not important in the majority. Though localized RVOT abnormalities are noted in some..RV abaltion can be succesful in odd case.

11. What happens to the ST segment in Brugada during exercise stress?

ST-segment may normalize in some. A stress test can help to risk stratify.  Subramanian M, J Cardiovasc Electrophysiol. 2017 Jun;28(6):677-683.0

12. Which drug is probably best for Brugada as of now?

Quininde , A fairly specific blocker of Ito current. However, it needs to be used diligently. Management of Brugada Syndrome: Belhassen B, Rahkovich M, Michowitz Y, Glick A, Viskin S Circ Arrhythm Electrophysiol. 2015 Dec; 8(6):1393-402.

13. Is ICD definitive therapy?

Obviously not. But, definitely life-saving in high-risk survivors. I guess definitive therapy is possible for future generations through the science of genetic reprogramming of Na+ channels. (Of course, our planet shouldn’t succumb to man-made climatic arrhythmia, by then ) 

14. Does widespread genetic testing & screening of families help in the management and reduce anxiety?

Cracking the genomic code of cardiac ion channels is the ultimate sophistication (Blueprint of fate ?) However, there is no guarantee this information is going to ease out the family members who harbor a genocopy with or without a phenocopy. 

15. Is Brugada getting undue attention in cardiology literature compared to many other common arrhythmias?

      You can answer this …………………………………….

 

Further reading

Li KHC, Lee S, Yin C, et al. Brugada syndrome: A comprehensive review of pathophysiological mechanisms and risk stratification strategies [published correction appears in Int J Cardiol Heart Vasc. 2020 Dec 19;32:100699]. Int J Cardiol Heart Vasc. 2020;26:100468. Published 2020 Jan 21. doi:10.1016/j.ijcha.2020.100468

 

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Posted in cardiac electrophysiology, cardiology -Therapeutics, Cardiology -unresolved questions, Cardiology-Arrhythmias, early repolarisation syndrome, Electro physiology, Electrocardiography-ECG, ICD and Pacemakers | Tagged amiodarone for brugada, brugada syndrome |

Cardiac failure Info desk :Diuretics never save lives, while Dapagliflozin does it in style !

December 17, 2021 by dr s venkatesan

An Interaction in IMCU

How is Mr. K, who was shifted from ward 102 ?

Yes sir, It was acute decompensated LV failure, Patient was in impending pulmonary edema. In fact, he developed. He is fine now,

How did he come around? He was too sick I thought.

“Just pushed 60 mg Frusemide IV, luckily he also had good BP, so with an infusion of NTG, titrated Carvedilol a little bit, he came out nicely. I guess it is Ischemic DCM”.

“Good, You have done a nice job”

“Don’t make me embarrassed sir. It is such a routine in our ER. 

To make him curious, I asked “Which drug do you think that saved him”?

“Obviously, Frusemide sir. He was frothing out. I thought he will require a ventilator. It was a matter of 20 minutes, sort of flushing out 500 ml lung fluid through the urine”.

“No, you are wrong. As a professor and cardiologist, I need to tell you this. Diuretics never save lives heart failure. 

Sir, I guess, you are not kidding. Does this statement apply to acute heart failure? We have saved 100s of lives with Frusemide,  both in acute, acute on chronic, and even in chronic cardiac failures with metolazone.

Hmmm, I agree with you my dear student, Frusemide has saved not hundreds but lakhs of lives in the past decades in all forms of heart failure. It continues to do this fabulous job even now. But, don’t say it in exams or scientific forums. It has no evidence to show survival benefits. You can’t credit a drug without evidence. Also realize, saving lives by unscientific means by a cheap generic is not something to boast upon. We need the blessings of RCTs, or Kaplans Mayer curves, or Forrest blobbograms. Unfortunately . that is the current principle of practice of medicine.

But sir, who is preventing whom, to do such studies. Why they are not comparing diuretics one to one with these modern drugs of inotropes, calcium modulators, or SGLTis, etc? 

I am not sure. My guess is, there are no good friends in the cardiac failure research community for this old warrior drug. 

Loop diuretics 

Till 1960s, toxic mercurial compunds was the only option to drain water in heart failures. The Invention of  Na+/K+ /Cl channel blocker Frusemide, ( In the thick ascending limb of the loop of Henle) is the single most important event, that changed the way we manage cardiac failure in both acute and chronic settings. Still, the current evidence creators hesitate to call it a life-saving drug,

The meteoric rise of SGLT-2 Inhibitors 

Meanwhile, a few micrometers down the hairpin bend of Henle, drugs called phlorizin are doing wonders. These Apple root barks derivatives were since been invaded by Glyflozins Industry. They are made into a powerful glycosuric drug that drags water out of the system along with glucose. This seems to be the biggest revolution in cardiac pharmacology ever since DaVinci drew the heart and Harvey made it functional. I think we need a supercomputer to count the number of papers and analyze the data from Dapa & Empaglyflosin. It is now concluded officially, as an evidence-based life saver in HF.

I asked one Gen X Pharma-geek, “How do these magic drugs perform this miracle in heart failure”? He said beamingly, It is not merely Glyco-diuresis, as you academicians think, it is some mystery action from heaven, still not decoded. What a revelation I thought.

Continuing Medical Education: Choosing the correct path is never easy!

Final message 

Loop diuretics are powerful drugs that aid the failing heart to reduce both pre and after-load. It is a fact, indiscriminate use of these drugs leads to some electrolytes and metabolic issues. But, hiding behind a hazy and shaky evidence base, and trying to ridicule these life-sustaining drugs, is the height of senselessness in cardiac failure literature.

Reference 

(There is a tug of war of evidence between benefits and risks. I guess someone will bring out the truth, which is written clearly on the walls)

1. Chris J Kapelios, Konstantinos Malliaras, Elisabeth Kaldara, Stella Vakrou, John N Nanas, Loop diuretics for chronic heart failure: a foe in disguise of a friend?, European Heart Journal – Cardiovascular Pharmacotherapy, Volume 4, Issue 1, January 2018, Pages 54–63, https://doi.org/10.1093/ehjcvp/pvx020

2.Faris R, Flather M, Purcell H, Henein M, Poole-Wilson P, Coats A. Current evidence supporting the role of diuretics in heart failure: a meta-analysis of randomized controlled trials. Int J Cardiol. 2002 Feb;82(2):149-58. doi: 10.1016/s0167-5273(01)00600-3. PMID: 11853901.

Postamble

It is to be noted,Eplerenone (EPHESUS trial )  & Finerinone  (FIDELIO-DKD trial) are new generation  K + sparing diuretics and mineralocorticoid antagonists may have better cardioprotection in cardiac failure.(Part of RAAS blockade)

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Posted in cardiac failure, Cardiology -guidelines, cardiology -Therapeutics, cardiology wisdom, cardiology-ethics, Cardiology-Land mark studies, Ethics in Medicine, evidence based cardiology | Tagged acc aha esc guidelines on heart failure, bumatanide, Cardiac failure therapeutics, dapa hf, dapaglyflozin, does diuretic save lives in heart failure, flaws of evidence based medicine, history of frusemide, meta analysis of diuretics in cardiac failure, toresemide vs frusemide |

What is the true success for a scientist ?

November 26, 2021 by dr s venkatesan

What is the true success in a scientific career?

It is not the number of publications in journals or getting those big awards or memberships in prestigious scientific societies. True success is “something else,” says the Nobel Medical Laureate  Dr Willam Kaelin 

Great thoughts. Just wondering, what are those elements beyond our controls he was alluding to?

 

Video courtesy and thanks : http://www.nobel.org

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Posted in bio ethics, Histroy of medicine, Medcal research, Medical education, Medical ethics, medical quotes | Tagged ethics in medical research, ethics in medicine, greatest award in medicine, medical quote, nobel prize in medicine, publish or perish, what is success in scientific world |

Sudden cardiac death of an Indian superstar and the “Non-academic aftermath”

November 4, 2021 by dr s venkatesan

A young Indian superstar actor Punnet Rajkumar, suffered a sudden cardiac death last week during a workout at his gym. We don’t really know what happened, was it really a conventional heart attack ? or simply an exercise Induced arrhythmia or an isometric dissecting injury to the coronary arterial (or Aortic) wall. Only a postmortem would have thrown some light. (I am not sure what the ER room ECG showed though) He had excellent physical fitness and was following a good healthy lifestyle. One possibility is extreme physical exertion.

It is ironic, while a sedentary lifestyle is a chronic coronary risk factor, excessive physical activity in the background of emotional stress can be turn out to be an acute risk factor. (This is not to frighten all those young and energetic, it only conveys a simple message. Moderation is a must in any indulgences in life)

AHA has made an elaborate scientific statement on this Issue.

                         https://doi.org/10.1161/CIR.0000000000000749

Meanwhile, the entire nation went into cardio-panic mode and TV media houses have become free cardiology consultation rooms. How many will realize sudden cardiac arrest and heart attacks can be totally two different entities. Further, who can teach the public, that endpoint of any life has to be cardiac arrest or a standstill. How unscientific does it sound when someone suggests a CT angiogram for all aged over 40 years ? Guess, who will enjoy whipping and sustaining such a frenzy.

Here is a precise article in Indian express that puts this episode into perspective.

https://indianexpress.com/article/opinion/columns/puneeth-rajkumar-death-doctors-hearth-attack-health-7606581/

The author is Dr. Ganesan Karthikeyan, professor of cardiology at AIIMS with a Global reputation.

 

 

 

 

 

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Posted in acute coronary syndrome, Cardiology -unresolved questions, RIsk factors, wisdom in cardiology | Tagged aha guidelines acc physical activity exertion, coronary risk factors, scd |

Paradoxical Low flow-Low gradient- Aortic stenosis: What is the paradox & why does it happen?

October 17, 2021 by dr s venkatesan

Aortic stenosis evaluation was simple in our days. Gradients across the valve were the key. Now, we have more parameters to bother about. Dynamic AVOs, flow state, resting LV function, contractile reserves, GLS, dobutamine response, etc. MRI assessment will soon overtake echocardiography. 

Hemodynamics of flow across LVOT. MRI 4D volumetric model of normal Aortic stenotic flow in the bicuspid valve (On the left). The more we know, the more we tend to miss! Image courtesy: Northwestern Medicine

The current AS algorithms, though scientific, I am afraid, appear much complicated with some frightening terminologies at least for the beginner. One such category is PLF-LG-AG.

Let us first answer this. What is LG-AS?

We diagnose a case of significant aortic stenosis but desperately miss to pick an adequate gradient across the valve. It is indeed a low gradient AS, still, you are not convinced, since the 2D look of the valve looks severe. Then you find the culprit. It is the dysfunctional ventricle pulling down the gradient. This is called  LG-AS.(one type )

*What is paradoxical -Low flow-Low gradient Aortic stenosis? (PLF-LG AS)

Now, we have another patient. Again it is  LG-AS, but the LV function and EF are normal. Now, you get confused and label it as PLF-LG-AS. 

PLF-LG AS is known to account for approximately one-third of patients with severe AS and preserved LV EF.PLF-LG severe AS is defined by AVA <1.0 cm², indexed AVA <0.6 cm²/m², mean gradient <40 mmHg, LV EF ≥50%, and low transvalvular flow (indexed stroke volume <35 mL/m²).

What is the paradox?

AS is severe, but the gradient is not showing at the valve. Wait, don’t think that is the paradox, since this can happen in any category of LG-AS.  So, the real paradox in PLF-LG-AS denotes to the fact that the gradient is low, in spite of normal LV  function (Rather, normal EF %)

Why the paradox? Why gradient is not showing? (In spite of good Ejection fraction ?) 

• Reduced stroke volume increased afterload due to associated HT are the major hemodynamic mechanisms of PLF-LG AS.
• The low-flow state can be related to small LV cavity 
• Significant diastolic dysfunction (Associated Amyloidosis is a new age problem kid on the block. EF is not the only parameter that can compromise the flow you know !)
• Atrial fibrillation (Ofcourse some cycles will pick up the high gradients, but are they spuriously low or high is the question  ) 
• Associated mitral valve disease leaks, as well as blocks, will ration the flow to LVOT.

*Finally, every cardiologist should be aware of the following two subsets that could wrongly enter this conundrum of PLF-LG-AS  without much fanfare but with lots of implications.

1. Most importantly, technical issues are the key confounders. Malaligned  LV / LVOT with that of distorted out-of-plane AVO is the commonest cause of failure to pick up the gradient. (Never diagnose PLF-LG-AS  without confirming it is not due to technical ). A tip: Don’t complete AS doppler study without a meticulous search for a good doppler signal from the suprasternal/right parasternal window. 

2. Next one can be named with a provocative term “Paranoid aortic stenosis*”. Once, a  fellow was reporting a shabby-looking calcific valve as low gradient, severe AS with normal LV function. He made this diagnosis solely based on AVO. Later, when it was assessed more scrupulously it turned out to be a true mild aortic stenosis, and none of the decorative echo features he was showing were really pathological. It was an error in the aortic valve area calculation due to LVOT area/VTI measurement errors that got mathematically amplified. An important teaching point emerged from this echo lab fiasco. Mind you, any true mild aortic stenosis (If the area calculation is wrong for some reason) will readily fulfill the criteria of PLF-LG-AS. One simple tip: Never diagnose severe Aortic stenosis without significant LVH.

What is the role of Doubtamine stress echo in PLF-LG-AS ?

It does help in both forms of LG-AS. You need to read about the contractile reserve, the response of dobutamine to flow (Cardiac index), gradient, and the valve area.

How to manage PLF-LG-AS ?

Many of them might be argued to end up in TAVR. So, follow the guidelines carefully but don’t apply them blindly

Final message 

In the evaluation of Aortic stenosis let’s make things simple. Gradients are indeed important. But, realize Doppler gives only pressure data. Converting them to flow and volume data is always error-prone. Instead, let us believe our eyes too.(Need not always depend on o MDCT vision)  Concentrate more on LV morphology, valve pathology, and careful assessment of LV function, finally take a decision to intervene based on true symptomatology and comorbidity.

Reference 

1. For the most authentic knowledge base

2.An excellent review on the topic 

Guzzetti Ezequiel Frontiers in Cardiovascular Medicine 2020

Further thoughts

Is there a “high flow-high gradient”- True mild AS?

High gradients across the AV  generally do not cause much confusion. If the mean gradient is > 40mmhg Aortic stenosis is always severe. Is that right ?. I think so. Exercise-induced paradoxical high flow high gradient AS as an entity is not reported as such. But, what really can happen in high output states, hyper contractile ventricles with high EF? We have observed doppler gradients overestimate the severity of Aortic stenosis. I think there is some dynamic component even in the so-called fixed valvular AS that alters the gradient in response to flow. Do we have proof for this?  OMG, it’s right there in echo lab every day, we are failing to notice it. Look at the AS gradients during AF. It is changing every beat, right.

 

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Posted in Aortic diseases, aortic stenosis | Tagged amyloidosis in aortic stenosis, ASE ACC AHA ESC guidelines for aortic stenosis, dobutamine stress in aortic stenosis, doppler error in aortic stenosis, grading severity of aortic stenosis, hypertension and aortic stenosis, low flow due to lv malalignment, low gradient aortic stenosis, paradoxical low flow low gradient aortic stenosis, sigmoid ivs lvh, suboptimal doppler signal in aortic stenosis, suprasternal window in aortic stenosis, tavr for aortic stenosis, tavr for paradoxical log flow low gradient stenosis |

Issues in diagnosing grade 1 diastolic dysfunction: Pearls and Perils

October 7, 2021 by dr s venkatesan

Doppler E/A ratio reversal is probably the most reported abnormality in clinical echocardiography. We are also pleased to label it as a grade 1 diastolic dysfunction. Making a significant population who come for regular health checks anxious and worried.

Sharing a presentation from the Annual conference ECHO INDIA 2019, I participated in a symposium on Diastolic dysfunction.

Topic : Issues in diagnosing grade 1 diastolic dysfunction: Pearls and Perils

How did we get into this academic trap? Should we continue this practice?

The current ASE guidelines 2016 have a clear message. It has taken off the E/A ratio from the Initial screening for diastolic dysfunction.

Summary & Final message 

Are we ready for the change? By understanding a simple concept, one can reduce the incidence of indiscriminate diagnosis of grade 1 diastolic dysfunction.

• E/A ratio apparently has a no role in diagnosing diastolic dysfunction in the normal population who have normal EF %.
• Hence, never report E/A ratio in Isolation as grade 1 diastolic dysfunction.
• However, in patients with HFrEF it does help in triaging diastolic dysfunction.
• Always look for symptoms and 2D features  (Unexplained dyspnea, LA enlargement, LVH ) before considering diastolic dysfunction.

*For advanced readers and researchers grade 1 diastolic dysfunction does have a deep meaning and always continues to puzzle.

Patient corner

For all those anxious patients who ramble around with a report of grade 1 diastolic dysfunction, I can assure you this. Please realize, 9/10 times, this is just a decorative echocardiography abnormality meant to add some spice to the report  does not have any significance.

*Will post a PPT presentation shortly.

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Posted in Cardiology-Echocardiography, Diastolic dysfunction, Echocardiography-hemodynamics | Tagged classification of diastolic dysfunction, diastolic dysfunction, diastolic dysfunction ppt, echoindia, grade 1 dd, HFpEF, indian academy of echocardiography, what is grae 1 diastolic dysfunction |

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• The contents of the this blog is being published as Kindle E book , as per the request of many of the readers. Every article will continue to be open source in this site. Again I shall reiterate the book format is not aimed at any commercial intent. It is only to facilitate learning in a single book format Here is the link to book
  https://amzn.in/d/euhL5vu

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