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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

 

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

Top Cardiology and Heart Disease Blogs in 2021

January 1, 2022 by dr s venkatesan

Surprised to find this site, in the 5th slot in the global rankings by feedspot search engine.

Never Imagined, when I started my scribblings way back in 2008 , It will be listed along with American heart asssociation, BMJ and others in top 10.

I need to thank the readers who make this happen.

Thank you all.

(PS :I am not sure on what basis these rankings were done though, still it adds some energy, that keeps this site running)

https://blog.feedspot.com/heart_blogs/

Posted in Uncategorized |

A new year brings “New hope”

January 1, 2022 by dr s venkatesan

After a hectic two years , let us pray & believe, the good old times will be back in our life.

Posted in Uncategorized |

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)

Posted in cardiac failure, Cardiology -guidelines, cardiology -Therapeutics, cardiology wisdom, cardiology-ethics, Cardiology-Land mark studies, Ethics in Medicine, evidence based cardiology | Tagged , , , , , , , , , |

A presentation on atrial fibrillation : Old wine in Old bottle

December 12, 2021 by dr s venkatesan

Link to PDF download 

Good news: Nothing much has changed since 2008

  • Recognizing the clinical importance of AF and the need to rule out a systemic cause is the key, Further, a genuine bedside debate about the pros and cons of simple vs aggressive treatment discussion is welcome.
  • The nomenclature issue of valvular vs non-valvular has finally seemed to have settled. The latter is banished for good reason. (Funny to note Aortic valve  was considered as not a valve for  so long !)
  • The rate vs rhythm control debate still favors the former. (AFFIRM/RACE)
  • Stroke prevention is the concern  &  anticoagulation is the mainstay. OAC/DAPT /triple therapy has evolved a little more in the last decade. Though stoke is a major concern, we rarely see neurologists & cardiologists debate closely on risk profiling issues of such patients. (at least in this part of the world.)
  • Whether we have conquered AF or not we have become experts in creating an unlimited number of bleeding risk scores. Understanding and applying them at the bedside need special memory and expertise.
  • On the combative front, ablation strategies, however, advanced they look, are vested with the risk of injuring the surrounding structures. My biased opinion is that the risks are prohibitive except in very refractory and troublesome AFs. (with all these 4D, contact, cryo, etc)  Recall the CABANA study. We are beginning to understand, the true embryological face of pulmonary veins insertion points is so variable, and residual sleeves are very rampant that will sustain the AF even after an apparently successful ablation.
  • LAA appendage closure studies again don’t look rosy as the device itself is prone to thrombus at least in the early periprocedural period. (Watchman requires more security and protection than the Inmates !)

Final message 

AF is a simple arrhythmia in 9/10 patients. Please, let us not complicate it. We must ensure, systemic and non-permanent forms of AF should not drain our cardiac resources. We shall follow basic principles of managing a cardiac arrhythmia that will suffice in the majority. An occasional patient needs to be referred to an EP specialist.  

A new look at AF risk estimation for stroke

doi:10.1001/jamacardio.2021.3709

Posted in Atrial fibrillation | Tagged , , , |

An Important work in Clinical cardiology : The hidden gem of “Diamond & Forrester” !

December 1, 2021 by dr s venkatesan

     If anyone asks to shortlist the best papers that were, ever published in clinical cardiology, I am sure, this one will reach the top ten. It was 1979, the field of cardiology is just waiting to explode. CAD was managed primarily with drugs and occasional CABGs.  Coronary angiograms were an academic luxury. Both thrombolysis and PCI were unknown. Fortunately, Clinical cardiology was still alive and kicking. Dr. George Diamond and  Dr. James Forrester from  Cedars Sinai, New York worked together to bring this masterpiece. How and when to suspect CAD in the general population? For the first time probability was applied as a diagnostic tool. 

Link to the NEJM Paper

The paper begins by analysing basic clinical symptoms, risk factors, then gradually dwell deep into the population-based likelihood ratio, of CAD with the help of stress ECG, Thallium, and fluoroscopic coronary calcium. It finally ends up with a magical fusion of the  Bayesian theorem into clinical medicine. It essentially taught us how to accrue scattered knowledge, clinical judgment, and diagnostic acumen among physicians in a community and aggregate them to a powerful statistical evidence base.

A popular Inference from the DK model still asked in cardiology boards

It’s more than four decades since this paper was published. There have been some concerns about DF classification in the current era.  It was compared with the new Duke risk and found to be less valuable in the low-risk CAD population.(Wasfy MM, et all AJC 2011)  The concept of pre-test probability deciding the diagnostic value of screening tests is very much valid. We need to recalibrate the DF scale for the current population and new generation screening methods like MDCT etc..(Gibbons et al Jamanetwork 2021 )

Forget the pros and cons, DF study told us the importance of clinical judgment in the decision making process. Now, we are living in a glamorous new world of cardiology. Cath labs have become our 24/7 office suits, always in hot pursuit for instant fix solutions. Still, we often find ourselves desperately blinking at the doors of EBM, for the elusive answers to some critical queries. Why the same intervention seems to work in one large study and totally go wanting in another? (MITRA-FR vs COAPT)

Where are we erring?

The problem is the way evidence is created. It is often made up of data collected from poorly framed questions and methods, which are incompletely collected or wrongly interpreted. I wish, Bayesian theorem derivatives also address the probability of how pure is the pre-test (research) evidence base available in a scientific community. The core of truth in statistical science lies in, how we understand and define the number needed to treat, (NNT) and the number needed to harm (NNH) with any treatment or diagnostic modality.

Final message 

Artificial intelligence and machine learning are projected to be the next big thing in medical science However, the probability of machines prevailing over, human clinical acumen, backed by a sound knowledge base and observation skills appears very minimal. Let us see. Meanwhile, I wish every young cardiologist to go through this paper by D&F to get enlightened.  

Reference

1.Diamond GA, Forrester JS. Analysis of probability as an aid in the clinical diagnosis of coronary-artery disease. N Engl J Med. 1979 Jun 14;300(24):1350-8. doi: 10.1056/NEJM197906143002402

2,Wasfy MM, Brady TJ, Abbara S,  Comparison of the Diamond-Forrester method and Duke Clinical Score to predict obstructive coronary artery disease by computed tomographic angiography. Am J Cardiol. 2012 Apr 1;109(7):998-1004. doi: 10.1016/j.amjcard.2011.11.028. 

3.Gibbons RJ, Miller TD. Declining Accuracy of the Traditional Diamond-Forrester Estimates of Pretest Probability of Coronary Artery Disease: Time for New Methods. JAMA Intern Med. 2021;181(5):579–580. doi:10.1001/jamainternmed.2021.0171

Further reading 

1.The Duo of D & F didn’t stop with that. They went on to make produce another fabulous paper on the hemodynamic classification of STEMI. Which is discussed elsewhere

Dr. Diamond & Dr . Forrester

 

 

Posted in Uncategorized |

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

Posted in bio ethics, Histroy of medicine, Medcal research, Medical education, Medical ethics, medical quotes | Tagged , , , , , , |

FAME 3 fails to defame CABG, cardiologists need not worry though !

November 5, 2021 by dr s venkatesan

News: Series of clinical trials fail to clear the ongoing confusion in the business of cardiac revascularization.FAME 3 is the new addition. 

Caution: A non-academic journal review

There is no secret, about this cold war happening in an incognito mode for territorial rights between cardiologists and cardiac surgeons in glamorous cardiac suits for the past two decades. Of course, we keep believing this is a friendly fight in the overall interest of CAD patients. The ultimate winner should be the patient, not anyone else. Will that happen? Will anyone will allow that to happen? I am not sure.

The FAME3 is a stunning large study from 50 centers FFR guided multivessel PCI, that failed to dethrone CABG (or at least it wanted to sit along with it) I am not a seasoned statistician but definitely can’t understand the logic behind the methodology* and the choice of words in the conclusion from a paper published from a renowned journal.

 

 

(*I can recall an article about Non-inferiority trial  from Lancet (Ref 1) )

FAME 3 aftermaths: A dizzy Interpretation

Before accepting the fact that, FFR guided PCI wasn’t able to show its superiority or to unable to prove its non-Inferiority, while CABG was clearly found to be non-inferior, (rather superior) to PCI, we should take into account an important caveat in the concept of FFR itself, which has at least half a dozen serious hyperemic and non-hyperemic flaws that demanded a more superior,non-hyperemic indices like iFR, RFR, qFR, etc.

Those of you who still believe PCI would be an undisputed modality in multivessel CAD  should take up the challenge and disprove the superiority of CABG by doing the same FAME 3 subset with iFR and other stuff. (Eagerly waiting for the hypothetical iFAME 4 trial)

One more way to Interpret FAME 3: How can we accept FFR guided multivessel PCI as inferior, unless we have an FFR guided CABG (FAME 3 didn’t do this) to compare? Can you guess if only pre-CABG FFR was mandatory criteria, that would have excluded or included important grafts, what would have been the impact of CABG? This is a more dramatic suggestion, that will say sorry to FFR,( the old physiological friend,) and label it as a new villain.

Final message 

Multivessel PCI still has a long way to go before trying to dethrone CABG.  But, strictly scientific cardiologists need not worry much and they can continue to indulge multivessel PCI without FFR, which is no longer unscientific ! Thanks to FAME 3. I think one of the Important indirect consequences (?purpose) of FAME 3 would be, playing the end game for FFR.

Reference

https://doi.org/10.1016/S0140-6736(07)61604-3

Posted in Cardiology -Therapeutic dilemma, Cardiology -unresolved questions, Ethics in Medicine, fame study ffr, Fracional flow reserve | Tagged , , , , |

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.

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.

 

 

 

 

 

Posted in acute coronary syndrome, Cardiology -unresolved questions, RIsk factors, wisdom in cardiology | Tagged , , |

ISCHEMIA trial is a tough nut to crack : Don’t lose heart, we will some how tame it !

November 2, 2021 by dr s venkatesan

There are a whole lot of scientists trying to jailbreak and expose the limitations of the hugely popular ISCHEMIA trial which put the emergency breaks in the way we used to practice cardiology. Not everyone is happy. While few are ready to apply the brake, many continue to love the accelerator.

This study (Ref 1)  talks about an important issue. How much of the CAD  populations in the real world will match the ISCHEMIA trial population? It concludes it is just 32%.  It suggests caution to the cardiologists to understand this trial from a proper perspective. Don’t give too much importance, lest we may end up with Inappropriate non-intervention. 

Sounds too good? 

But is it real?

The authors of ISCHEMIA have countered this claim. (Ref 2)If we include all mild and moderate symptom cohort Ischemia study population is very much relevant in the true world and, actually constitutes about 68 % .

Final message 

Clinical trials are the greatest gift of science and EBM. But why is that …it never fails to confuse us at each and every step, while we accumulate tons and tons of evidence.

I wish someone do a mega four-limbed study on what really our patients are getting in the overall CAD care.

  1. Inappropriate non-intervention 
  2. Appropriate Interventions 
  3. Inappropriate interventions
  4. Appropriate non-Intervention.

I could easily guess the winning theme of this hypothetical trial. (That’s not good news though) However, response 4  If practiced in the right spirits would have the maximum impact on global cardiovascular health in terms of both healing and saving.

Reference

1.Chatterjee S, Fanaroff AC, Parzynski C, et al. Comparison of patients undergoing percutaneous coronary intervention in contemporary U.S. practice with ISCHEMIA trial population. J Am Coll Cardiol Intv. 2021;14:2344-2349.

2.Maron DJ, Bangalore S, Hochman JS. The glass is at least half full. J Am Coll Cardiol Intv. 2021;14:2350-2352.

 

Posted in Uncategorized | Tagged , , , , |

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