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Archive for the ‘cardiology -Therapeutics’ Category

“We have a 24/7 cath lab with an open door policy. Our cardiologist arrives at 15 minutes’ notice. Door to balloon time is less than 60-90 minutes”, 

“Great, so, you can always offer a successful treatment for STEMI”

“No, that we can never guarantee.” 

 “Oh, It Is not the answer, I  expected”

“I agree, it sounds disappointing, but. truths are less pleasing. What I am trying to say is, there are a number of factors other than the availability of a grand cath lab and agile and effortless hands, that try to reperfuse the myocardium in distress.  I agree, we do save lives occasionally in a dramatic fashion. Recently we resuscitated an almost dead man with CPR and ECMO-guided PCI. But, most times it turns out to be just a customary ritual that takes us to the legal and therapeutic  endpoint* of STEMI management”

*Both salvage & non-salvage

“I didn’t get you, Can you explain further?

See this curve and try to understand it yourself. (I would say, this is the ultimate curve to understand in the entire field of coronary care)

Can you guess what will be the outcome for C to B, or B to A ?  In the real world, a substantial number of interventions take place at an Invisible point E beyond A  Source: Gersh BJ, Stone GW, White HD, Holmes DR Jr. Pharmacological facilitation of primary percutaneous coronary intervention for acute myocardial infarction: is the slope of the curve the shape of the future? JAMA. 2005;293:979–86

Slippery slopes and edgy Interventions

At what point the patient lands up in the curve & at what point the interventional cardiologist intervenes (or does not intervene) matters the most. 

The gaps between benefit and harm can change in a few strokes of time. The reperfusion tamasha can get more curious if we realize both the slope of the curve & its absolute position are dynamic. It can shift to the right or left with reference to the patient’s Initial medications, MVo2 confounders, the quantum of collateral circulation, myocardial hypoxia threshold,  previous ischemic episodes, conditioning, etc. So, basically, we are reacting to events and trying to rush up things. Don’t worry about all this. Cardiologists have every expertise and equipment to tackle untoward events.

STEMI is not always myocardium under fire

Finally, and most importantly STEMI, though a cardiac emergency. all should not be equated with the house(myocardium) on fire analogy. It can also be a spontaneously aborting, settling, or evolving, self-extinguished controlled fire, and the myocardium may take it easy. All that it requires is some deep ischemic slumber. Don’t try to poke it with all our violent hardware at one go in the name of salvaging. What is required is proper CCU care to take care of potential arrhythmia, angina, or failure. One may create more damage if trying to dowse non-existing flames furiously, which expresses in the form of reperfusion Injury and no-reflow to the myocardium. (Which might have reperfused at leisure without experiencing the injury.)

It is worth pondering over this question.

Why does even an apparently well-timed primary PCI of IRA leave behind a significant LV dysfunction or even a  scar? This is a clear case of “successful PCI failed reperfusion syndrome”. It is better cardiology community defines successful primary PCI with reference to predischarge  LV function, not on the IRA patency and mystery endpoint called TIMI 3 flow.

Final message

Cath lab doors that are open 24/7,  with experienced cardiologists may matter little if we are double-blinded against multiple scientific and non-scientific factors that are visible as well as invisible. 

Counterpoint

How good is late PCI? Are you not aware benefits of the open artery hypothesis?

You need to learn a lot man, before posting such posts.

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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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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 54–63https://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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Why ISCHEMIA trial conclusions often make us nervous?

Because, we know we can’t follow the lessons from it with true intent, as many of us are near slaves to Invisible Interventional forces in some form or other.

I would think, ISCHEMIA trial in one sense was a wasted effort. We always knew OMT is superior to any sort of PCI in stable CAD  (Backed up with COURAGE /BARI 2D/and of course the deadly exposure by ORBITA )

Anyway, we did ISCHEMIA for the sake of deniers, with huge public funding to prove the truth as truth.

Still, I am sure ISCHEMIA will be looked down, by most elite Intervenionlists. For the rest, it becomes a tough fight with their conscience. 

A recent review on European cardiology review 

Final message 

I don’t know, how many more trials would be required to tell us the same story all over again. Hope we grow enough COURAGE to follow the ISCHEMIA lessons. Let us (try to ) make a full stop on this issue.

 

 

 

 

 

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Some of the questions  addressed  in this presentation

1.What happens to fetal blood pressure during maternal hypotension how good is fetal autoregulation?

2.Why is LSCS increasingly preferred mode of delivery in heart disease complicating pregnancy challenging the traditional scientific concept?

3.What is likely hood of patients with moderate mitral stenosis developing pulmonary edema during prolonged 2nd stage of labor?

3.What is the missing link between PIH and PPCM? How prepartum cardiomyopathy differs from postpartum?

4.Is Eisenemneger really an absolute contraindication for pregnancy?

5. How can we continue VKAs warfarin or Acitrom throughout pregnancy? What are the potential problems of double switching one at 6th week from VKA to Heparin and again from heparin to VKA  at  12th week?

Hope, the man-made hematological bridge in pregnancy has been finally liberated from confusion (Who is saying not yet?)

 

6. On what evidence base the safety margin of 5mg cutoff for Warfarin and 3mg for Acitorm was decided?

7. Who is insisting on us to do Anti-Xa monitoring for LMWH in pregnancy? Is it really needed? What does the American society of hematology say?  (ASH guidelines for VTE in pregancy 2018) Why we don’t insist on Xa estimation in acute coronary syndrome?

8. What is the inflection point of at which risk of termination is almost at equipoise with continuing pregnancy in various heart diseases.

A GIF run-through of the presentation.

PDF & video version will be posted

 

The ultimate reference 

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How many times you have treated cardiac arrhythmia in both emergency & non-emergency situations?

Infinite times.

How many times did you really bother to know the mechanism of a given arrhythmia before ordering medication or shocking?

Hmm,.. let me think. (Except for AVNRT/ AVRT, and few VTs, very rarely I have worried about the mechanism  !)

Why is it so? because treatment takes priority and we are able to tame the arrhythmia even without knowing the real mechanism.

The following slide is a gross summary of the cardiac arrhythmia mechanism

Understanding cardiac arrhythmia is vitally important for a few reasons in a few settings.

  • In acute settings, we need to know automatic tachycardias will not respond to shocks. Reentry tachycardias will respond more promptly. (Of course, we may not know it till we shock ) Calcium blockers like verapamil might block triggered activity in MAT. Overdrive pacing is the answer for many automatic tachycardias and some refractory reentrant tachycardias (ATP protocols in ICD has taught us this ) 
  • In the chronic setting when you contemplate mapping, locating, and ablating arrhythmias, mechanisms are important. The task here is locating slow conduction paths and decoding the diastolic circuit around the scar  (If you plan ICD, knowledge about mechanism  becomes redundant again)

  • Finally, knowing the mechanism of arrhythmia is a fascination by itself to help understand the great subject called cardiac electrophysiology, where 100s of ion channels work nonstop drawing the action potential on a moment to moment basis sustaining our life.

A challenge

Can you localize a VT and find the mechanism in a patient who is Ischemic /hypoxic and acidotic? You can never do it. Please note, most polymorphic VTs can’t be localized. The mechanism is either automaticity, trigger activity, or even micro-reentry. You need to shock and look for the causes.(Link to How does the treatment of monomorphic VT differ from Polymorphic VT? )

Final message

Should we need to know about the mechanism of arrhythmia we treat?  Definitely yes, if you have that passion to know the truth, or else just order Amiodarone or shock and check out of CCU. (Of course, we have a very good option of calling EP consult the next day.)

 A review article on mechannism of cardiac arrhymias

Rev Esp Cardiol. 2012;65(2):174–185

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           Practice of cardiology is simple as long we don’t dwell deep into coronary physiology.

One of my patients asked, why he was told his total occlusion in LAD appears safer now, which was subtotal a few months ago.I told him, it is indeed true. It is the fear of subtotal disease that’s prone to a fresh coronary event. In total occlusion, chances of that happening are less or nil.

 

How can you say 100% block is safe?  Is that always true?

No, it’s not always true. He was surprised when I said it is not 100 %, even 90% lesion can be safe if it’s not causing significant angina and responding to OMT. Of course, It is the morphology and stability of the lesion that will dictate* the outcome in the subtotal occlusion. If the lesion is stable, FFR is good >.8 (TMT is poor man’s FFR equivalent )  you can leave it as it is. Doing OCT /Virtual histology /NIR spectroscopy to define the vulnerability of plaque is neither practical nor desirable (Extreme academics is injurious to health) 

So it is not the degree of the block that’s going to matter, but the effects of that block on distal circulation that will decide the rules of the myocardial revascularisation game. But unfortunately, both you, (the patients) we (the cardiologist) are finding it so difficult to come to terms with this basic truth in spite of multiple guidelines. 

 

Meanwhile, CTO however makes it much easier to make a decision. One need not bother the content of CTO unless you plan an Intervention. I guess there is no FFR for CTO. Are we aware of any studies that have quantified antegrade flow across a 10% patent LAD and compare it with the Collateral flow in LAD in 100% CTO?

We have long glorified a concept of the open artery hypothesis. (Mainly in Post STEMI though) No one has dared to test and compare a hypothesis that a closed artery might still score over the open in at least some of the subsets of stable CAD. Such a study can never be ethically forbidden after all its a well-observed truth in the real world. 

Reference 

Trials on CTO  revascularisation DECISION CT (Not useful )   EURO-CTO  (May be useful) 

 

 

 

EURO CTO https://academic.oup.com/eurheartj/advance-article-abstract/doi/10.1093/eurheartj/ehy220/4990878?redirectedFrom=fulltext

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This post was originally written in 2013.

A middle-aged man with STEMI  came to our CCU.  It is just another case of STEMI and asked my fellow to lyse.

Anterior STEM ecg

But it was not the case . He, told me, Sir, the patient had a syncope following chest pain and he has injured his face and Jaw. He was actively bleeding. When I saw this face, it was indeed  frightening.Strptokinase induced bleeding

What shall we do ? When a patient  with STEMI presents with bleeding facial Injury

  1. Rush for Immediate PCI (Which was  of course not possible in our place as it happened out of office hours! )
  2. Take that ultimate risk and thrombolysis
  3. Give only heparin ( Many times it is as good as  lysis )

We took a (bold ? ) decision to thrombolyse with streptokinase.(After  a CT scan which ruled out any Intracranial bleed like hematoma etc) Clopidogrel was also given.

absolute contrindication for thrombolysis facial trauma

Patient continued to bleed in the initial 3 hours and was oozing in the next 12 hours. Blood transfusion was contemplated, but it was not required. Dental surgeon opinion was sought, his teeth were pulled and a compressive bandage was applied.It arrested the bleeding.The ECG settled down.LV function was almost normal with minimal wall motion defect. He is posted for a coronary angiogram later.

Final message

 There may not be anything called “Absolute contraindication” everything appears relative

I presented this in the weekly clinical meet,  with a tag line of  How to save a patient, apparently by violating a standard guideline. Not surprisingly, It evoked laughter amusement from learned physicians. I wasn’t. Guidelines are meant to guide us agreed.They can not command us. They are not legally binding documents as well! Many lives can be saved if only we have the courage to overrule when it’s required.

Afterthought

Had this patient has bled to death during lysis what would have happened to the treating doctor? (or )If the patient has died due to MI, because of deferred thrombolysis, what would be the line of argument?

2020 update.

This case scenario is a non-issue as of today. With so much experience, we straight away do PCI . Just manage the oral bleeding if any.

 

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The Country of mine with 140 crore population, is under complete lockdown mode. We are anxiously tense in one aspect, but enjoying the free time due to the peculiar “Corona effect” on cardiac emergencies.

Unable to understand you . . . please go away

What happened to our 24/7 busy CCU ? Does it happen only in my hospital? Can’t be. Let me check it right now. I called my fellow, who has since become a leading cardiologist in the nearby town.

guidelines

I have since called many of my close contacts. In both Government and private hospitals. The pooled data were analyzed in a virtual cloud memory. I am fairly convinced, our observation was indeed true.

The following can be considered as near facts.

  • There have been at least 50% minimum dip of Overall ACS cases. It even went down to 80%reduction in a few places
  • Even UA/NSTEMI showed a significant drop.
  • There was general hesitancy to do primary PCI even if it’s technically Indicated.
  • All most all STEMI were lysed. Heparin was liberally used.
  • Many patients preferred telephonic consultations.ECGs were reported over mobile platforms
  • None of the back pains & gastric pains were admitted as atypical chest pain.
  • Most cardiologists closed down their regular OPD
  • For the first time, Govt institutions were considered worthy to refer.

Why ACS Incidence nose dived?

  1. Under recognition?
  2. Under-reported ?
  3. Low Incidence?
  4. Low rate of referral?

STEMI that goes under-recognized and unreported? The consensus was, it’s less important factor as currently, very few are unaware of the Importance of chest pain and widespread availability of emergency services 108/911

Does that mean real incidence has Indeed come down?

The global atherosclerotic burden,(the substrate for STEMI) in the society is nearly constant. Still, the incidence of ACS has declined dramatically in the lockdown period. This conveys an important message and compels a search (research)

The plaques that are waiting to rupture in the population somehow getting a reprieve. Mind you, the presence of a risky plaque in LAD alone won’t cause a STEMI. It needs a trigger. The day to day physical stress, spikes of catecholamine, emotional swings, traffic pollution etc. The only plausible explanation appears to be the vulnerable patients along with their plaques are also locked up inside its Intimo-medial home. (Armchairs and bed rests can not only treat STEMI , they can prevent it too !)

Why the incidence of NSTEMI /UA has also come down?

Again, the same factors might operate. But, more likely self-stabilizing pseudo / Low-risk ACS is a distinct possibility.

A significant chunk of UA /?CSA/suspected NSTEMI patients come from referrals by GPs.The biggest pool of cases for cath labs comes from this group of noncardiac/Atypical chest pain syndromes*. Which shows some Incidental (In)significant lesions that subsequently becomes a cardiac emergency.

Since they have reduced their consultations the numbers have quite significantly reduced.

*Chronic CAD masquerading as ACS is not a forbidden concept

Final message

We are taught some important lifetime lessons in cardiac practice by this 20 nm, lifeless RNA particles.

1. The bulk of the ACS in the society is triggered by the day to day stress of the fast and furious “Just do it” world. The mitigating effect of social lockdown on physical and emotional stress on plaque dynamics on the incidence of ACS will be a big research subject in the coming months.

2. More importantly, It has exposed the existence of one more hidden epidemic in the community “manufactured coronary emergencies” propagated by a resistant cardio tropic virus that has disseminated deep into evidence-based cardiology. Let us cleanse this virus too after finishing off the Corona.

Postamble

It’s just a crazy opinion from a scribbling, blogger. However, I am sure, It’s only a matter of time, great journals like NEJM, JAMA, and Lancet will be screaming the same truths in a more palatable evidence-based manner.

Meanwhile, I can see early signs of restlessness(withdrawal) among us waiting for early release from the lock-up and resume the customary mode of evidence-based cardiology practice.

As I complete this write up . . . .surprised to find this report from TCT MD. Similarities if found, could only be coincidental.

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