Dr.S.Venkatesan MD

Archive for the ‘Cardiology -guidelines’ Category

STEMI secrets : Honesty is still Intact in “Harrison text book” of medicine

Posted in acute coroanry syndrome, Cardiology -guidelines, Cardiology -Therapeutic dilemma, Cardiology -unresolved questions, cardiology-ethics, Primary -PCI, Thrombolysis, Thrombolysis -Tips, tagged euro pcr, Harrison principles of internal medicine, management issues in cad, Primary PCI vs Fibrinolysis, scai acc aha esc guideliens, stemi secrets, tct md, tips and tricks in priamry pci, tips in acs on September 1, 2022|

Why didn’t you do it … for this patient?

 “I thought, he was not the right patient for the procedure. I believe, what I did was the correct decision. Why all this fuzz? after all, the patient is doing so well without that procedure,.. are you worried about that? 

“No, I need an explanation, we have a fully functional cath lab in our center. The patient came in the right window period. Still, you haven’t offered the best mode of treatment”.

“I can reiterate it again sir. Just because a lab is available 24/7, it doesn’t make all patients eligible for a  PCI. I think I didn’t commit a professional misdemeanor when I decided in favor of fibrinolysis. In fact, I would be guilty had I rushed him to the cath lab, just to satisfy the misplaced scientific position we have decided to adopt. If you think, I am culpable for successfully treating a patient without taking the patient to the cath lab, you may proceed with the penal action.

Before that, I would request you to please read the current edition of this book we all revere. (Which continues to mentor physicians all over the globe for the past 50 years)

 

The current edition of Harrison 2022 is just out. I thought, there is something great learning point in Cardiology chapter, specifically about the reperfusion strategies in STEMI

My hearty thanks to the editors of the chapter for the crystal clear expression about this much-debated procedure* and specifically choosing the word “PCI appears* to be more effective ” (even) if it is done in experienced persons in dedicated centers. The choice of the word used by the authors is Intentional and must be applauded. This message must be propagated to all our fellow physicians. What a way to convey an important truth pertaining to the management of the most common cardiac emergency, while many in the elite specialty are so dogmatic in their assertion without verifying the reality.

*  The verdict is still under the jury even after 3 decades, since the PAMI days of the early 1990s. Thank you, Harrison. What a gentle, but a righteous way to express an opinion about a procedure that is apparently enjoying a larger-than-life image based on a handful of studies and a flawed meta-analysis.

Final message 

Primary PCI is just an alternate form of treatment to fibrinolysis in STEMI. Both are equipoise in the majority of patients. Extreme care and diligence are required to harvest the small benefit the PCI seems to provide.  There are lots of ” if and buts” that decide the success of this procedure. Get trained, and do it selectively for those who really need it.

Postamble

You may call yourself a super-specialist. But, please realize, If you have any doubt about key management strategies, never feel shy to take a cue from Internal medicine books. The greatness of these warrior books is that, it comes devoid of all those scientific clutters backed by premature evidence. 

 

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Curve of wisdom in ACS : Open Cath lab doors may mean nothing , if the windows are closed !

Posted in acute coroanry syndrome, acute coronary syndrome, Cardiology -Criteria, Cardiology -guidelines, cardiology -Therapeutics, Cardiology -unresolved questions, tagged acc aha esc scai gudilines, acs, acs management, evidence based cardiology, open artery hypothesis, primary PCI vs thrombolysis, reperfusion, reperfusion injury, stemi, time window in acs on February 1, 2022|

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

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 on December 17, 2021|

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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How to misunderstand health economics ?

Posted in Cardiology -guidelines, Ethics in Medicine, Social medicine, wisdom in cardiology, tagged comparative effectiveness, cost effectiveness, cost ineffectiveness, drsvenkatesan, evidence based medicine, health budget of a country, health care indices, health care wastage, health economics, junk science, medical quote best, outcome analysis, quality of health care on June 28, 2021|

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Acute “Corona” syndrome : Glad to know plaques are also in lockdown mode !

Posted in acute coronary syndrome, Cardiology -guidelines, Cardiology -Interventional -PCI, cardiology -Therapeutics, Ethics in Medicine, Uncategorized, tagged Acute corona vs coronary syndrome, ethics in cardiology, evidence based cardiology on April 3, 2020|

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.

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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Early thrombolysis knocks out pPCI yet again . . . this time from Shanghai !

Posted in Cardiology -guidelines, cardiology -Therapeutics, cardiology journals, tagged EARLY MYO trial circulation, ppci vs thrombolysis, primary PCI vs thrombolysis, stream trial on October 18, 2017| 3 Comments »

Primary PCI (pPCI) is a  glorious revascularization strategy for STEMI practiced for over 2 decades  but still has not proved its perceived mettle convincingly as a large population based strategy. In the mean time, the utility value  of  thrombolysis  was systematically  (Intentionally too! )  downgraded in the minds of both academic and public mind.

Truth can’t be buried for long. Series of revelations are coming up restoring the superiority of early thrombolysis over pPCI even in PCI capable centers.

In 2013, the high Impact STREAM trial argued  for pharmacoinvasive approach within 3 hrs as it was at equipoise with a pPCI. Now, EARLY -MYO  from China vouch  for pharmaco- Invasive approach  till 6 hours. (Just published in Circulation September 2017 )

 

 I think we need to wait for some more time , for another prevailing  falsehood that need to be busted ,(Looking  out for some straight thinking new generation cardiologist to do it !)

What is that ?

Many of us have misunderstood(rather made to !)  that pharmaco Invasive has a defined therapeutic endpoint ie taming  & stenting the IRA . This is absolute ignorance  happening even in state of the art centres ,ironically this beleaguered concept is  backed by peer-reviewed papers from premier journals. The fact of the matter is , If thrombolysis is stunningly successful (Which at the least happens in 50 % ) one can stop with that , it’s also a therapeutic endpoint at least for time being .

Is coronary angiogram a baseline test like ECG ?

That’s what current cardiologists with cutting edge knowledge  seem to believe !  Do you agree ! I am sure I’m not !

 Patients with STEMI who had successful thrombolysis who had an  apparently uncomplicated course (Assessed by strict clinical ECG, ECHO criteria) need not go for coronary angiogram in the immediate future.In fact some good guidelines strongly argue for it and call it as Ischemia driven PCI ! but very few seem to respect that concept.)This will not only contain the cost and ensure the vast majority of Inappropriate (  scientific quackery) coronary plumping activity in human race.

Searching for an elusive data ! Can some one help ?

I have been searching for data , from all those major pharmaco invasive studies (Which is not being reported /shared or analysed )

How many  patients in the “success cohort” after thrombolysis  who subsequently land up with urgent PCI related complications when trying to stent an already reperfused IRA or while tackling  coexisting Innocent or non-innocent non IRA lesions ?

* Complications and adverse events  may be acceptable in patients who had failed thrombolysis or who are  unstable  but even minor adverse events are forbidden in patient with a truly successful and asymptomatic patient.

Final message

So called scientific facts have very short half life !  for the simple reason they are let loose in human domain prematurely !

Reference 

1.Efficacy and Safety of a Pharmaco-Invasive Strategy With Half-Dose Alteplase Versus Primary Angioplasty in ST-Segment–Elevation Myocardial Infarction Jun Pu, Song Ding, Heng Ge, Yaling Han, Jinchen Guo, Rong Lin, Xi Su, Heng Zhang, Lianglong Chen and Ben He EARLY-MYO Investigators  Circulation. 2017;136:1462-1473

2.Paul W. Armstrong,  Anthony H. Gershlick,   for the STREAM Investigative Fibrinolysis or Primary PCI in ST-Segment Elevation Myocardial Infarction .  Team N Engl J Med 2013; 368:1379-1387April 11, 201

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