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Archive for the ‘Cardiology -unresolved questions’ Category

Missing links in IHD : What is the relationship between Ischemia & cardiac arrhythmias ?

Posted in Cardiology -unresolved questions, Cardiology-Arrhythmias, tagged on January 5, 2023|

The term Ischemic heart disease (IHD) was once very popular, but many abandoned it as it became an academic cliche.  CAD & CAHD are the other terms that are equally popular and prevalent. Stable IHD was in vogue till recently, which was again replaced by “chronic coronary syndrome’ now. Honestly, I feel the original term IHD to be restored however outdated it may look. it encompasses the entire spectrum of clinical cardiac disorders.

Manifestation of Ischemia heart disease 

  1. Angina
  2. Infarction
  3. Cardiac failure
  4. Arrhythmias 
  5. Silent ischemia
  6. Sudden cardiac death

 The purpose of this post is to share some thoughts on the link between Ischemia and cardiac arrhythmia. 

 

 

What is the relation between  Ischemia and cardiac arrhythmia (especially VT)

A.Strong relation

B.Weak relation 

C.No relation 

D. Recurrent ischemia protects against arrhythmia.

The fact that. acute Ischemia triggers primary VT and VF and is the leading cause of electrical death is sufficient to fix the answer without any doubt. But, the  truth is, the link between Ischemia and cardiac arrhythmia is more complex  

If we could agree ischemia is a powerful trigger of ventricular arrhythmia, will every patient with chronic stable angina be at risk of  VT after walking a certain distance?  

So, where does cardiac arrhythmia fall in the Ischemic cascade of events? the fact that chronic ischemia on exertion rarely precipitates an arrhythmia conveys a strong hidden message. 

Coming back to, STEMI where the arrhythmic risk is powerful, still, if the same acute ischemia, presents as UA/NSTEMI, with severe compromise of resting blood flow, it doesn’t trigger a VT usually. This fact should baffle us and question why even acute ischemia carries low arrhythmic risk except when it happens with STEMI.

The potential mechanisms of lack of VT in UA* (No evidence /Class C evidence) 

  • In UA, ischemia is primarily subendocardial, and the neuronal innervation which is more in the epicardial plexus fails to get stimulated. This is in contrast to what happens in STEMI. Here It is transmural ischemia and the sub-epicardial is always involved.
  • In this context, the high prevalence of VT in Prinzmeal angina where there is subepicardial injury is a point to be noted. In young NSTEMI/STEMI crossover entities like Wallens and De-winters, there is a high adrenergic drive, which triggers the VT rather than ischemia per-se.
  • Finally, even in STEMI, only a minority of 15-20 % of myocardium become arrhythmogenic and face fatal complications. What protects the rest of the 75 %? is genetics, epigenetics, or fate.? 

The practical implication of this question

  1. The VT in ischemic cardiomyopathy is related more, to the scar burden, strategically placed islands of dead and live tissues, and the overall severity of LV dysfunction. This makes the Ischemic VT, as a term,  could be a misnomer.  In fact, it is the viable ischemic tissue that is a powerful trigger.
  2. If baseline chronic ischemia is less likely to trigger any VT, revascularisation in chronic CAD (PCI/CABG) is unlikely to give relief from it as well.

Anti-arrhythmic adaptation in chronic Ischemia 

We know about ischemic preconditioning and angina relief. It may apply to arrhythmic preconditions as well. Recurrent ischemia, while we expect to elevate the arrhythmic risk, it is a curious and exciting possibility it might work as an “anti-arrhythmia vaccination” at the molecular level. 

Final message 

So, what is the true relation between ischemia and cardiac arrhythmia?  

It is not as strong as one would believe it to be( Except in the early hours of STEMI and a very small subset of NSTEMI.

Curiously, in certain lucky beings, recurrent baseline ischemia may protect against future arrhythmias.

Reference 

1.A V Ghuran, A J Camm, Ischaemic heart disease presenting as arrhythmias, British Medical Bulletin, Volume 59, Issue 1, October 2001, Pages 193–210, https://doi.org/10.1093/bmb/59.1.193

2.Janse MJ, Wit AL. Electrophysiological mechanisms of ventricular arrhythmias resulting from myocardial ischemia and infarction. Physiol Rev 1989:  69 ; 1049 –169

Few more questions worth pondering 

Why do certain VTs struggle to become sustained?

Will discuss this later (Will need to talk about the diameter of the primary Rotor, the Curvature of rotors and source-sink mismatch, etc. )

How often  Ischemia triggers AF?

I haven’t heard of Ischemic SVT, or ischemic AF much. Trying to accumulate more Info on this.

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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 , , , , , , , , 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 , , , , , , , , , 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

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Knowledge check in Brugada syndrome : A rapid fire session

Posted in cardiac electrophysiology, cardiology -Therapeutics, Cardiology -unresolved questions, Cardiology-Arrhythmias, early repolarisation syndrome, Electro physiology, Electrocardiography-ECG, ICD and Pacemakers, tagged , on January 5, 2022|

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

Posted in Cardiology -Therapeutic dilemma, Cardiology -unresolved questions, Ethics in Medicine, fame study ffr, Fracional flow reserve, tagged , , , , on November 5, 2021|

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

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

Posted in acute coronary syndrome, Cardiology -unresolved questions, RIsk factors, wisdom in cardiology, tagged , , on November 4, 2021|

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.

 

 

 

 

 

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How did all those calcium entered my father’s coronary artery doctor ?

Posted in Cardiology -unresolved questions, tagged , , , , , , , , , , on September 3, 2021|

“It was severe double vessel disease &  turned out to be a complex angioplasty in LAD ” 

Why doctor? what happened?

It was a hard lesion, there was plenty of calcium deposits. It was not clearly visible in the angiogram. I had to do IVUS. Curiously, the calcium was clustered in all the three planes of the vessel ( intima the media and adventitia) and they projected into the lumen blocking the path.

Image collage representation purpose

Thank you, doctor,  how did you manage to remove it,?

It was a real struggle. I had to break the calcium shell before deploying the stent. (What we refer to as lesion preparation). I thought Initially I can displace it with high-pressure balloon inflation, I went up to 40 ATM pressure,  finally needed a  rotational ablation with a burr.  ( IVL -Intravascular ultrasound was an option, but may not have helped either because of heavy Intimal load, Angiosculpts, and the cutting balloons (Wolverines) we don’t have)  

Was it a risky procedure?

Yes, of course, see the sharp burr rotating 150 thousand resolution per second hugging the coronary artery without damaging it

By the way, why did he accumulate so much calcium inside doctor? Can it be due to his daily calcium supplement doctor?

Oh – my ? that is important new Info. I think that wasn’t noted in the case file. Tell me more, How long did he take it? 

I think he is taking it for long years. He is rather obsessed with it, consumes lots of calcium in his diet as well. He was also taking vitamin D as it once went down to 15 ng/ml. He needed to strengthen his bone which was porotic in the Dexa scan. Was that a problem now? But his serum calcium was always normal, Then, from where does, this calcium enter my dad’s coronary artery doctor?

I am sorry I  don’t know the answer so far. Now, your dad seems to teach me a lesson. It has to enter from the bloodstream or happen de nova due to degeneration. Calcium along with phosphate is a tightly regulated metabolism.They are closely linked to diet, bone, renal and endocrine glands function. We don’t understand how there can be a no-relationship between blood calcium and coronary arterial calcium. Again plaque calcium and serum calcium may or may not correlate. Understand our knowledge base with which we treat you. 

That’s ok doctor. But do you think,  should he stop calcium & vitamin D tablets from now on?  

Hmm, you keep asking tough questions. I will be a fool if I asked you to continue right!

Please go through this article from Jhon Hopkins and decide ( & MESA study 10 year follow on calcium supplement Ref 2)

Final message

The human body is a wonderful machine. Calcium is a life-sustaining ion present in each of the 75 trillion cells we have. We are programmed to handle all elements except in a fraction when true pathology strikes. Never try to outsmart our natural homeostasis with unnecessary and unsolicited chemicals. Indiscriminate calcium supplements are definitely an unfriendly guest for the coronary artery.

Now, Is it just a coincidence?  the new epidemic of coronary microcalcification detected by CT scans(What is your Agatston’s score buddy ?) is matching with a steady increase in per capita consumption of calcium and vitamin D tablets.

Reference

1.Anderson JJB, Kruszka B, Delaney JAC, et al. Calcium intake from diet and supplements and the risk of coronary artery calcification and its progression among older adults: 10-year follow-up of the Multi-Ethnic Study of Atherosclerosis (MESA). J Am Heart Assoc. 2016;5:e003815.

2.Myung SK, Kim HB, Lee YJ, Choi YJ, Oh SW. Calcium Supplements and Risk of Cardiovascular Disease: A Meta-Analysis of Clinical Trials. Nutrients. 2021 Jan 26;13(2):368. doi: 10.3390/nu13020368. PMID: 33530332; PMCID: PMC7910980

For advanced readers

1. Does calcium stabilise a lesion or destabilize a lesion?

It does both .

2. Is CT calcium score correlate with serum calcium?

Yes, it does.Ref : Sanghoon Shin,  European Heart Journal, Volume 33, Issue 22, November 2012, Pages 2873–2881, https://doi.org/10.1093/eurheartj/ehs152

3. What are the various types of coronary calcium? Which is a more tricky lesion? 

 

 

Image courtesy -Abbot A calcific nodule is the tricky one, as it can be tiny still result in invisible stent malapposition inviting future problems.

 

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Why ISCHEMIA trial conclusions often make us nervous ?

Posted in Cardiology -Criteria, cardiology -Therapeutics, Cardiology -unresolved questions, Comparative efficacy, tagged , , , on July 6, 2021|

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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Heart disease in pregnancy: Overview & management

Posted in cardiology -pregnancy, Cardiology -Therapeutic dilemma, cardiology -Therapeutics, Cardiology -unresolved questions, Pregnancy and heart, pregnancy and heart disease, tagged , , , , , , , , , , , , on April 2, 2021|

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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Issues in thrombolysis: There may not be anything called “Absolute contraindication”

Posted in bio ethics, Cardiology -Therapeutic dilemma, cardiology -Therapeutics, Cardiology -unresolved questions, Cardiology Risk assesment, cardiology- coronary care, Cardiology-Coronary artery disese, Primary PCI, Thrombolysis, tagged , , , on May 16, 2020| Leave a Comment »

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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