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Archive for the ‘acute coronary syndrome’ Category

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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I have never found it difficult to retrogradely cross a dangerous epicardial collateral in complex CTO. Delivering a twin stent in a partial culotte strategy for a bifurc lesion has never tested my talents. Stenting a left main across the LAD, jailing the LCX with OCT support is my favorite time pass. Crushing a calcium infested diffuse long lesion with diamond-tipped ablator appear as breezy as shopping in a mall.

But this one is really challenging 

What is that?

Understanding these four studies (Ref 1-4 ). They dogmatically say medical management confers definitive protection in chronic coronary syndromes. It stretches our limits of Imaginary Intelligence! How can a near tight coronary obstruction sitting right across your eyes, be left untouched? The latest one seems to suggest we can even ignore FFR positive lesions.

COURAGE BARI 2D ORBITA ISCHEMIA DRSVENKATESAN SHD CHRONIC STABLE HEART DISEASE PTCA PCI ACC ESC SCAI 2GUIDLEINES

It requires 4 negative forces . . . to bring one big positive Impact!

I don’t understand who is funding these negative trials and glorify it, and trying to defame the talents in me. All these studies have a huge lacuna. They conveniently exclude high-risk cases and allowed liberal cross over to PCI later on. Even the just-released ISCHEMIA trial had 38 % patient with no angina. (But why they received PCI ?) How to Interpret these trials and extract the true conclusion? .One consolation is, I know these negative trials have a very short memory and expiry date. Very soon I shall be liberated from the clutches of this negativism.

Even as I scribble this, my inner conscious is telling a completely different story. I agree we do Indulge a lot in stable Ischemic Heart disease. (SIHD).  I am yet to be clear what exactly we mean by SIHD. How is that near 90 % mid LAD guy ran 12 met exercise with negligible perfusion defect and still FFR was .7 ?

OMG, save me from this academic conundrum and help to acquire true wisdom.

Reference

1.Weintraub WS, Spertus JA, Kolm P, Maron DJ, Zhang Z, Jurkovitz C, et al. For the COURAGE Trial Research Group. Effect of PCI on quality of life in patients with stable coronary disease. N Engl J Med. 2008;359(7):677–687. [PubMed[]

2.BARI 2D Study Group. Frye RL, August P, Brooks MM, Hardison RM, Kelsey SF, MacGregor JM, et al. A randomized trial of therapies for type 2 diabetes and coronary artery disease. N Engl J Med. 2009;360(24):2503–2515. [PMC free article] [PubMed[]

3.Al-Lamee R, Thompson D, Dehbi HM, Sen S, Tang K, Davies J, et al. ORBITA Investigators Percutaneous coronary intervention in stable angina (ORBITA): a double-blind, randomised controlled trial. Lancet. 2018;391(10115):31–40. [PubMed[]

4. International Study of Comparative Health Effectiveness With Medical and Invasive Approaches – ISCHEMIA

 

 

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Background STEMI knowledge check : Evidence-based Ignorance

I think , It is unfortunate, In the management of STEMI , the two popular strategies of myocardial reperfusion is made to fight with each other as if they are perennial enemies for over two decades. Suddenly, someone with a rare coronary insight thought, why fight each other , they can have a friendly hug and work together. That brought the concept of pharmco -Invasive approach or strategy(PIA) backed up by STREAM, FAST-MI, and TRANSFER AMI studies.Yes, it appears to work well and devoid of all the early adverse events of pPCI. (Much to the dismay of ardent fans of Primary PCI )

*May I add one more shocker of a fact . Deep subset data mining from the above trials did show very early lysis may even act as a perfect stand-alone therapy negating the need for acutely one pharmaco Invasive PCI altogether.(Which was never published) Don’t get alarmed the concept is nothing but , the good old lysis , followed by leisure & elective Ischemia guided PCI in all uncomplicated STEMI.

Now coming to the FAQ in Cardiology Boards: Why is the time window for PIA is 3 to 24 hrs ?

The simple answer for an uncomplicated fellow is “published studies have shown benefit only in this time window. If you do PCI early (,<3h) after lysis paradoxically both bleeding and pro-thrombotic complication over the stented lesions are more common. The upper limit is 24 hrs , since by that time we lose all the potential for myocardial salvage”

End-

Larger version of the answer

(Advanced readers who are willing to get confused, may read further)

1. Lysis and immediate PCI doesn’t go well at least in trial world. (FINESSE study, by Ellis et all NEJM 2008) Though cardiologists tend to blame lysis (effect of) to Interfere with their hand skills, it can very well be the opposite. The PCI undo the true benefit of lysis. For cardiologists to accrue maximum benefit in the early time window, they need to be too fast, in the process, they accelerate and fuse adverse events of both modalities.

2. The time window 3 to 24h could simply be evidence-based empiricism. In the major STREAM trial, invasive limb happened between 6 and 16 hours only. We stretched both in the top and bottom in the time clock and made it 3 to 24 hours with other trial data.

3. One realistic reason could be this. It requires a minimum of three hours for a patient to reach a place of coronary Invasion after lysis. So one may argue its time allowance for transport .It comes in handy at times.

4 .If the patient reaches earlier, we need to delay the PCI intentionally to please the evidence based medicine. Mind you, every minute delay increases the chance of no reflow as the microvasculature goes for edematous and porous death.

5. Please note, the time window for pharmaco Invasive strategy will go for a tail spin if the initial lysis is failed. Here, we have to rush I guess. Mind you, In this situation, the evidence based blaming that early PCI increases the adverse events immediately following lysis goes topsy turvy . This is where , we should recall old studies of routine rescue PCI (without clinical criteria) rarely succeeded to correct failed thrombolysis (SWIFT trial)

6.Now, why not PCI after 24hrs? The game can be played reversed if you document ongoing Ischemia in IRA or Non IRA, one may do it . The problem arises when the flawed thought process of a cardiologist could legally justify all PCI beyond 24 h /class 3 Indication after STEMI.The argument goes like this. I think this patient has residual silent Ischemia in- spite of severe LV dysfunction (Suspicion is the justification, to which ,unfortunately no one can dispute) It only suggests open artery hypothesis is still trying to raise from the graveyard more than a decade after its near burial.

Final message

To all those energetic, evidence-based cardiac physicians, we all know coronary care is all about time. In fact, we need to be blessed much more than a sense of time. There is something called medically( or spontaneously )stabilized ACS.  Please realise , “timely and safe intervention” for your patients could simply mean either playing the time button slow/ fast / slow or fast forward / pause or simply shutdown the cath lab, reach home early and enjoy some music or movie in your favorite streaming player.

Reference

1.Ellis SG, Tendera M, De Belder MA, FINESSE Investigators Facilitated PCI in patients with ST-elevation myocardial infarction. N Engl J Med. 2008;358(21):2205–2217. [PubMed]

2. Armstrong PW, Gershlick AH, Goldstein STREAM Investigative Team Fibrinolysis or primary PCI in ST-segment elevation myocardial infarction. N Engl J Med. 2013;368(15):1379–1387. [PubMed]

3. Danchin N, Puymirat E, Steg PG, T, on behalf of the FAST-MI 2005 investigators Five-year survival in patients with ST-segment-elevation myocardial infarction according to modalities of reperfusion therapy: the French Registry on Acute ST-Elevation and Non-ST-Elevation Myocardial Infarction (FAST-MI) 2005 Circulation. 2014;129(16):1629–1636. [PubMed]

4. Cantor WJ, Fitchett D, Borgundvaag B, TRANSFER-AMI Trial Investigators Routine early angioplasty after fibrinolysis for acute myocardial infarction. N Engl J Med. 2009;360(26):2705–2718.. [PubMed]
5.. Bonnefoy E, Steg PG, Boutitie F, , CAPTIM Investigators Comparison of primary angioplasty and pre-hospital fibrinolysis in acute myocardial infarction (CAPTIM) trial: a 5-year follow-up. Eur Heart J. 2009;30(13):1598–1606. . [PubMed]

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A middle aged women , with acute onset left sided chest pain and ECG changes was seen by a general physician. He had little hesitation in labeling the patient as  ACS( To be precious he reported the ECG as lateral wall Ischemia) and asked for an echocardiogram to rule out a heart attack  (This is how cardiology is practiced in many areas) .

This patient came to my lab  for the Echocardiogram .The echo window was poor , It showed a structurally normal heart and there was no pericardial effusion. I suspected something systemically wrong in this patient and asked for a X ray chest .

Subsequent scrutiny of this  patient revealed she had moderate left tuberculous effusion. ECG changes are attributed to this. We know pericardial disease can cause ECG changes that mimic ACS. While pericarditis can elevate the ST segment. Can pleuritis without effusion cause ECG changes.  What is the demarcation point between pleural from pericardial surface ?

What are the ECG features of pleural effusion ?

  • Low voltage qrs.
  • Poor R wave or even q waves
  • QRS axis shifts are due to true anatomical / electrical shifts
  • T wave inversion as in this patient

Mechanism of T wave inversion in plural effusion.

T wave represents ventricular repolarisation. To be frank I am not able to give an exact mechanism of such  defects in pleural effusion.

The following mechanisms are  suggested

  1. Left sided pleural effusion can closely mimic pericardial effusion .One can get low voltage QRS in lateral chest leads .
  2. Anatomically I would guess the plural fluid also hugs the heart and the inflamed pleuro-pericardial Interface (Is there fibrous continuity ?) result in some degree of epicardial interference or reversal in electrical polarity.
  3. The true effects of mediastinal shifts with large effusions  on ECG is not clear(Lead V 3 and V4 may pick V5 / V6 signals in left sided effusions )
  4. Fluid altering the electrical conduction property
  5. Associated minimal pericardial effusion and  effectively causing epi-pericarditis as a part of poly-serositis .
  6. After ruling out all plausibility one may think primary ischemic changes as well.

Teaching points and potential error

To label  a left-sided pleuritic pain with ECG changes as ACS can never be considered as a serious error.However , rushing such patients to cath lab or   lytic therapy along with heparin leads to more trouble. ER physicians should always keep in mind T wave inversion in isolation is indeed a rare cause* of ischemia. Still,  as a physician first , we need to have a check list to rule out common non cardiac conditions. Pneumothorax is one another entity that can exactly mimic a STEMI with ST segment shifts and q waves.It’s also possible left sided pleural effusions produce q waves and mimic an old MI as this case report reveals.(Constatine A Manthous Chest 1993)

I think  X-ray chest is least used modality in a coronary care unit for various reasons . Still ,the utility of which can never be undermined and should be used diligently . 

*Of course we shouldn’t  forget a sinister form of ACS  referred to as Wellen’s LAD  syndrome which may present with dynamic T inversion.

Reference

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Evening cardiac clinic is generally a relaxing place until an occasional patient  with vague chest discomfort present with this sort of an ECG .

He was a 68 y old hypertensive and was on Tablet Amlodipine .After a cursory look at his ECG , eyes wandered to look for some specifics. Suddenly ,my  ECG reading skill was stretched . Is it really LVH ? or Ischemia ? I asked for any old ECG which he couldn’t provide. I had to blink  more than a moment , before asking him to describe his chest pain in detail one more time . I got almost convinced it was not ACS  since he was having only localized pain over left side of chest. Still , I didn’t have the courage to send him home. An Echo was done.

Curious to know what the Echo showed ?

 

Yes , you also probably guessed right . It is LVH and there is no wall motion defect either.

How to differentiate between Ischemia and LVH ?

This is a common question asked in the board exams.There are number of ECG clues to differentiate the two .Mostly it will help  fellows  to pass exams. Academics rarely comes to your rescue when patients land with  chest pain  especially at odd hours.

Find the answer in this link

https://drsvenkatesan.com/2009/12/12/how-to-differentiate-lv-strain-pattern-from-primary-lv-ischemia/

 

Now comes the real twister , Does presence of LVH  exclude Ischemia in any way ?

Why can’t be ACS in a patient with LVH ?

When I posed these questions , some one suggested global longitudinal strain  with speckle  tracking to rule out ischemic wall motion defect, my resident suggested  high sensitivity Troponin and Ischemia modified albumin.

Whatever is the technological assistance , one thing  is certain,  we need to finally fall back  on patient’s symptoms . Unstable angina is neither an ECG diagnosis nor biochemical  or Echo diagnosis . (Its all about patient description about his angina , that clinches the  diagnosis !)

It remains a fact normal spot Troponin can never rule out  ACS on time ,( Even patients with unstable angina who  harbor  tight  LAD lesion can be both ECG /Enzyme negative )

When we are not sure ,the traditional coronary care dictum  shall operate .It demands admit, observe, with serial ECGs and enzymes. This protocol cant’t be followed strictly for a variety of reasons . We may have to rely entirely on our clinical Intuition accrued over the years.

A modern-day cardiologist might have a different dictum .The simplest solution in such situations is a diagnostic radial snap shot coronary angiogram .It is an easy way out  . . . , and avoids the trouble of spending wasteful minutes of personal conversation with the patient .The ethics of outsourcing history taking , patient record review or even clinical examination has pushed the definition of professional competence in coronary care into murky grey zone.

One more reason we should hesitate to rush these patient to cath lab is the detection of  incidental insignificant CAD (Which will loom larger than life when they are wheeled in from  ER)  that will  lead on to  further inappropriate chain of events.

How relevant is clinical acumen in modern era ?

Clinical acumen in medicine can never be taught in class rooms or read in text books. It is the innate ability to  combine  knowledge, experience ,skill  and  lastly (and most importantly) courage to ignore conflicting and pervasive data from new generation Investigations. Instead of helping us ,they often directly affect our increasingly vulnerable native medical cognition.

Even if some one is blessed with a good clinical acumen it seems to have little value many times as power of Investigations and fear of missing a event will prevail over it ! I have been victim of this phenomenon many times and not able to follow what my mind preach me !

What happened to this patient ?

I had to admit him against my  wish (Of course I was safe!)  He too got admitted reluctantly and was observed till morning , spent Rs 5000 for pack of investigations and stay , was discharged without any issues with a diagnosis of simple Hypertension and LVH.

The non academic bug  didn’t stop there  . . . again  contrary to my conscience  I had to suggest  optional coronary angiogram to rule out true CAD as a precautionary statutory advisory !

 

Counterpoint 

How do you know this is really not CAD  ? I won’t believe unless and until I see the CAG and its normal.

Ok, Let me post his angiogram if he decides to  undergo it.

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 When half a dozen guidelines from extremely evidence based “Esteemed cardiac societies”  decide to confront an Incomprehensive cardiologist , there is no other way , but to create  a personalised i-Guidelines on STEMI !

*(i-Idiotic)

 

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Some of the noise bites from a busy cath lab after a  mid noon angioplasty

         Oh’  that  looks bad , whats that projecting !

There is some haziness too ,

            Make sure its not a flap,

  Better to do IVUS or should I OCT ?

           Shall I  post dilate with NCB ?

Should we cover with  another stent ?

           I think we can manage with Tirofiban or Reopro 

Call the chief ! suggested a first year resident,that seemed to be the most reasonable noise bite among all .Yes, the final command came from the chief cardiologist after a 10 second glance over the workstation ,”Guys,  forget it , . . its acceptable  pinching, DAPT will take care of it , just ensure adequate ACT till night , put the next case . . .on table” !

That’s fairly common chat session in any high volume cath centres (Which ended abruptly  in this case with the chief’s uttering)

Does any body know  what the chief meant by  the term pinching ?

  • Is it the  pinch of Intimal fold ?
  • Is it pinch of plaque ?
  • Is it a flap ?
  • Is it a plaque prolapse within the strut ?
  • Or just a evaginated thrombus
  • A subintimal calcium speck ?
  • A longitudinal stent deformation?

Any one knows the histology ? Is there any natural history  study of such pinching ?

Iam afraid no one knows . But common sense tell us it can be anything  between a totally benign entity to  Imminent nidus  for an acute stent thrombosis , depending upon the patient’s destiny and physician’s luck !

How does one make a decision in such an uncertain situation ?

The decision to leave that pinching is taken by any  cardiologist  based on his past experience or  Inexperience or both. Some do IVUS/OCT , many don’t . Whatever the decision  ( empirical or scientific ) its  going to be tentative  and  outcome is any body’s guess.

Final message

Coronary arterial pinching is a dangerous cath lab slang used exclusively by expert Interventional cardiologists , often after a hurried PCI ! It may sound  innocuous .To label a protruding plaque as a “safe pinch”demands heavy courage that is an essential requirement  for a successful Interventional  cardiologist , which most of them are blessed with !

Reference 

1.No Reference as such :There is no specific study about histology of coronary pinching  .Though , IVUS and OCT data are available for various post PCI shadows , it never addresses the issue of pinching specifically as no one is clear about what they mean by it.  Hence ,we are planning to decode this long pending mystery with our own  PINCH-iVUS  study.

2.This article from Circulation Imaging  new generation IVUS could reveal  histology of pinching

f5-large

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