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Archive for December, 2018

ACS mimickers in ER : Wish I call it “Ischemic” pleural effusion ?

Posted in acute coronary syndrome, tagged , , , , , on December 28, 2018| Leave a Comment »

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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The crazy science of coronary reperfusion : When TIMI 1 & 2 beats “TIMI 3” in the myocardial salvage race . . . cardiologists get confused !

Posted in Uncategorized on December 8, 2018|

The prime job of cardiologists is to restore coronary blood flow in an emergency fashion. While we do this with reasonable success ,there is still a missing link between our Initial aim and achieved goal.

It’s all too common situation in any busy cath lab , to see two similar STEMI patients with identical time window & proximal LAD as IRA , in totally different scenarios. In the first patient we find a trickle of flow in LAD , who is relatively comfortable  with normal LV function (In whom , emergency primary PCI might appear redundant.) While the other patient , even after rapidly established TIMI 3 flow , LV wouldn’t look good at all . All our efforts to reperfuse is found wanting.  Ultimately LV goes in a downward spiral , ends up in irreversible cardiogenic shock or fatality inspite of Impellas, ECMOs and other LV assist exotica !

 

intra-coroanry-thrombus (2)

I can promise , you can never guess from the angiogram whether this ACS patient was very much comfortable or he is in cardiogenic shock on ventilator  unless I reveal the history. Am I right ? That is the mystery of coronary circulation and hence its so critical to serve the myocardium what it wants ? Never treat a coronary artery in isolation !

What is the possible explanation ?

The first trickle (Say TIMI 1 which is usually spontaneous or lytic related ) is the one that’s going keep the muscle viable and possibly prolong the time window for the subsequent reperfusion strategies .Hence it is the timely TIMI 1 or 2 is much more critical than delayed TIMI 3 (Still rapid).

Time window woos :

Who fixed the reperfusion  time window as  6 to 12 hours ? Do you know on what basis  the acceptable delay of 30 to 60 mts related to primary PCI ? was made acceptable by  cardiology community ?  If you analyse the published data both are highly contentious and empirical. ( Suggest you scrutiny the data from DANAM2 , PRAGUE and AIR PAMI and come to your own conclusion) (*These are the 3 sacred studies done with few thousand patients  that redefined our approach  to STEMI and gave the licence to waste the golden hour ! )

I remember reading  the Robins pathology book (Bible of  pathology William Boyd as well ) in early days of medical school myocardium may die even within 1 hour with wavy necrosis, contraction bands etc. Looking back some times I  wonder how the clinicians have conveniently prolonged time window with whims and fancies of science Intact.

Concurring with the pathologists , we have learnt some harsh lessons inside the cath labs. One of them is that even ultra fast pPCI can fail to salvage  myocardium, meaning that time is not the ultimate thing in our race. (There should be other important determinants )

A brief journey back into our pathology classes : Have a look at this table 

Time window in stemi 6 hour 12 hour or 90 minutes

Please note, Irreversible Injury might happen any time after 30 minutes .Of course it can vary . But, the question is how are you going to identify these patients with  ultra short  time windows? source : Robbins Basic Pathology 9th Edition.Elsevier

Other factors that influence myocardial cell survival

Re-perfusion is not a single edged sword 

We may wish the concept of re-perfusion Injury is a myth : Unfortunately it is not ! Myocardium doesn’t relish (not always) the return of circulation in full dose. (May be it’s laying and taking the much needed rest with the initial Injury!)

Reperfused myocardium

Sudden gushes of blood leads to extravasation into the interstitium (due to damaged capillaries)  increases the Intra myocardial resistance and obstructs the microvascular flow. We have  witnessed more than a handful of patients going for cardiac arrest once IRA is opened (of course,  we might be  able to resuscitate many of  them )

Myocardial hypoxia resistance time

Please realise ,true  STEMI clock starts not with onset of symptoms but with time of total occlusion.There is more than subtle difference between the two. Onset of total occlusion to symptom time is not a well explored or understood Interval. We take it for granted that the onset of symptoms coincides with total occlusion.

But in multi vessel CAD, even a CTO can cause a STEMI through loss of distal collaterals. Further ,the presence and absence of pre-infarction angina (PIA*) , ischemic pre-conditioning (IPC*) sensitizing effect of  remote CAD , manifest vs recruitable  collaterals  all these make the fixed time windows with which we did our land mark studies of PCI / lysis academically  questionable.

* Both PIA  IPC are master confounders in the true time window calculations .We don’t know whether its due to ischemia tolerating myocytes or pain tolerating nerve fibres  responsible for this varying presentations.But the mystery is certain , when we  realise the angiographic  spectrum of ACS can range from silent ATOs to painful CTOs

Final message

Is timely reperfusion (and its favorable effect ) lies in God’s domain ? If you we  believe myocardial susceptibility , arrhymogenicity and recovery to hypoxia is genetically determined ,then the difference between fate and science Is much narrower than we think .Its appears we can change the former with the later with both positive and negative outcomes. So ,the  “f”  word may not be a forbidden at-least in the STEMI management. It resides not only  within the human genomic codecs written with double-helical nucleic acid fonts . . . but also  in the nimble and restless hands of both novice and experienced interventionists !

                       

A study proposal 

Let me make a hypothetical statement .A significant subset of patients with STEMI have ultra short myocardial survival and we are unable to identify these hypoxia challenged hearts where primary PCI related delay could be a myocardial sin. Any one willing to prove or disprove this hypothesis ? If some body take this quixotically important study in STEMI management please give me some credit as a contributor !

 

 

 

 

 

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