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Archive for the ‘Cardiology – Animations’ Category

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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Reading X -ray chest can be as blind as a bat flying in the dark . It needs lots of Imagination . (Many times the blindness continues to cath lab as well  during structural interventions is a different story !)

Yes ,its true  any one can recognise a cardiomegaly in X-ray  . . . but  Which chamber is responsible for cardiomegaly ? and quantifying each ones contribution to the increased CTR is the critical question. 

We know the 4 chambers in the heart are arranged in a complex pre-specified  (Antero -superior and right to left orientation ) still , the CT ratio in X-RAY chest is based on the diameter formed by two chambers only ie right atrium and left ventricle.

However, any of the 4  chamber enlargement can increase  CT ratio in pathological conditions.

  • LV enlargement is the most common cause for cardiomegaly as it is the normally  border forming.(DCM, Aortic valve, HT diseases)
  • RV can do it when it enlarger grossly forming the left heart border(COPD, Severe pulmonary hypertension of any cause)
  • RA can enlarge to both pressure and volume overload.(CHF, with RVF)
  • LA is least likely to be border forming as it is midline structure .Since It tends to enlarge posteriorly and superiorly it rarely enlarges sideways. Occasionally In severe mitral stenosis it can enlarge to the right and cross the right heart border causing the classical shadow in shadow.

Since I have struggled with X ray orientation of heart chambers in my early days (Still i do sometimes!) Just thought , why we are not fusing a X-ray with a given patients echocardiogram that will help understand the chamber anatomy .

Fusion Image of X ray chest PA view with apical 4 chamber in ECHO. (Rotated to specified angle to match heart border)

Note : The Left atrium is not only left of RA , its also posterior and superior to RA.This makes the IAS  not actually  pure right left to relationship but also a slight  infero to superior and antero posterior  orientation.(This can be realised when we puncture the IAS from RA side the needle goes more of superior)

X ray chest left lateral view is  fused with para- sternal long axis view. Please note this is not true anatomical correlates. The RV shown in echo is actually RVOT but in X-ray its more of RV body .

* A note of caution : The fused Images are rough attempt to co-register x-ray with echo. There is sophisticated software in some new generation cath labs to mix fluro images with live TEE data that aid in Interventions.

Postample
A bedside Instant point of care echo is becoming a norm in clinical cardiology practice. Why bother about  X-ray then ? Agreed to that point to a certain extent. But, I used to tell my (amused ) students that technology based lazy learning doesn’t help build a strong scientific  foundation which would ultimately threaten the patient care one day !

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Ventricular pressure volume loop is an Important ( often feared !) concept to learn for cardiology fellows . . . I would say , It is not that hard to understand !

These loops tell us the secret  hemodynamic story of a 300 gram “mass of muscle” called the heart  and how It handles about 100 ml of blood every beat and successfully ejects around 70 ml into Aorta and Pulmonary artery *

108356heart_beating

While doing this life sustaining job , It would seem the heart muscle  conducts a perfect, non stop, hemodynamic orchestra with 4 electro-mechanically coupled phases which is depicted as classical ventricular pressure volume  loop. Mind you, this loop is plotted pressure volume data from a single heart beat and it can’t be time correlated with heart sounds or ECG as the two parameters loop around in same time cycle.

Watch this animation , carefully and read the appearing annotation that come along with each phase.That should suffice to understand the basic. (For Audio version go the video link in the reference )

Modified from a clipping from Giphy.com.Original source of this Image is not located. Whoever has done this thanks and it’s a great attempt.(I have tried a fusion Image of doppler mitral Inflow in diastole and Aortic pressure curve during ssytole to bring PV loop an anatomical perspective.)

*Note: When we say PV loop it means about by LV by default . We do have seperate RV ,LA (even RA?) PV loops.

Is there clinical application for  PV loops ?

It may not have any direct use , but understanding  how a ventricle works in normal conditions or at distress especially during acute decompensations or after surgery  is vital. With modern gadgets like LV assist devices,  Impella used widely and to assess hemodynamic efficiency of transplanted (Very soon total artificial hearts) , PV loop analysis of both RV/LV will be critical.

Is there any simple Lab modality that can draw this Loop curve instantaneously ?

echocardiography lab methods for ventricular pressure volume loop

 

Very few companies make it . AdInstruments that make power lab monitors, enable us to visualise PV loops invasively .

 

Can we get PV loops non invasively by Echocardiography ?

Echocardiography  provide us both volume  and pressure data.With improving accuracy of data it should be possible to plot the loop manually with some effort. (Still , we can’t get pressure in all points of cardiac cycle )

I guess, sooner 3D volumetric machines with automated online doppler pressure data across the valves  can help us draw the ultimate LV functional  curve live on real time.If that happens cardiologists will be further enriched and hemodynamically enlightened !

Final message

The shape , size , timing and the slopes of this loop  givs us vital info about the functional aspects of ventricle. First one should understand the normal loop , then , we can dwell on the effects of acute and chronic lesions like regurgitations, cardiomyopathy ,cardiogenic shock etc.

Reference 

An excellent knwoledge base on the topic with a  video 

Dr. Richard E. Klabunde, PhD

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Failure of  enocardardial  cushions  to separate and reach the  predesignated destination  ie  right and left AV valve is the basic embryological feature in AV canal defect .This brings whole AV ring  down and stretches the distance between  the semi-lunar valve (especially aortic)  with that of LV , thus elongating  the LVOT into a classical  goose neck deformity.The defect  has a profound  impact on how the AV node and its branches penetrate the ill-formed AV junctional tissue and fan out into the ventricle. There are  four basic issues  that are responsible for the various conduction defects in AV canal defect.

  1. Postero- inferior  displacement of the A-V node is the key abnormality .
  2. Hence  AV node penetrates the ventricle at the level of crux which is abnormal .This results in short his bundle  (AV node short of compressed with His  early direct origin of the left bundle branching)
  3.  Left bundle branching system by itself is also abnormal  with hypoplasia   left anterior bundle branches.
  4.  Right bundle branch is relatively long and elongated

Physiological effects

  1. Prolonged PR interval (50%)
  2. QRS  axis shift can be extreme right or left , but superior direction is a rule .Typically its around -180 . Left axis deviation is distinct in downs syndrome (Counter-clock wise rotation q in lead 1 and  AVL ) .It should be learnt , the ECG features (due to  anatomical defects in AV conduction system  ) can be be  easily modified by the hemodynamic stress of  ventricles  due to associated conditions and classical pattern may non exist )
  3. Surprisingly high grade AV blocks are rare (“viz a viz” LTGV )

Electro-physiology

Short HV interval is documented  in AV canal defects inspite of prolonged PR due to small his bundle length.

membranous ventricular septum 2

conduction system in av canal defect vsd

A large Inlet VSD , simply takes over the place meant for the conducting system and its pushed down and out

Reference

Robert Feldt from Mayo clinic did excellent work about this issue and published in Circulation, Volume XLII, September 1970

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Left main ostial lesion remains a  challenging task .A new stent design is  proposed here.

The lesion

Left main  ostial  stenting lesion003

The hardware 

left main ostial coronary stent drsvenkatesan

The technique

Left main  ostial  stenting lesion002

Final message

This thought came  when I  recently encountered a patient with a left main ostial  stent which was projecting well into aortic root .It is an open access patency ,whoever is capable of converting this idea  to a clinically applicable technique is welcome to proceed !

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Click over the Image  for animation

ptca balloon for PTMC inoue 002

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Cannon waves occur when Atria contracts against a closing tricuspid valve of  right ventricle .( There  would be a equivalent left atrial cannon which  goes into pulmonary vein as well  , it is discussed elsewhere !)

Cannon waves  happen only when P waves fall within QT interval in ECG as QT represents the electro-mechanical systole of  ventricles.  (Since P wave represents atrial systole , it is simple to understand when it falls within QT both atria and ventricular contractions collide to produce a cannon wave into the neck or pulmonary veins.)

The following two images of cannon waves  taken from the legend  Dr Paul woods own tracing  .

irregular cannon waves in jvp  complete heart block

regular cannon waves in jvp  svt avnrt  11 va conduction  002

Regular cannon waves

Occur during SVT  with 1:1 VA conduction.*

1 : 1  VA conduction  can be considered as  absence of  AV dissociation  (Rather  disciplined  VA association with every beat ) This is essential to create a hemodynamic  milieu for regular cannon waves.

* In AVNRT , VA conduction in strict  sense  is a misnomer  .It is simply a retrograde conduction thorough  the AV node .

Irregular cannon waves 

  1. Complete heart block .
  2. Multiple random VPDs
  3. Some patients with VT.*(Who are those patients ?  Those with AV dissociation when retrograde “P” wave falls  within QT interval cannon occurs. As expected this occurs in random fashion  which makes  the cannon fire irregular.

Can we get regular cannon in VT ?

Yes , but rare . As explained earlier this can happen only if AV  association occur on a retrograde fashion.

Further reading in this site

What-is-a-cannon-sound  , how is it related to cannon wave ?

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