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A 75-year-old male post CABG with severe LV dysfunction and ICD and dual-chamber pacer in situ presented with NSTEMI.

An angiogram revealed something, and he got this form of treatment. ? What is it?

Image and case courtesy Patel R, Ghadiam H, Patel P, et al. (April 05, 2020) Angina Leading to Metal in the Heart: An Interesting Case of Saphenous Vein Graft Coiling. Cureus 12(4): e7546. doi:10.7759/cureus.7546

Features of SVG venous graft aneurysm

Graft aneurysm what are the risks?

  • Thrombosis
  • Recurrent ACS
  • Rupture 

Management 

  • Vascular plug
  • Multiple coils  (Does coil occlusion offer a permanent cure?  I can’t think so )
  • Covered stent
  • None. No Intervention Just OAC & observe, follow up can be a good option and can beat all above three in many patients.

Reference

1.Ramirez FD, Hibbert B, Simard T, Pourdjabbar A, Wilson KR, Hibbert R, Kazmi M, Hawken S, Ruel M, Labinaz M, et al. Natural history and management of aortocoronary saphenous vein graft aneurysms: a systematic review of published cases. Circulation 2012;126:2248–2256.CrossrefMedlineGoogle Schola

2.Dieter RS, Patel AK, Yandow D, Pacanowski JP Jr, Bhattacharya A, Gimelli G, Kosolcharoen P, Russell D. Conservative vs. invasive treatment of aortocoronary saphenous vein graft aneurysms: treatment algorithm based upon a large series. Cardiovasc Surg 2003;11:507–513.CrossrefMedlineGoogle Scholar

3.Nolke L, McGovern E, Wood AE: Saphenous vein graft aneurysms; the true, false and ugly!. Interact Cardiovasc Thorac Surg. 2004, 3:631-633. 10.1016/j.icvts.2004.07.011

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TAVR is a game-changing structural interventional procedure that delivers an Aortic valve percutaneously. With hardware and expertise constantly Improving, excellent outcomes are common. However, this video clip reminds us, nothing can be taken for granted in any Intervention. (Sharing a Twitter feed Courtesy Raffaele Piccolo)

Why did this complication happen? Hardware, technique, or a fragile Aorta?  or just bad time  The fatal perforation seems to have occurred near the distal arch, with no visible signs of porcelain Aorta or gothic aortic arch. What could have been done? Could an ultra-fast deployment of a covered stent with ECMO support possible? Extremely difficult task.

Further reading 

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Evidence-based medicine (EBM) is being projected as a scientific God’s secret specialty. Physicians who don’t follow EBM are considered unfit non-professionals. Presumably, in pursuit of truth, all those glamorous official bodies in cardiology bring out umpteen number of protocols, guidelines, advisories, and recommendations.

The blueprint for EBM

We have the famous 3 levels of recommendation backed up by different levels of evidence. Many of us trust these as the jury’s final verdict for most illnesses in cardiology. I would like to bring one particular issue about this hugely popular model of EBM. It is about one specific class of Indication referred to as 2b. The other day, there was an intense argument for an ICD in a young HCM patient and CRT in DCM based on this 2b stuff. Kindly request all of you to pause for a moment and introspect. We can realize, class 2b plays a mischievous game in EBM with the English language “may and may not”. It tries to push subconsciously an interventional bias from equipoise, in spite of lack of good evidence and clear divergence of opinion and a possible trend towards harm.

Further, there is widespread reluctance in many cardiac workgroups to refer class 3 recommendations as an absolute (or at least relative contraindication) It was strange to note one of my colleagues argued that,  class 3 is also a fair recommendation, to accept or reject is in our domain. I was initially shocked to hear that but had to agree with him ultimately as we realized a significant chunk of interventions we do, like delayed PCI > 24 hrs, CTOs, and chronic stable belongs to the proud class 3 recommendation. The debate came to a funny end when a senior cardiologist confessed somehow class 3 seemed to be a lesser evil than even class 2B.

Final message

For the sake of our patients, we need to bring an urgent reform in the EBM. Let us merge class 2b with class 3 and put it in a single basket and keep it out of reach to all tempting stakeholders. We shall display only class 1 in our therapeutic showcase.

Counterpoint

(*Dynamic recommendations is the norm in science, as we accumulate evidence with time.. Agreed, let us do this silently in research labs. Don’t bring it to practical guidelines. No, can’t agree. Freedom to indulge with an experimental modality in a no-option patient must always be there as we are able to give the benefit of doubt to these helpless patients. This is a valid argument but we must not forget even in dire situations  good option need not be a compulsive action, it can be in action as well)

 

 

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“Third wave? what is that”

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Basic science lessons are promptly forgotten by the time we reach the final year of medical school. How about recalling them decades into clinical practice ? The mechanism of systemic edema revolves around the interplay between hydrostatic pressure, colloid pressure, interstitial pressure. However, In the pulmonary circuit, it gets a little more complex. Acute pulmonary edema begins to occur at around 18mmhg  PCWP. What is special about this number 18? Nothing great. The lung begins to ooze when the LVEDP/LA mean pressure exceeds the colloid osmotic pressure, (that keeps fluid in situ) within the pulmonary capillaries, which is about 18mmhg. Interstitial fluid begins to collect as the basal rales go onto develop frank alveolar edema at 25mmhg. Of course, chronic situations like mitral stenosis both lymphatic reserve and thickened interstitial fibrotic process keep threshold still higher) 

To simplify, whatever be the mechanism on the left heart, during acute pulmonary edema for the lungs to get flooded, we need a well-functioning right ventricle. If only the RV has enough wisdom*, it should take the cue and slow down and help the LV out by reducing its preload. (RV’s afterload is LV’s preload right )

We know, the lungs are protected from congestion in a number of chronic right ventricular diseases, pericardial disorders, severe PH. This happens in RV infarction. This lung-protective effect might explain the heterogeneous nature of outcome in RVMI (bad to excellent) 

Final message

We know, the commonest cause of pulmonary edema is due to acute LVF. Now add one more mechanism in the genesis/and or maintenance of pulmonary edema. Vigorously contracting, RV is equally culpable. 

Here is an Important paper that discusses the key role of RV in the precipitation of acute pulmonary edema.

Some more questions relevant to this topic

1.What is the effect of RV dysfunction on paroxysmal nocturnal dyspnea & orthopnea? 

2.Explain class 3 Forrester’s hemodynamic grading of acute MI. (Why PCWP goes down in grade 3 compared to grade 2?)

 

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Nearly a century ago, Carl Wiggers helped us understand the dynamics of cardiac cycle with a historical diagram depicting systole and diastole. We know diastole has 4 phases. They are  IVRT(nil)  early rapid filling,(70%) diastasis,(0-5%) atrial contraction(25%) (Percentage filling within the brackets)

What is mid diastole?

The easiest way to define mid diastole is to divide diastole into three parts with reference to time and call the mid-third as mid-diastole. (.5 seconds/ divided by 3). But, Physiologically we can’t do that. Even hemodynamically there is no distinct mid diastole as diastole is divided into 4 phases as described earlier. When there are 4 parts how can we slice out mid diastole without an overlap? 

So, what shall we do? Technically which is the best period to be referred to as mid diastole?

Maybe diastasis. In this period either little or no flow occurs. HR heavily influence the duration of diastasis. Cardiologists especially during auscultation created the concept of calling anything happening after mitral valve opening as mid diastole. ie after IVRT which equals* A2-MV opening interval (In the true sense,  it must be the early diastole that can begin with mitral valve opening for physiologists, but for cardiologists, it begins with aortic valve closure because we can hear only closing sounds)

What happens in mitral stenosis? 

Any significant obstruction of the mitral valve, the gradient builds up immediately after the mitral valve opens. The murmur gains momentum in the early rapid filling phase of diastole, gradient spills over to fill the diastasis, and finally accelerates in pre-systole to end up in loud S 1.

 Is there really an early diastolic murmur in mitral stenosis?

  (I can’t agree. We were never taught that way)

Yes for sure. In fact, it can be the dominant murmur in many, since the early rapid filling phase of diastole contributes 70% of filling. In mitral stenosis, the early diastolic gradient will always be present. So. mitral stenosis murmur indeed begins in early diastole and extends further depending upon the severity.

If there is really an EDM in mitral stenosis, why do we still keep calling it MDM?  

Just by tradition and for convenience. Auscultatory mid-diastole is different from hemodynamic mid diastole. This irony occurs because murmur descriptions are based not on time but on phases. So, by convention, a murmur that does not occupy the IVRT phase is labeled as MDM. This also helps us to differentiate MDM of mitral stenosis from aortic regurgitation which has the exclusive rights to be called an early diastolic murmur.(Since it occupies the IVRT phase) 

Final message

This is probably a too-long post to unmask a trivial nomenclature issue in the diastolic murmur of mitral stenosis. Still, it’s worthwhile to understand this. The word “mid in MDM” is arbitrarily used and doesn’t really reflect either the time or the true hemodynamics. In fact, the same reasoning is applicable for any flow murmur across the mitral valve that is inappropriately referred to as MDM. 

Caution  

*Let me not confuse the youngsters especially undergraduates. MDM of mitral stenosis will remain as MDM in exam halls. It will never become EDM as that of AR where the murmur starts in the IVRT phase. 

 

For advanced readers

What is the earliest murmur to appear in mitral stenosis?

The first noise comes in the early part of diastole or late presystolic when atria contracts. Never in true mid diastole and gets filled up the in mid part as the disease progresses. So, we can have mitral stenosis without murmur in mid diastole. The morphology of murmur can best be understood when we correlate with Doppler echo profiles.

Is MDM of mitral stenosis crescendo or decresedo or both ?

Normally in diastole crescendo murmurs are uncommon as pressures are falling.( Ventricular contraction only can generate crescendo pressures.) Still, In mitral stenosis, there is minimal crescendo at the onset even when the  E velocity decelerates. However, there is a definite presystolic accentuation with atrial contraction which can also be referred to as late diastolic crescendo. 

*Is IVRT the same as the A2-OS interval? 

It is almost the same but not the same. Find out the difference.

 

Further reading

ongley1955

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Further reading 

Here is a book from Dr. Ralf Sundberg, a former general and transplant surgeon, a prolific researcher from the prestigious Karolinska Institue, is trying hard to spill some not-so-sweet truths. A must-read, especially for the heavily biased optimistic scientists.

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The relationship between Aorta & PA is the key to diagnose many complex congenital heart diseases. Here is a simplified illustration for gross understanding. Please refer to other sources for complete review.

 

Further reading

CONGENITAL HEART DISEASE| VOLUME 118, ISSUE 9P1390-1398, What Determines Whether the Great Arteries Are Normally or Abnormally Related?   https://doi.org/10.1016/j.amjcard.2016.07.050

 

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Caution: Some language 

News

It is heartening to note the apex body that is leading the fight against Covid in India, has responded well. It has either recalled or censured many of the Investigations & drugs, procedures that were used in this pandemic. (Not because they are futile, but they also resulted in a meaningless escalation of cost and possibly worsened the outcome)

So, what?

Beware, “non-scientific mutations” are common in medical research even in ordinary times. It is omnipresent now, and no surprise they end up as a premature evidence base. The consequences of this can be as adverse as the viral variants we fear. The global economic drain of this pandemic is definitely more than what it really deserves. The bulk of resources consumed by Remdesviers, Tociluzumabs, Ivermectins, etc. will easily cross few billions. Further, it is estimated 100s of millions were spent on Indiscriminate diagnostics like CT scans and, Interleukins, D dimers, and even RTPCRs that made a mountain out of a mole. Infinite doses of antibiotics are diligently prescribed for a viral disease knowing fully well it won’t work. One estimate In India says 800 crores worth of Zinc and vitamins were sold over the counter. (The same budget for 1000 bedded state of art hospital!) Heartless marketing. It was painful to watch hard-earned savings was siphoned from not so wealthy & poor for a simple hospital stay.

 It must be acknowledged the Government (both state and central) is doing an exemplary job taking care of both private and public health against all odds. However, on a global scale, It is unfortunate many Governments of low GDP countries were politically compelled to spend on flimsy interventions for a self-expiring pandemic. If only these funds are diverted properly, that would help us build permanent health Infrastructure in each of the underdeveloped districts. The only thing, that’s worthy to spend now, is towards the largescale manufacturing of a quality vaccine. Health economists from WHO shall genuinely audit the global expenditure of this pandemic that will help tackle future pandemics better.

(In)conclusion

The virus has decided to play its own game with humanity for whatever reason. The great news is that the vaccine is working. We hope the virus will show enough mercy and leave us shortly. Please follow the required covid hygiene and learn to live in a  personal lockdown mode so that countries need not shut down. Meanwhile, a strict embargo on excessive covid related information in the public domain seems as critical as the vaccine. (the demarcation between true knowledge and misinformation is as blurred as one could Imagine)

Postamble 

Wishing for a  smooth landing with abundant common sense (Image courtesy TIME magazine )

Happy days will be here again soon. But, never forget the harsh lessons taught by this tiny virus .“We must learn to cohabitate on this planet along with other lives peacefully. If we are adamant, God is likely to lose his patience and may not hesitate to discard us permanently “

 

 

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3D printing technology is growing at a rapid pace. Both cardiologists and cardiac surgeons are expected to benefit a lot.It helps us in understanding deformed anatomy in complex congenital heart disease as well as planning for synthetic cardiac implants. 

Currently, the technology is limited only by the chemical material used to print the heart and its components. The American chemical society is working at it to create more realistic heart models. Once we master this,  biological printing with synthetic tissue equivalents is the ultimate aim. 

Major Indications

  • Planning cardiac reconstructive surgeries in congenital heart disease. 
  • Aortic grafts in Marfan syndrome and other endovascular grafts.
  • Valve prototyping

What could be possible in the future?

A dream possibility is that, 3D printing of a patient’s own coronary artery that is diseased with an exact replica that may either act as a surgical graft or deliverable percutaneously.

It is 3D cloning of a coronary artery with a live blood flow experimental setting.(Image clipped from above video)

Final message

It is a merger of biology, chemistry, tissue engineering, and computing. Already it is used in specific conditions.(How about ordering a designer RVOT in severe TOF ?) We are approaching fascinating times in cardiology. Of course, everything would come at a price. We can reap the benefits of this path-breaking progress in science, if and only if, technology is regulated well, Indications are liberally coated with common sense.

Reference

A review article on 3D printing in cardiology Nature review 

Giannopoulos 2016

 

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