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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 

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)

 

 

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.

 

 

 

 

 

“Third wave? what is that”

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?)

 

Syncope is one of the common, yet difficult symptoms to evaluate especially in the elderly. Post-prandial syncope is one condition likely to be missed out.As the name suggests It has a distinct relationship with food intake. Mild fall in postprandial BP is an expected response but if it exceeds a  limit* syncope is triggered. (*Highly variable)

Hemodynamics of Postprandial state

  1. Normally splanchnic circulation demands up to a 25%  increase in blood volume after a moderately large meal. 
  2. When this happens there must be compensatory vasoconstriction elsewhere especially in muscles. Lack of this response results in inappropriate falls in SVR. (The second mechanism is more constant and can be disproportionate to fall of BP)
  3. The mediators for this are either neurogenic or hormonal or both.
  4. Gastrointestinal mediator (Vasoactive Intestinal polypeptide dysregulation) is thought to play a major role. 

From Jansen et al  Archives of Internal medicine 1995

When does it occur?

It can manifest as early as 15 minutes, up to 2 hrs. The fall in systolic  BP is around 20mmhg. More common with large, hot meals. The fact that it can occur up to 2 hrs post meals, there is a likelyhood we might overlook it in history.

Other differential diagnoses 

Management 

There is no specific therapy. Some of the following might be effective.

  • Caffeine,
  • Somatostatin,
  • Acarbose,( α-Glucosidase Inhibitor ) 
  • Avoiding acute high carbohydrate intake.
  • A psychogenic component can be noted in a few that is attenuated by cognitive-behavioral therapy.
  • Midoridine, an Alpha¹ receptor stimulant  can be surprisingly more effective in some who have overlap with orthostatic hypo  (Cleve Clin J Med. 2010 May; 77(5): 298–306.)

Final message

Postprandial hypotension/syncope is a less recognized entity. As always, history is the most important diagnostic tool in the evaluation of syncope, which comes free of cost as well. The diagnostic yield is much greater than sophisticated Holter and event monitors.

Please note, there is a much more prevalent, lesser version of this condition, ie postprandial dizziness or giddiness. However, as already stated there is a significant overlap between orthostatic hypotension and postprandial syncope. It’s worth ruling out diabetes and autonomic dysfunction, (even subclinical Parkinsons) in elders with such symptoms. 

Reference

Here is a  comprehensive and elegant study (I think, It is only one of that kind on this topic )

1.Jansen RWMM, Connelly CM, Kelley-Gagnon MM, Parker JA, Lipsitz LA. Postprandial Hypotension in Elderly Patients With Unexplained Syncope. Arch Intern Med. 1995;155(9):945–952.

Postprandial hypotension Jansen1995

 

 

 

 

 

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

 

 

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.

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