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A consult with a 62-year-old patient in my office 

Hi, welcome?  What is your problem?

Nothing doctor. I am good. 

What brings you here then?

I used to have angina before. Now, I am fine doctor but confused after undergoing this angiogram. I need an opinion.

How is your exercise capacity?

I do walk, work, and able to do almost all regular activities.

Why did you do this angiogram then? 

Had to undergo this after a doubtful stress test, Now, I am told by at least 2 eminent cardiologists, that I am having just one functional coronary artery, and it is dangerous for the all-important LAD to live at the mercy of RCA. They said they will try to fix it with wires first or CABG if it failed.

After explaining the excellent backup from RCA to LAD, I told him, “Yes, most scientific cardiologists are not trained to respect collateral circulations, in spite of the fact, many CTOs fall under class 3 (contra)Indication for revascularisation. I must admit I am not that scientific but it ensures my patients don’t really suffer unnecessarily”

“Make a pardon doctor, I didn’t get you, What I am  supposed to do ?” 

I don’t know why I was so blunt in my response  “If you believe me, forget the lesion. If you don’t, get it stented or go for CABG as per the majority advice of the eminent “. I am sorry. I think I cleared your confusion.

-end-

 

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Heart is a dynamic organ, so any auscultation by default becomes dynamic. Still, what we mean by dynamic auscultation is, to look(hear) carefully at what happens to the sounds and murmurs during different phases of respiration*, posture and induced hemodynamic stress by altering preload, and afterload, etc. (* Some of us may not consider respiratory changes as part of dynamic auscultation, But, it is to be noted even spontaneous respiration is subtle dynamism and is reflected in JVP as well as second sound mobility. While forceful breath-holding or exhalation can dramatically shut down & release venous return from entering the thorax.This is the basis of the most popular maneuver of Valsalva.

I know, dynamic auscultation is a lost art. For fellows, the only issue that seems to bother is to understand the dynamic auscultation in various types of LVOT obstruction, MVPS , and to differentiate  aortic from pulmonary regurgitation murmurs, with or without VSD, RVOT/LVOT vascular /Valvular clicks etc

Here is an old presentation (2010) of mine from the archive.

One of the great resources on this topic is from Dr Delman. Hope this book is available. There is one more exclusive atlas by Delman & Stein dynamic auscultation with phonocardiographic and pulse correlation 

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Embryology

Sinus venosus ASD (also referred to as SVC ASD)  is a defect in the failure of the sinoatrial orifice to lateralize completely to the right side during atrial septation.Left venous valve, as well as the septum secundum, fails to fuse with the roof of the atria creating interatrial communication. During this process, the developing pulmonary vein overshoot to the right side making PAPVD a mandatory add-on defect. (Harley ,Thorax 1958 ) It can be referred to as embryonal venous migration defect at the level of RA. In the same sense, it is not a true defect in IAS but a defect in septation between SVC/PV. It may also be referred to as unroofing of RUPV. The so-called Inter atrial communication actually is the confluence point of RUPV/SVC/RA.(See TEE images below) 

We know, in SVC ASD-commonest associated anomaly is PAPVC . It is not an ideal term to use though, instead, it is encouraged to use the term PAPVD (drainage) . Technically true PAPVC can not be connected to RA cavity as PV can connect either to cardinal or vitelline vein only. This distinction is helpful when we search for additional PAPVCs cranial to SVC. Sometimes we might recognize this error only after closure of SVC ASD. 

Should we close SVC ASD ? How do we close?

Age, natural history, symptoms, the quantum of shunt will answer an occasional troubling query , “should we close it at all? Surgery is the standard approach till now. What makes device closure popular? Two reasons 1.Patient /or parent’s fear of surgery  2.Cardiologist’s urge for innovative Interventional procedures. (The fact that a simple covered stent will do the job is too tempting to make an attempt) However,please note, the procedure is not at all simple as one would Imagine.

Anatomical prerequisite for device closure 

The defect must fulfill some critical anatomical essentials.  

  • It should be an isolated defect.
  • RA should not be grossly enlarged
  • Re-routing of RUPV to LA should be possible 
  • A significant circumference of RUPV should be committed to LA.
  • There should not be downward extension involving septum secundum making it an SVC + OS ASD 

Technical issues

  • Self-expanding vs balloon expanding stent (Anyone may be chosen)
  • Stent flare-up SVC RA junction crucial
  • Must ensure  RUPV doesn’t get compressed with device.

  • Forces that hold the SVC end of the stent is very important. Sometimes It may require a second proximal stent just to prevent migration of the first stent.
  • Live LA pressure and RUPV monitoring may be critical to recognize PV ostial compromise. For this, a transeptal puncture may be required (Ironically creating another mini ASD !)

 

Finally, and most importantly follow-up is mandatory with device closure since the stent is on the venous circuit as RA, SVC thrombosis expected. (Anticoagulation protocol not clearly  defined as of now )

Final message 

Device closure for SVC ASD is a good Innovation. A perfectly delivered covered stent at the RA/SVC junction will do the trick. However, In my  opinion, surgeons do a neat(More complete)  job It is time-tested. Single or double patch or warden procedure may be done.(Ref 2)

Reference 

1.Hinnerk Hansen, Phuoc Duong, Salim .M. Jivanji, A. Qureshi, Eric Rosenthal Transcatheter Correction of Superior Sinus Venosus Atrial Septal Defects as an Alternative to Surgical Treatment J Am Coll Cardiol. 2020 Mar, 75 (11) 1266-1278.

2.Warden HE, Gustafson RA, Tarnay TJ, Neal WA. An alternative method for repair of partial anomalous pulmonary venous connection to the superior vena cava. Ann Thorac Surg 1984;38:601-5. 

 

https://doi.org/10.1016/j.pedneo.2019.06.013

 

https://doi.org/10.1016/j.athoracsur.2020.03.113

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Two queries that linger in the medical profession for a long. I am afraid they aren’t addressed specifically by the stakeholders.

Question 1 

Foe a moment, let us assume there is no option to answer all three are equally important. Medical colleges are supposedly Godly places where high-quality noble professionals would germinate, let into the community thereupon, to heal the ill and suffering. The teaching faculty has a huge responsibility. They must ensure that students are transformed into responsible caregivers in the first place. They should be made to understand that the knowledge they acquire has a short half-life and medical education is all about continuous learning and unlearning. Unless teaching and research are morally genuine and scientifically perfect, the things we do in the name of patient care is going to be redundant. Hope you got the answer right!

 

Question 2

Now that, we got the answer to the question 1, here is a more difficult question. 

Out of the four, only one addresses the skill and expertise. The rest of the three generally happen away from the bedside. The answer is strikingly clear I guess.

 

Postamble

I agree the answers to these queries can be extremely sensitive, and contentious for many of us. Little deeper lies the truth. Hope, the quote from the much-stigmatized father of modern medicine  “Primum non-nocere” will help find the answer. 

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Bicaval view is an Important TEE view to visualize, the LA, IAS, and right atrium. I used to have some trouble getting oriented to this view. Hence this post. It is obtained in the 90-120 degree view at the mid esophageal position. Imagine the patient is lying on his left side and the probe comes from above down between the spine and heart to the LA from within the esophagus. This is the best view to see IAS in the profile.(Subcostal TTE can also do it) Note how the LA hugs the right atrium which is actually an ill-defined (In TEE I mean) common meeting point of both IVC and SVC. Also important is the relationship of RUPV with SVC & the horizontally running RPA sitting right over the top of LA.

The relationship between RUPV and SVC is crucial in device closure of large ASD, especially in sinus venous defect.

Clinical Importance of this view

  • Very useful in ASD rim morphology especially in the posterosuperior rim.
  • Delineates clearly the defect boundaries in SVC ASD.

Sinus venosus defect: Image source not known. Thanks to the creator.

  • This view doesn’t miss even the smallest PFO (With Contrast )
  • Can be used to guide IAS puncture in structural heart Interventions.
  • IVC /SVC mass extension into RA well visualized.

RA myxoma attached to septum: Image source -Michael Essandoh from Research gate

Final message

Getting oriented to TEE  planes and images is so useful in structural heart interventions, like TAVRs, mitral clip, LAA occluder, tandem heart, valve in valves, etc. It is indeed a tough exercise and requires re-learning of cardiac anatomy with fluoroscopic overlay*.I wish, I go back and sit with first-year medical school students and start all over again.

*Current hybrid cath labs do provide Echo/Fluro co-registration, still it demands core 3D anatomical Imagination.

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PCI is effective in relieving angina,  what does it do to LV dysfunction?

This is a fundamental query in the principles of revascularisation of CAD . The term LV dysfunction can convey a bizarre meaning.It can constitute any of the combinations of the following.Cell death, necrosis, scarring, fully dead, partially dead, partially viable, apoptotic cells that are clustered across various myocardial segments. These cells are interwoven with fibrotic interstitium. Microvascular integrity is also altered.

Cells stretch, slip and slide with one another. Contractile architecture is lost. This is referred to as remodeling.In the process, the ventricle gets dilated. Wall stress increases, LVEDP raises. Patient may go for progressive failure.The whole concept of chronic myocyte loss is due to the process called programmed cell death.

Does PCI cancel this pre-planned program?

The answer seems to be a clear ” No” (Of course few studies do show some improvement ) It is becoming clear,  chronic ischemic juggernaut moves on. The mechanical spiral effect on the myocardium will go unabated whether you rectify the small residual ischemia or not), However, tissue engineering, anti-fibrotic drugs, cell repair molecules, stem cell assistance are attractive approaches to prevent or treat ischemic cardiomyopathy in the future.

If PCI can’t do it what about CABG ?

Read the STICH trial in Ref 2

Point of clarification

Revascularisation does have a role in salvaging the myocardium and improves LV function when done before irreversible damage has happened. When does it happen? To be precise, within 24 hrs of IRA occlusion. This is all about knowing the science of myocardial viability. Of course, In (un)real world this 24 h deadline is the least respected time window because cath lab viability directly competes with myocardial.

Reference

 

 

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The branching pattern of the human cardio-vascular tree is as unique as one’s fingerprint. One such hugely variable anatomy is the SA nodal blood supply.

Certain salient features

  • Variation can be seen in origin, course, and termination.
  • Now it is estimated to arise from RCA in 70% (Moved up from 55% in old studies )
  • From LCX (25%)
  • Dual SA node supply(5%)
  • Direct from Aorta

It is heartening to find this good anatomical review on this topic.

A) From the Right Coronary Artery; (B) From the Left Circumflex Artery (proximal); (C) From the Left Circumflex Artery (distal); (D) From the Left Coronary Artery; (E) From the Aorta; (F) Dual origin from the Right Coronary Artery and the Left Circumflex Artery. Image source : Vikse J, PLoS ONE 11(2): e0148331

Implication for the surgeon

The whereabouts of this tiny, yet important artery is critical to the surgeons’ as they incise and explore the atrial roof. (A gateway, that gives access to so many cardiac surgeries) The SA nodal artery mostly goes retro caval but it can be peri-caval or even anterior to SVC.

This image shows (a,b,c) the course in relation to SVC, Developmentally as the venous pole go posteriorly to fix the SA artery behind it.Image source : Vikse J, PLoS ONE 11(2): e0148331

For the Interventional cardiologist

A rare but distinct mechanical compression of SA node artery is reported with large ASD closure device. The plane of compression is usually occurring in the superior aspect of IAS when the SA node artery cross over the RA to reach the SA node. Should be suspected whenever unusual bradycardia occurs during the manipulation of the device or just after deployment. Always mind the delicate gap  between the antero superior rim and disc where SA nodal artery is likely to trespass.

AV node Ischemia with ASD device

With precise imaging modalities, new secrets are emerging. Additional AV node arteries from proximal RCA is documented.This is a surprising learning point for us. This artery is referred to as the right superior descending artery, which provides an alternative blood supply to the AV node from the proximal right coronary artery. The transient compromise of this hitherto unknown AV nodal twigs by the ASD device cause AV blocks. With this new info, we also got an answer to one more lingering question, why would disproportionate bradycardias are observed in inferior MI even when distal RCA is flowing well. We can’t blame high vagal tone always.

SA node compression by ASD device amplatzer

A CT angiogram showing how the ASD device encroaches the SA node artery. Image Source:Tsunehisa Yamamoto JACC 2016 (Linkedbelow)

The original article has an excellent video clipping of how an ASD device hugs the SA node at the superior edge of ASD.

Final message

Human anatomy is not the subject meant to be read in the first-year medical school cadavers, & forget thereafter. Surprisingly. the field of anatomy is also evolving with new mysteries exposed by modern imaging.SA nodal arterial blood supply is one such interesting aspect of cardiac anatomy. Young fellows in cardiology shall pursue further anatomical dark spaces in the heart (One such topic is how cardiac lymphatics compete with the venous system in draining cardiac interstitium)

Reference

Vikse J, Henry BM, Roy J, RamakrishnanPK, Hsieh WC, Walocha JA, et al. (2016) AnatomicalVariations in the Sinoatrial Nodal Artery: A Meta-Analysis and Clinical Considerations. PLoS ONE 11(2): e0148331

It’s gratifying a unique and committed group exclusively doing research in Anatomy. It Department of Anatomy, Jagiellonian University Medical College, Krakow Poland.

http://www.eba.cm.uj.edu.pl/

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Corona has triggered the scare of the century, even among the scientifically savvy brave men & women. The scale of the panic was unprecedented. However, one positive outcome of this pandemic was, this 20 nm RNA particle forced many of us, to ponder over the true purpose of life. It demanded a course correction in those who found one. Now, after 9 months Corona, in its second wave seems to be somewhat kind to humanity. The case fatality rate is dropping to nearly one-tenth of its peak in the first wave. 

 

 

 

 

Where is the evidence coming from?

Apart from our own personal experience from 1500 bedded corona hospital, this paper reports data from 53 countries.

 

Note, the red covid mortality curves are not matching the black positive waves (Both Europe and Asia)

Link to the original article https://doi.org/10.1111/tbed.13819

The possible reasons for the low case fatality rate.(Personal observation)

  1. Viral apologetic  behavior*
  2. Second wave affecting more healthy younger who fight it better.
  3. Less panic in the health care delivery system
  4. Though there is no specific therapy, at least some basic treatment strategies are in place.(Timely steroids & mindful oxygen did the trick)
  5. Initial aggression out of Ignorance (ie ventilator deaths) has largely ceased.
  6.  RT-PCR(which helped In diagnosing /isolating ), CT scans,(helped in grading) the Remdesvirs(gave peace of mind ) the Tocilizumab(did nothing great ) has at best played a minuscule role at a huge cost.

Among all these factors, which do you think is the most important contributor to a declining fatality?

The single important factor could be, “The virus has decided unilaterally to forgive the frightened human beings, and become less virile“.(At least in those people who sincerely respected the viral might by wearing masks and other paraphernalia) Sorry, for uttering this forbidden stuff in science, still it could well be the truth. 

If corona is losing its sting & steam what would be the realistic role of the vaccine? What is the likelihood of vaccine getting false credit*?If we are allowed to be optimistic, Corona in all likelihood is waiting to say goodbye after a feeble third or fourth wave. All these are speculative, still, one thing looks positive. Unlike the much-quoted fact about the Spanish flu of 1920, which resulted in more damage in the second wave, which is unlikely to happen with corona.

Disclaimer

* This article never intends to undermine the importance of preventive measures and vaccines for this worst pandemic in recent human history.

Counterpoint 

The decline in case fatality is may not be uniform as fresh data from Europe suggest. It’s hyperbole to expect corona’s second wave to bring good news. It is largely left to the people’s behavior to contain the pandemic than to get a pardon from the virus. 

 

 

 

 

 

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In CKD, LVH is a near-constant feature with echo showing thick, bright echoes from IVS. The LV mass increases, partly due to physiological hypertrophy ,also contributed by deposits of uremic middle molecules and fluid collection in the interstitium as myocardial edema.This, is recognised as T 2 weighted MRI signals. Chronic fluid stasis may progress to myocardial fibrosis. (Kidney Blood Press Res 2018;43:134–142 )  

Effect of Frusemide on myocardial edema 

We know, loop diuretics cause aggressive depletion of ECF volume and to a lesser extent Interstitial fluid. The effect of diuretic on myocardial water content is a poorly studied parameter.(Still more visible to a shrewd echocardiographer)

Effect of dialysis

While the effect of diuretics on myocardial edema is not consistent, however, we have observed definite regression of myocardial thickness, mass, and rigidity following dialysis. This transforms into a better LV systolic and diastolic function. At least in one patient, we have observed  the E velocity shrunk more than 50% the next day following dialysis pushing them to lower grades of HFpEF( A potential study topic.)

Final message 

The Improvement of the functional class of CKD patients immediately after dialysis is not only attributable to the removal of excess fluid and toxic uremic molecules, regression of myocardial edema plays an important role.

Further reading

Trinh E, Chan C, T: Intensive Home Hemodialysis Results in Regression of Left Ventricular Hypertrophy and Better Clinical Outcomes. Am J Nephrol 2016;44:300-307.

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