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No doubt, the heart is a biological wonder with its non-stop pump function. Still, it cannot function as a continuous rotary pump like the electrical motors do. It has no other option but to contract in a pulsatile manner. However, the mean pressure in circulation is fairly constant, flow is kept continuous, and fairly laminar. This is made possible by the built-in elastic pressure in the aorta and the poorly understood but vitally important parameter vascular tone. Aging widens the pulse pressure due to dissipation of vascular tone. Atrial fibrillation adds new bizarre dynamism to this pulsatility and challenges the aortic wall’s competence and compliance further. This is the basic mechanism behind the classical description of an irregularly irregular pulse in AF. The pulse can be  so unpredictable, it was originally referred to as acute confusional status of heart (Delirium cordis)

What is the effect of AF on systolic, diastolic, and mean blood pressure?

In AF systolic BP varies considerably from beat to beat. Diastolic BP does show some changes but less obvious. So far mean pressure fluctuations in AF have not been given much significance.  

Clinical significance of AF on the brain: Thinking beyond stroke 

From a stroke perspective rate and rhythm control did not show much difference. The prime reason for AFFIRM  trial not showing benefit with rhythm control was embolic stroke was much more common from sources other than left atrium proper and hence the usage of oral anticoagulants was more important than rhythm control in overall stroke control. 

Now, an important study trying to look at this hitherto ignored aspect( Andrea Saglietto,  EP Europace, 2021). It raises concern about the impact of AF on long-term cerebral function. Should we restart the debate in favor of rhythm control? No doubt, the pulmonary venous electrophysiologists will be too glad to welcome this concept.

Now, we have new evidence based on near-infrared spectroscopy AF does cause unpredictable beat-to-beat changes in cerebral microcirculation that leads to neurocognitive dysfunction. It is possible there can be a breach in cerebral autoregulation limits in a significant number of post-long RR  beats. We may soon look forward to a new entity of “dementia cordis“as a sequel to chronic AF.  

 

Reference

1.Andrea Saglietto, Stefania Scarsoglio, Daniela Canova, et al Increased beat-to-beat variability of cerebral microcirculatory perfusion during atrial fibrillation: a near-infrared spectroscopy study, EP Europace, 2021;, euab070, 

 

 

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Here is an uncommon story of a patient with palpitation,SVT , Troponin +ve, and suspected ACS.

Palpitation in ER ⇒ {Tachycardia +Troponin positive ≠ ACS}

Mechanism of troponin elevation following any SVT

  • At high heart rates (>200) myocardium is subjected to non-Ischemic mechanical strain & squeeze. Minute amounts of Troponin is let out like a myocardial juice into the circulation (Like atrial natriuretic peptide release which causes polyuria during AVNRT)
  • Tropinin releases have been shown to correlate with both heart rate and duration of ST depression (Subendocardial strain /AVRT left lateral pathways)
  • Short diastole induced low coronary perfusion pressure and a true transient (but insignificant) Ischemia
  • Finally, SVT (especially in the elderly) is a natural “exercise stress test” equivalent, ST depression with Troponin positivity is a true marker of significant epicardial CAD

Significance

False alarm of ACS is the most important issue. (Except one study which showed a different conclusion Chow GV, Prognostic significance of cardiac troponin I level in hospitalized patients presenting with supraventricular tachycardia. Medicine (Baltimore) 2010;89:141–148. doi: 10.1097/MD.0b013e3181dddb3b. [PubMed]

Note: If AVNRT occurs with aberrancy, or AVRT presents as antidromic tachycardia with a wide qrs tachycardia the confounding effect is perfect as it can no way be differentiated from true Ischemic VT or atrial fibrillation.

Final message

It is no ER room secret that a single spot Troponin value has lost its credibility considerably in segregating ACS from non-ACS conditions. It is falsely elevated in a long list of cardiac and noncardiac conditions. It is a worthy point of learning, among the cardiac conditions, the commonest cause for false elevation is during any tachycardia. This should be kept in mind. Because a patient with chest pain who present with benign palpitation due to prior SVT (Arrival ECG could be normal) a false raise can trigger a chain of inappropriate reaction that may land the spot even in the cath lab.

Postample

In spite of these limitations, non-diagnostic ECGs, we expect Troponin and CPK to guide us in chest pain screening. We now have added one more marker, high sensitivity Troponin Assays. Let us believe, it doesn’t add to more confusion. I think the main purpose of these biomarkers in the future, would be to arrest the habit of using cath lab as triaging place for chest pain instead of ER room. (A brief review from ACC https://www.acc.org/latest-in-cardiology/articles/2017/08/07/07/46/a-brief-review-of-troponin-testing-for-clinicians)

Reference

1.Troponin elevation in supraventricular tachycardia: primary dependence on heart rate. Ben Yedder N, Roux JF, Paredes FA Can J Cardiol. 2011 Jan-Feb; 27(1):105-9. [PubMed] [Ref list]

2.Kanjwal K, Imran N, Grubb B, Kanjwal Y. Troponin elevation in patients with various tachycardias and normal epicardial coronaries. Indian Pacing Electrophysiol J. 2008;8(3):172-174. Published 2008 Aug 1.
3.Carlberg DJ, Tsuchitani S, Barlotta KS, Brady WJ. Serum troponin testing in patients with paroxysmal supraventricular tachycardia: outcome after ED care. Am J Emerg Med. 2011;29:545–548. doi: 10.1016/j.ajem.2010.01.041. [PubMed] [CrossRef] []

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This question might squeeze the collective coronary knowledge of any cardiologist. (At least, it does for me !)

What is an intermediate coronary lesion? (ICL) 

Traditionally it is an “angio-ocular reflex” measurement of coronary arterial diameter stenosis that lies between 40 to 70% (Mind you, 70 diameter stenosis is 90% area. So, we must be clear what we really mean in any revascularisation debate).

Above one is the simplest expression of ICL. (* While 70% cutoff is fairly constant, the lower limit 40% is still not a settled issue. It can even be 30 %. I think we haven’t yet named the lesions 1 to 39%. It is the spectrum that contains  Coronary erosions, ulcers, luminal irregularity, or the evasive term minimal CAD  )

Many sub-classes exist in ICL.

  1. Should ICL definition be different in proximal LAD? (A 40% PDA or OM2 lesion is not the same as 50% LAD right.Maybe we need to artery specific redefinition, left main we did it already)
  2. It can be de nova chronic (most common ) Acute  /subacute, acute recanalization (Each has a different management strategy)
  3. What about ICL with good TIMI 3 flow. Mostly safe and can be ignored?
  4. Should we bother to know the content of ICL? It could be a minor plaque or just thickened and narrowed arterial wall or even layered thrombus.
  5. Is it isolated ICL?  When ICL occurs in isolation it gets more attention is natural to ignore if ICLs are noted along with other critical lesions nearby. The risk of ignoring or risk of including ICL in the final angiogram reports is unquantified. 
  6. When two ICLs lie by next to each other (Tandem ICL) will you add the stenosis resistance in series? Does the length matter.(Can we measure net FFR ?) 
  7. Is it symptomatic vs asymptomatic? (very difficult query )In stable non-Infarct CAD Internedaite lesions do not obstruct flow, but Post ACS it is the distal microvasculature that determines the epicardial flow. so even intermediate lesion resist flow.
  8. ICLs in ecstatic segments pose a special issue. Adding to this Galovian positive remodeling mask the true plaque burden(Currently liberal use of OAC like warfarin are used in ectatic vessels with ICLs)
  9. By the way, is it true, ICLs are more prone for  ACS?  We believe it based on small studies and sort of biased teaching. Of course, there is some truth in it, but in a larger sense, it is not correct thinking. ICLs by sheer number overtake the critical lesions in terms of Incidence. So more ICLs present as ACS. But in, pure pathological terms flow-limiting lesions do carry more risk for ACS. (Of course, calcification might stabilize a few of them, and convert them to CCS) . For argument’s sake, if we agree ICLs are more prone for ACS, we should first fix these lesions than the more tighter ones.(Any guidelines forthcoming ?)
  10. Finally, the most important query Is the ICL vulnerable, or is it flow-limiting? (read below)

Imaging and physiology

CAG is just a shadow of contrast luminogram. Further, the contrast flowing across a lesion cannot be equated with the true velocity of blood flow. So, what shall we do? How do we overcome the limitations of CAG shadow? We need to go after more glamorous shadows like IVUS and OCT. They do suffer from myopia and hypermetropia respectively. Still, they are good enough to reveal important info like the content of lesions like calcium thrombus with acceptable precision, etc. The thickness of the fibrous cap (TCFA) is a current marker of vulnerability. This thickness is dynamic as do plaque liquefaction. We are looking ahead to the days of virtual histology and plaque metabolism by NIR spectroscopy. Decisions based on a single one-time snapshot from intermediate lesions would largely be meaningless. 

What about physiology? FFR, iFR,(Adenosine free)  QFR (Based on TIMI frame count) offer a more scientific assessment of flow across the lesion. Still, it is not clear. An elegantly made study is available that depicts the relation between stenosis and FFR.

Realtionship between diameter stenois snd FFR. Note even a 30% lesion has low FFR and wide variation a 70% lesion show on either side of cut off .8Does Routine Pressure Wire Assessment Influence Management Strategy at Coronary Angiography for Diagnosis of Chest Pain? The RIPCORD Study Nick Curzen circulation cardio vascular Interventions 2014.

Relationship between diameter stenosis snd FFR. Note, even a 30% lesion can have a low FFR, and a 70% lesion show the FFR to scatter on either side of the cut-off value .8 . So, what does it mean?  We have simply shifted our ocular bias to objective flow bias. Does Routine Pressure Wire Assessment Influence Management Strategy at Coronary Angiography for Diagnosis of Chest Pain? The RIPCORD Study Nick Curzen circulation cardiovascular Interventions 2014.

What is the effect of statin on ICL?

There is no specific large-scale study that looked into this. Plaque regression and stabilization are expected in most ICL with intensive statin regimens. (Seung-JungPark et al  JACC 2016) It reduces new-onset TCFA. Will it increase the cap thickness? It can be assessed by the OCT study. (Maybe it is already available will search for it ). PCSK & Inclisiran should do it if not a statin. 

Final message

Coming to the title question, the term ICL means nothing without the clinical background and the angiographic setting it is detected. Realize, the intermediate lesions don’t Imply intermediate risk. We can’t do  IVUS or OCT in all intermediate lesions. Even if we detect vulnerability in a 50% lesion, treatment will remain mostly intensive medical management. (There is absolutely no good evidence to show stents stabilize vulnerable plaque that does not limit flow ) 

So, the best approach to all those billions of ubiquitous ICLs scattered across the human coronary landscape is to stabilize it OMT( Open-minded medical therapy), lifestyle modification (taking style out of life), reassurance, and propagation of peace that will passively the plaques. Imaging and FFR can do wonders in an elite minority population at a considerable cost. (However, for the sake of demystifying atherosclerosis we should continue research with such modalities, sparingly though )  

Reference

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Click to access RICM_41_1_0.pdf

 

 

 

 

 

 

 

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ASD device closure has become a de-facto modality for most ostium secundum defects(<35mm). The stupendous success of this procedure is attributed to careful pre and Intra-procedural Imaging, new generation hardware and of course the ever-improving expertise among Interventional cardiologists.

Still, there is one issue that is bothersome. It is the late complications of this device and the need for follow-up (Unlike surgery where close and forget option seems real and confer lot of comforts) The delayed mechanical complications are now extremely rare still  follow up of these patients is advised.

What is the mechanism of Aortic erosion in ASD device closure ?

The IAS is a dynamic structure. (Ask any echoc’ardiographer ,how ASD size varies with cardiac cycle.) The device should sit right across all rims including the  Aortic rim . If the device if larger , and if the Aortic rim is less it has on other option but to splay over the Aorta . Enthusiastic young cardiologists should be aware this splaying is not in our control at all. Not all splaying are good and safe as well. If its not smooth and if the septum is mal-aligned there could be friction Injury to Aorta. A very early manifestation of device dislodgement and later a trickle of  pericardial effusion. This should be watched for. (Please be reminded a early pericardial minimal effusion due to sudden shrinkage of RA, RV and due to some unknown hypersensitivity response ? can confuse us )

Link between deficient Aortic rim and Erosion : An unsettled Issue (But , we settled it ! )

One issue that is poorly understood is, many Interventional cardiologists believe strongly that the length (and even quality) of Aortic rim is the least important and need not to be respected. I am still not clear on what basis this piece of Interventional literature came in. This is exactly is the reason even novices take liberty and large devices are implanted casually encroaching the Aorta. Though most cardiologists shrug of this risk of Aortic rim deficiency and subsequent erosion,  at least one study clearly showed a serious link between the two. I feel the issue is not yet settled and demands re-scrutiny.

This presentation was made in Tamil Nadu Interventional (TIC)council meet at held recently

 

This image has an empty alt attribute; its file name is aortic-erosion-2-1.gif

Link to the PPT presentation aortic erosion 2

Final message 

After going through all relevant literature as on 2019 , the incidence of aortic erosion is rare but the fear is real (Many feel it is paranoid and largely unfounded ) I won’t agree though.The message must be, a good quality Aortic rim is important too.

However, a properly sized device, perfectly delivered with good Image assistance by a trained cardiologist in a high volume center (? >25/year) shall prevail over surgery in most patients with ASD. 

Reference

 
 
 
 
 
Further issues : Stroke risk with ASD device 
 

One more Issue with ASD closure device is delayed embolic episodes from thrombus attached to device. This is prevented by  routine anti platelet drugs practiced by certain Institutions .The new generation devices (Occlutech Germany) has modified the LA side of the disc (No Hub) to reduce this risk

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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 meant, your collateral circulation is good enough and you may not need any intervention.

Are you sure doctor?

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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