Dr.S.Venkatesan MD

An unusal conversation with a flamboyant student fellow,

---

May I know , What is the normal Pericardial thickness, ?

Which pericardium you mean sir ? ,Parietal or visceral?

Would like to know both .

It is variable sheet of tissue .You want the thinnest part or thickest part ?

Don’t beat around the bush .Tell some answer.

You want, autopsy thickness, or real life thickness as surgeon sees it ?

I want it in practical Imaging modality

Do you want Echo, CT or MRI thickness ?

I should say , its too much for a first-year fellow in reverse questioning!

Ok relax sir, shall I tell the systolic or diastolic thickness?

So, you decided to spoil my day.

Ok, one final clarification sir,, you want thickenss over anterior RV aspect or over posterior atria ?

You are getting on my nerves. Thankyou, will you please leave the class .

---

Yes, pericardial anatomy ,can indeed make us crazy. Let us try to get some answer .

Whenever some one is asking about pericardial thickness, it generally mean the parietal,thicker fibrous outer layer. It’s about 1 to 4 mm*, never more than 3 -4 mm .As we can see, it is a highly variable sheet of folded tissue with different adherent surfaces. The visceral pericardium is very much less than 1 mm, in fact,it need to be measured in microns. It is called the epicardium and adheres seamlessly to the myocardium with intervening fat. (Sub epicardial fat)

Ref: Normal pericardium measures 0.4–1.0 mm thick in autopsy studies but normal pericardium measures 1.2 mm in diastole and 1.7 mm in systole on MRI studies [1].It is sort of surprising finding, to note pericardium also thickens in systole.

Mind you, echo over estimate the thickness, and its crudest form of measurement and should not be relied upon.Even CT over estimates.MRI is currently closer to true thickness.

In constrictive pericarditis, which pericardium compresses the heart?

In effusive constrictive pericarditis, organized fluid makes the two layers stick together and makes it thick, making it difficult to differentiate the two layers in any imaging modality. Hence, the answer is that both layers together compress the heart, but the fibrous layer is primarily responsible and exerts more pressure per inch.

Can epicardium per-se thicken with normal thickness of parietal pericardium?

We are not clear about it. The rarity of constriction in viral myo-pericardiits comparred to tuberculous suggest isolated epiicardial constriction is rare as epicardium is sngle sheet of cell .In wonder inflitrative pericarits might occur arsoing pure feom epeicardium following myo or epimyo caritis. . I dont know , may occur in some myopericardits.We need to ask Dr Renu virmani.

(*Answer to this question might alos explain why rheumtic pericardiits doesnt cause constriction as it doesnt involve fibrous pericardium )

Does sub-epicardial fat make epicardium appear thick ? How to differntiate it ?

This is a tough one to diffferentiate . There have been cases of constrictive physiology due to epicardial fat (Effusive-constrictive pericarditis with massive epicardial fat A Goto, M Lancet September 01, 2001)

One final question: Is it the thickness or the elastance /resistance of the pericardium that determines the likelihood of constriction?

Pericardial histology and elastance are more important. We know, that transient constriction with normal pericardial thickness is a very well recognized entity. (Haley JH,JACC 2004)

Final message

Never under-estimate the importance of pericardial anatomy. It can go as deep as its recesses and the tortuous sinuses. Try reading this wonderful review by Rodriguez.(Ref 1) I guess it might have taken tons of time to write such a great article. Don’t excuse yourself to waste 20 minutes in between your angioplasty times.

Reference

1.Bogaert J, Francone M. Cardiovascular magnetic resonance in pericardial diseases. J Cardiovasc Magn Reson. 2009 May 4;11(1):14. doi: 10.1186/1532-429X-11-14. PMID: 19413898; PMCID: PMC2685792.

2.Haley JH, transient constrictive pericarditis: causes and natural history. J Am Coll Cardiol. 2004 Jan 21;43(2):271-5. 147

STREAM trial (New Engl J Med 2013) was a sort of paradigm-creating study, that made Pharamco-Invasive approach – PIA an authentic via-media strategy, trying to accure benefits from both lysis and PCI in the management of STEMI.

However, one question remained. Does PIA work safely in the elderly, where bleeding risks are higher? Do they tolerate the double whammy of P and I ? Both procedures keep the blood clotting process tentative for a prolonged period of time.

Emprical usage of half dose lysis is not new, is existingn, for more than 4 decades, right from streptokinase days.

Now the multi-center STREAM-2 trial , released from Belgium , Published in the current issue of Circulation, asked this specific query on the efficacy of half dose Tenecteplace in PIA.

Both strategies had almost similar outcome with 87 % TIMI flow, implying elderly people , are reciveing twice the dose of lytics without any true benefits, but enhancing other risk.

Final message

The conclusions are not surprising. Our empirical thoughts have now, become acceptable sort of evidence. So , let us go ahead with this renewed PIA strategy and proceed with half dose of Tenecteplase ln elderly ( A liberal cut off of >60 years) without any guilt.

Meanwhile, the STREAM team has one more important job to do. So far, no one has the guts to test “P” vs “PIA” in the current era, in a large scale ( ie proceed with “I” if and only if “P“has failed. After all , if P is successful, that has resulted in good TIMI 3, and normal LV function there is no need for I )

Hope, somebody or institution get that courage and funds to design a STREAM- -3 trial comparing three distinct strategies, ie stand-alone TNK vs PIA, & pPCI and make it a reality. I am sure, it will bring surprise and very likely a pleasant one for all stake holders.

(Why should the number 65 bother us in TCFA-detected by OCT? Does this number really deserve that respect? Trying to find some truths from 8 questions with & without evidence.)

1. Does TCFA really make a plaque vulnerable?

A.Yes

B. No

C. Maybe

Answer: Yes & Maybe. But there seem to be more important factors other than TCFA for a plaque to become vulnerable making TCFA not really a big deal.

2. TCFP is more common in which lesions?

A.Flow limiting lesion

B.Nonflow limiting lesion

C.No relationship between TCFA and flow

Answer: No relation, rather a random relationship.

3. What is the natural history of TCFA?

A.Get ruptured

B.Static

C.Get thickened

D.Further thinning

Answer: If someone can answer this query accurately, he can be rewarded Nobel Prize, in Lipidology

There are some studies available though.

Ref : This 2023 paper adds some anxious content to those who ignore TCFA. Long-term outcomes of patients with normal fractional flow reserve and thin-cap fibroatheroma EuroIntervention 2023;18:e1099-e1107. DOI: 10.4244/EIJ-D-22-00306

 4. What to do with FFR-negative(FFR>.9), TCFA-positive lesions (tcfa<50mic)? Does stenting TCFA make it less vulnerable?

No. Stents and scaffolds were never invented to make a plaque less vulnerable.

5. How is TCFA different in stable CAD from ACS situation?

They are very different. In the ACS situation, TCFA (Whether the cap is intact or not ) needs immediate attention. Does it mean immediate stenting? No, it is not. (But unfortunately, it is what happens in the reality.) Thrombus and its lytic products add a new dimension of risk for recurrent ACS. High-dose statins are critical here. Stenting is so tempting, and logic and science are in direct conflict here.

6. Do statins increase the thickness of TCFA?

A.No

B.Yes

C.Possibly yes.

Answer: Statin does have some action on the cap. there is no such thing as if the cap increase from 65 to 100 micron the plaque is safe. More than thickness, it stabilizes and hardens the contents that are being capped. European Heart Journal – Cardiovascular Imaging (2017) 0, 1–8 doi:10.1093/ehjci/jex102

7. Which is possibly, the thickest cap over an atheroma?

Intimal calcification on the luminal side is the thickest cap (like a helmeted plaque) that protects from any traumatic injury from blood components. (Sub Intimal calcific nodules may behave differently though)

8. If calcium is the safest cap in chronic CAD,, why do cardiologists, attack it with all sorts of weapons?

This is where “excessive knowledge along with academic ego‘ in incognito mode plays spoilsport with our hidden wisdom.

Calcium is an uninvited guest that directly challenges our might and talent, and interferes with placing a stent. No surprise, we take up this fight personally, and destroy, shock, drill, or displace it at any cost. Of course, tackling calcium* is required in very selected patients; it should never be done just because it interferes with the deployment of a stent. (We need to periodically remind ourselves, that PCI is not synonymous with stent implantation; stentless PCI is also possible.)

*Calcium and coronary artery is not a simple topic to understand. How can one agree with the above content, when there are innumerable studies that say a high CT calcium score is directly related to plaque burden. Mind you CT calcium score has little correlation with intimal plaque rupture.

TCFA: Should we worry?

TCFA is a concept born out of cutting-edge coronary Imaging technology OCT. After a decade of experience, we realize we can’t hunt & count these caps among the vast plaque burden. The 65-micron cap is just an anxiety-provoking number. Forget the cap. They are often Innocent.

Looking beyond TCA

What is beneath the cap and the biomechanical forces in the pool of tissue underneath, ultimately matter. The fluidity of the necrotic core and the ferocity of the angry macrophages, MMPs, as well as the triggers from within the lumen like the shear stress of blood plays a major role. We also know that diabetic glycation injury widens inter endothelial gap. We have sufficient reasons to assume, that the sharp edges of LDL molecules, hit the endothelium at a high mean BP along with neural triggers from the peri adventitial sympathetic network that injects the final catecholamine blow to the endothelium.

Final message

No technology can answer the above queries or predict the events. So be at peace with all basic precautions and risk factor regulation.

Reference

1.EuroIntervention 2023;18:e1099-e1107. DOI: 10.4244/EIJ-D-22-00306

2.European Heart Journal – Cardiovascular Imaging (2017) 0, 1–8 doi:10.1093/ehjci/jex102

Image courtesey : Sekhar, S. et al Canadian Journal of Cardiology, 2015 (Ref 2)

Coronary stent infection (CSI) is no longer a rare and fancy diagnosis. It is increasingly recognized and is equivalent to infective endocarditis. Though CSI appear simple & practical terminology, Infective endo-coronary arteritis may be the ideal term for this device-related infection.

Any prolonged fever following PCI must be investigated with this condition in mind. Unlike other forms of infective endocarditis, vegetations are rare, or do not occur . Instead, the infection erodes endothelium, often leading to the development of an infective aneurysm. Staphylococcus infections seems to more common. Though host immunity is a factor, it is possible inadequate cathlab sterility plays a major role.

Diagnosis

Conventional IE criteria may not be fulfilled. PET scanning helps us to detect & map the active inflammation in the peri-stent area.(See the Image) The PET criteria to define significant inflammation are not yet standardized. One possible differential diagnosis to CSI is, acute or subacute allergic stent rejection.(Not Kuonis syndrome)

Treatment

Is complex, and carries a high mortality rate. It is best to manage it without any aggressive intervention. Physical removal of the infectious focus, along with the stent, may seem like an ideal option.

However, real-world scenarios often preclude this option as exceptional surgical expertise and team work is needed as in this report (Ref 3)

Reference

There is an excellent meta-analysis on this rare entity by Nagendra Boopathy and others from my place Chennai (Ref 1)

1.Ramakumar V, Thakur A, Abdulkader RS, Claessen B, Anandaram A, Palraj R, Aravamudan VM, Thoddi Ramamurthy M, Dangas G, Senguttuvan NB. Coronary Stent Infections – A Systematic Review and Meta-Analysis. Cardiovasc Revasc Med. 2023 Sep;54:16-24. doi: 10.1016/j.carrev.2023.02.021. Epub 2023 Mar 8. PMID: 36906449.

2.Sekhar, S., Vupputuri, A., Nair, R. C., Palaniswamy, S. S., & Natarajan, K. U. (2016). Coronary Stent Infection Successfully Diagnosed Using 18F-Flurodeoxyglucose Positron Emission Tomography Computed Tomography. Canadian Journal of Cardiology, 32(12), 1575.e1–1575.e3. doi:10.1016/j.cjca.2015.10.022

3.B.G.K. Sudhakar,Pseudomonas aeruginosa septicemia resulting in coronary stent infection and coronary artery aneurysm and acute infective endocarditis of mitral valve causing severe mitral regurgitation- A case report, IHJ Cardiovascular Case Reports (CVCR),Volume 2, Issue 3,2018,Pages 191-195,

The heart is a mechanical pump, still electrically wired delicately and extensively, right from the SA node to the vast Purkinje network, which is activated by sequential propagation. Myocardial contraction occurs with amazing electro-mechanical coordination with millisecond precision. If the wiring line is interrupted, it is natural to expect some bumpy rides. This local delay often manifests as, wall motion abnormality.

WMA is commonly occurs in LBBB .What about LAFB ? LAFB is a term used if one of the fascicles of the left bundle is delayed or completely cut off. Wall motion defects are also expected in LAFB, but most of us do not give importance to it. If new-generation echo machines with speckle tracking imaging are used, these desynchronies can be identified.(Ref 1)

One of the reasons for LAFB-induced WMA is missed often, is that the plane of desynchrony is in an odd omni plane. The anterior fascicular delay is an electrical imbalance between the notoriously placed posterior fascicle, tending to deflect the electricity a few milliseconds early towards the crux. This results in desynchrony between the remote base ie the crux of the heart to the summit of the heart, which is difficult to pick up in conventional TTE views. Of course, if LAFB is proximal and complete, one may still get a clear-cut WMA. If RBBB is associated, WMA is definite and mimics an MI.

Clinical implications

Our experience suggests WMA in LAFB is not clinically significant, except when it is mistaken for an ACS event. Poor R wave in V1 to V3 is a feature of LAFB cann add more uncertainity.

It can also interfere with accruing or assessing the true benefits of CRT with biventricular or His bundle pacing.

Final message

It is true ,wall motion defect in echocardiography will raise an immediate alarm for every cardiologist.But, we must also realise there are atleast a dozen causes for it, other than ACS. It is prudent to know ,nonischemic electrical wall motion defects can occur in LAFB too, and cause diagnostic doubts. (Many fold rare though, when compared to LBBB)

Reference

Leeters IP, Davis A, Zusterzeel R, Atwater B, Risum N, Søgaard P, Klem I, Nijveldt R, Wagner GS, Gorgels AP, Kisslo J. Left ventricular regional contraction abnormalities by echocardiographic speckle tracking in combined right bundle branch with left anterior fascicular block compared to left bundle branch block. J Electrocardiol. 2016 May-Jun;49(3):353-61. doi: 10.1016/j.jelectrocard.2016.02.002. Epub 2016 Feb 10. PMID: 26931516.