(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.

ECG diagnosis any one can make. The second part of the question needs some thoughts.

Dissecting the ECG* diagnosis

1.It is Atrial fibrillation with fast ventricular rate, with signifcant ST depression in V 4, V5, V6 .This could Indicate few things.

2.Preexisting LVH with AF

3.AF with new onset ST depression. This would mean an emergency (or may not) if it is an thromotic ACS high risk UA with posssible left main. But, one should bear in mind AF is an Natural atrial stress test , and ST depression could simply be a marker of tight fixed, stable lesion, (without a thrombus) that would require an elective Intervention.

4.Coming to the The ST elevation in AVR, many strongly believe it is a marker of left main disease. (Still, we can’t call it as AVR- STEMI, because it may just represent reciprocal ST elevation to any sort of ST depression in lead V5/V6 that includes benign LVH )

5.Look for ST elevation in lead V1 whenever you have ST lifts up in AVR. If V1 is isolectric , left main is very unlikely

The second part of the question.

I am sure, ruling out CAD without angiogram will be labeled as outright crazy. No cardiologist in their right sense will do that, I guess. Still, we could do it in this case. What did we forget in this discussion so far? We got lost in the electrical debate and failed to address the fundamentals. Why did this patient come to the hospital, requiring an ECG?

What did the clinical examination reveal?

While the cardiologist could not rule out CAD, the calm patient, complaining only of palpitations, ruled out a potential emergency chain reaction. Furthermore, a crescendo murmur in the aortic area sealed the issue. Yes, it is moderate aortic stenosis confirmed by an old GP’s prescription slip. She is being evaluated again for the severity of AS, treated with rate-controlling drugs for AF, since there was no acute heart failure or angina.

One more question

Why AF is not precipitating left heart failure even in patients with aortic stenosis ?

The concept of Left atrial functional reserve is a seperate topic, that will answer this query.

Final message

You don’t require an urgent cath lab mobilization to rule out CAD, even in a patient with a frightening ST segment, stuttering amongst irregular tachycardia. Always listen to the patient and have enough patience to look into the old records.. For that, we need to realize, we have to allow the patient to talk.

Postamble.

Presence of AS in no way rules out a CAD.Both can co exist. But if severe AS occurs with significant CAD, absence of angina is exceptional.

Discussing lifestyle modification is an essential cliché in every preventive cardiology consult, For most, it still means good nutrition exercise, and stress relief. It is true, that the average human longevity has increased considerably in the last century. However, this apparent gain in life expectancy by the stunning discoveries in science ( 10 years ?) has already been eaten up, by the self-inflicted,  poor styles in life. The new kid on the block, i.e. social media is playing a powerful amplifying effect.

Spot a new entry in lifestyle interventions.

Here is a fresh list of lifestyle modifications from the latest edition textbook of heart disease by Dr.Braunwald, considered the bible of Cardiology. Not at all surprised, to note the new entrant at the bottom of the list. 

Yes,  It is asking us to consider moving out, from the lovely city life to the countryside, and gift a pure and peaceful life to our vascular endothelium, which is devoid of PM2.5, NO2, Carbon monoxide (CO) Sulphur dioxide (SO2), etc.

Final message

I would expect the World Health Organization (WHO)  to declare ” unregulated urbanization” as a  communicable disease and include it in the ICD code sooner or later. (Air pollution is a masquerading term though!) .The urgency is real, since the apparent gain in life, due to modern medical therapeutics is getting rapidly eroded.

No more evidence is required to emphasize the fact, that enforced rural living is going to be an important CVD Intervention for the future. If someone (or any organization ) is still doing research to confirm this, please realize you are wasting time, stop it, and get on with corrective action along with the WHO’s other SDG goals. 

Reference

1.Emily J. Flies, Suzanne Mavoa, Graeme R. Zosky Urban-associated diseases: Candidate diseases, environmental risk factors, and a path forward,  Environment International, Volume 133, Part A, 2019,

2.Das, M., Pal, S. and Ghosh, A. (2008), Rural urban differences of cardiovascular disease risk factors in adult Asian Indians. Am. J. Hum. Biol., 20: 440-445.