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Decision making  for PCI in chronic CAD continues to be delicate. This is especially true, if the lesion is Intermediate and the plaque vulnerablity is susepcted.

How to tackle this stress positive Intermediate LAD lesion. Functional capacity good. Non-diabetic, mildly elevated lipids. Now, continuing medical management with intensive lipid control is the best possible management. (We have evidence for medical management being good even in significant 90% lesion) Above is a case report from https://www.acc.org/education-and-meetings/patient-case-quizzes/medical-therapy-for-cad

Reassurance is a revascularization equivalent

Sharing a similar experience with one of my patients in his early fifties. After getting a fairly convincing consultation, he accepted medical management. However, guided by both NI & AI, he sought a second opinion to confirm whether my assurance was indeed correct. He underwent FFR and OCT, and both he and his plaque became vulnerable. The FFR was normal. He was too intelligent to ask about the FFR – Stress test discordance, for which his cardiologist had no answer. Still, they did not advise a PCI and the decision was left to him, respecting the current patient-oriented guidelines.

The patient went home empowered but spent sleepless nights, fearing about potential fissures,  in the life sustaining fibrous cap.He believed that he was at the mercy of a 75-micron thin cap covering his plaque. In one of the anxious days,in the following week , he got admitted himself in a posh downtown cardiac center. A as per the guidelines, the patient chose his own pathway for a PCI. Cardiologists obliged piously to his wishes. Now, he feels better. He says he is happy to undergo a self prescribed stent.

I was glad, he had the courtesy to come back and showed the results. I learnt. it costed him 6 Lakhs and his insurance covered it fully. I realised , my 30 minutes reassurance was busted by the insurance card in few minutes. I wasn’t surprised.It’s okay, it’s all in the game. I learned it long ago. Fear* (either spontaneous or induced), the power to decide & affordability are the most powerful determinants of any inappropriate medical procedure.

Learning cardiology from UN & WHO

We have United Nations and WHO, the two global guardians. Any one with average intelligence will agree, these instituions can never bring either peace or health to this world.Let us ensure, the practice guidelines of cardiology doesn’t go that way. We boast ourselves, that we have a strongly evidence based vigorously scrutinized cardiology practice framework. How true it is ? Are we hiding behind pateint preference, and pushing  science to the  background ? Let us be transparent. I think it’s time, the powerful bodies like ACC/ESC should connect all the missing dots. .One important issue  is,  fear or anxiety-driven PCI, which usually overtakes other true indications.

Final message

In an ideal world , reassurance and GDMT , if properly done, should be a revascularization equivalent in most CAD patients .The  reality is, fear* prevails over reassurance, for a variety of reasons.

Postamble

*Anxiety thrives well, in an environment of uncertainty. It is mutually inclusive among both patients and physicians.However  most Professional physicians are expected to tackle it. Still many struggle. Patient : What if the block worsens? Physician: What if the patient comes back with an event and oh .. my pride and practice?  May be, physicians are not to be blamed much. I think. it is all about a unexplained,  biased human mind set. Even a death during an inapproproate Intervention is pardoned off, but an error, raising out of an appropriate medical mangment is rarely forgiven.

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“Every Interventional Cardiologist, realistically, need to be a preventive neurologist too!”

The concept a permanent ascending aortic porous membrane filter (PAA-PMF) is an extrapolation of the idea of mechanical thrombus capture, as proven by IVC filters for venous embolism prevention . Also we do have and temporary intra-aortic filters like Sentinel , Embol-X for arterial particulate capture.

Device Concept

The PAA-PMF would feature a self-expanding nitinol frame, with a fully porous head end. The device can be heparin-coated polyester or polyurethane mesh membrane, deployable via 12-14 Fr femoral sheath, similar to IVC filter designs but should be optimized for aortic pressures. Suggested pore size of 100-125 μm targets >100 μm emboli, akin to Embol-X filtration efficacy in capturing 95% of particulates (atheroma, fibrin) during aortic declamping. The essential requirement is that the porous membrane should not create an impedance gradient. How feasible it is, to be tested. Conical shape, the radial force will ensure good ascending aortic wall apposition.

Device location site

Site of placement is critical. Proximal ascending aorta, 2-3 cm distal to sinotubular junction/proximal to brachiocephalic trunk, as in Embol-X for maximal cardiac/aortic debris interception without coronary/arch compromis

Potential indications

(Only in patients with very high risk of cardioembolic stroke)

1.Chronic stroke reduction in patients with MVR/AVR/TAVR/MAVR

2.High-risk mobile LV mural thrombus

3.Chronic AF with visible and invisible clots in LA

4..High-risk procoagulant conditions with recurrent embolism

Definite Risks

*Occlusion and hemodynamic compromise is the most crucial issue. However, when compared to the incidence IVC filter clogging, the high pressure aortic flow is likely to self-wash the device (as happens in a prosthetic aortic valve)

Trapped emboli may enter into coronary circulation is a possibility. Putting a filter at ascending aorta precludes left heart catheterization.

*Migration , Hemolysis are other expected complications.

Intense anticoagulation would be required to prevent occlusion of the filte . (Still, stopping it temporarily doe not not increase the risk of stroke)

Final message : Is it Worth for a Preclinical trial ?

We do have temporary aortic filters. The concept of permanent or semi-permanent filters is largely theoretical, with potential risks being more than benefits. The device can take care of only cardio-aortic embolic stroke.

However, considering so many complex, risky intracardiac and intravascular devices being tested on a daily basis, it is not a big deal for the current generation of interventional cardiologists to try this.

More than our interventional appetite, we really need a device that prevents stroke in a permanent fashion. It is definitely worthy to do initial studies in a porcine model. Would be glad , if Edwards, Abbot or Medtronic and other new Innovators respond to this.

References

  1. Shammas NW, et al. Intra-Aortic Filtration: Capturing Particulate Emboli during Cardiopulmonary Bypass. NIH. 2004. Available from: https://pmc.ncbi.nlm.nih.gov/articles/PMC1351822/
  2. Shammas NW, et al. Embol-X Intra-Aortic Filtration System: Capturing Particulate Emboli in the Cardiac Surgery Patient. NIH. 2004. Available from: https://pmc.ncbi.nlm.nih.gov/articles/PMC4682540/
  3. PCI Mag. Revolutionary Anti-Thrombogenic Coating for Stents Promises Safer, Faster Healing. 2024. Available from: https://www.pcimag.com/articles/112641-revolutionary-anti-thrombogenic-coating-for-stents-promises-safer-faster-healing
  4. Kaufman JA, et al. Radiologists’ Field Guide to Retrievable and Convertible Inferior Vena Cava Filters. AJR. 2019. Available from: https://ajronline.org/doi/10.2214/AJR.19.21722
  5. Cleveland Clinic. Vena Cava Filters: Purpose & Placement. 2025. Available from: https://my.clevelandclinic.org/health/treatments/17609-vena-cava-filters
  6. Bilal H, et al. Complications of Inferior Vena Caval Filters. NIH. 1997. Available from: https://pmc.ncbi.nlm.nih.gov/articles/PMC3036364/
  7. Alpaslan M, et al. Embolic Protection Devices in Transcatheter Aortic Valve Implantation. NIH. 2025. Available from: https://pmc.ncbi.nlm.nih.gov/articles/PMC12194329/
  8. Almanza DC, et al. Comparative Review of Large Animal Models for Suitability of Cardiovascular Devices. IJMS. 2024. Available from: https://ijms.info/IJMS/article/view/763/1645
  9. Mohammadi H, et al. Simulation of blood flow in the abdominal aorta considering hyperelasticity of the wall. J Carme. 2021. Available from: https://jcarme.sru.ac.ir/article_1223.html
  10. Ketha S, et al. Comparative Review of Large Animal Models for Suitability of Cardiovascular Devices. IJMS. 2019. Available from: https://ijms.info/IJMS/article/download/763/1644?inline=1

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We know TAVI is in the striking distance , to literally take over most aortic valve interventions. From a humble beginning from very high surgical risk with prohibitive comorbidity, now it has almost touched the totally asymptomatic, relatively morbid-free patients. Thanks to the hardware, expertise, and motivation from multiple forces.

While the numbers increase, still the debate between SAVR and TAVR is riddled with speculation, skepticism, and absolute confidence. (Reason: TAVI is a passively fixed valve in a blind procedure at a self-selected annular plane, with no option to remove the crushed native leaflet debris and the resultant complications. Lastly, TAVI’s lifespan* is currently less than half of a mechanical valve. *Expected to improve with polymer valves)

The latest trial to join the litereture is EARLY TAVR in October 2024

Here is a brief, personal comment about the paper for non-academic consumption. Look carefully at the 15th second of the video. Pause it, look at the number over there on the bar of unplanned hospitalisation.

It is a staggering 41.7% in clinical surveillance group, twice more than TAVI group, pathologically tilting the conclusion of the study.

Video source and courtesy https://youtu.be/3wwQEEG4aWg

By the way, what is that unplanned hospital admission? Who is planning that admission in the asymptomatic control group? If 41% of people in the clinical surveillance group needed hospital admission, what does it mean? Does that mean clinical surveillance was so poor that they were rushed to the hospital despite being asymptomatic and stable in the surveillance period?

Why should totally asymptomatic patients get admitted in the control arm, in such huge numbers? You can presume what could be the reason. My guess is too sinister.

Another issue plaguing the RCTs for decades, is continuing even in 2025. That is putting together death, stroke, and unplanned hospital admission as a combined endpoint in the same basket. This is the familiar old cheat story i.e., used to intentionally torture the truth.

Final message

Any student with basic sense of statisitcs can interpret the result of this landmark trial from NEJM correctly. The question we need to ask is, what are the triggers for those unplanned hospital admissions?

Further, it is good for NEJM (and the medical community) not to accept any papers, if the studys’ endpoints are not appropriate or defined with the intention to manipulate, which happens in many sponsored trials.

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Statins belong to a group of drugs, stolen and reengineered from the blueprint of natural Chinese red yeast rice (Monocoline K) in the late 1980s. The rest is the remarkable history in the pharma industry.

Statins directly interrupt the cholesterol synthesis by blocking HMG-CoA within the hepatocytes. It significantly lowers the LDL, fights human vascular atherosclerosis. It makes the plaque either regress, prevent progress, make it harder and in the process make them less vulnerable . There are innumerable studies that document the evidence. Statin has become a must-prescribe drug in any one with clinically established CAD or even in concealed CAD. Guidelines are available to prescribe statins various intensity, depending on the risk profile.

Which statin ?

There has been a long list of statins. Many of them have retired from the ring .Currently, the fight is between Atorvastatin, a Rosuvastatin. Like Pepsi vs. Coke.

Note the graphic ,A meteoric rise of one drug since 2005 . (Can you guess the reason ?)

ATRORVA or ROSUVA Which one should I choose ?

There is very little “one to one” comparison study between Rosuvastatin and Atorvastatin .The gap in the pros and cons are narrow. Following points are observed, without much dispute.

1.Rosuvaststin is more powerful.

2.Plaque stabilisation effect is not different((Satrun, study NEJM 2011 based on IVUS)

3.New onset diabetic risk is more likely with Rosuvastatin

4.Worsening of cataract is also more with Rosuvastatin

5.Atrovastatin has some additional benefits in lowering triglycerides. (Bakker-Arkema RG, JAMA. 1996)

No one is dare enough to give strong verdict . Surprised to find one this month. BMJ has come out with a possible answer. It is called LODESTAR trial (Ref 1)

Mechanism of new onset diabetes with statins (REF 3)

It can be 7% with Rosuvastatin (less with Atorvastatin). We think, statins act primarily within the hepatocytes where cholesterol synthesis takes place, but they also have an eye on the pancreatic β-cells as well. It down-regulates GLUT-4 in adipocytes, and results in compromised insulin signalling. Furthermore, statins’ impact on epigenetics may also contribute to statin-induced T2DM via differential expression of microRNAs.

Mechanism of cataract with statins (Ref 2)

The cells lining that line the lens are dynamic and require cholesterol on a day-to-day basis. Statins inhibit proper epithelial cell development within the crystalline lens, where cholesterol biosynthesis is critical to maintain transparency and structure of the lens.

Final message

So, is it Atorvastatin or Rosuvastatin? It is left to you.

Mind you, “no statin at all” is the best option if circumstances and risk profile allows. Statins are never considered life-saving staple drugs in our fight with CAD and atherosclerosis. We, along with our scientists might may make you feel like that. Lipids can be controlled within desirable means exclusively with diet and exercise in most of the population* .

(*Forget about statins in the last 5000 years of known human existence, so many great people have lived a long and successful life in this world, without even knowing there is an organ called the heart that is responsible for the circulatory system)

Reference

1.Lee YJ, Hong SJ, Kang WC, Hong BK, Lee JY, Lee JB, Cho HJ, Yoon J, Lee SJ, Ahn CM, Kim JS, Kim BK, Ko YG, Choi D, Jang Y, Hong MK; LODESTAR investigators. Rosuvastatin versus atorvastatin treatment in adults with coronary artery disease: secondary analysis of the randomised LODESTAR trial. BMJ. 2023 Oct 18;383:e075837. doi: 10.1136/bmj-2023-075837. PMID: 37852649; PMCID: PMC10583134.

2.Leuschen J, et al Association of statin use with cataracts: a propensity score-matched analysis. JAMA Ophthalmol. 2013 Nov;131(11):1427-34.)

3.Carmena R, Betteridge DJ. Diabetogenic Action of Statins: Mechanisms. Curr Atheroscler Rep. 2019 Apr 30;21(6):23. doi: 10.1007/s11883-019-0780-z. PMID: 31037345.

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There are numerous complex grading for bifurcation lesions available.

The one proposed by Medina is simple and most useful.

In this grading three segments

  • Proximal main vessel
  • Distal main vessel
  • Branch vessel

Are given a code 0, and 1 if  lesion is present or absent .

This grading gives simple and fast method to label a bifurcatiuon lesion and to asssess the response to PCI. The only issue here is the individual  lesions are not graded , for example branch vessel ostium just involved about 20 % is not addressed . Further TIMI flow in these vessels may also be incorporated

How medina grading can be used to assess effectiveness of

angioplasty  ?

A patient with 1.1.1  after the treatment should revert back to 0.0.0.  if converted into 0.0.(.5) may indicate a residual side branch lesion  .5 shall indicate 50% residual lesion, .3 , 30% etc

 

What is the best management strategy for bifurcation lesions?

The topic has been discussed extensively for over a decade in various forums.

Though the lesions and intervention techniques  appear complex the basic concept is simple.

Following is the 8 point algorithm

1. Assess the bifurcation lesion accurately.

2. Apply the general rule and ask the first question whether PCI is neccessary at all ? if decided for PCI

3. Stent the main vessel.Protect the side branch.  

4. Dilate the side branch with a balloon.(KIss or through the struts) 

5. Very rarely,  if the side vessel is more significant and large  stent it and balloon the main vessel.

6. Use drug eluting stents with caution .

7. Resist the temptation of using two stents unless the situation demands and is absolutely required.

8. Never attempt to do bifurcation angioplasty during ACS as apart of primary angioplasty.( Unless you’re extremely competent, even then aim of primary PCI is to salvage myocarium quickly , not to provide TIMI 3 flow in non IRA vessel.)

Dr.S.Venkatesan.Madras medical college.Chennai.

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                                   ACS   is the  most common cardiac emergency .  Management of STEMI is relatively straight forward.  The  only decision that to be taken is the  modality of reperfusion. (Primary PCI   or thrombolysis.) There is no need to risk stratify  STEMI on arrival. All STEMI patients are considered high risk on admission. Whereas  NSTEMI consists of  a heterogeneous  population. They need to be   triaged into low intermediate  or high risk categorizes on arrival.There is two management  approaches for unstable angina .All high risk UA should enter early invasive strategy . And low risk and intermediate risk group will get early conservative management. 

                                       The principle of management of  UA differ from STEMI in a fundamental way , as there is no issue of myocardial salvage in UA .The primary aim is to provide relief from pain and prevent an MI. So in the strict sense there is no time window in unstable angina /NSTEMI.

 

                                       But it is generally considered 48 hours is the time limit for an early invasive approach.If the patient has crossed this time there is apparently no great difference in outcome for conservative and invasive approach. 

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