scai | Dr.S.Venkatesan MD

Posts Tagged ‘scai’

An “Intriguing concept” in STEMI care: Pre-hospital thrombolysis is great, while In-hospital lysis is a suspect !

Posted in Uncategorized, tagged acc, acs, dr s venkatesan, esc, guidelines, lancet, madras medical college, nejm, pre hospital thrombolysis, scai, stemi on June 12, 2026|

Human myocardium does not read hospital sign boards . It simply doesn’t bother whether thrombolysis is done in a moving van or a stationary room . When confronted with a life threatening emergency , all that it demands is quickness with which it is administered. Yet, in modern interventional cardiology, a same thrombolytic drug transforms from a life-saver into a forbidden clinical error, depending on whether it was injected in an moving ambulance or in the emergency Department.

This is the comical, yet tragic, irony of modern STEMI care.

Pre-hospital lysis is celebrated as a great strategy , while ultra fast in hospital lysis even within the “golden hour” is frowned upon as low-quality treatment.

At the heart of this paradox lies , the cult like status of primary PCI .It is true, pPCI has been etched as the gold standard of ACS care. However, most of the experienced cardiologist* know its perceived supremacy is not absolute ,largely attributed to the seductive power cath lab . (* Few have the courage to admit it )

Respect the myocardium not the cath lab

The efficacy thrombolysis is strictly a function of time, not geography. Landmark data from the CAPTIM trial explicitly demonstrated that when thrombolysis is administered within this early window, mortality rates are equivalent, and in some subsets superior, to immediate pPCI.

The current system of care willingly accepts this when a paramedic administers the drug but reprimands a physical if he does the same in his CCU .Why ? We seem to suffer from a misplaced academic arrogance that demands , fate of every coronary event must be decided only in cath lab. Any thing else is considered as deviation from the standard of care

Final message

It is time to change how we use the terms “pre-hospital” and “in-hospital” thrombolysis and replace them with a simple terminology . Symptom to Reperfusion Time. If a patient presents to a pPCI-capable center within the first hour standalone, ultra-fast ER lysis should be made an established, protocol equivalent to pre-hospital care, which is at equipoise with (un)disputed gold standard of pPCI as per the landmark study of CAPTIM.

Postamble

It is heartening to note In-hospital thrombolysis continues to be dominate mode of reperfusion at any point of time, inspite of the negativity surrounding it. Can we take this as a proof of real mettle of pPCI ?

References

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How is that ? A self prescribed PCI (s-PCI) , is an accepted professional medical decision

Posted in Uncategorized, tagged acc, aha, bari 2 d, bmj, courage, esc, fear driven pci, ffr, ffr driven pci, guideliens cad, indication 2a vs 2b, indication for pci in cad, insurance driven pci, iscehmia driven pci, jama net work, lancet, nejm, oct, pci, scai, symptom driven pci on March 7, 2026|

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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How do mitral valve balance its Tethering and Closing Forces ?

Posted in Uncategorized, tagged coapt study, eccentric cs concentric mr, jacc, lancet, lub dub, macr, Mechanism of mitral regurgitation, mitra clip, mitral annulus, nejm, role of stethoscope in current era, scai, TAVR, teer, tethering cs closing forces in mitral valve on January 3, 2026|

Preamble : The Lubs & Dubs

The lubs and dubs, along with some added sounds are the only language, the heart can speak in health and distress. It’s a worrying story altogether, gradually many of us are becoming “cardiac illiterates” as we struggle to read , its gentle communication. it is not our fault. Stethoscopes are reduced to become a social marker of being a doctor. We may excuse ourselves, even if we can’t differentiate a systolic from diastolic murmur, after all, hand held echo machines, instantly tell the diagnosis.

( After reading this article, fellows are expected to understand why the first heart sound in MR (ie the lubs,) are mostly soft, some times normal or even loud in certain conditions)

Now, let us go to the mitral valve dynamics

How many of us are aware, there is a big science of physics and biology operating when the mitral valve perfectly closes at the level of the annulus, with each systole , balancing different sets of known and unknown forces.

In this article, we will see how these two sets of forces mitral valve tethering and closing forces balance out each other to seal the mitral valve and what happens when the forces begin to fight each other.

Balance of Tethering and Closing Forces in Mitral Valve Coaptation

The mitral valve (MV) coaptation refers to the edge-to-edge apposition of the anterior and posterior leaflets during systole, ensuring a competent seal to prevent regurgitation. This process is governed by a delicate balance between tethering forces (which restrain leaflet motion to prevent prolapse into the left atrium) and closing forces (which approximate the leaflets for sealing).

Tethering forces: These are primarily transmitted through the chordae tendineae from the papillary muscles (PMs) to the leaflet free edges and bellies, pulling the leaflets apically and laterally toward the left ventricular (LV) apex. They arise from:
Closing forces: These are driven by the transmitral pressure gradient during systole, where rising LV pressure (generated by LV contraction) exceeds left atrial (LA) pressure, pushing the leaflets together. The force is proportional to the LV dP/dt (rate of pressure rise) and peaks in midsystole.
Balancing mechanism: Coaptation occurs when closing forces overcome tethering, enabling leaflets to meet with sufficient overlap (coaptation length >8 mm typically). Imbalance favors regurgitation: excessive tethering (e.g., from PM displacement) causes apical tenting and incomplete closure; insufficient closing (e.g., low LV contractility) fails to seal the orifice. In health, the forces are synchronized with systole, with closing forces dominating midsystole to minimize the effective regurgitant orifice area (EROA).

Paradoxes in the Balancing Mechanism

MV mechanics exhibit several counterintuitive paradoxes, where adaptive or dysfunctional responses lead to outcomes opposite to expectations. These highlight the interplay of geometry, contractility, and force transmission:

Paradoxical systolic PM elongation: Normally, PMs shorten during systole (1 cm) to offset annular descent and maintain annulopapillary balance. Post-myocardial infarction (MI), scarred or ischemic PMs paradoxically elongate driven by transmitral pressure tension. This decreases annulopapillary distance, attenuates tethering, and reduces MR severity—contrary to the intuition that PM weakness worsens regurgitation. However, extreme elongation risks leaflet prolapse, flipping the paradox to increased MR.
PM dysfunction attenuating ischemic MR: In isolated dysfunction, reduced PM contraction intuitively increases slack chordae and prolapse risk. Yet, in localized basal inferior LV remodeling, PM dysfunction (measured as reduced longitudinal systolic strain) inversely correlates with MR fraction attenuating MR by limiting excessive tethering. This holds only with certain level of remodeling . Gross and asymmetrical remodeling can exaggerate tethering and increase the MR.
Dynamic EROA reduction despite peak driving pressure: MR often peaks early systole (when closing forces are low and tethering dominates) but paradoxically decreases midsystole, even as LV pressure (driving force) maximizes. This occurs because rising closing forces (transmitral gradient) overcome tethering, shrinking the orifice mimicking reduced regurgitation when it should worsen.Thgis mechansim can some times seen when MR jet is bi-fid in doppler tracing.
Imbalanced chordal forces causing focal prolapse: In acute ischemic MR (e.g., posterior wall ischemia), tethering redistributes unevenly: tension drops in ischemic-side chordae but rises on the nonischemic side causing focal tenting and relative prolapse on the ischemic commissure. This creates an eccentric jet despite global LV contraction.

This article clearly tells us that the forces acting on the mitral valve apparatus are so complex. The conceptual model of tethering and closing forces may be oversimplified. There are variable interactions between them. More importantly, the atrial forces also influence and intrude into these forces. Realize that MV competence is not just about force magnitude but their vectorial distribution and timing, often amplified by LV geometry changes.

Final message

As cardiologists and surgeons, we must realize the fact, how important it is to analyze both anatomy and the physiological impact when we rush to clip, cut, or repair it with annuloplasty and subvalvular interventions.

*Sometimes, it might even be tempting to do mitral valve replacement, even when it is not indicated, because we need not bother about all these dizzy mechanics and physics of MR jet forces.

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Permanent Aortic filter : A pre-clinical proposal for PAA-PMF, device for long term stroke prevention

Posted in Uncategorized, tagged acc, aortic filter, circualtion research, embol x, esc, innovations in cardiology, ivc filter, laaa occluder, lancet jacc interventions, nejm, PAA-PMF, permanent aortic filter, scai, sentinel device, stroke prevention, TAVR, triguard on December 24, 2025|

“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

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/
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/
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
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
Cleveland Clinic. Vena Cava Filters: Purpose & Placement. 2025. Available from: https://my.clevelandclinic.org/health/treatments/17609-vena-cava-filters
Bilal H, et al. Complications of Inferior Vena Caval Filters. NIH. 1997. Available from: https://pmc.ncbi.nlm.nih.gov/articles/PMC3036364/
Alpaslan M, et al. Embolic Protection Devices in Transcatheter Aortic Valve Implantation. NIH. 2025. Available from: https://pmc.ncbi.nlm.nih.gov/articles/PMC12194329/
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
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
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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“Non-superiority” trial of sub-optimal PCI vs OMT : A proposal for a study design

Posted in Uncategorized, tagged aha acc guidlines, cardiology fellows research topic, cardiology research propsal, cardiology research topic, courage, dm cardiology fellows research, esc, fellows research topic, ischemia, non inferiority trials, non-superiority trials, omt vs gdmt, omt vs pci, optimal pci, orbita, pci, PCI VS medical management, ptca, scai, suboptimal pci, suboptimalpci vs omt on February 3, 2025|

The therapeutics of coronary stenosis has become a technogical wonder, interwoven with statistical wordplay in the last few decades. PCI is sitting pretty at its peak glory.The term OMT or GDMT is a popular terminology, but realistically exist only in guidelines.

It is a strange academic habit among cardiologists, that they have subdivided medical management into optimal and suboptimal. Meanwhile, we haven’t seen any papers from cardiology forums that classify PCI according to its quality. How many of use a term like optimal PCI or guideline-directed PCI (O-PCI, GDPCI). Every PCI, by default, is perceived as good by our flawed coronary intellect.

A single patient experience

Let me share a patient consult from a remote town of north India. He is a STEMI patient (1 year old) with mild LV dysfunction and thinning of IVS and anterior wall. His CAG showed a significant looking, yet non-flow limiting LAD lesion without any troubling symptoms. I came to know he had consulted two institutions and was apparently not happy with their approach (In his own words, “They seem to be primarily interested in caging my LAD than listening to me”).

Somebody has suggested my name. He called me over the phone for a consult. I asked him remain there to follow his doctor’s advice. But, he flew some 2000 km to meet me. He was so knowledgeable and was aware of everything I wanted to tell. Like, viability, scars, futility, and benefits of revascularization, imaging-assisted PCI, impact of PCI on exercise capacity, importance of risk factor management, etc.

I told him, “In my opinion, you have technically a single vessel disease that can be managed well with drugs. But if PCI is to be done, it should be done in a proficient manner, as the lesion looked hard and was close to the LAD ostium, trespassing LCX as well.” I stressed the importance of a professionally done procedure with enough expertise and follow-up maintenance care.

He was not entirely satisfied with my response. He wanted a clear yes or no! . I told him, “If you have full trust, continue with the drugs at full intensity and do a stress test after 3 months. otherwise, if you keep getting even the slightest doubt and anxiety over the hidden blocks, go for a stent immediately at a good Institution. (My conscience said the latter half of my advice was unwarranted, but I had to; after all, me too need a protective mechanism)

He left my clinic profusley thanking me. I am not sure , how my consult was useful for him and what he is going to decide.

Academic lessons from this patient.

1.Patient fear factor over coronary blocks may be the ultimate game changer. Cardiologists should try to mitigate this fear and at the least should not be an amplifier to this emotion.

2.Leaving tricky profesionaly complex decisions to the patient, is an easy escape route for us, however it comes very close to professional incompetence. (Of course, we do this on a routine basis, approved by the modern medical guidelines, ethics, and legal system, in the name of patient empowerment)

3.Finally, we can grow a potential research hypothesis. A sub-optimal PCI is non-superior to OMT.It is curious there is no study available to compare sub-optimal PCI to OMT. We must also realize there is nothing called standalone PCI. Without concomitant OMT, PCI is a dud. Every young cardiology fellow need to etch this fact in their cortical cardiac memory. OMT often turns out to be the savior of stents, but the latter ruthlessly steals the credit.

Postamble

I could find one study analyzing suboptimal stenting (Ref 1), but it didn’t compare it with OMT. Suddenly, as I finish writing this, a big fact struck me hard, i.e., even a well-done PCI in sophisticated core labs with meticulous care struggled to beat OMT in a barrage of landmark trials (like COURAGE, ISCHEMIA, ORBITA). What is the big deal to analyze suboptimal PCI vs OMT?

Prati F, Romagnoli E, Gatto L, La Manna A, . Clinical Impact of Suboptimal Stenting and Residual Intrastent Plaque/Thrombus Protrusion in Patients With Acute Coronary Syndrome: The CLI-OPCI ACS Substudy Circ Cardiovasc Interv. 2016 Dec;9(12):e003726. .

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Distal vs proximal strut crossing in BFL : Who is trying to sustain the confusion ?

Posted in Uncategorized, tagged bifurcation lesion, crosssing side branch, dk crush, ebc club, esc acc aha esc, jailed side branch, scai, single or two stent strategies on July 4, 2023|

Anyone who is flushed with millions can become a member of “The Hurlinghamin” London or the “Yacht” in Monaco, or any other glamorous clubs in the world. But, EBC* is different. Only cardiologists are privileged to enter. EBC is obviously unique. It is the only club addressing exclusively a subset CAD, ie bifurcation coronary lesions. Apart from immense pride and academic entertainment, it teaches us some deep technical points. (By the way, BFL* is a minuscule spoke in the gigantic wheels of global atherosclerosis)

Approach to BFL

90% of BFL still require only drugs or humble single stent or a provisional second stent strategy. However, as per basic rules of human intellect, lesser problems continue to bother us and consume our precise time. This continues, even after realisng , there are 6 complex two stent strategies that doubles up complications.

(*EBC -European Bifurcation club .BFL-Bifurcation lesion)

We will address one unique issue in BFL. May not be a major clinical issue .Still, it’s worth it. It is about the side branch crossing after the intentional jailing of the side branch.

Let us answer this query first

Pure science: Observations from Bench test (Text from Ref 1)

In contrast to provisional stenting in which re-crossing through a distal strut is desirable, initial re-crossing the crushed SB stent in the DK crush technique should be done through a proximal stent strut to minimise the risk of SB stent deformation. A theoretical exception could include bifurcations with a particularly narrow angle for which proximal re-crossing may shift more struts towards the MV, leading to a less desirable, longer neocarina. The 2^nd recrossing should be done through a distal strut.

Bench testing is clear. Still , Why this confusion ?

We are all talking about theory in bench testing in stable non-hemodynamic conditions that lacks a biological carina and the dynamics of plaques. We are aware that there are at least 5 virtual ostia in every bifurcation arena (or trifurcation) . The qunatum and direction of plaque sharing occurs with a random effect. We also know the final kissing either cements these plaques perfectly or unsettles in a most bizarre way. So, these strut crossing stuff, are more of an imaginary bio-engineering principles. Whichever strut you cross, do it slowly, gently dilate it to the maximum within the polygonal confluence and good approximation. Don’t get too much carried away , even live online OCT guidance do not guarantee a perfect crossing.

Final message

The answer to the title question seems to be (me), one need not hair-split much on the site of crossing at the side branch. Fortunately, in whatever way, we weave the metallic mesh*, at the epicenter of the coronary highway, it is the natural secretagogues like TPa, Nitric oxide, PGI-2, along with DAPT decides the patient’s genomic fate.

*An appeal to all EBC club members.Before embarking upon a compex PCI on a stable patient , please think for one last time , whether your patient might do well, only with medicines.

Referecne

1.Hall AB, Chavez I, Garcia S, Gössl M, Poulose A, Sorajja P, Wang Y, Louvard Y, Chatzizisis YS, Banerjee S, Xenogiannis I, Burke MN, Brilakis ES; Collaborators. Double kissing crush bifurcation stenting: step-by-step troubleshooting. EuroIntervention. 2021 Jul 20;17(4):e317-e325. doi: 10.4244/EIJ-D-19-00721. PMID: 32310131; PMCID: PMC8919516.

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What is double barrel stenting ?

Posted in Cardiology -Interventional -PCI, tagged cabg, circulation, complex pci, distal left main, double barrel stenting, europcr, India live coronary, interventional cardiology, jacc, left main stenting, live pci work shop, pci, proximaleft main, ptca, scai, tctmd, trifurcation lesion, unprotected left main on February 13, 2011| Leave a Comment »

It is a complex PCI procedure meant for high risk bifurcation /Trifurcation lesions
Two stents are simultaneously deployed.
It aims to prevent sudden acute occlusion of one of the major branches .
It is not an easy procedure , and be used only in rare circumstances .
Distal left main and ostio proximal LAD/LCX is a classical example.
Navigation can be difficult , only well experienced operators should attempt it.

*Is there a ready made two lumen stent available ?

The image is meant for concept purpose only !

It is one of the techniques available to stent unprotected left main

An excellent review in ACC intervention journal for unprotected left main .

Click on the Image to reach the article

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Ignorance based cardiology :How often a coronary artery reject a stent ?

Posted in Cardiology -unresolved questions, cardiology- coronary care, Cardiology-Coronary artery disese, Infrequently asked questions in cardiology (iFAQs), tagged coronary stent, cypher, evidence based cardiology, guidelines, jama, nejm, nstemi, onlionejacc, paclitaxel, pci, primary pci, rescue pci, scai, stemi, sub acute stent thrombosis on August 5, 2009| 9 Comments »

Fundamental principle of human biological system is to live in harmony with nature and environment.Each cell has a unique reaction when it comes into contact with external material. This reaction can be acute or chronic , local or systemic. The most severe form of allergy is called anaphylaxis that can result in instantaneous loss of life. There is a whole gamut of disorders that resulted in a separate speciality called allergic medicine .

Further ,the transplantation science have taught us an organ or cell can be rejected at any point of time after implantation (Hyperacute -chronic) .With advancement of science we have started implanting a variety of devices with complex metallurgy ,inside human body, metal clips, prosthesis, valves, wires, etc .How the body handles them .The consequences can be a mild reaction to major ones occasionally.

Consider ,a local allergy due to a orthopedic prosthesis in one of the leg bones is far less serious than a metal within a coronary artery irritating the intima .

Remember hypersensitivity reactions can be severe . This lady reacted like this to a sandal slipper -A fiery red infiltration

Imagine if a stented coronary artery react like this what would be the possible consequence ?

In susceptible individuals , can a metal cause

Intimal hyperemia

Intimal induration

Intimo-medial edema following stent deployment

Why drug eluting stents are more prone for hypersensitivity ?

The answer is simple , while metal allergy is a comparatively rare phenomenon, the drugs we coat and the polymers used are many fold likely to result in hypersensitivity reaction.

While the world is worried more about penicillin , sulpha allergy which occurs in 1 in 100000 , we tend to ignore the metal and drug reactions within the tender coronary arteries.

What is the clinical expression of stent hypersensitivity ?

It is often a coronary event in the acute phase and restenosis in chronic phase.

How much of acute stent thrombosis is related to stent allergy mediated reaction ?

The exact incidence will never be known. It could be high. Whenever a sudden unexpected early stent occlusion can be a suspect .

Is stent allergy a local reaction or systemic reaction ?

It is most often local .The drugs the stent elute can elicit a systemic reaction occasionally.

So what can be done to prevent this complication ?

Drug companies in it’s package regularly include the warning message ! What does it imply to have a caution on the covers ? .This warning simply represent about our ignorance in this issue. We presume it is a minor problem.

Questions unanswered

How does a cardiac patient knows whether he is hypersensitive to stainless steel or nickel ?

Is it practical to have a stent allergic test in every patient before PCI ?

Is routine administration of corticosteroids for few days after PCI an answer ?

Reference

R.Virmani , circulation 2004

http://circ.ahajournals.org/cgi/content/full/109/6/701?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=stent+%27allergy%22+&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT

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How to tackle CTO ? Japan shows the way – Welcome to the world of complex cardiovascular interventions !

Posted in Uncategorized, tagged CCT JAPAN, chronic total occlusion, complex pci, cto, front runner, gaurd wire, ptca, scai, tctmd on August 1, 2009| Leave a Comment »

Annual workshops for interventional cardiologists has been hugely popular events.They have become the forum for all technological breakthroughs. Some of the popular ones are

Japanese have gained a unique place in complex cardiovascular therapeutics interventions especially in chronic occlusions.

Landmark article for CTO crossing

www.cct.gr.jp/2003/wirehand/index.html

How to reach Japan ?

Click below

CCT2010

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Coronary hemodynamics in 100% occlusion ?

Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, cardiology- coronary care, Uncategorized, tagged 100% lad, 100% rca, chronic total occlusion, coronary artery, coronary collateral circulation, courage study, cto, des, europcr online, jacc, nejm, nstemi, oat study, open artery hypothesis, pci, plain balloon angioplasty, primary pci, ptca, scai, stemi, stents, tctmd, thrombolysis, toat study on July 15, 2009| 8 Comments »

Total coronary artery occlusion is a common finding in CAD especially in chronic stable angina. Normal coronary blood flow is 5 % of cardiac output that amounts to 250-300ml/mt.At an average heart rate of 70/mt , each beat injects about 5cc blood into the coronary circulation.This is shared between two coronary arteries. This means , only few CC (2-3cc) of blood enters each coronary artery with each cardiac cycle .

When one of coronary artery is totally occluded what happens to the coronary

blood flow ?

A.Total coronary blood flow can be be maintained normal at rest as it forms only about 5% of cardiac output (or it is only slightly reduced )

B. It is believed , the unobstructed coronary artery could receive the blood meant for the contralateral coronary artery. This possibly explains the increased coronary artery diameter in the non obstructed artery.

C. It’s nature’s wish , that the contralateral coronary artery shall share 50% of it’s blood through collaterals if available.

D.If collaterals are not formed it , the unobstructed coronary artery may be over perfused with double the amount of blood flow.

E. Some times , the collaterals steal much more than what the obstructed coronary artery deserves and make the feeding coronary artery ischemic. This is many times observed in total RCA occlusion with well formed collaterals from LAD/LCX.

F.The collateral flow in CTO also depend on whether flow is directed from LAD system to RCA or from RCA -LAD system. The LAD is better placed to assist RCA than vice versa.This is for two reasons.1.LAD blood flow is higher than RCA so it can share it.2.The driving pressure is more from LAD -RCA , as RCA can receive blood flow even during diastole .

F.During exertion , the coronary hemodynamics become further complex.The collateral’s are traditionally thought to be less than adequate during times of exercise.But it is more of a perception than solid scientific data.This rule may be applicable in only certain group of patients. We know CTO patients with very good exercise tolerance who have documented collateral’s.

G.Collaterals can be either visible or invisible by CAG. The strength of collateral circulation is not in it’s visibility but it’s capacity to dilate and respond to neuro humoral mediators at times of demand. Currently , there is lot to be desired regarding our knowledge about the physiology of visible collaterals , no need to mention about invisible collaterals !

Final message

The above statements are based on logics and observations .

Is it not a irony in cardiac literature , where thousands of articles are coming out every month to tackle totally occluded coronary artery(CTOs) , there is very little data regarding the coronary hemodynamics in chronic total occlusion . How does a patient with CTO can manage a active life with only one functioning coronary artery ?

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Dr.S.Venkatesan MD

Expressions in cardiology

Posts Tagged ‘scai’