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A Proposal for a Randomized Trial on Covered Stents in Complex, friable, TCFA driven, Acute Coronary Syndromes : The SEAL-TCFA trial

Posted in Uncategorized, tagged , , , , , , , , , , on June 17, 2025|

Covered stents are exclusively reserved for coronary artery perforations. Yes, that’s what we think. There has been limited exploration regarding the value of covering the complex lesions, which could prevent future coronary events .

It is possible, covered stents might play a extended role , other than perforations as in complex .friable thin capped lesions . As of June 2025 , haven’t found any such study in cardiology literature.

Ref : Kilic ID, Fabris E, Serdoz R, Caiazzo G, Foin N, Abou-Sherif S, Di Mario C. Coronary covered stents. EuroIntervention. 2016 Nov 20;12(10):1288-1295. .

The recently released PREVENT study argued for PCI for patients with vulnerable high risk plaque. Ironically , it is found plaques with very thin cap ie <50microns are at risk of rupture by the radial stress of struts in the immediate or late follow up.

The thought of this study came when we witnessed high recurrent events, due to plaque prolapse, TCFA injury, new plaque ruptures, micro emboli. no reflow etc in patients with complex lesions.

Any past studies done on this aspect ?

There have been some attempts to use covered stents in degenerated venous grafts. Also, the M-Guard stent system was used in the past to seal thrombus during primary PCI. Both showed mixed results. (Gracida 2015)

Are we ready for a trial with a far fetched Imagination ?

What about jacketing and sandwiching the coronary lumen internally with a synthetic layer of tissue? That can potentially prevent recurring events indefinitely. (It is like making a native coronary artery into a Teflon-coated tube.) The proposal may look crazy until we find a inert layer of synthetic tissue to false roof the coronary lumen. But someone can make a start.

Final message

Covered stents are not just meant to arrest blood leaking outwards, in case of perforation , it can also be used seal high risk plaques, that ruptures and leaks its content into the lumen.

*In the following document, a brief outline and proposal is written about such a study. Whoever wants to do such a study, may use it. I wish I could be an external adviser, as I am no longer attached to a teaching hospital or research center.

SEAL-TCFADownload

Postamble

Before , we begin such a study, one may look at the long term outcome of patients who had already received covered stents for perforations. This is important because, PTFE’s pro-thrombotic potential and need for additional vigilance is yet to be defined.

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What is the relationship between Orthopnea and RV function ?

Posted in Uncategorized, tagged , , , , , on June 15, 2025|

Paroxysmal nocturnal dyspnea and orthopnea are cardinal symptoms of heart failure. The difference between the two has been extensively discussed and debated in medical literature. The key difference is in the time lag that occurs in PND , while orthopnea occur immediately. However, we never looked into PND & Orthopnea with reference LV, RV or biventricular failure.

The fact that Orthopnea occur immediately, raises many critical queries.

It is presumed that the increase in venous return in a recumbent posture immediately causes lung congestion and stimulates pulmonary receptors (J or non-J?) which results in dyspnea. The fact that orthopnea is relieved by sitting posture demands still more explanation. Is it volume-dependent lung congestion, or volume and stretch-dependent RV mechanic receptor stimulation? (or both) I think it is difficult to answer that question.

We get some indirect clues in bed side, by experience. In many patients with Chronic RV dysfunction , orthopnea seems to be less, making it likely pulmonary origin. At the same time, if RV dysfunction is new or acute, it is the raised RVEDP, that is responsible.

Now , we have a problem . Is orthopnea related (more )to RV or LV dysfunction ?

It can have complex inter dependent relationship. In fact, the degree of pulmonary hypertension, the septal push (Reverse Bernheimer effect ) can further confound. Severe RV dysfunction alters the V:Q ratio of lungs, and a also a mismatch between RV vs LV stroke volume.

Final message

The origin of Orthopnea is determined by the status of both RV and LV function. They can either congest or decongest the lung. Realize, in a severely dysfunctional biventricular failure, it is the fine balance between them that keeps the lung dry or wet.

The importance of RV mechanoreceptors and their pathways to dyspnea centers are less understood. While the mechanism of orthopnea is intertwined between the functions of the two ventricles, PND is fairly specific for acute elevation of LVEDP and resultant alveolar interstitial edema. Mind you , orthopnea can occur with totally dry lungs, if its origin is from RV, while it is a rarity in patients with PND.

Post-amble

Time lagged Orthopnea : A proposal for new clinical entity.

We have also seen patients with RV dysfunction mimic PND when they develop dyspnea say 15 to 30 minutes after lying down. Fellows should go back in time and try to re-look and analyze gaps in our understanding of cardinal symptoms.

A small study is easily possible about the incidence of PND and orthopnea in patients with cardiac failure with reference to right and left ventricular function.

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Forbidden thoughts in medical science : Should we Include un-intentional medical errors, as part of disease process ?

Posted in Uncategorized on June 5, 2025|

Final message

Since, we can’t sue science for its impurity , or a misbehaving bacteria , an inadequate imaging machine or manipulated health care system,poor doctors have become, the only visible targets.

Related topic

Martin A Makary BMJ 2016;353:i2139 doi: 10.1136/bmj.i2139

Next query in medical ethics

What is the permissible level of error rate, for a medical professional?

Governments can err, Courts can err, pilots can err, meteorologists can err, sportsmen can err, but …

Wish , the prestigious British journal of medical ethics write a position paper on this.

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Can we report ECGs without seeing the patient and knowing their symptoms ?

Posted in Uncategorized on June 4, 2025|

Every day, 100s of physicians and cardiologists are asked to report ECG either physically or on-line .In India, they do it for some paltry benefits from stand alone labs , hospitals , institutional protocol or by sheer compulsion.

When only ECG is reported ,the physicians are often blind to the indications for which it is taken . The symptoms of the patient or the past history is rarely available. It is a sorry state of affairs and many of us do this, fully aware of the consequences – a normal ECG can’t rule out an ACS in at least 10 % of times.

Now, here is an ECG of a 40 year old male, on my table for reporting. No other info is available.

How should I report it ? Can I refuse to report ?

There were five options

A.ECG Normal

B.ECG within normal limits, with non specific ST/T changes

C.ECG shows ST elevation Infero- lateral leads. To rule out ACS

D. Early repolarization pattern

E. I refuse to report, until clinical data is made available.

My report: ECG within normal limits. (Shows ERS pattern with non specific ST elevation in Infero-lateral leads.To correlate clinically, and advised a physician consult. )

One of my colleagues commented, that I lacked the guts to comment the above ECG as normal. The contention is, ERS pattern occurs in up to 20% of the young population, and it evokes unnecessary anxiety. How do I know he is pain free ?However, I agreed with my colleague. It is indeed ERS by all means. But,how long ?, we can be carriers of proxy anxiety, for the sake of our patients. Further, by no means ERS gives immunity to ACS. (What happens to the ST segment of ERS during ACS is a different query to be answered.)

(*Later on I came to know this guy had epigastric pain, and was simultaneously evaluated for CAD which was excluded . Mind you, mistaking ERS pattern for ACS is an age old problem. About 5% of thrombolysis in ISIS -2 study(1988) turned out to be in patients with possible ERS)

Final message

Can we report an ECG without knowing the patient and his symptoms ?

It is a foundational question in clinical medicine. The answer to which can shake the way, we practice cardiology. It is indeed unprofessional* of a physician to report an ECG without knowing the patient status. But we do it every day , can’t avoid it. But ,let us at-least insist the ECG lab guys to note down the symptoms or /the purpose for which it is taken (like a regular health check or pre-op evaluation, etc).

*Of course , to escape from a potential miss, we should atleast write, ECG to be correlated clinically and with past records.

Post-amble

We are in the AI era. ECGs are read by data-hungry machines. If you think there are AI models that can match a million ECG patterns and detect an ACS in milliseconds, sorry, you are sadly mistaken. Unless and until patients’ entire history is fed into humanized machines, (that had undergone 8 years of rigorous cardiology training) the risk of missing a diagnosis is significant.

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Balloon vs Self expandable TAVI : Essential differences

Posted in Uncategorized, tagged , on May 20, 2025|

The following table was created , when there was a dispute in one of my lectures , when I told self expanding valves has more” Net-radial force”on the annular arena. It was pointed out, I was wrong and contrary to the published literature . Yes, may be, but could agree only partly on this. The physics of radial force/stress can be under stood only, if we classify it with reference to time , ie at the time of deployment vs long term stress. Also,the type of metal and the intrinsic potential energy stored in self expanding stent.By the way, this enhanced radial force is supposed reduce the PVL in SEV.

Note : One curious fact is often ignored. All self expandable valves, can be balloon expanded further, if there is a need. While, a balloon expandable valves can never acquire the properties of a self expanding valve.( Toutouzas K, The DIRECT Trial. JACC Cardiovasc Interv. 2019 )

TAVI : Current status

TAVI is considered by many (not all) as the revolution of this century ,in the field of Interventional cardiology .More than a million valves are implanted so for .TAVI as a concept is sustaining and trying to prove the test of time (Of course with lots of ifs and but)

The indications for TAVI has come down drastically ,from very high risk subsets to even low risk patients, without corresponding reduction in complications. (Consider this : Para valvular leaks in surgical AVR can be low as 1-3% while it can be as high as 40% ) Still TAVR has that magnetic attraction for a simple reason it avoids surgery.

Unfortunately, the technology has not seen much innovation beyond the PARTNER .We get to see so many clones of self-expanding and balloon-expanding platforms are crowding the market ,with extra skirts , sleeves, design for coronary access etc. Meanwhile, we have vastly improved in expertise, delivery hardware and managing complications.

However, until we develop methods to remove the native valve debri from the aortic root , it is very hard to bring an outcome, that is equipoise to surgical valve replacement. Future designs will look into active fixing valves with polymer-based leaflets to increase the longevity of the valve, which is, currently less than 50% of mechanical valves.

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What is the relationship between number of Aortic leaflets and number of Aortic sinuses ?

Posted in Uncategorized, tagged , , , , , , , , , , , , , on May 20, 2025|

Simple answer : If one leaflet is absent (True embryonal agenesis of anlagen) then corresponding sinus also fails to germinate. So number of leaflet is equal to number of sinus.This implies,In normal Tricuspid aortic valve there are three Aortic sinuses. In Bi-cuspid Aortic valve there are two Aortic sinuses depending on the absent leaflet (Generally R & L sinus present)

But, reality is complex : (Apparently , there can be no relation between the leaflet and cusp) Here, a distinction is made between truly absent leaflet to fused BCAV. In fused BCAV (ie with or without raphe )the number of sinus can be three like a normal Aortic root .

Is fusion line same as Raphe ?

Usually yes. Raphe is a raised ridge which is a marker of fusion plane But, cardiac morphology never allows us to take things easy. To complicatt our thinking, the fusion can be smooth and perfect without a ridge or raphe. This raphe less fusion makes it difficult whether we are dealing with true geno-phenotypically BCAV or simply fusion phenotypes of what should have been a genotypic- tricuspid valves . There is a simple clue in this complex scenario .In the later case it is identified by presence of three sinus. Does this make simple our understanding right ?( I am not sure, the above understanding is correct , this is how I Interpreted. (Please, clarify if some one finds it wrong)

The two famous classification of Aortic leaflet 1.Siever 2.Micahlena

Why is the number of cusps important ?

It decides the type of TAVI valves and location of implant.

Fortunately, we have a consensus nomenclature system for Aortic valve leaflets

  1. BCAV types are defined as fused BCAV,
  2. Two-sinus BCAV,
  3. Partial-fusion (or forme fruste) BCAV.

The fused BCAV type is the most common type (90-95% of BAV cases); and is characterized by two of three cusps appearing fused within three distinguishable sinuses of Valsalva; frequently but not always with a congenital fibrous ridge (raphe) between the fused cusps.

  • Right-left fusion is most common (70-80%). The right-left phenotype also is most common across all variations of aortic valve dysfunction (AS or AR) and aortic phenotypes (normal aorta, dilated root, dilated ascending aorta, dilated arch).
  • Right-nonfusion is second most common (20-30%), and in adults is associated with a higher prevalence of AS and of progressive AR.
  • Left-non fusion is least common (3-5%).

The two-sinus BCAV type is uncommon (5% of BAV cases), with two cusps of roughly equal size within two sinuses of Valsalva.

  • Laterolateral (side-to-side) two-sinus BAV has one coronary artery arising from each sinus.
  • Anteroposterior (front and back) two-sinus BAV can have one coronary artery arising from each sinus or both coronaries arising from the anterior sinus.

The partial-fusion BCAV ( forme fruste) type is more recently recognized and of unknown prevalence. The appearance is similar to a typical tricuspid aortic valve, but with <50% fusion between two cusps at the commissural base forming a mini-raphe.

Next query :

What are differences between raphe and commissure ?

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Rare cardiac emergencies: Air entrapment in pericardial space

Posted in Uncategorized, tagged , , on May 16, 2025|

Acute onset dyspnea can surprise us to any extent. Sharing a old video case report from the archive.

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Proximal native vessel disease progression : Is it good or bad following CABG ?

Posted in Uncategorized, tagged , , , on May 15, 2025|

No doctor will want any disease to progress in their patients. But, coronary revascularization is an enigma. Cardiologists take every step to regress the atherosclerotic process and be meticulous in maintaining antegrade flow across the left main and proximal LAD or LCX. They double up their caution after PCI in left main or proximal segments.

Meanwhile, our cardiac surgeons do enjoy a unique liberty. In fact it is a luxury, i.e., they can afford to forget the status of proximal disease. What they want is the patency of the graft, integrity of the anastomotic site, and distal vessel status. Atherosclerosis being essentially a proximal disease, surgeons have all the more reason to be blessed. Of course, it should have been disciplined well-done CABG.

Do they ever wish for proximal vessel disease progression ?

What a non-sensical question, dude ?. Don’t get shocked. I was told, many of surgeons would, indeed be happy with that, as it tends to divert more flow to the graft, and long term patency is better. There are many instances when they close the antegrade flow, if it is interfering with graft flow during the surgery itself. .

Final message

Cardiologists strive hard to heal at ground zero where vessels are traumatized. Worrying day in and day out, after putting a scaffold. Surgeons simply fly over it, laughing at the lesions. So, what is the lesson from this post? When making critical decisions on coronary revascularization, think twice .Make a learned decision for every given patient.

Counterpoint

Native vessel progression do have adverse outcomes even after CABG, provided it occurs in the non by-passed vessel or when it occurs distal to the bypass circuit. Please ,don’t take a wrong message that progression of atherosclerosis is welcome post CABG. Every post-CABG patient should follow the same OMT and lifestyle modifications to reduce the burden of atherosclerosis in a larger sense. What this article refers to, is mainly about the influence of disproportionately high antegrade flow on graft survival. Surgeons do prescribe statin after CABG routinely , not withstanding the results of ACTIVE study (Ref 2) which showed high Intensity statin following CABG, had little influence on graft patency.

Reference

1.Jabagi H, Chong AY, So D, Glineur D, Rubens FD. Native Coronary Disease Progression Post Coronary Artery Bypass Grafting. Cardiovasc Revasc Med. 2020 Mar;21(3):295-302. doi: 10.1016/j.carrev.2019.05.017. Epub 2019 May 24. PMID: 31204241.

2Kulik A, Abreu AM, Boronat V, Ruel M. Intensive versus moderate statin therapy and early graft occlusion after coronary bypass surgery: The Aggressive Cholesterol Therapy to Inhibit Vein Graft Events randomized clinical trial. J Thorac Cardiovasc Surg 2018;Jul 21:

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Dyspnea , Is it from the heart or lungs ? : A land mark paper in Internal medicine, JAMA 1982.

Posted in Uncategorized on May 14, 2025|

Dyspnea is one of the commonest symptoms in medical practice. Whatever be the trigger, ultimately, it is a sensory perception, felt at the level of the cortex (to be specific, the Amygdala nucleus) decides the intensity . The initiating receptor usually arises from the muscle spindles , due to mismatch in the length and tension . These spindles are located widespread in intercostal and other respiratory muscles. The afferent pathways are complex, as are the brain stem processing centers and cortical modifications—all matters.

(* A proposed definition with mechanism :Both physiological and pathological dyspnea are the unpleasant breathing awareness (In time), till for the oxygen debt is repaid to the depleted mitochondrial, ATP treasury , for the cost of excess respiratory work done, is one popular definition )

The complexity of the neural circuit for dyspnea can be judged, even if the cranial or spinal pathways i.e., vagus or spinal transection, dyspnea is not fully relieved (experiments on post-vagotomy, quadriplegic patients, and transverse myelitis). The answer might look simple in one way. Please mind, we don’t need an intact nervous system to carry afferent dyspnea signals to the brain centers. It can simply be carried by blood, to the central chemoreceptor in biochemical form.

The uniqueness of this symptom is , it can be entirely physiological , or a harbinger of Instant fatality as in acute pulmonary embolism or LVF. Resting dyspnea is always a concern, unlike exertional which has more benign cause. As a cardiologist, we always equate dyspnea to elevated LVEDP and possible LVF . Though RV failure can also cause dyspnea.

Generally, young fellows might ignore non -cardiac non- pulmonary cause of dyspnea. It is better to reemphasize ,the commonest cause of dyspnea missed in ERs and ICUs are metabolic or systemic in nature . (We have seen Kusmaul’s breathing of DKA raising false cardiac alarm )

 Systemic causes of dyspnea (With normal PCWP)

  • Metabolic dyspnea*
  • Bio-chemical dyspnea*
  • Anemia*
  • Most lung diseases

*Chemo receptors are as important as baro- recptors of heart and J receptors in lungs

Is cardiac dyspnea possible with normal PCWP ?

 Pre capillary Pulmonary HT (Isolated Arterial PH) 

 RV infarction.

Classical Hypoxic dyspnes in cyanotic heart disease (TOF,)

Any RV failure , can trigger RV baro-receptors(similar to LV but less concentrated)

Final message

Dyspnea: is it from the heart or lungs? This popular debate has been going on for decades and was answered in a landmark review published four decades ago.(JAMA 1982).Every one of us, must go through this to understand critical cause of dyspnea that arise from heart and lungs.

However, if the question is, which is the commonest cause for exertional dyspnea? Is it from the heart or lungs? The answer is neither of the two. The commonest cause of dyspnea as a whole is neither from the heart nor lungs. It is probably anemia, physical deconditioning, fragility, or sluggish systemic skeletal muscle respiratory status due to a sedentary lifestyle. This explains why a marathon runner can run 42 km without stopping, while a healthy middle-aged man struggles to climb even three floors because of sedentary activity.

Reference

 1.Wasserman K. Dyspnea on exertion. Is it the heart or the lungs? JAMA. 1982 Oct 22;248(16):2039-43. doi: 10.1001/jama.248.16.2039. PMID: 6811770.

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Why DEBs are eluting Paclitaxel, while DES are eluting Sirolimus ?

Posted in Uncategorized on May 13, 2025|

A brief review

Paclitaxel: Is a highly lipophilic, and rapidly absorbed by vessel walls and retained for days to weeks, making it ideal for DEBs, which deliver the drug during brief balloon inflation (30–60 seconds). Its cytotoxic action, disrupting microtubules and arresting cells in the M-phase, effectively inhibits neointimal hyperplasia without requiring prolonged drug release.

Sirolimus: Less lipophilic, sirolimus requires sustained release to achieve therapeutic levels, as it acts cytostatically by inhibiting the mTOR pathway, arresting cells in the G1 phase. This suits DESs, which provide continuous drug elution over weeks via polymer coatings. Its lower tissue retention makes it less effective for short-contact DEBs.

Paclitaxel hurts the endothelium with DES, but it heals with DEB ? How is this possible ?

Paclitaxel’s association with delayed healing and inflammation raised concerns about long-term safety in DESs, particularly after reports of late and very late stent thrombosis. It is abandoned in DES platform.

Paclitaxel born again as DEB avatar

It is claimed, Paclitaxel’s rapid uptake and lipophilicity make it suitable for DEBs, while sirolimus’s need for sustained release and favorable long-term profile suits DESs. It is very hard to believe, the published evidence, however robust they are. Only thing I can guess is, Paclitaxel enjoys a safety net in DEB , as the drug disappears so quickly before any useful effect or side effect could manifest. Ongoing research into sirolimus-coated balloons may shift this paradigm. Till then, we have to trust Paclitaxel, that remains the standard for DEBs due to pure scientific reasons.

Final message

Paclitaxel, which was at its crowning glory during the SYNTAX times , was phased out in DES due to various/ serious untoward effects.

Please bear with this highly biased opinion. I suspect, as a face-saving measure, the industry accommodated Paclitaxel into the DEB platform when it was chucked out of DES. I think we must learn to find truthful pathways of research.

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