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HF is the inability (or reduced ability) to supply oxygen and other nutrients to fulfill the body’s demands. In the process, the heart either fights or flights, and results in symptoms due to hemodynamic alterations, or adversities of neuro-hormonal activation.

Now, what is Anemia? Anemia is a condition with reduced or dysfunctional RBCs. that directly interferes with oxygen delivery to tissues. It is not at all a coincidence, the core functions of the heart and blood are strikingly similar and intertwined. While the heart is the powerhouse of the circulatory system, without good-quality blood, the greatness of this vital organ becomes redundant.

 

A failing heart & compromised blood, throws up a double challenge, to the fundamental function of the circulatory system and results in impaired cellular oxygen delivery.

 

Fortunately, RBC and Hemoglobin have an adequate reserve, and real metabolic issues happen only after a 30 %  reduction in hemoglobin. During this time the heart works more to compensate by maintaining high output. When HB falls less than 6 to 7 grams the heart itself suffers from hypoxia and goes for intrinsic failure. So, when anemia coexists with cardiomyopathy imagine the tissue’s plight.

Anemia in Heart failure 

 

While there are many links between anemia and heart failure few things are worth emphasizing. It can be discussed in 4 categories.

  1. Primary anemia that results in heart failure is a separate topic and comes under high-output HF.
  2. Anemia as a part of the same disease process as heart failure. (Anemia of chronic illness) 
  3. Nutritional anemia associated with common forms of heart failure (Ischemic and non-ischemic DCM) 
  4. Anemia of CKD and coexisting heart failure 

*Category 2 is often missed, while category 3 is often ignored

Prevalence of anemia in HF.. Up to 30%. (Iron deficiency anemia is the most common)

Diagnosis: Criteria Ferritin less than100 or 100-299 μg/L with transferrin saturation <20%). 

What is the optimal Hb %?  Should be 13 grams

Iron deficiency is much more than anemia 

It is worthwhile to go back to the basics, anemia is just one aspect of iron deficiency. Humans live their life, essentially inside the breathing chambers of mitochondria in each of the 12 trillion cells.  Without an adequate iron supply, the citric acid cycle will come to a creeping halt. It is now recognized, altered mitochondrial function is one of the key peripheral defects in HF. (Ref 1) Iron deficiency could be an Incidental marker for a more important tissue deficit elsewhere. 

What do the trials say about the role of routine Iron supplements in HF?

As usual, trials blink with data on either side of the truth. Small studies suggested benefits. But large studies with Iron supplements and Erhytopoitn analogs failed to show benefits. IRON-OUT, RED -HF (Ref 2,3) . But in a popular study from the Lancet , showed ferric carboxymaltose improved the outcome. (Ponikowski P,l. Lancet. 2020 Dec 12;396(10266):1895-1904).

Final message

We, as modern-day cardiologists are always pre-occupied with measures to improve LV ejection fraction at any cost (Since we fell into a false knowledge trap of defining HF solely on the basis of  EF% ) To make HF patients walk 30 meters extra in a 6-minute walk test we have complex and costly procedures like CRT, Mitra clips, and IAS flow regulators,  etc.

However, experience tells us there are many parameters other than EF that can improve functional capacity and quality of life. Breathing exercise is the best example. Let’s add one more to this list. A simple correction of anemia with iron can make your cardiac failure patient walk many blocks more. Trials are not consistently confirming this though. Don’t bother them,  just have a try. If prescribing tablet iron without evidence bothers you with scientific guilt, ask your patient to take a diet with rich iron content and see the difference.

For advanced readers

Anemia and  Aortic afterload: The apparent advantage

There is one curious concept. Anemia makes the blood thin. Reason lowered viscosity. As a consequence afterload falls. , hypoxia-induced peripheral vasodilatation and enhanced nitric oxide activity also contribute to this.  Vasodilatation also involves the recruitment of microvessels and, in the case of chronic anemia, stimulation of angiogenesis. So, anemia apparently has a double edge, and one of them seems to be beneficial.

We must also beware, the risk of iron overload is genuine in some of these patients with HF. This makes us wonder, in ancient times venesection was used for so many undisclosed illnesses, which might include heart disease as well.

Reference

1. Melenovsky  V, Petrak  J, Mracek  T,  et al.  Myocardial iron content and mitochondrial function in human heart failure.  Eur J Heart Fail. 2017;19(4):522-530

2. Lewis GD, Malhotra R, Hernandez AF, et al. Effect of Oral Iron Repletion on Exercise Capacity in Patients With Heart Failure With Reduced Ejection Fraction and Iron DeficiencyThe IRON OUT HF Randomized Clinical TrialJAMA. 2017;317(19):1958–1966. doi:10.1001/jama.2017.5427

3. Swedberg K, Young JB, Anand IS, Cheng S, Desai AS, Diaz R, Maggioni AP, McMurray JJ, O’Connor C, Pfeffer MA, Solomon SD, Sun Y, Tendera M, van Veldhuisen DJ; RED-HF Committees; RED-HF Investigators. Treatment of anemia with darbepoetin alfa in systolic heart failure. N Engl J Med. 2013 Mar 28;368(13):1210-9. doi: 10.1056/NEJMoa1214865. Epub 2013 Mar 10. PMID: 23473338.

 

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We have enough evidence to question the superiority of the presumably best practice in cardiac pacing namely dual chamber pacing. Apparently, the DDD failed to show gross benefits in both  AV block as well as sinus node dysfunction. (UKPACE, MODE-Selection Trial) in studies done nearly two decades ago.

It is 2022. Here is one more study in the Indian heart journal, coming up from JIPMER Pondycherry,on this concept. It is an intelligently designed cross-over study. The same patients were switched between DDD and VVI modes. This study reaffirmed the lack of appreciable hemodynamic and clinical benefits with DDD mode yet again. 

We have also contributed a little on this issue. It was found cardiac failure in VVI pacing was not a real big issue in the long-term follow-up. We presented and published in world congrees of cardiology Dubai 2012, and Circulation journal. 

How is that? A dual chamber pacer with AV synchrony fails to show a hemodynamic benefit?

The answer is simple..VV desynchrony is a common denominator for both VVI and DDD pacers. Providing AV synchrony without VV synchrony doesn’t make real sense in the long term to overcome the altered physiology, Still, DDD pacing continues to enjoy a popular mandate by hiding behind a vague outcome measure called quality of life.

What is the physiological pacing then?

Just because, DDD and  VVI pacers are equipoise,  can we presume the new pacing kid LBBB pacing would be physiological? We wish so, but unless and until we replicate the entire conducting system right from SA, and the AV node which includes many miles length of delicate Purkinje cables, every pacing system we use is currently pathological. (If that sounds too harsh, let’s make it non-physiological)

Having said that, VVI pacing is one of the most remarkable Inventions in medical science since the last century, that plays God’s own function and gives a new lease of life to all those patients with critical AV blocks and trouble some SNDs.

Final message

It may be difficult to digest for true scientists. Restoring the atrial booster pump is not bringing in the desired benefits. It is clear that VVI pacing will never become obsolete. This fact was established long before. We must argue and wonder, why we need to keep proving a scientific truth again and again?  There could be a good justification too. Real-time cardiologist behavioral patterns clearly tell us, as a genre, they often struggle to get detached from futile modalities even after good published evidence (PCI for CTO, Revascularisation for Ischemic DCM, are a few more examples)

 

 

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“Never take your eyes off the monitor and the pressure curve” It is one of the basic instructions given to the fellows & technicians as they start engaging the coronary artery and Intubating the coronary ostium in their early cath lab postings. There are two commonly heard noise bites in the cath lab for the beginner. 1. Damping 2.Ventricularization.

Damping

It is the deformation of the normal arterial pressure curve, with a blunting of both systolic and diastolic pressure that drops compared to aortic pressure. Extreme damping can mimic a straight line with few wavy undulations. It means the forward flow is impeded as the catheter might be blocking the coronary flow at least partially, if not completely. Immediate pull back and adjustment of catheter is required to prevent adverse events that includes cardiac arrest. (Of course, catheter kinks, blocks, and air in a circuit are to be ruled out first)

Mechanism of damping

  1. The catheter tip is too large for the ostium.(Technical)
  2. A left main or RCA ostial lesion*(Most significant clinically)
  3. The coronary artery wall is thin and goes for spasm
  4. Catheter diameter is too small and glides into the coronary artery (The catheter tip hitches against the lateral wall of the coronary artery often over a plaque, a silently staged perfect setting for a dissection )

Unique features in RCA damping

In RCA, damping could simply mean it has engaged conus branch. Damping is more common in RCA and it tends to get sucked in deeper for two reasons. We know , the RCA catheter is not preformed, the tip seeks the ostium, looking for a negative pulling pressure from within the RCA. Further, unlike the LCA, the flow in RCA is continuous in both systole and diastole. Another possible factor is the inspiratory swings of RV transmural pressure is more than LV.

Transient bradycardia due to compromise of SA /AV nodal flow is common. It is well known that RVOT is a thin and VPD-prone zone , compared toLVOT. Hence it is more vulnerable to ischemia and triggers a VT/VF if damping is prolonged in RCA.

Ventricularization

This is tracing during the engaging of a left main ostial stenosis. The diastolic pressure drops on the third complex, and the pulse pressure becomes large . Note the small “a ” wave slur as well near the diastolic nadir. The aortic pressure curve is restored once tip adjustment is done. Image courtesy Thoraci key.https://thoracickey.com/coronary-angiography-3/

It simply means the pressure curve starts looking like a ventricular pressure curve. The issue is not that simple. It is still a mystery, how could the coronary artery pick up ventricular pressure. In fact, it doesn’t. It was initially thought to be either deformed aortic pressure or a wedged coronary artery pressure .or a combination of the two.

It s now accepted it’s due to total occlusion of the coronary artery the ventricle muscle sucks the catheter and pulls the diastolic pressure markedly down even lower than LVEDP. The systolic pressure also falls but not much of it is noticed.The fact that ventriculaization happens less commonly with RCA gave us a clue to its mechanism. (Most of the RCA travels over RV and since RV muscle mass wields less negative suction force )

How to differentiate true LV location from ventricularization?

If the catheter enters the LV cavity, the systolic pressure will match that of aortic systolic pressure and diastole will reach the LVEDP. In ventricularization there can be a slight drop of the systolic pressure, but the diastolic is the one goes far down. Further, the ascending limb is shallower, the descending limb is steeper in coronary ventricularization. Apart from this if we carefully look “a” waves will be visible in ventricularisation in the late diastolic phase.(Could it be the modified Incisura ?)

Relationship between damping and ventricularization ?

Discussing damping and ventricularization together is more of an academic tradition. Please realize, both may not be two exclusive entities. In fact, they can occur at the same time, or sequentially or interchangeably if the catheter tip swings back to partial to total occlusion and vice versa. if complete wedging occurs it becomes ventriculariszation.

Which is more dangerous damping or ventricularization?

How can you ask such a question? Both can be harbingers of serious hemodynamic issues if ignored and accidentally injected, The dreaded one is the dissection. Apart from mechanical injury, Injecting dye during damping or ventricularization causes dye stasis, and may trigger VT or VF if it is prolonged. There is a biochemical component too. As the contrast swirls around for a few seconds it can cause transient hypocalcemia by chelating this cation.

I don’t have a clear answer to the above query. In my understanding, forceful injections during ventricularization could be more riskier as injection happens over a total occlusion in a wedged position and dye has direct access to the microcirculatory bed. It is true, expert cardiologists do shoot in damped positions occasionally to see the anatomy quickly. They may be your mentors, still don’t learn this trick, till you become a true expert (Famously referred to as hit and run technique)

How to overcome these pressure curve malformations?

Most times, it is a simple technical artifact issue. Deep Intubation with an oversized catheter could be the commonest cause in the otherwise normal coronary artery. Proper catheter sizing, angle of alignment, and adjustment is the key. If it is a spasm nitroglycerine might help. Using catheters with side-hole perfusion catheters is an option in difficult anatomies. Mind you, side holed guide is a two-edged weapon, it can mask true hemodynamic adversaries by falsely showing a good aortic pressure tracing.

(One of the good cath lab habits is to have a look around the patient face at least once in a while when performing complex procedures. We have many times recognized serious hemodynamic issues only after the patient starts behaving bizarrely due to hypotension. Pressure curves can fool you, but patience will never.)

Final message

Recognizing abnormal waveforms during engagement is a crucial step for the beginner (Experts can’t ignore though) Please remember LMCA stenosis should be the default alarm for any damped pressure curve as you engage the LCA. If you take things casually consequences can be lethal for the patient as well as the consultant in charge.(Fellows can’t take it lighter though). It is an undisclosed fact, that many of the serious complications in the cath lab happen not out of ignorance or lack of expertise, but because of ignoring some basic principles and lack of cath lab discipline.

Reference

1.Baim DS, ed. Grossman’s Cardiac Catheterization, Angiography, and Intervention. 7th ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2006. 2. Judkins MP. Selective coronary arteriography, a percutaneous transfemoral technique. Radiology 1967;89:815.

2.T Pacold I, Hwang MH, Piao ZE, . The mechanism and significance of ventricularization of intracoronary pressure during coronary angiography.Am Heart J. 1989 Dec;118(6):1160-

3.A good review from Journal of Invasive cardiology .

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A forbidden quote in medical science

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Though all of us are aware, the incidence of heart failure is increasing exponentially and is the leading cause of global disease mortality, what we fail to understand is, we still lack a good definition cardiac failure. 

Defining HF based on EF% is convenient but adds more complexity, and is less scientific too. Still, as of now, we have adopted this. I think, one of the important factors that apparently increased the incidence of HF is the creation of an entity called HFpEF. (Formerly diastolic heart failure)

Thanks to ESC, we have a consensus document, which has defined HFpEF based on functional, morphological, and biochemical features. This is a more refined model from the original Mayo clinic H2FpEF score.

Both are given below.

 

Mayo criteria
The problem with both these criteria is the disproportionate importance given to AF. The knowledge gap here is, AF can be initiated at any degree of increased atrial strain which can independently raise LA mean pressure without persistent elevation of LVEDP. We recognize now, left atrial obesity (fatty atrium)  is a powerful trigger of AF, still, in this situation, an Innocent LV may get blamed with a tag of HFpEF. Likewise, many HFpEF may turn out to be primary  LA dysfunction than LV failure. To make things more confusing(scientific) for diagnosing true HFpPEF, we may soon need to look into LA-EF as well. (LA-HFpEF)

Can we diagnose clinically significant HFpEF, without pulmonary hypertension?


In my understanding, the answer is No.

Looking at the two schemes (Mayo & ESC) one thing is clear. Pulmonary hypertension is the key hemodynamic expression of HFpEF. It could be either resting and persistent or exertional and transient.t is obvious the PH in HFpEF is post-capillary. (The modern term for pulmonary venous HT). Mind you, while PVH is mandatory to diagnose HFpEF, PAH (precapillary ) is also observed in most patients with significant HFpEF. This is the reason TR jet velocity is included as one of the criteria.  (To make things simple, we may need to create a new classification of HFpEF, ie resting vs exertional HFpEF.This is what the diastolic stress testing is all about.)

Final message

It is back to basics & time to dig into the fundamentals, of what exactly we mean by heart failure. Is the elevation of LV filling pressure alone sufficient? Should it happen at rest or at exertion, and whether neuroendocrine activation is necessary? Is RASS activation similar in both HFrEF and HFpEF? Try to find the answer to this. How often does HFpEF fulfill Framingham’s criteria of HF.? ( Löfström et al  ESC Heart Fail. 2019) 

Trying to understand the nuances of HFpEF, I think, we can make a statement,- HFpEF can not be diagnosed without pulmonary hypertension. It makes a lot of sense the P in the H2FpEF  scoring system denotes PH, however, It is assigned only a single point, which needs revision. In fact, there is a strong case to argue and make it an essential criterion.

Paradoxically & curiously HF with reduced ejection fraction (which is the most common form of HF) doesn’t require the presence of PAH to diagnose it. This issue may also be examined.

Reference 

1.How to Diagnose Heart Failure With Preserved Ejection Fraction: The HFA–PEFF Diagnostic Algorithm: A Consensus Recommendation From the Heart Failure Association (HFA) of the European Society of Cardiology (ESC). Eur Heart J 2019;40:3297-3317.

2.Löfström U, Hage C, Savarese G, Donal E, Daubert JC, Lund LH, Linde C. Prognostic impact of Framingham heart failure criteria in heart failure with preserved ejection fraction. ESC Heart Fail. 2019 Aug;6(4):830-839. doi: 10.1002/ehf2.12458. Epub 2019 Jun 17. PMID: 31207140; PMCID: PMC6676283.

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Does the Aortic root contract or relax during ventricular systole? Some time back, I asked this question in one of my classes for the fellows and found no takers. Not even a guess? I realized later, it was indeed a tough question. The heart is not the only dynamic organ, as we generally believe. The entire aorta which is an extension of the left ventricle has to be dynamic according to the physics of ventricular-arterial coupling and the momentum of blood flow.

What happens to the aortic dimension with systole?

Even prior to systole, there is evidence, the aorta gets ready to receive the blood from the LV. So, the Aortic root must be larger at the onset of systole. (Ref 2 ) It is been generally agreed now, that the systolic dimension is slightly more by a few mm. That is why aortic dimensions are measured in peak systole as per the American society of echocardiography.

There has been an opposite argument as well. The diastolic aortic dimension could be larger, as the aortic valve is in the closed position and the aortic root distended, & becomes a reservoir of blood that’s meant to be distributed during diastole. What determines the aortic dimension on a moment-to-moment basis?  Is it the, LV contractility, pressure, or volume, or the compliance of the aortic wall that determines the aortic dimension and pulsatility? How does a prosthetic valve alter this?

So, what exactly happens to the aortic dimension during the cardiac cycle ? 

A wonderfully done study from University Medical Center Utrecht, The Netherlands throws some important facts with their analysis of ECG-gated CT scans in 108 Aortas.(Ref 1)

It is surprising, to note the aortic root behaves independently. It either contracts or relaxes with a range of 4 mm swing on either side of the systole and diastole. Another stunning fact is, it remains static in a significant number. (One possible explanation is the true aortic annulus is less dynamic because it is bordered by the fibrous skeleton, while the rest of the aortic root only can distend or shrink )

Clinical implication of aortic pulsatility

The implication of knowing (or not knowing )the dynamism of the aorta can be huge.

  • Age-related stiffening and onset of systolic hypertension
  • Aortic diameter, pulsatility, and shear stress are the key parameters in initiating dissection and its propagation
  • Choosing the right sized valve for AVR
  • Current interventional heart-throb TAVI involves just a passive placement of the valve in the aortic root. Imagine what will happen, if the foundations are excessively dynamic and shaky   

It is surprising, even after decades of vascular research, we lack clarity on what exactly happens to aortic root during various phases of the cardiac cycle. (Currently, paravalvular leak, & migration of TAVI remains a major worry, which has a direct relationship with pulsatility of the aortic root ) One thing is obvious,.Young cardiologists have a lot of work to do in this arena.

Final message

 Though the aorta is a direct extension of LVOT, its vaso-motion doesn’t seem to be in complete sync with the cardiac cycle. It tends to have an independent behavior, out of phase with the heart. 

As per available evidence, the aortic root dimension can either increase, decrease, or be static in response to LV contractility.

Reference

1.de Heer LM, Budde RP, Mali WP, de Vos AM, van Herwerden LA, Kluin J. Aortic root dimension changes during systole and diastole: evaluation with ECG-gated multidetector row computed tomography. Int J Cardiovasc Imaging. 2011 Dec;27(8):1195-204.

2. Pang DC, Choo SJ, Luo HH, et al. Significant increase of aortic root volume and commissural occurs prior to aortic valve opening. J Heart Valve Dis. 2000;9:9–15. [PubMed] [Google Scholar]

3. Vesely I. Aortic root dilation prior to valve opening is explained by passive hemodynamics. J Heart Valve Dis. 2000;9:16–20. [PubMed] [Google Scholar]

 

 

 

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Welcome to Kuna island. The Kuna Indians are really unique people. living off Panama, right in the isthmus connecting North and south America, The Kunas reside in the San Blas archipelago comprising about 360 islands, of which about 60 are populated by them. They have lived on these islands for centuries, but their exact origin is not completely understood.

 

These innocent tribes have taught an important lesson in human blood pressure regulation, vascular biology, and salt sensitivity. We know, that high blood pressure, is a maximally researched entity in medical science in terms of etiology, vascular effects, and its control. Still, we don’t know, what are the limits of normal BP for human beings. The debate will not end until we are clear about, whether human beings evolved from monkeys or emerged as de-nova organisms. Recent studies have revealed a remarkably low level of mitochondrial gene diversity in monkeys, suggesting that there has been remarkably little genetic admixture. (Ref 2)

What we know from 3000-years-old human history is, blood pressure is directly related to the physical work done by us and the diet we eat. While salt is considered pro hypertension, physical activity is a much more important determinant in bringing it down. Normal BP in a pre-civilized world was low compared to a civilized population. They also enjoyed better vascular health. Where is the evidence? It comes from the life cycle of Kuna Indians. Here is a very unique paper published in the Hypertension journal.(Ref 1) Three cheers to the authors for confirming this long pending speculation with meticulous data collection. (See the Image)

What was special in Kuna’s diet that prevented cardiovascular events? It is been shown in the study by Hollenberg, their diet contained rich in cocoa and flavonoids that made the difference.(The salt consumption was still high though)

As Kuna’s moved out from their primitive lifestyle to first, the  Kuna Nega,(a suburb) and subsequently to a fast-paced Panama city. See the impact on their systole and diastolic stress on the heart. The loss of protective effect of the native diet is obvious.

Final message

Lifestyle is the buzzword today. It is a by-product of the new civilized world that will define human health. The human vascular tree tries to sync with a new lifestyle pushing the BP curve to the north. The true normal BP for denova-human beings may still be very much lower than what we believe. A crazy suggestion was made, that human BP should match that of non-sedentary monkeys.  I Hope, we get more evidence later for such hyperboles. As of now, we have to accept, hypertension is largely due to disorder in human civilization, development, and prosperity.

 How about embracing the styleless lives of native Kunas to take control of our vascular health.

Reference

1.Hollenberg, Norman K.; Martinez, Gregorio; . “Aging, Acculturation, Salt Intake, and Hypertension in the Kuna of Panama”  Hypertension29 (1 Pt 2): 171–176.

 

BROWN (S.), ATKINS (C.), BAGLEY (R.), CARR (A.), COWGILL, DAVIDSON (M.), EGNER (B.), ELLIOTT (J.), HENIK (R.), LABATO
(M.), LITTMAN (M.), POLZIN (D.), ROSS (L.), SNYDER (P.), STEPIEN (R.) – Guidelines for the Identification, Evaluation, and
Management of Systemic Hypertension in Dogs and Cats. J Vet Inern Med, 2007, 21: 542-558

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This is the story of PCI to LAD from the customary bifurcation workshop for the budding experts, which ended up with a compulsive final OCT run-through, triggering a debate on what to do with the side branch.

What shall we do next?
  1. Just balloon dilate the distal strut
  2. Would consider a second stent. Maybe a TAP  depending upon LCX morphology
  3. At this stage, I would like to know the FFR or iFR across LCX Jail.
  4. Get rid of this OCT, Let me have look at regular CAG. I bet I can make a better decision.
  5. Leave it alone if the clinical status & profile is good

Leave it alone? Is it not an incomplete Job?

Definitely incomplete. Please realize, No job is complete in interventional cardiology. If we believe so, it exposes our Ignorance ( & some arrogance). Intentional side branch jailing is an integral part of  PCI techniques. Are we not ignoring day in and day out. 

Someone in the audience asked Why did you do OCT at all? 

The chief operator quipped “You can’t ask this silly question in a scientific workshop. We bought the OCT kit to improve the quality of PCI. We are proud of it. Really feel blessed to use it and I am sure my patients will benefit from it”. We have to agree with him. These new Imaging techniques though give us extra high-definition, but it comes with troubling revelations with their new vision. If you are pathologically honest and believe in empowering patients, it is absolutely necessary to convey the following facts in the discharge record as well. It would be something like this, “There was a 120-micron strut crossing the LCX ostium, that might continuously impede a chunk of platelets & RBCs every beat, for the rest of your life and might enhance the risk for thrombosis. (Of course, DAPT will take care of it and ask the patient not to worry)” 

OCT: One-minute review

OCT is Indeed a stunning Innovation. It can be useful in all 3 phases of PCI. 1. Assessment and preparation of lesion bed. 2. during stent deployment and optimization. ,3. Post-stenting follow up. The technology has grown so fast, now angiographic co-registration and longitudinal frame reconstruction comes inbuilt. It required 3 versions of LUMEN study and a 4 th one (LUMEN 4 ) is yet to come, expected in 2022  to prove the worthiness (or worthlessness)  of OCT. 

One attractively named DOCTORS study asked the specific question directly (Does Optical Coherence Tomography Optimize Results of Stenting)”  This is from NSTEMI patients .read yourself for the conclusion. It is not convincing to me.  Meneveau N.,  DOCTORS study (Does Optical Coherence Tomography Optimize Results of Stenting)”Circulation 2016134: 906.

Mind you, OCT is not only an expertise-dependent procedure, it also has important imaging limitations. It has low penetration max 2mm, can not differentiate lipids from calcium, shadowing behind red thrombus is an issue and most importantly it may miss the external elastic lamina (EEL) and measurement errors are real. 

Cost-effectiveness

If an imaging technique to assess a stent *(*Still waiting to prove its worthiness) could cost more than the device itself, realize how good our economic intellect is. Just because your lab has an OCT console, it need not transform into a technically perfect PCI. There are at least half a dozen factors other than Imaging that matters. 

Final message

OCT is a breakthrough technology that needs to be used judiciously and it definitely helps us understand the nuances of coronary stenting, especially in complex lesion subsets, and its mechanical and histological contents. However, let us not propagate a false message, that without OCT we can’t perform a perfect PCI. Give due respect to all those sharp-eyed interventional cardiologists with good techniques, who can do a better job, beating the HD vision of OCT, with their native blindness. 

Reference 

https://eurointervention.pcronline.com/article/intracoronary-optical-coherence-tomography-state-of-the-art-and-future-directions

Post-amble

Can you guess how many PCIs are done with OCT guidance globally?

It is less than 5 %. In India, it must be, I guess it is < 2% So, we are living in a terrifying world of coronary interventions, where  98 % of PCI is happening blindly, sub-optimally, and unscientifically., Data from CLI-OPCI registry adds more panic:  Centro per la Lotta Contro l’Infarto – Optimisation of Percutaneous Coronary Intervention (CLI-OPCI) registry:  It says device-oriented cardiovascular event (DOSE) is high with OCT detected sub-optimal  PCI.

So, what are we going to tell our patients who will undergo PCI (undergone) without OCT guidance in the past, present, and future?

Simply ask them to forget this OCT stuff. Just reassure them. Nothing will happen.

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