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One of my colleagues was joking ,nowadays patients force us to read or even educate us . I completely concurred with him.


Doctor, do you have any investigation to know how much is the plaque burden in my coronary artery?

Yes. Sure , we have many modalities, right from CT calcium , OCT, IVUS, NIR, etc.

How would I know , which one of them is high risk and vulnerable ? I recently read in Forbes Sunday health supplement, It says ,it is better to know the thickness of the cap covering the plaque. It further says, about the risks of having a thin cap .(TCFA-Thin cap fibro atheroma.) Can you prescribe some tests to find out the thickness of these caps doctor ?

There you go, into the perils of hyper- education of modern society. So, you want me to teach you the molecular biology of Atherosclerosis ,right ?


Yes, now cardiologists and basic scientists are armed with unprecedented tools of intra-coronary imaging, like OCT, IVUS, NIR spectroscopy, etc. to decode the histological, biochemical, pathological secrets within the atherosclerotic plaques. Atherosclerosis is not a worrisome issue as long as it is contained deep within the vessel wall and doesn’t encroach the lumen. However, plaques, which are close to the lumen, are more prone to empty its contents into the lumen by a fissure or rupture triggering an event. In that sense, you have a reason to worry about TCA. Itis very much logical to expect the cap hat covers the plaque to protects and reduce the risk of its rupture.

This was a very attractive concept and we were able to analyse it with intracoronary optical coherence light-based imaging. For some time we really felt TCFA is really a marker of vulnerability. Now, we realize the concept of TCFA, has a thin layer of truth intertwined in a thick layer of myth .(Lee KY, Chang K. Understanding Vulnerable Plaques: Current Status and Future Directions. Korean Circ J. 2019 Dec;49(12):1115-1122. doi: 10.4070/kcj.2019.0211. )

In physiological state ,it is amazing to note, how a single layer of endothelial cell is able to withstand a lifetime of vascular stress. A plaque is covered by a thin cap that includes a endothelium (In tact in many plaque) While this layer is good enough to protect exudation of its content irrespective of the nature of lacquer content. A contrasting corollary is , a much thicker Aorta dissects without even a plaque if the pressure injury is more. TCFA are stressed from both abluminal and luminal aspect. Does it balance these forces ?

TCFA are defined as fibrous caps with less than 65 microns . The importance of this thickness is being questioned for two reasons now.

1,Technoloigical limitations of measuring cap thickness : False positive thin caps , false positive thick caps are equally common.

Factors influencing cap thickness

1.Superficial macrophages, ,

2.Loose connective tissue,

3.Punctate foam cells, and

4.Smooth muscle cell infiltration of the fibrous cap

5.Tangential light dropout(Ref 2)

2.The second one is a more fundamental flaw in our understanding. TCFC, after all could be just as innocent as any other plaque. This is based on the observation many of the thin capped plaques remain indolent while thick capped become a culprit . Cap thickness is just one of potential parameter of vulnerability, but many others known and unknown factors and forces operate on the plaque and make this TCFA simply irrelevant.

Some queries for advanced readers

What are the chances of a Thick cap fibro atheroma (ThCFA) getting ruptured ?

65 micron is not God prescribed cut off point . A simple adrenaline surge and eccentric plaque shoulder can be destabilized. A sudden shearing stress of intracoronary hypertensive spike can crack a 650 micron cap. On the contrary, even if the cap is thin , but the content it holds are non-necrotic , rupture is rare event and vice versa.

What are biological events that follow the rupture ?

Not every rupture leads to an ACS. The highly armed anti-coagulant and anti fibrinolytic system has enough resources to clear of the contents.(Unless it is over-whelmed ,which can be called as an act of God or a response to our past deeds)

Relationship between CT calcium score and TCFA

It is highly plausible, high calcium in plaques indicate, most caps are thickened and hardened. Though calcium score is a popular estimate of plaque burden, it is still a weak link to our ignorance and knowledge towards prevention of cardiac events.

Does TCFA prone for more coronary erosion ?

Though logic would suggest so, it appears , there is no meaningful relationship between them.

Does statins increase Thickness of TCFA ?

Yes. They are claimed in many studies. This is important, all patients need to take Statin to stabiles the plaque overall (Takarada wt al. Atherosclerosis. 2009 Feb;202(2):491-7.) More recently PCSK blockers Alirocumab was shown to increase TCFA at lesion levels study by NIRS (PACMAN-AMI study)

Final message

Coming to the question raised by the patient . My frank reply would be

“Never worry my dear patient total plaque burden or calcium scores. I would say, even the fear-mongering with blood levels of lipid sub-fraction, is an exaggerated state of pathological health consciousness. Life is short .We have better things to accomplish. The least we can bother in our life, is how to increase the thickness TCFA. Even if we find the total numbers of TCFA, what are we going to do with that info? My guess is ,the propensity of TCFA to damage your heart is 1000-fold less than the anxiety (associated with it) eroding some other innocuous plaque .

The chances of plaque misbehavior is as unpredictable as, the probability of a scale 4 Richter quake striking and shaking the basement of your house. So, instead of worrying about these TCFAs, concentrate on your work, about your lifestyle, stress, eating habits, and stop reading too much from all these health supplements. After all, please remember much greater men like Abraham Lincoln and Mahatma Gandhi lived a stellar life , in the grand old era when no one knew what was cholesterol and lipids.”

Reference

1.van Soest G, Regar E, Goderie TP, Gonzalo N, Koljenović S, van Leenders GJ, Serruys PW, van der Steen AF.Pitfalls in plaque characterization by OCT: image artifacts in native coronary arteries. JACC Cardiovasc Imaging. 2011; 4:810–813.

2.Phipps JE, Hoyt T, Vela D, Wang T, Michalek JE, Buja LM, Jang IK, Milner TE, Feldman MD. Diagnosis of Thin-Capped Fibroatheromas in Intravascular Optical Coherence Tomography Images: Effects of Light Scattering. Circ Cardiovasc Interv. 2016 Jul;9(7):10.1161/CIRCINTERVENTIONS.115.003163 e003163. doi: 10.1161/CIRCINTERVENTIONS.115.003163. PMID: 27406987; PMCID: PMC4946571.

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*Caution : Language -Harsh. Likely-hood of truth : High


The flamboyant genius of Andreas Roland Gruntzig, from Zurich gifted us the path-breaking treatment modality for coronary stenosis five decades ago. After a series of experiments in animals and peripheral vessels, he proved with a single patient N-1 study that effectively treated refractory LAD angina in a 38-year-old man in 1977. (Ref 1)

That’s when PTCA/PCI arrived in the clinical cardiology arena. After some initial hiccups, it was non stop success story supported by metal scaffold. Within a span of five to ten years, the concept spread globally. No one has questioned the efficacy of PCI for true angina with a critical lesion.

The costly aftermath

Over the last three decades, PCI armed with a variety of technologies and expanded with explosive indications, has grown into a monster intervention (including the life-saving primary PCI). In the process, the abuse prevailed over the use, causing considerable damage. So, we desperately required to break this inappropriate menace with evidence base like COURAGE, ISCHEMIA, BARI-2D, These studies tried to apply some breaks, but the force was weak and couldn’t abolish a pseudo-academic vice. Something happened in 2018 , the ORBITA trial .It sent real shock waves to the Interventional community. Contrary to the usual behavior of such studies, the ghost of ORBITA appeared to roam longer in the cardiology academia than expected. We needed a quick fix.


What happened ? ORBITA-2 came in 2023 . It said in no unequivocal terms , that PCI also can be a first option in CSA. It is no way inferior to OMT. What was the necessity to do ORIBTIA 2 so soon ? When do you do a placebo controlled sham study ?

We do such studies when we suspect ,the very efficacy of the modality. What we really wanted to know for a long time , was whether PCI really beats medical therapy in stable angina of moderate or severe intensity with at least one critical lesion. ORBITA-1 was an excellent and Innovative trial, that answered the above query without any doubt, that PCI has no add on value over medical therapy in chronic CAD.

In whatever angle we look , ORBITA-2 looks a redundant one (EuroIntervention. 2022 the rationale for ORBITA- 2 ) It appears to my crooked mind, the primary aim of the ORBITA -2 is to neutralize the negative publicity (positive for the patient) the original ORBITA did. There seems to be a non-academic indication for doing this study to undo the damage done by ORBITA-1 .The irony is, almost the same team has done this study, that diluted the positive impact of the original ORBITA. If my utterances are true, such studies have no place in academia .Not only it is proving a redundant point but also let loose a wrong message , that PCI and medical therapy have equivalent effect and one can choose whatever they wish.

Final message

In an important sense, ORIBITA 2 is one among the same old study to defame the OMT. Unfortunately, the power of mis-communication is always greater than power of right-communication. ORBITA 2 looks a redundant study and serves no new purpose except to say PCI can also relieve angina in a tight lesion, which Gruentzig proved 50 years ago.

Post-amble

I wrote this post a year ago, was hesitant to post. Come September 2024. Surprised to read this defiant article against ORBITA-2 from this Impactful journal of Circulation Cardiovascular Quality Outcomes.

Reference

1.Gruntzig A. Transluminal dilatation of coronary-artery stenosis. Lancet. 1978 Feb 4;1(8058):263.

Echocardiography, the ultrasonic vision, with which we are able to directly visualize the heart is a monumental discovery ,gifted to us by Edler & Hertz in the 1950s. These high frequency sound interacts with myocytes in a variety of ways like penetration ,reflection, ab & adsorption, back scattering etc. It has further evolved , at the tissue level diagnostic like 3D speckle ,and strain etc .

With all all these advancements ,how good is echocardiography in ruling out (or in) reversible /treatable HCM mimickers or their molecular subsets.

Recognizing non-sarcomeric Hypertrophic Cardiomyopathy (HCM) by echocardiography is one such task .It can be challenging, but here are some clues to help:

  1. Unusual hypertrophy patterns: Non-sarcomeric HCM may exhibit atypical hypertrophy patterns, such as:
    • Mid-ventricular hypertrophy
    • Apical hypertrophy
    • Hypertrophy in the right ventricle
  2. Absence of systolic anterior motion (SAM): Unlike sarcomeric HCM, non-sarcomeric HCM may not exhibit SAM of the mitral valve.
  3. Normal or reduced left ventricular outflow tract (LVOT) gradient: Non-sarcomeric HCM may not have a significant LVOT obstruction.
  4. Presence of fibrosis or scar tissue: Look for signs of fibrosis or scar tissue on echocardiography, such as:
    • Bright or patchy appearance in the myocardium
    • Increased echogenicity
  5. Abnormal myocardial texture: Non-sarcomeric HCM may exhibit an abnormal myocardial texture, such as:
    • Speckled or “ground-glass” appearance
  6. Other structural abnormalities: Some non-sarcomeric HCM cases may exhibit other structural abnormalities, such as:
    • Mitral valve abnormalities
    • Tricuspid valve abnormalities
    • Right ventricular abnormalities

Ref : Sarcomeric versus Non-Sarcomeric HCM June 2023 Cardiogenetics 13(2):92-105

Some specific echocardiographic features of non-sarcomeric HCM include:

  • Fabry disease: Typically shows a “binary” appearance of the myocardium, with a bright and dark pattern.
  • Amyloidosis: Often exhibits a “granular sparkling” appearance of the myocardium.
  • Cardiac sarcoidosis: May show a “starry sky” appearance due to myocardial fibrosis.

Please keep in mind, that echocardiography should be complemented with clinical evaluation, genetic testing, and other diagnostic tools to confirm the diagnosis.

Amyloid -HCM coexistence

Medical pathology is never a pure science.It can make our assessment topsy turvy at any moment .One such rare phenomenon is amyloid getting deposited in a patient with classical inherited HOCM. (Boyangzi Li, Cardiac AA amyloidosis in a patient with obstructive hypertrophic cardiomyopathy,
Cardiovascular Pathology, Volume 48, 2020,
)

A comment on deep genetic profiling

Genetic studies in HOCM are academically exciting  and professionally gratifying. From the patient perspective, it provides  an opportunity to treat any reversible or treatable enzyme disorders(Ref 1 Migalastat for Fabry’s disease & Tifamidis and Patisiran in TTR Amyloidosis) .

But, the benefits of deep genetic testing has to be carefully harvested as there is a troubling trade off, due to the hitherto hidden prognostic anxiety, these genetic breakthroughs bring along.

Final message

Contrary to the belief , a carefully interpreted echocardiography along with clinical profile will be able to recognise sarcomeric HCM in most situations.But, it is still weak in ruling in a non- sarcomeric HCM.

Reference

1.McCafferty EH, Scott LJ. Migalastat: A Review in Fabry Disease. Drugs. 2019 Apr;79(5):543-554. doi: 10.1007/s40265-019-01090-4. Erratum in: Drugs. 2019 Aug;79(12):1363. doi: 10.1007/s40265-019-01166-1. PMID: 30875019; PMCID: PMC6647464.

2.The small interfering mRNA drug , is an interstitial protein excretory drug in TTR amyloid.

CAPTIM trial was published in 2002, which left a gospel truth in the science of myocardial reperfusion (two decades gone now). It is a sad academic story ,most of the interventional cardiology community shrugged it off as a non-event. After CAPTIM , there were several other studies that tried to reiterate the same. The fact of the matter is, in the art and science of reperfusion, all that glitters may not be gold at the myocardium level.

Yes, we do have a tiny advantage of pPCI in terms of complete revascularisation. But it was blown out of proportion, backed by small but glamorous studies. However, the true benefits are hidden in a timely early reperfusion, best done at out-of-hospital (or even in-hospital*) with the emergency crew’s assistance.

Since Intravenous lysis looks too simplistic, that do not need expertise, and lacks a commercial trail, it is wrongly depicted as inferior management strategy in STEMI

Every one of us is equally responsible for this sorry state of affairs. In many countries, the hub-and-spoke model is struggling to deliver. The spokes often fail in their duty to begin the reperfusion, (Perceived low quality treatment and peer pressure) while the further delay happens at the hub , that earn the wrath of the myocardium ultimately. In this context, we need a movement to revive the pre-hospital thrombolysis. This is what CAPTIM told us.

No one knows how the pPCI related delay was legally ratified and academically accepted by the elite cardiology forums. Some poorly designed small cohort RCTS are responsible for this. There were some sensible moves too later on. To counter the logistic limitation of pPCI came the pharmaco-invasive strategy backed upby STREAM, FAST-MI trials etc. Still, no one is able to undo the disproportionate popularity of pPCI .At best, It has a miniscule 1 % edge in the outcome if performed on time, at a expertise intensive place. (Efficiency of thrombolysis is highly reproducible. It is a fact, an ambulance crew is able to equal or even surpass the expertise of cardiologists in terms of absolute myocardial salvage) )

Now, it is heartening to read a meta-analysis addressing pre-hospital thrombolysis, done from my part of the country. This paper is published by Dr. R. Bharathkumar, and his team. He is one of our senior colleague, mentor and former professor of Stanley Medical College. Chennai. With this study ,they have successfully proved an existing truth, in a more refreshing and authoritative manner (Ref 1 )

I am here with sharing this full paper. Readers can infer their own conclusion. Would like to to highlight two important new points told in this paper in a gentle way, yet conveying a powerful message.

1. Much surprisingly, the guideline recommended the “door to needle time” in pPCI is achieved only in a fraction of the population in real world. (NRMI data Ref 2)

2.There is a differential Impact of PCI related delay on the myocardium with reference to IRA. In LAD STEMI time is more crucial. The permissible limit is 40mts not the traditional 90-120 minutes (Ref 3)

Final message

The perceived superiority of pPCI over any other modality of reperfusion is not absolute*. The above paper reemphasize this one more time ,with strong evidence aggregation .I wish ,this paper deserves a more prominent place in major journals like Lancet or JACC or even NEJM.

Meanwhile, we should not make sweeping statements, that tend to convey a wrong idea, which makes pPCI look invincible at all points in ACS time line. The irony is , many of us strongly believe, it is worth loosing the golden hour in lieu of perceived superiority pPCI . This shatters the concept of “time is muscle ” Thanks to the evidence based cardiology.

Counterpoint

*PCI in the setting of ACS do have a critical life saving role in certain subsets of ACS, that can never be undermined . What is being debated is the true benefits of this revolutionary intervention as a population level strategy.

Reference

1,Ramadoss, Barathkumar1; Pari, Arun2; Santhi, Sharanya Shre Ezhil3; Ravi, Sailatha4; Ramanan, Ezhilarasan4. Strategy to Reduce Mortality Rates of ST-elevation Acute Myocardial Infarction Using Prehospital Thrombolysis: A Meta-analysis. Research in Cardiovascular Medicine 13(2):p 48-57, Apr–Jun 2024. | DOI: 10.4103/rcm.rcm_1_24

2.Nallamothu BK, Bates ER, Herrin J, Wang Y, Bradley EH, Krumholz HM, et al. Times to treatment in transfer patients undergoing primary percutaneous coronary intervention in the United States: National registry of myocardial infarction (NRMI)-3/4 analysis. Circulation 2005;111:761-7.

3.Pinto DS, Kirtane AJ, Nallamothu BK, Murphy SA, Cohen DJ, Laham RJ, et al. Hospital delays in reperfusion for ST-elevation myocardial infarction: Implications when selecting a reperfusion
strategy. Circulation 2006;114:2019-25

This ECG can help you find an answer .HR is 50/mt. Find the PR interval .It is also printed right there.

What happens to PR Interval in sinus Bradycardia ?

A. Remains normal

B. Prolonged but within normal

C. Prolonged beyond normal

D. Depends on the cause of Sinus bradycardia

Answer

When cardiac cycle slows down, every interval must get prolonged. PR interval is no exception. If you apply that rule the answer would be simple (Its B ).But this question has much more issues hidden into it. In this ECG it touches on the doors of first degree AV blcok. Normally PR doesn,t stretch that far in isolated benign sinus bradycardia.

Sinus rate is determined by SA nodal, funny pacemaker current(if) .The rate of which is determined by the delicate balance between sympathetic and para-sympathetic signal flux. The dynamicity of the slope of phase 4 , ie spontaneous resting membrane is another key determinant apart from sift in the density of mean P cell firing focus .(see below)

The sinus rate depends upon the cranio- caudal shift that occur within specialized tissue .(10-15mm slender the basmati rice shaped SA node)

When do PR interval prolong in sinus bradycardia ?

The commonest cause of sinus bradycardia is due to increased vagal tone . It is no secret , vagal tone do Influence AV node as much as it does the SA node . So, what can we expect ? Logically .the AV node must also slow down . But does it happen really ?

No, most of the time the AV nodal delay doesn’t not occur in sinus bradycardia . Does that mean the vagal spill over do not reach the AV node ? It does, but the fact is, the reduced heart rate attenuates the normally prevalent decremental conduction property of AV node. So we do not expect a prolonged PR in sinus bradycardia.

However, if PR interval is prolonged in sinus bradycardia , we can except silent pathological states like , sinus node dysfunction where AV node can also be affected. Also, prolongation of PR is very common in ACS situations in Infero- posterior (RCA/LCX) territory where both SA and AV nodes are simultaneously targeted.

Prolonged PR in bradycardia some times is a hemodynamic necessity as ventricular filling time is prolonged.

Clinical Implication

It is a good habit to have rapid glance at PR interval in every patient with sinus bradycardia. This will ensure a rare miss of AV nodal dysfunction .

Final message

PR interval is normal or show little prolongation in most of sinus bradycardia. If it is prolonged, without any circumstantial evidence for enhanced vagotonia , then, it could indicate some thing wrong in the conduction system. Atropine test might help us out in differentiating true vagotonia from intrinsic delay.

Who said this non-sensible statement? ( I guess ,this would be the first response from many cardiologists !) If you feel the same, then this post might not be for you.

Relationship between Ischemia and arrhythmia

While the relationship between Ischemia and VT is really complex, the term “Ischemic VT” itself adds more twists. Its all about timing, intensity of Ischemia , associated factors and finally the baseline arrhythmic risk that includes the mystery defects in myocyte gap junctions and ion channels.

Following are some of the observations.

Primary VT

This is the true Ischemic VT. Even here, it is the associated factors, like hypoxia or acidosis are the triggers which of course are resultant of Ischemia. There are further problems . Even critical Ischemia, as in high grade unstable angina, rarely Initiate a VT, while STEMI seems to have the exclusive rights to trigger it , by its ability to produce acute transmural ischemia . (Note: Whether primary VT occurs before or after myocardial necrosis is not clear) There is evidence to prove, susceptibility to VT at times of Ischemia is in the genetic make-up of ion channels, as pointed out by famous French electrophysiologist Haïssaguerre. (NEJM 2008)

Post Infarct VT : (24 hrs to 2 weeks ,an empirical criteria we use)

This can be called as Ischemic, still we ‘wouldn’t know whether the arrhythmia is originating from dead or live tissue. It can even be combined Ischemic-Scar VT

Late Ischemic VT

These are the typical scar – substrate -mediated ,micro/macro reentry VT .The strip of tissue on the border zones of conflict (between viability and non viability is always restless (Gaza strip of VT?) This is rarely amenable to revascularization, unless some one is able make that area 0% Ischemic , which is a highly improbable scenario. The alternate option is diagonally opposite .EP guys are empowered with a deadly solution, and authorized to shoot down focus (or isolate) instead of the futility of revascularisation. (Please note, this doesn’t work and should not be attempted in early ischemic VT, though few case reports of RF ablations during VT storm li- Juan Qu et al AMJS 2924 )

Final message

The relationship between Ischemia and VT is poorly understood, (rather than to say complex.) It is true ,acute Ischemic VTs has more closer relation with Ischemia, often settles down with prompt revascularization.

In chronic VT , shooting down the ischemic focus by ablation is more likely to extinguish the arrhythmia ,rather than revascularization. This is because partial revascularization irritates the viable myocardium and keep the ischemic focus active. ( Class C evidence) ICD though a revolutionary technology to prevent a SCD in these circumstance it makes a poor choice to reduce the arrhythmic burden .At best , it is just a back up device to tackle the escaped VTs in spite of RF ablation and drugs.

Reference

1.Haïssaguerre M, Hocini M, Cheniti G, Duchateau J, Structural Alterations Underlying a Subset of Unexplained Sudden Cardiac Death. Circ Arrhythm Electrophysiol. 2018 Jul;11(7):e006120. doi: 10.1161/CIRCEP.117.006120. PMID: 30002064; PMCID: PMC7661047.

If you understand the pericardial anatomy fully, you can call yourself real master of clinical anatomy. (Ref 3,4) We know, it is a complex protective cover over the heart , that has three layers with a unique relation with one another. The outer one is tough conical bag .It has an embryologically distinct origin .It develops from septum transversum and sits over the diaphragm tightly, to which it shares the same embryological origin. While the inner serosal layer (rather cavity) splits into two layers and encloses the heart .Though this serosal layers develop from a different mesenchymal tissue , it is biological wonder both fuse in perfect harmony. , The developing heart bends, folds and loops within the serosal cavity.

The inner one embraces the heart fully forming epicardium (otherwise called visceral pericardium) and reflects back after covering great vessels .While reflecting back it is firmly attached to inner surface of fibrous pericardium forming the pericardial cavity . Never confuse parietal layer of serous pericardium with the thick outer fibrous pericardium, though both are gelled together. Since heart is not a strict globular organ, the hug of visceral pericardium over the heart is not uniform and complete , especially over the great vessels enter or leave the heart (Hilum of the heart). Hence it folds , and forms two sinuses and recesses.

What happens with pericardial Inflammation ?

Inflammatory pericarditis can occur in differential fashion. For example, the most common chronic pericarditis tuberculosis affects the fibrinous layer. Post MI pericarditis involves the epicardium. It is vital to understand epicardium is thin and transparent sheet of tissue , one may not split it from the heart. It is also important to know coronary arteries run under this thin visceral pericardium( ie sub epicardial) So anatomically , In constrictive pericarditis , the immediate target would appear to be the coronary artery , than the myocardium . But, what really happens ? Let us Introspect on this.

In CP which layer exerts the force of constriction ?

Macroscopically ,It would be a dramatic sight to see the heart caged within hard shell of pericardial mass. To be frank, we can never make a distinction between the three layers once its thickened. Which layer is the triggering force, that promotes adhesion and compression is also not clear. We presume, the thick fibrous layer is villain de chief. (This we learnt , by observing rheumatic heart disease pathology ,wherein pericarditis , never evolve into constriction as it doesn’t affect the thick fibrous layer) .The inflamed exudative pericardial fluid doubling up as a glue to stick all three layers is a true possibility.

Whatever happens, once the inflammation become chronic, it goes on steadily and begin to compress (rather restrict in diastole). At this stage, anti- inflammatory drugs like NSAIDS, colchicine or specific anti-tuberculous drugs along with a bit of steroids can arrest or slow down the pathological process and prevent this deadly disease. The phenomenon of transient constriction with normal thickness pericardium is also reported.

The normal and the pathologically thickened constrictive pericardium

The quantum of constrictive force widely varies in different areas of the heart. Obviously, the thickened pericardium hurts the heart in diastole . Right side of the heart is more vulnerable because of its thin wall and the low pressure beneath . However the constriction process continues over, anterior, lateral , posterior and even the AV groves The sinus the recesses can also become obliterated .

Does the coronary artery gets compressed ?

When the whole heart become as hard as a cricket ball , what do you expect the fate of coronary artery would be ? Fortunately, it escapes in many . But, the threat of compression or calcific (ice-berg) injury is always there. There has been many reports of patients with angina in CP (Ref 1). Here is case report from India , where a calcific pericardium exerts a vice like tightening over LCX. (Ref 2)

This is not surprising, when we know, at late stages the pericardium can even infiltrate the myocardium.

Video showing diastolic compression in constriction source : Christopoulos G, Stulak JM, Oh JK, Prasad A. Diastolic Coronary Artery Compression in Constrictive Pericarditis. JACC Case Rep. 2020 May 6;2(5):825-827. doi: 10.1016/j.jaccas.2020.01.009. PMID: 34317356; PMCID: PMC8301696.

How do the coronary artery often escapes in CP ?

One important reason is , unlike myocardial bridge here the artery gets compressed in diastole , with a passive distending pressure from LV cavity rather than active constrictive force.(See the above video) The diastolic coronary arterial pressure rarely goes below intrapericardial space pressure , which in fact is obliterated. Still, the point to be noted is, mass effect can still result in non hemodynamic compression.

Final message

Fortunately, coronary arteries often escape from serious pressure effects of constriction but the threat is real especially in late stages .It can happen either by the calcific spurs in the pericardium or diffuse pressure effect or tight ring like localized constriction. While de-nova coronary Involvement is far less common, the operating surgeon needs to take extreme care to avoid it during surgery . Surgical pericardiectomy is either partial or total caries considerable mortality even today. Total pericardiectomy is myth at best. Few pieces of adherent pericardium are left over especially in the posterior aspect.

There is a landmark study from Mayo clinic, with data from over 1000 pericardiectmy surgeries ,over eight decades . Every cardiologist and cardiac surgeon must read this to understand the nuances of pericardial surgery (Murashita Ann Thorac Surg. 2017) Now Robots are being tried to assist in this delicate surgery (CTS-NET 2023 Total Robotic Pericardiectomy for Constrictive Pericarditis)

Reference

1.Mahé I, Braunberger E, Bergmann JF. Angina caused by calcific constrictive pericarditis. Ann Intern Med. 2002 Dec 17;137(12):1012-3. doi: 10.7326/0003-4819-137-12-200212170-00036. PMID: 12484734.

2.Rajagopal, MD, DM • Sreenivasa Narayana Raju, MDConstrictive Calcific Pericarditis Causing Coronary Artery Compression Radiology 2021; 299:539 • https://doi.org/10.1148/radiol.2021203726

Two Excellent reference for comprehensive knowledge in pericardial anatomy

3.Rodriguez ER, Tan CD. Structure and Anatomy of the Human Pericardium. Prog Cardiovasc Dis. 2017 Jan-Feb;59(4):327-340. doi: 10.1016/j.pcad.2016.12.010. Epub 2017 Jan 4. PMID: 28062264.

4. E.Rene Rodriguez ,Carmela D.Tan Structure of the human pericardium and responses to pathological processes JACC 2016

*Lifestyle definition

 A set of attitudes, habits, or possessions associated with a particular person or group. and such attitudes, etc, are regarded as fashionable or desirable.

Final message

Communicable disease need not be an Infectious disease like covid. The word “Communicable” shall soon convey a new meaning, to the enlightened. Adverse life styles ,disseminated into the community that vigorously propagate CVD, has every reason to be referred to as a ‘Neo non-infectious pandemic”

Postamble

In the strict sense, CVD is not a communicable disease ,rather the risk factors are …but technically it is.

Reference

1.Rippe JM. Lifestyle Strategies for Risk Factor Reduction, Prevention, and Treatment of Cardiovascular Disease. Am J Lifestyle Med. 2018 Dec 2;13(2):204-212. doi: 10.1177/1559827618812395. PMID: 30800027; PMCID: PMC6378495.

3.A comprehensive narrative review

1.What is the response of RV to pressure overload ?

A. Dilatation

B. Hypertrophy

C Both occur together

D. Hypertrophy is the Initial response, followed by dilatation

Answer :

Since we believe RV’s behavior is generally opposite to that of LV , many would tick, dilatation as the first response. This may be correct when there is acute raise in RV after load, as in PE. However, It is surprising even in chronic pulmonary hypertension , the degree of RVH is not constant and homogenous .This is because , different parts of RV chamber has different wall thickness .Further, the pressure distribution from PA to RV is uneven. The co-existing TR confounds the loading conditions. It is not yet clear, how the RV would respond to raised PA pressure. In the bed side, we are seeing both flight(dilate) ot fight (RVH) reactions from RV (more often the former than the later) It is possible RV behavior is be pre-programed and built into the genes of the contractile proteins.

It is worthwhile to note, RVH is constant feature in non pulmonary hypertension related “after-load” conditions as in valvular or sub valvular PS. This is more to do failure of regression of RV mass early after birth, rather than the actual effect of high after load. Another point is purely technical. RVH is measured in RV free wall, in subcostal view in diastole and inspiratory phase.(upper limit is 4mm) Many of us could miss RVH in routine echocardiography unless specifically looked for.

2.Which is the first echocardiographic parameter to get impaired when RV fails ?

A. RV FAC (Fractional area change)

B.TAPSE

C. RV Ejection fraction

D.RV longitudinal strain

E. RV S

Answer : I am not very sure about the right answer , but TAPSE is last to get Impaired .(Still, we celebrate it like anything is a different story) Many believe transverse functional Indices like FAC is impaired early. and is less influenzed by the spurious spill over of Left ventricular contractile force in transannular plane (Which augments longitudinal functional Index like TAPSE),

The following illustration (From Ref 2 ) summarizes all RV functional parameter in a succinct fashion. Fellows must be familiar with at-least half of them.( RIMP is less practical and error prone can be ignored)

Reference

1.Gorter TM, van Veldhuisen DJ, Bauersachs et al Right heart dysfunction and failure in heart failure with preserved ejection fraction: mechanisms and management. Position statement on behalf of the Heart Failure Association of the European Society of Cardiology. Eur J Heart Fail. 2018 Jan;20(1):16-37. doi: 10.1002/ejhf.1029. Epub 2017 Oct 16. PMID: 29044932.

2.Harjola VP, Mebazaa A, Celutkiene J, Bettex D, ET AL  Contemporary management of acute right ventricular failure: a statement from the Heart Failure Association and the Working Group on Pulmonary Circulation and Right Ventricular Function of the European Society of Cardiology. Eur J Heart Fail 2016; 18: 226