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Archive for September, 2024

PCI for stable angina : Sham trials are welcome, but not OMT shaming trials !

Posted in Uncategorized on September 23, 2024|

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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.

2.Rasha Al-Lamee, David Thompson, Hakim-Moulay De et al Percutaneous coronary intervention in stable angina (ORBITA): a double-blind, randomised controlled trial Lancet P 31-40, 06, 2018

3.Rajkumar CA, Foley MJ, Ahmed-Jushuf F, , Al-Lamee RK; ORBITA-2 Investigators. A Placebo-Controlled Trial of Percutaneous Coronary Intervention for Stable Angina. N Engl J Med. 2023 Dec 21;389(25):2319-2330. doi: 10.1056/NEJMoa2310610. Epub 2023 Nov 11. PMID: 38015442; PMCID: PMC7615400.CopyDownl

4.Boden WE, De Caterina R. ORBITA Trials Are Not Justification to Promote a PCI-First Strategy in Nonacute Myocardial Ischemic Syndromes. Circ Cardiovasc Qual Outcomes. 2024 Sep;17(9):e011268. doi: 10.1161/CIRCOUTCOMES.124.011268. Epub 2024 Sep 17. PMID: 39288214.

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A forbidden quote in medical science

Posted in Uncategorized, tagged , , , , , , , , , , , , on September 14, 2024|

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Can we differentiate “Sarcomeric vs non Sarcomeric HCM” by Echocardiography ?

Posted in Uncategorized on September 4, 2024|

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.

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The pseudo-superiority of pPCI is exposed one more time … but it will thrive!

Posted in Uncategorized, tagged , , , , , on September 1, 2024|

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

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What happens to PR Interval in Sinus bradycardia?

Posted in Uncategorized, tagged , , , on September 1, 2024|

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.

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