Dr.S.Venkatesan MD

No, we can never ever consider OMT, as a re-vascularisation equivalent .

February 25, 2024 by dr s venkatesan

Hi, welcome Mr George, I just reviewed your records. You have three blocks in your arteries supplying the heart.

Are they serious Doctor ?

Not really, but one of them appear tight

What should I do Doctor ? But, I am comfortable Doctor.

You may be. But I am not .You need to undergo some re-vascularisation procedure .

What do you mean by that Doctor ?

It means either a percutaneous coronary intervention with a stent or CABG.

Can I get my heart re-vascularised by drugs alone Doctor ?

No we can’t . Hmmm , wait, we do have something called OMT/GDMT. Can you put on hold for some time Mr George, you have asked a real tough question.Let me recollect something from my forgotten basics clinical lessons.

The Illusion of myocardial re-vascularisation

PTCA is sort of repair work done over the blocked area that restores the traffic(blood) flow. while CABG, diverts flow from the congestion or road closure, along a by- pass road, which rejoin the main road later. These are called re-vascularisation procedures. Please note, both of them, never bother to find the status of micro-vascular integrity which form 95% of net coronary vascular surface area.

Hiding behind the technicalities

PCI demands reduction in percentage  stenosis , resulting in pre-defined minimal luminal area (MLA), maximizing net luminal gain, & restoration of TIMI 3 flow in all three coronary arteries .These are the popular scientific parameters. For CABG we aim at good and complete, uninterrupted short and long term distal flow.

However ,we have some effective clinical and pathological markers too, for effective re-vascularisation They are  clinical well being and good functional capacity , relief from chest-pain, reduction of plaque volume, plaque stabilisation, maintenance of  collaterals , microvascular patency ,  reduction of recurrent events .The irony in CAD management  is  in many patients who are on only drugs , clinical endpoints can be achieved without the above mentioned technical end points ! ( As we have learnt from the OAT, COURAGE trials which dramatically showed arterial patency is nothing or little to do with major  clinical end points )

Final message

Scientific minds can not accept certain things which are less glamorous and unassuming. Simply swallowing few drugs can never make us(both physicians and patients) believe it can be an equivalent to PCI/CABG .

Intentionally or unintentionally , we have made PCI and CABG appear invincible and conferred the sole-rights to be referred to as re-vascularsation procedures , Realistically looking medical  therapy also provide good revascualrisation (re-or neo) especially where it is needed ie in the coronary micro circulation.

Hence forth, in the overall interest of  CAD community , and with good scientific basis “It is good to emphasise to our patients optimal medical management of CAD  is  also one form of re-vascularization This will help us to neutralise the unfair” Semantic  advantage” the PCI and CABG enjoys.

Reference : Apart from the heavily quoted classics of COURAGE, BARI-2D, ISCHEMIA, ORBITA 1 etc. (Please note ORBITA -2 is not an antidote to ORBITA-1) ,Read this 1.AVERT study :Atorvastatin equals PCI .2.Regular exercise equivalent to PCI (ESC 2009) .Will try to get the link for this soon.

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When medical conferences become an “Edutainment Industry” the speciality of Cardiology leads from front !

February 22, 2024 by dr s venkatesan

Recently , I received two e-mail invite for two major conferences one in India other in Europe.

Once upon a time, in 1990s we as fellows used to attend these conference for Rs 1000 (15 Euros/Dollors). Now it is 50-75 thousands (5000-7500 % increase) Even few years ago it was affordable. I don’t know how many of us can think to attend such conferences. Definitely not me. What prevents these guys to keep the cost nominal. Certainly, inflation is not the reason. Air tickets and hotel room tariffs has just raised 50-100%.over the same period

if you look closely into the above menu card, Indian tariffs would tell a crazy story .When global purchasing power parity ratio is applied, Rs50000 will be equal to approximately 6000 Euros (*Factor of 8 for each Dollar). Which in realty, fix this Indian conference cost, at a true equivalence of 4.8 Lakhs.

Final message

My professor used to say, teaching and learning should be spontaneous, and never be a commodity. Can you guess who is fixing these conference fees beyond the reach of a lay student & doctor ? Some of you might know the true reason. The regulatory bodies are just helpless. There is a direct link between a MBBS seat costing 1 crore in our country , to these jacked up conference costs. The moment greed enters, we become a party to un-professional scheme of things, however good is our expertise and knowledge .

There is a joke going on in India, if you can find one cardiologist who pays the registration fees from his pocket, he shall be awarded highest professional award . I am sure, there will be few eligible souls who defy the rule of the current academic landscape.Let these conferences, be dedicated to them.

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Why ICDs are less effective in Non Ischemic DCM ?

February 20, 2024 by dr s venkatesan

We wish, our understanding about cardiac contractile physiology is deep and nearly complete. Heart is an irreversibly coupled electro-mechanical organ , right from the fetal days until the final heart beat. In myocardial pathology, the genesis and sustainability of ventricular arrhythmia are intricately related to the degree of LV dysfunction of any cause.

SCD is the leading cause of mortality in heart failure. Tackling SCD was in God’s domain, until the brilliance of Dr. Michel Mirowski shrunk the defibrillator and implanted it under the chest in 1980. (Dr. MM’s s a unique and inspiring story, from Poland amidst the holocaust times, right up to his invention at Johns Hopkins)

Why ICD for SCD ?

Beta blockers and Amiodarone remain good options for mitigating SCD. (Of course, Amiodarone has a huge baggage of side effects.) But, as you know machines always beat drugs. After multiple RCTs, we found any severe LV dysfunction (EF <30%) requires an ICD to reduce SCD. Though MADIT trial required an inducibility of VT, MADIT-2 told us that just the presence of LV dysfunction is sufficient.

Since then, ICDs have proliferated globally, of course with multiple collateral issues. As we navigated the cardiac EP terrain further, we found that all is not well. ICDs faced some foundational questions regarding its utility value vs. risk . ICD explanation epidemic in the past was a true story. Still, Mirowski”s electrical kid survived the test of time and evolved with great technological innovations from companies like Medtronic, Guidant, Abbot etc. It has, now grown into 45 year old wonder device, that can wake up the heart from death . (Wish ,the Nobel committee has Dr Mirowski’s name in their podetial posthumous prize list)

ICD usage with reference to DCM sub types

One factor frequently debated about ICD is its efficacy with reference to the etiology of LV dysfunction. Many studies indicated this factor could tilt the balance of risk to benefit of ICD in a critical way. ICDs are more useful in Ischemic DCM than non ischemic DCM is a recently observed penomenon ,though we are not sure yet . SCD-HeFT trial (NEJM 2005) did show some benefits in N-DCM, but it was only in class 2 stage. Then came the DANISH study, which made us strongly believe ICDs in Non-Ischemic DCM are not a really useful intervention. (N Engl J Med 2016; 375:1221-1230)

Why ICD doesn’t work well in NDCM ?

Since IDCM patient had more SCD events , ICD is more likely to be useful in ischemic DCM than non ischemic is a distinct possibility (Higgins AY, . Am J Cardiol. 2020)

The un-disputable fact is ischemic DCM has a target to treat, though it is termed as cardiomyopathy. While most of non-ischemic DCM are truly global muscle disease with primary or secondary with known or unknown disease process, unless we are able to correct the etiological factor, these patients are not going to do well in spite of ICD.

The differentiation between DCM and NDCM itself is not a simple task. Overlaps do occur. (An important clue is NDCM involves both ventricles equally and subendocardial sparing almost always suggests NDCM)

Final message

It seems to be a fact, ICD are less useful in NDCM. The simple reason could be we can address the ischemia a potential arrhythmic target by some form of revascularization in IDCM. The second reason is, NDCM is a progressive primary muscle disease.

Still, our understanding is largely incomplete. ICDs don’t exhibit partiality. By default, they try to give a new lease of life to any episode of pulseless VT/VF whether it is from IDCM or NDCM. (Please remember we don’t deny an ICD for a sarcoid cardiomyopathy or end-stage HCM just because they are non-ischemic. in origin )

Post-amble

An unfriendly fight between CRT & ICD

The science of LV dysfunction and the need for ICD got complicated when CRT entered the scene a decade ago. CRT is indicated when a LV is dilated with poorly coordinating contractions due to conduction system malfunction, that stretch the QRS complex either LBBB or monophasic RBBB or combination both BBBs(Masquerading)

Since, the indication between ICD and CRT overlapped, industry guys taught us some cardiology lessons, They offered the option of fusing the two together and called it CRT-D & CRT- P. Please note CRT-P is nothing but the glorified version of plain old CRT (The P could mean either the dual /BV or the mono ventricular (RV) default back up pacing.)

The choice between CRT -P and D has taken more curious turns. Since we are not clear whether the incidence of SCD is reduced by CRT or ICD. This paper from Egypt address this issue in an exemplary manner. (Ref 4).

Now, there are more than handful of papers that show CRT-P per se can reduce the SCD events significantly by reverse re modeling of LV and improvement of LV function. Currently, we have started to believe CRT-D may not be indicated in many and could in fact add more electrical side effects.

It is ironical, currently the issue of in-appropriate ICD/CRT-D implantation appears more important than the well known adversary of inappropriate shocks. Both of them needs some meaningful attention. It is worthwhile to to note ,If we address the former the later issue cease to exist. Let the global EP think tank introspect and to refine and redefine the Indications of CRT-D.

Reference

1.Bardy GH, Lee KL, Mark DB, Poole JE, Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT) Investigators. Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure. N Engl J Med. 2005 Jan 20;352(3):225-37.

2.Køber L, Thune JJ, Nielsen JC, Haarbo J, DANISH Investigators. Defibrillator Implantation in Patients with Nonischemic Systolic Heart Failure. N Engl J Med. 2016 Sep 29;375(13):1221-30.

DANISH 10 year follow up re-confirms it

3.Yafasova A, Butt JH, Elming MB, . Long-Term Follow-Up of DANISH (The Danish Study to Assess the Efficacy of ICDs in Patients With Nonischemic Systolic Heart Failure on Mortality). Circulation. 2022 Feb 8;145(6):427-436.

4. CRT -P vs CRT-D

Samy M, Hamdy RM. Arrhythmic and mortality outcomes in patients with dilated cardiomyopathy receiving cardiac resynchronization therapy without defibrillator. Indian Pacing Electrophysiol J. 2023 Nov-Dec;23(6):171-176.

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Posted in Uncategorized | Tagged crt device, crt-p vs crt-d, danish trial, ischemic dcm, madit trial, non ischemic dcm |

Predicting myocardial viability from surface ECG following MI

February 14, 2024 by dr s venkatesan

Once upon a time, long, long ago, cardiologists used to be worried about akinetic segments, scars, dead tissue, and Q waves before attempting revascularization by either PCI or CABG. Now, the concept of myocardial viability has become a cliché ( rather demeaning) at least within the cath labs. Currently ,we follow a self administered whip . Every post-MI patient should be considered for revascularization as a default strategy irrespective of the level of dysfunction or scarring .This can happen either in the IRA territory or non-IRA territory or both.

This strategy is now dis-armed with fresh evidence in the form of REVIVE -BRICS trial. However, there could be some distinct errors in the way many Interpreted this study. (Read here about REVIVE tral Perera D, Ryan et al JAMA Cardiol. 2023). One reason viability testing lost its sheen is the fact, identifying the extent of viablity requires a complex battery of tests. If we have simple clues on bed side, the adoptation of this concept would not have become a challenge.

Lets go back and learn something from the year 1999

For those cardiologists who believe myocardial viability is still an important factor before revascularization, let me pull out a 30 year-old study from the University of Aberdeen, UK, that looked into the humble ECG to detect viability. The authors went beyond just observing presence or absence of Q waves .It conveys a great learning point.

Modified from Al-Mohammad A, et al Heart. 1999 Dec;82(6):663-7. (Ref 1)  Matching means non-viable myocardium  (Tissue looks akinetic or scar-like, while PET concurs and shows lack of metabolic activity. This is referred to as matching, and the segment is non-viable) Mismatch means viable myocardium (Tissue appear dead by akinetic Echo but metabolism intact ie a mismatch implying viability )

It is worthy to note, the authors looked specifically over the segments that subtended Q waves and looked for viability matching. It was correlated with a PET scan, the gold standard for viability testing even now.

The results were important and insightful. What we infer from this study is actually a simple message. In post-MI patients, even with the burden of q-waves, if the return wave overshoots the baseline and inscribes some sort of r-wave (Qr, QR, qR patterns), there is a high possibility of viable tissue when compared to QS wave. It is a new lesson from a old paper for me. , ie any R is good whether it is preceded by q or not.

It is good to recall ,other simple clues to the presence of viable myocardial tissue, such as presence of angina, M-mode wall thickening. Not to forget other modalities like, well preserved sub endocardial function by speckle tracking echo, dobutamine-stress, myocardial contrast echo, and LGE-MRI.

Final message

As on 2024, the concept of myocardial viability testing has not vanished. We must ensure, not to pass on a incorrect message to generation next cardiologists, that viability tests are outdated and obsolete.

Reference

1.Al-Mohammad A, Norton MY, Mahy IR, Patel JC, Welch AE, Mikecz P, Walton S. Can the surface electrocardiogram be used to predict myocardial viability? Heart. 1999 Dec;82(6):663-7. doi: 10.1136/hrt.82.6.663. PMID: 10573488; PMCID: PMC1729205.

2.Perera D, Ryan M, Morgan HP, et al. Viability and Outcomes With Revascularization or Medical Therapy in Ischemic Ventricular Dysfunction: A Prespecified Secondary Analysis of the REVIVED-BCIS2 Trial. JAMA Cardiol. 2023;8(12):1154–1161. doi:10.1001/jamacardio.2023.3803

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Posted in Uncategorized | Tagged acc aha esc guidelines, ECG predictors of myocardial viablity, MYOCARDIAL VIABLITY, PET SCAN FOR VIABLITY, REVIVE BRICS STUDY |

Which doctor treats “Y-36” disease ?

February 11, 2024 by dr s venkatesan

The ICD-11 , the latest code lists nearly 15000 diseases. Have a look at this much celebrated (respected ?) list put up by the world health organization There are so many entities in the list , that are man made and solution is right there in our minds.

Zoom your eyes on the red rectangle.

Impact of Y-36

Y-36 is a contagious endemic, transmitted by power, pride and foolishness . Y-36 along with violence is a perennial disease and a leading cause of global mortality. It not only take lives, it inflicts huge , irreversible financial , economic cost.

What is infective agent Y-36?

One suggestion would be Y-36 may be subclassified under DSM manual as well , as a psychiatric disease of individuals or heads of state , and policy makers.

How do you prevent Y-36 ?

We have hundreds of pharma companies working on small interfering RNA, and other biologicals, monoclonal vaccines etc. There is not even one organization (except the one, 39 storied struggling lab on the banks of East River, New York City) attempting to find a potent polyvalent WACV-Y36 (War and Violence Cleansing Vaccine) against Y-36.

It is likely, the need and feasibility for such a vaccine will become redundant, as much of the humanity will be eliminated well before it is invented.

Final message

What could be the message for the Interventional cardiologist from this ? Nothing ? .No, there is something.They need to ensure, any of their aggressive interventions accidentally end up as a Y-36 equivalent without their knowledge & intention. (I say this because , many consider , we are at war with atherosclerosis , the core pathology in CAD . War always has collateral damage.)

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A NOTIONal truth : Surgical AVR deteriorates faster than TAVI, for some mysterious reasons!

February 10, 2024 by dr s venkatesan

Reviewing NOTION study, the Nordic TAVI 10 year follow up has just been released (Ref 1) :

Caution :Non-academic content

This study reports the long-term outcome in low-risk individuals who required AVR. The study basically compared the blind and passive deployment of bio-prosthetic aortic valve aided by the catheter skills of new-age cardiologists with sophisticated image backup versus Open surgical replacement of the aortic valve by experienced cardiac surgeons, after meticulously removing and debriding the native leaflets and suturing the prosthetic valve permanently in the optimal target site under direct vision.

Study summary

Conclusion

The study results finds the valve deployed percutaneously under semi- blind vision, was equipoise with SAVR done under direct vision. The surprise however is, TAVI was superior to cardiac surgeons in multiple aspects .The mysterious finding is TAVI had less Structural valve dysfunction, and possibly low bio valvular failure (BVF), if Kaplan -Myer curve trend is little extrapolated. No doubt ,the Aortic interventional world is applauding and everyone is joining the party.

Now, some academic queries ?

1.Did the trial compared best practices of TAVI & SAVR ?

No. Because it was done in 2010-2013. (Which grew faster TAVI or SAVR in the last10 years ? in terms of both hardware and expertise . How it will impact now ?)

2..Was the outcome assessment blinded ?

No

3.Why there is 50 % cardio vascular and 60% all cause mortality in both groups even though they belong to low risk category ?

Don’t know. Not clear.

4.Why the gradient was high in SAVR in the follow up ?

There are two important factors. More than 98% of TAVI patients had a valve sized 26–31 mm, while 98% of SAVR patients received a size 19–25 mm . Apart from valve size aortic annular enlargement before SAVR was not done in majority, there by enhancing the gradient and valve mis-match.(Note :The TAVI begins at 26mm and SAVR ends at 25mm. For how many of you this looks odd ?)

4a. Was doppler velocity index measured in all to assess EOA in follow up ?

No. It was not mandatory.

5..Is it Ok to define structural valve dysfunction(SVD) based on gradient alone ? Did TEE/CT follow up imaging done ?

No. Flow is physiology. Sub physiological valve destruction very much possible without affecting gradient.

6.The rate of severe SVD was higher after SAVR. Is there any meaningful explanation why surgeons valve deteriorated fast ? 

No .

7.Was CAD accounted for outcome difference ?

No .CAD patients were excluded.

8.Did this study address technical issues in performing PCI with new onset CAD and its possible impact in outcome

No. TAVI induced coronary ostial encroachment not reported.

9.Why didn’t they use bi-leaflet mechanical valves in SAVR group ?

Don’t know .(*One possible reason is given in the foot notes)

10.Is this study still valid ?

Sorry,  I don’t know.

Final message

Whatever is written here, NOTION will remain a great study with a 10 year meticulous follow up . As a cardiologist, very soon we will be allowed legally to choose TAVI even in more younger , low risk cohort of Aortic stenosis without co-morbid conditions. Still, if you put patient first approach ,CAUTION should precede NOTION .

* One version of answer for question 9 , would be TAVI vs Bi-leaflet St-Judes study was in-fact proposed, but was apparently not approved for (un)ethical reasons, of comparing a short living bio-valve valve with a long lasting mechanical valve.

Reference

1.Hans Gustav Hørsted Thyregod, Troels Højsgaard Jørgensen, Nikolaj Ihlemann, Daniel Andreas Steinbrüchel, Henrik Nissen, Bo Juel Kjeldsen, Petur Petursson, Ole De Backer, Peter Skov Olsen, Lars Søndergaard, Transcatheter or surgical aortic valve implantation: 10-year outcomes of the NOTION trial, European Heart Journal, 2024;, ehae043, https://doi.org/10.1093/eurheartj/ehae043

2.TCT -MD article from the INTEGRITY group / Link 2

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Posted in Uncategorized | Tagged acc aha esc guidlines, aortic stenosis, Aortic valve replacement, avr, core valve, edward sapien, notion 10 year follow up, notion trial, partner, savr, st judes valve, surtavi, tavi tavr in low risk category, uk tavi |

What is the correlation between number of doctors in a society & health of population ?

February 6, 2024 by dr s venkatesan

This query is lingering ever since I entered the medical profession. Though, this question might appear absurd , no correct answer is found yet .When we search the literature, the relationship between doctors and health can be 1.linear, 2.non linear, and 3. even inverse . 1 & 2 are ok 3 is forbidden.

However, to put it in a nut-shell, healthiness of a society is little to do with Doctor population alone, is well known and I think it needs no proof. The following scattergram gives some idea about the Issue.

Where to get answer for this controversial question ? Great times we are in. We have taught the machines to think. To clarify this query. I began a conversation with Chat GPT.

Hi Mr GPT , hope you do well in spite of non stop bombardment of queries to you .Let me begin this What is the relationship between number of doctors in a society and the healthiness of the society ?

Chat GPT: Welcome and thanks , always willing to help. The relationship between the number of doctors in a society and the overall healthiness of the society is not strictly linear. While having an adequate number of doctors is essential for providing medical care and improving health outcomes, it is only one factor among many that influence the health of a society.

The health of a society is a complex and multifaceted concept that depends on various factors such as access to healthcare services, education, socioeconomic conditions, lifestyle choices, public health policies, and cultural factors. . Having an appropriate doctor-to-patient ratio is generally associated with better healthcare delivery and outcomes.

However, simply increasing the number of doctors does not guarantee a healthier society. Health of a society is influenced by factors beyond medical care, such as nutrition, sanitation, environmental factors, and social determinants of health.

It’s important to consider that correlation does not imply causation. While there may be a positive correlation between the number of doctors and the healthiness of a society in some cases, it does not necessarily mean that more doctors directly cause a society to be healthier.

Therefore, while the presence of an adequate number of doctors is important for a healthy society, it is just one piece of the larger puzzle,

Can I expect a straight forward answer to my question does increasing doctors assure a healthy society ?

Yes or No ?

ChatGPT : I must admit , the straightforward answer to your question is “No.”

So, If you supply more and more doctors into a society without taking into other factors what will be the consequences ?

ChatGPT: If you were to increase the number of doctors in a society without considering other factors, several consequences could arise. It’s important to note that this scenario assumes an oversupply of doctors without addressing the broader healthcare system, infrastructure, and other healthcare-related aspects. Here are a few potential consequences:

1. Unemployment and underemployment: An oversupply of doctors can lead to increased competition for available positions. This may result in some doctors being unemployed or underemployed, not utilizing their skills and knowledge effectively.
2. Brain drain and resource allocation: If there is an excess of doctors in a particular region or country, some doctors may choose to emigrate or seek employment opportunities elsewhere, resulting in a brain drain. This can lead to imbalances in healthcare provision and exacerbate shortages in other areas or specialties that require attention.
3. Strain on healthcare resources: Increasing the number of doctors without considering the availability of healthcare infrastructure, equipment, and resources may strain the existing healthcare system. Hospitals, clinics, and medical facilities may struggle to accommodate the influx of doctors and provide adequate resources for patient care.
4. Cost implications: The increased number of doctors without addressing other healthcare system factors can have cost implications. Expanding the healthcare workforce may lead to higher expenditures on salaries, training, and infrastructure. These costs could potentially burden the healthcare system and, ultimately, affect healthcare accessibility and affordability.
5. Specialty imbalances: An oversupply of doctors can result in imbalances in the distribution of specialties. For example, there might be an excessive number of doctors in certain areas, such as dermatology or plastic surgery, while shortages persist in other essential areas like primary care or rural medicine.

It’s crucial to note that a well-functioning healthcare system requires a comprehensive approach that goes beyond the number of doctors. Factors such as healthcare infrastructure, access to healthcare services, equitable distribution of resources, quality of care, and preventive health measures need to be considered for an effective and efficient healthcare system.

In this scenario , is there a possibility of detrimental effect on health if excess doctors are present who want to compete for patients and there by increasing inappropriate treatment?

ChatGPT : In the scenario you described, where there is an oversupply of doctors competing for patients, there is indeed a possibility of detrimental effects on health. This situation can potentially lead to inappropriate treatment and its associated consequences.

Thank you, for answering my 30-year-long query. “I am sure many may not accept your version.” Though your answer concurs with my perception, I can’t accept the current state of affairs. There is a strong push from among global authorities to increase the number of doctors (especially specialists) without a deep understanding of the reality. (Even the WHO is in a state of confusion, how best the enforced modernity in medical care is to be followed. It is a wild truth , at-least 60-75% of the work the doctors do, can be done by trained nursing professionals or paramedics, and in the near future, AI-powered med-bots)

Reference

1. Nolte, Ellen, Mckee, MartinDoes : Book Title : Health Care Save Lives? Avoidable Mortality Revisited ,2004
2.Crivelli L, Domenighetti G.The physician/population ratio in Switzerland: the impact of its regional variation on mortality, health expenditures and user’s satisfaction. Cah Sociol Demogr Med.
2003;43(3):397-425

Next query

Does nurse -population ratio correlate better with health of a society than D-P ratio ?

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Posted in Uncategorized | Tagged doctors, health, healthcare, medicine |

Why is Aspirin, everyone’s nemesis ?

February 1, 2024 by dr s venkatesan

Here is a current review on a topic, which needs some Introspection

For a kid, A stands for apple in kindergarten, while in the school of cardiac pharmacology, A would sound as Aspirin. Such is the importance of this drug, known for its obedient, predictable efficiency in the entire spectrum of CAD right from primary prevention of CAD to emergent primary angioplasty in Cath lab. Most of us will also agree, It is a work horse drug, not only for the cardiologists , but has been an anchor drug in as many critical general medical therapeutics, wherever platelets are to be passivated.

We are well aware of molecular basis of this drugs action. Aspirin impacts most points in the core axis of platelet adhesion , activation and aggregation either directly or indirectly .(Though, its just a COX 1 blocker) Its efficiency is backed by countless papers with authenticated evidence.

Final message

“Now, we, realize Aspirin is being targeted and facing potential elimination “

Why is this happening ?

Aspirin acts by just blocking thromboxane mediated platelet activation , it doesn’t antagonize adenosine triggered activation, hence it is useless is the argument. Some how, our thought faculty is intruded , and unable to realize, the same question can be played in reverse .

P2-Y12 blockers in whatever form & fashion ,helplessly watch thromboxane A2 promoting platelets activation , isn’t ? Please understand, many cases of Clopidogrel and Ticagrelor resistance is apparently related to lack of assistance from the Aspirin .(Genetic P450 heterogenicity story doesn’t explain this fully )

The other concern is Aspirin increases the bleeding risk. It is a perfect irony , this argument is exactly opposite the one discussed above, Implying Aspirin could be a more powerful anti-platelet agent.

It is a duty of every one of us, to find the true reasons for such a bias against Aspirin. However strong the evidence base, (that is being created) It is very difficult to believe , Aspirin is shown the exit door for academic reasons.

Post test

If you want to convert Dual-APT to Mono-APT , which will you jettison ?

A.Aspirin

B.Clopidogrel

C.Ticagrelor

D.Whatever the guideline say.

E.Will leave it to the patient to decide.

Reference

1.Piera Capranzano, David Moliterno, Davide Capodanno, Aspirin-free antiplatelet strategies after percutaneous coronary interventions, European Heart Journal, 2024;, ehad876, https://doi.org/10.1093/eurheartj/ehad876

.

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Posted in Uncategorized | Tagged acc aha guidelines, aspirin, bias-against-aspirin, dapt, esc guidelines, mapt |

Major research papers from NEJM in 2023

January 25, 2024 by dr s venkatesan

Here is a pleasant surprise, a collectors issue of NEJM year book 2023, is made available free (even for non subscribers, in its website) .It is fascinating to know how fast the Internal medicine has grown. For the busy cardiologists, this will a be refreshing reminder, that there are other important organs and specialties do exist in medicine , with equal breakthroughs and Innovations.

It is indeed an amazing , whirlwind tour of medicine for all those who see medical science as single holistic specialty. It has articles, ranging from from simple clinical studies on postpartum hemorrhage (E-MOTIVE study) from deep inside Africa by Melinda Gate foundation, to Dupilumab for COPD, a stunning monoclonal antibody inhibitor of IL-4 for COPD exacerbations. Shortening tuberculosis treatment with a strategy involving initial treatment with an 8-week Bedaquiline-linezolid regimen (TRUNCATE-TB study) is also a revelation.

Of-course, the mandatory cardiac topics do find a prominent place including the currently omnipresent drug GLP agonist Semaglutide for HFpEF (STEP-HFpEF study). Baxdrostat, an Aldosterone synthase antagonist for treatment-resistant Hypertension, appears promising (BrigHTN).

Final message

However, the crowning glory among all articles appear towards the end of the document, titled Combating misinformation as a core Function of Public Health.

Let me share the link to this PDF document here. Hope it allows open access and there are no copyright issues. Notable articles of 2023 from NEJM .

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Posted in Uncategorized | Tagged 2023 review articles, acc aha esc guidlines, an Aldosterone synthase antagonist for Treatment-Resistant Hypertension, Baxdrostat, bmj, E MOTIVE STUDY PPH, lancet, nejm, Of-course, semaglutide, TRUNCATE TB |

HDL dysfunction & It’s clinical Implication

January 21, 2024 by dr s venkatesan

High-density lipoproteins (HDLs) represent a class of lipids, very heterogeneous in structure, composition, and biological functions .The density is between 1.063 to 1.210. It has at least 5 sub-types. Normal HDL level in blood should be above 35mg (50-60mg Ideal). When it goes beyond 60 there is not much benefit to accrue and also some surprise findings are there.(Article will be linked soon)

We know ,HDL carries free cholesterol from peripheral cells, including macrophages and endothelial cells. After reaching the liver, HDL receptors in the hepatocellular surface, metabolize it into bile acid or neutral lipids, which are excreted as bile and feces. This is the much famous Reverse Cholesterol Transport(RCT) and the anti-atherosclerotic effect of HDL .It must be emphasized apart from RCT, it has antioxidant, anti-inflammatory, antithrombotic, and vasodilator actions. Two good reference : One is a book ,that was a surprise . (Review article on HDL) (A text book on HDL )

Structure and shape

HDLs are real complex lipids occurring as pseudomicellar, quasi-spherical lipidomes. It has at-least 80 different binding sites for various proteins and ligands. APO A1 is the major apo-lipoprotein which mediates its action.

In one way, it looks like an International Space Station orbiting in the bloodstream, with multiple docking and releasing points. We are far away, from understanding the role and function of various molecules that get either activated or deactivated either in the circulation or inside the cells. Unlike other sub fractions of lipid, HDL evades routine imaging by NMR or X-ray crystallography. This is one of the reasons we find it to understand this molecule fully.

HDL : The untold story !

Despite the evidence suggesting a clear inverse relationship between HDL cholesterol concentration and the risk for cardiovascular disease, plasma HDL cholesterol levels do not predict the functionality and composition of HDLs. It can change color from good to bad with a drop of a hat in various clinical situations.

Ref : Bonizzi A, Piuri G, Corsi F, Cazzola R, M HDL Dysfunctionality: Clinical Relevance of Quality Rather Than Quantity. Biomedicines. 2021 Jun 25;9(7):729.

Types of HDL dysfunction :

A combination of obesity & diabetes has high chance of pushing this molecule into bad times. There is evidence, (primarily in this setting) HDL undergoes structural changes, and exhibiting pro-inflammatory, pro-oxidant, prothrombotic, and pro-apoptotic properties. (Sounds more ominous than LDL is it not ?)

Glycolysation of HDL

Diabetics results in systemic glycation of all cells or whatever molecule the blood bathes in. We also know the core pathology of diabetic micro angiopathy and basement membrane defects in various target organs are due to this. glycation.

It is very much understandable, HDL also becomes a victim. the glycated HDL is reprogrammed and forgets its good intentions. It not only loses its original function of cholesterol efflux, it ends up facilitating the pro-atherosclerotic forces, by shaking hands with the villain LDL. (Front. Cardiovasc. Med., 27 May 2022 Sec. Lipids in Cardiovascular Disease Eduardo Z. Romo  Volume 9 – 2022) 

A rigid HDL : The key to HDL function lies not only in its structure but also in the shape. It need to be flexible .It is expected to change its shape like a chameleon, while ferrying the cholesterol to liver. It has multiple shapes to choose from, discoid to double helix , spherical as and when required. A rigid HDL struggles to perform its action. Docking and alignment issues with ApO A 1 and A 2 is also contribute to the molecular dysfunction.

Link between HDL and platelet : We are getting more surprises with the multifaceted nature of HDL. Its been demonstrated HDL degrades PAF(platelet activating facto quicker) . hence ,a dysfunctional HDL can change the hematological milieu to pro-coagulant state. European Heart Journal, Volume 44, Issue 16 2023, 1394–1407, 

How to know whether my HDL is functioning all right ?

HDL sub-fractions, APO A 2 are not routinely measured as clinical tool. As of now, there is no practical tests to know it. No worries. If we start thinking about every molecules’ integrity (Just, we have few billions of it ) life will be made miserable. Be-calm, carry on with your work .Trust your HDL, it will remain good for you. Take care of all risk factors and lifestyles that is within your control. This piece is written for the cardiology fellows to understand , the dichotomy between CAD and dyslipidemia.

Final message

*We must admit, as scientists we have had little understanding about HDL. Still, to the public we have passed on a possibly erratic message that HDL is a hero in our fight against CAD. This is purely based on, one of its action i.e., RCT. Maintaining HDL level as per guidelines is good, but the reassurance given by that number can be a superfluous.

*Meanwhile, the concept of Non/dysfunctional HDL can not be taken lightly, since there is considerable evidence to suggest it might transform into a hazardous one in an undefined span of time. This explains the poor correlation between dyslipidemia and CAD risk. More comprehensive research is required to progress further in the field of lipid biology.

Reference

1.HDL Dysfunction Is the Answer in the Sphinx’s Riddle?* Juan J. Badimon, PHD, Carlos G. Santos-Gallego,  JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY VOL. 66, NO. 13, 2015

2.Eren E, Yilmaz N, Aydin O. High Density Lipoprotein and it’s Dysfunction. Open Biochem J. 2012;6:78-93. doi: 10.2174/1874091X01206010078. Epub 2012 Jul 27. PMID: 22888373; PMCID: PMC3414806.

3Camont L et al (2011) Biological activities of HDL subpopulations and their relevance to
cardiovascular disease. Trends Mol Med 17(10):594–603

4Gordon SM et al (2011) High density lipoprotein: it’s not just about lipid transport anymore.
Trends Endocrinol Metab 22(1):9–15

5.Corina Serban, Danina Muntean, Dimitri P Mikhailids, Peter P Toth & Maciej Banach (2014) Dysfunctional HDL: the journey from savior to slayer, Clinical Lipidology, 9:1, 49-59, DOI: 10.2217/clp.13.83

6.Adelheid Kratzer, Hector Giral, Ulf Landmesser, High-density lipoproteins as modulators of endothelial cell functions: alterations in patients with coronary artery disease, Cardiovascular Research, Volume 103, Issue 3, 1 August 2014, Pages 350–361, https://doi.org/10.1093/cvr/cvu139

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