Dr.S.Venkatesan MD

What happens to CAC score after statin therapy ?

August 20, 2026 by dr s venkatesan

Patient No 1 :

“Doctor, you had  put  me on high dose statins since my CAC score was high. Now, my CAC is increased further. What is this ? should I not get anxious ?”

“No.Not at all . It is a good sign and it indicates your plaques are getting stabilised”

How is that possible ?

It is a therapeutic paradox. We start statins based on a CAC score in a low-risk population only to find the CAC score increase further in many people. In multiple analyses, we have seen the CAC score even increase up to 30 % . Feel happy about it, as we presume it is a sign of plaque stabilization.

That’s interesting Doctor. Now,.. Doctor, my dad already has a good CAC score of 300 , without statins he should be lucky , is it not ?

No you are wrong. “Natural CAC score is a marker of plaque burden, and we can never consider it as an index of stability, while the statin-induced high CAC score is absolute bliss &  index of pure stability“

Patient no 2 : My CAC is not increasing with statins , what to do ? Is it sign of statin failure ?

May be yes. I am not sure . It may indicate a poor response to statin and  inability to convert the plaques to its logical destination ie hardening and micro calcification.

Final message

Most coronary calcification whether God or statin made , imply that plaques are stable biologically. (Except the nodular /eruptive ones or those in  the shoulder region of the plaque, which can make a plaque physically stressed . Cardiologists  hate calcium essentially because, it is a hinderance to deploy a stent)

We rarely realise , how often we formulate important concepts in cardiology based on very superficial or incomplete knowledge

Reference

1.Dykun I, Lehmann N, Kälsch H, Möhlenkamp S, Moebus S, Budde T, Seibel R, Grönemeyer D, Jöckel KH, Erbel R, Mahabadi AA. Statin Medication Enhances Progression of Coronary Artery Calcification: The Heinz Nixdorf Recall Study. J Am Coll Cardiol. 2016 Nov 8;68(19):2123-2125. doi: 10.1016/j.jacc.2016.08.040. PMID: 27810054.

2.Henein M, Granåsen G, Wiklund U, Schmermund A, Guerci A, Erbel R, Raggi P. High dose and long-term statin therapy accelerate coronary artery calcification. Int J Cardiol. 2015 Apr 1;184:581-586. doi: 10.1016/j.ijcard.2015.02.072. Epub 2015 Feb 24. PMID: 25769003.

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Posted in Uncategorized | Tagged agatson score, cac score, dyslipdemia, indication for statin based on cac score, ldl, lipids, what happens to cac score after statins |

2026 AHA /ACC dyslipidemia guidelines : What is new ?

August 19, 2026 by dr s venkatesan

Eight point summary

1.PREVENT-ASCVD Equations: Replaces the older Pooled Cohort Equations with more accurate, contemporary equations for adults aged 30–79, establishing new risk thresholds to guide lipid-lowering therapy.

2.Reintroduction of Lipoprotein Goals: Returns to using absolute target goals for low-density lipoprotein cholesterol (LDL-C) and non-high-density lipoprotein cholesterol (non-HDL-C) to effectively monitor and guide treatment intensity.

3.Preferred LDL-C Estimation: Mandates the use of either the Martin/Hopkins or Sampson/NIH equations over the traditional Friedewald calculation to ensure superior accuracy across varying triglyceride levels.

4.Universal Lipoprotein(a) Screening: Recommends measuring Lp(a) concentration at least once in all adults to refine cardiovascular risk assessment, recognizing levels ≥125 nmol/L as a key risk-enhancing factor.

5.Targeted ApoB Measurement: Recommends measuring Apolipoprotein B to guide further treatment intensification once standard lipid goals are met, particularly in patients with diabetes, CKM syndrome, or elevated triglycerides.

6.CAC Score : Upgrades Coronary Artery Calcium (CAC) scoring to a Class 1 recommendation to guide decisions to withhold, postpone, or initiate therapy when primary prevention decisions remain uncertain.

7.Severe dyslipidemia : Standardizes the addition of non-statin therapies like ezetimibe, PCSK9 monoclonal antibodies, or bempedoic acid to maximally tolerated statins to reach aggressive absolute lipid goals.

8.Dietary Supplements Discouraged: Recommends against using over-the-counter dietary supplements (such as fish oil, cinnamon, garlic, or turmeric) to lower lipids due to inconsistent data and lack of proven clinical benefit.

Three questions

1.What are key difference between PREVENT vs PCE equations?

2.Which can be ranked as the the most important change in the new guidelines ?

LDL reduction with statins as primary prevention in low risk individuals , is a major change

3.Which can be termed as the most questionable recommendation ?

CT calcium scoring for identifying candidates for primary prevention.A CAC score Zero only is safe . The new guidelines say even if it is 1 , a moderate-intensity statin is reasonable to achieve a ≥30% to 49% reduction in LDL-C

Reference

Blumenthal RS, Morris PB, Gaudino 2026 ACC/AHA/AACVPR/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Dyslipidemia: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. J Am Coll Cardiol. 2026 May 19;87(19):2624-2757. doi: 10.1016/j.jacc.2025.11.016. Epub 2026 Mar 13. PMID: 41824590.

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Posted in Uncategorized | Tagged 2026 ACC/AHA GUIDELINES WHAT IS NEW ?, apo b 100, APO LIPOPROTEIN SMALL A, CAC SCORE ZERO VS 1, ESC LIPID GUIDLINES, inclisiran, PCSK, PRIMARY PRVENTION IN DYSLIPDEMIA |

Timing of valve replacement in AR vs MR : Why are they different ?

August 11, 2026 by dr s venkatesan

Timing of AVR and MVR in AR and MR has always elicited huge discussion in cardiology literature. Mind you, if the patient is symptomatic and there is LV dysfunction, it is absolutely easy to make a decision.Here, the question of timing doesn’t arise at all. (Of course, the symptoms and LV dysfunction should be confirmed to arise because of valve disease, not because of any other systemic disease, or LV dysfunction might be due to associated CAD. *I know a women who got her leakinging mitral valve replaced because she developed symptoms of dyspnea due to anemia .

Timing becomes a big issue only in patients with no symptoms at all. Some cardiologists put them on a treadmill. It is controversial, as anyone will develop symptoms. But , somehow, we should make it sure, patients are truly asymptomatic.

For long, we relying on some gospel echo parameters. I don’t how good they are. But , no one really knows,how and when the onset of LV dysfunction would be , and how it will progress. But, we are bound by the guidelines , as on today. There is some critical difference between the echo parameters , based on we intervene.

For mitral valve the threshold is lower. It needs early MVR for same degree of regurgitation as AR. It is proposed by the author for the benefit of fellows to easily remember the cut offs. It may be called as the 40:60 rule for MVR and 50:50 rule for AVR. The former denoting LVESD and later referring to LV EF %. The difference in echocardiographic thresholds arises because the two lesions cause fundamentally different hemodynamic loads on the left atrium and ventricle .(Read the legend in Image)

Final message

With mortality and morbidity for valve replacement steadily falling, it is likely more and more patients will be taken for surgery early. Of course, intervention guys are raring to go with percutaneous TAVR and TMVR, so the thresholds are expected to fall.

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Posted in Uncategorized | Tagged 40:60 rule for mvr, 50:50 rule for avr, acc aha esc guidelines for valvular heart disase, aortic and mitral reguritation, aortic regurgitation, dr svenkatesan, lv end systolic dimension in ar and mr, madras medical college, mitral regurgitation, optimal timing of avr and mvr, rule of thumb for avr and mvr, timing og avr and mvr in ar and mr, valvular heart disease, why normal ef is low is considered low in mr ? |

LAA device closure for AF : “Useless” or Use, less ?

August 9, 2026 by dr s venkatesan

Journal Club Review : LACC for AF

What is the brief conclusion of this important study from EUROPACE ?

This meta-analysis aggregates data from 6 randomized controlled trials involving over 7000 patients to answer a burning question. Should we aggressively plug LAA in lieu of OAC or DOAC in AF ?

The short answer from this meta-analysis is a resounding “no” if our primary clinical goal is preventing ischemic stroke

Link to the article

Some observations and comments about this study

For all those cardiologists and physicians who have huge trust on LAA closure for AF , this study delivers a remarkable reality check:

• The Stroke Incidence : The very purpose these devices are implanted is reduce it. But what happens ? Patients randomized to LAA closure suffered a 41% higher relative risk of ischemic stroke or systemic embolism compared to those on oral blood thinners.
• The Harm : In a 3-4-year follow-up period, the Number Needed to Harm (NNH) may not look significant. For every 100 patients given a shiny new implant, one additional patient will experience a stroke that a simple daily pill could have prevented.
• The Bleeding Trade-off: To its credit, LAAC successfully reduce the bleeding risk associated with OAC/DOAC

Will this study change the FDA approval and guidelines ? What will be the future of LAAC ?

No, Absolutely not. FDA is unlikely to react. It reviews devices based on their safety profiles for specific, indicated populations. Because these devices successfully reduce bleeding rates for patients with an absolute contraindication to blood thinners, their approval is legally and clinically sound.

The medical gadget eco-system works perfect. A device manufacturer proves that a LAA plug stops bleeding in a high-risk group. The device gets approved. Most of us fall for it and naturally shifts toward “liberal usage” as an easy, high cost alternative for patients who don’t want to take medication every day.

Final message 

It appears  LACC is  not a  useless device, but it need to  be used less .

With an estimated 400,000 implanted annually , it is too hard for us to say LAAC is useless. The future will inevitably bring next-generation devices with fancier anti-thrombotic coatings or redesigned plugs. Meanwhile, thousands of low-risk patients will continue to undergo unnecessary procedures , forcibly accepting the risk of increased stroke for the sake of convenience & glamor.

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Posted in Uncategorized | Tagged device management in af, laa device closure, watch man device |

Which one of the following is “least important” virtue to become great doctor ?

August 5, 2026 by dr s venkatesan

Which one of the following is least important to become great doctor ?

A. Compassion & Caring

B. Sincerity & Hard work

C. Knowledge & Skill

D.Honesty  & Integrity

Trying to answer

Yes I agree, It is brutal to frame such a question. If healing, and taking care of the suffering  mankind, is the primary purpose of the noble profession , after 4 decades in to the medical profession, realised a possible truth . “Knowledge and skills are vital, but sadly lags behind the other three by considerable distance” 

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Posted in Ethics in Medicine, Medical ethics | Tagged Hippocratic oath, medcial ethics, medical education, noble profession, who is a great doctor ? |

Welcome to one more “Naming- ceremony” in CAD

August 1, 2026 by dr s venkatesan

CAD : It is been called IHD, CCD, CAHD, CCS, etc. Now there is a new proposal from European Heart journal (with an Impact factor of 48 ) to change the nomenclature of chronic coronary syndrome to NAMIS : Non acute myocardial Ischemic syndrome (Ref 1)

What is the purpose & need to change the current terminology ?

The proposed AMIS and NAMIS classification shifts the clinical paradigm from coronary anatomy to myocardial function. For decades, terms like “coronary artery disease” overemphasized epicardial stenosis, neglecting the reality that ischemia frequently occurs without structural blockages. Data shows that up to 40% of symptomatic patients lack macroscopic obstructions, suffering instead from microvascular dysfunction, vasospasms, or myocardial bridges. This new term NAMIS can bring in the phenotypes like INOCA and MINOCA into the CCS without any conflict. Further, replacing vague adjectives like “stable” or “chronic” with “non-acute” reflects the high long-term residual risk of cardiac events. I also think, this new framework is meant to unify the European and American guidelines, where they use differing terminologies.

Counter Point : Do we really need this ?

Purpose of any new classification is , it should have a clear impact on patient management. But, we often find, scientific committees periodically take pride in changing the nomenclature akin to make a academic fashion statement .Within a few short years, we migrated from stable CAD to SIHD, switched to CCS , CCD etc . The fact is , for the patients it is the same angina for which they seek relief. They simply don’t bother whether doctor label their condition a syndrome or disease .

Reference

1.Boden WE, De Caterina R, Kaski JC, Bairey Merz N, Berry C, Marzilli M, Pepine CJ, Barbato E, Stefanini G, Prescott E, Steg PG, Bhatt DL, Hill JA, Crea F. Myocardial ischaemic syndromes: a new nomenclature to harmonize evolving international clinical practice guidelines. Eur Heart J. 2024 Sep 29;45(36):3701-3706. doi: 10.1093/eurheartj/ehae278. PMID: 39211956.

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Posted in Uncategorized | Tagged acc esc aha guidlines, ACS VS CCS, AMIS VS NAMIS, cahd, CCD, CCS, esc, EUROPEAN HEART JOURNAL, NOMENCLATURE OF CAD, nomenclature of heart disease, stemi vs nstemi |

“Apo A vs Apo (a) vs Lip (a) ” : Getting out of the notorious nomenclature trap in lipidology

July 27, 2026 by dr s venkatesan

It is an irony, we call the lipids as chief villains in the genesis of atherosclerosis and CAD. The fact of the matter is, it is the protein component that hides among the lipid jelly, with multiple folds and stinging tails, that ultimately help the LDL to penetrate the intact endothelium . These are called , apo-lipoprtiens. The fate of lipid molecules is determined by these apparently humble looking proteins .It must also be noted the even the goodness of HDL vanish if its apo-liprotein fails to co-operate . The Apo proteins are labeled differently in each sub fraction of lipids. Its Apo A 1 in HDL Apo B 100, in LDL and Apo C in VLDL.

Playing with English Alphabet A

Scientists can be casual , though not intentional when naming newly detected molecules. The major nomenclature issues are with Apo A , Apo a , Lip a These three entirely separate proteins with nearly identical names, should not be confused with. A subtle shift between a lowercase letter and a capital letter completely changes the meaning, taking us from a highly dangerous cardiovascular risk factor to a healthy, protective one.

Apolipoprotein A : This is a highly beneficial protein that defines the HDL function.(Ofcourse one must remember too much of HDL can be toxic as well .In fact when it exceeds 60 mg ,it will become dysfunctional, rather harmful.This is the U curve phenomenon of HDL)

Apolipoprotein(a) : This is the sticky, genetically fixed protein tail found only on Lipoprotein(a). It promotes blood clotting and triggers arterial inflammation.

Lp(a) : It is formed when a single Apo(a) protein tail binds to the Apolipoprotein B-100 (ApoB) wrapper of a standard LDL like particle. Because of this hybrid structure, Lp(a) possesses dual pathogenic properties. LDL core delivers cholesterol into the arterial wall, while the attached Apo(a) tail promotes localized inflammation and thrombosis . Lp(a) plasma levels are strictly determined by inheritance and remain highly stable throughout an individual’s life.

Lipoprotein(a) structure. Lp(a) is composed of two parts: one part is low-density lipoprotein (LDL)-like particles with apolipoprotein B100 (apo-B100), and the other part is the stinging tail apolipoprotein a [apo(a)]

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Among the above three molecules, lipoprotein(a) is the celebrated one kept in the limelight. It is strongly determined by genetics and is a predictor; rather, we can call it a marker of LDL virility (like Apo B 100). It is entirely produced in the liver, its level is claimed to be static lifelong. Obviously, it cannot be true, as it would heavily dependent on liver function. Further, different vendors have come into the market with this, and they have different normal ranges.

Final message

When reading the lipid molecules, please focus on the English . A capital A vs. small a makes a huge difference between harming and healing the patient. Of course, we must be thankful, as of now, we have don’t have no small b or small c Apolipoproteins in lipidology.

Reference

Tsimikas S. A Test in Context: Lipoprotein(a): Diagnosis, Prognosis, Controversies, and Emerging Therapies. J Am Coll Cardiol. 2017 Feb 14;69(6):692-711. doi: 10.1016/j.jacc.2016.11.042. PMID: 28183512.

Patel AP, Wang (汪敏先) M, Pirruccello JP, Ellinor PT, Ng K, Kathiresan S, Khera AV. Lp(a) (Lipoprotein[a]) Concentrations and Incident Atherosclerotic Cardiovascular Disease: New Insights From a Large National Biobank. Arterioscler Thromb Vasc Biol. 2021 Jan;41(1):465-474. doi: 10.1161/ATVBAHA.120.315291. Epub 2020 Oct 29. PMID: 33115266; PMCID: PMC7769893.

Lipid particle science

https://www.jacc.org/doi/10.1016/j.jacc.2023.11.008

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Posted in Uncategorized | Tagged apo A, Apo A 1, apo lip a, apolipoproteins |

The Invisible “solo fighter” for the NEET reforms in India !

July 24, 2026 by dr s venkatesan

India is sort of burning, with students on the streets for exam reforms.The problem started with the leakage of question paper for National Entrance and eligibility test for medical college( NEET) Government is on the back foot. The prime minster has come out, assured the students and their concern will be taken care of. Yes, it is true greedy cartels are exploiting the system. But, we are ignoring a big hidden moral failure in the whole issue.

However, It is very convenient to march through the streets pointing fingers at the state, but blaming the government alone is not enough to fix a rotting system. We love to demand absolute structural perfection from institutions while completely ignoring the mirror of reality. It is us, the public that fuel and maintain the corruption supply chain through a collective, desperate willingness to bypass merit at any cost.

Let’s be honest, even a un-breachable testing infrastructure cannot save an education system where parents and students are actively looking for illegal shortcuts. When families willingly treat leaked question papers as a premium commodity, they are not victims they are the core investors funding the black market. I wished, I could find at-least one banner conveying this fact too.Unfortunately, it can never happen.

True reform cannot happen through government orders alone. It requires a brutal confrontation with our own societal hypocrisy and a complete dismantling of the demand side of corruption.

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Posted in Uncategorized |

How often TAPSE misses RV dysfunction ?

July 16, 2026 by dr s venkatesan

TAPSE the most celebrated RV function index misses significant Right Ventricular (RV) dysfunction in an estimated 30 to 50% of patients. ( when relying solely on it).It fails to detect underlying impairment because it only measures the longitudinal shortening of the RV base, largely ignoring global chamber contraction.

Mechanism attributed to the unreliability of TAPSE

• Ventricular Interdependence: The RV motion is influenced by left ventricular function by the shared IVS contraction.
• Chronic Volume or Pressure Overload: Conditions like severe tricuspid regurgitation or pulmonary hypertension cause the RV to alter its contraction geometry. This leads to “pseudo-normalization, of TAPSE” it remains >1.7 cm despite dysfunction.
• Post-Cardiac Surgery: In patients who have undergone procedures involving pericardiotomy, TAPSE often drops drastically as post pericardiotomy the RV radial function exccedds longitudinal
• Loading Dependency : TAPSE is highly influenced by preload and afterload conditions.

The following table summarises the various components and it’s contribution to RV contractility.

*Contrary to the popular belief, there is overlap between free wall contraction and longitudinal contraction. In fact, there is no clear definition for RV free wall. Logic tells us, any part of RV which is not formed by IVS can be considered free.

*Importantly, Longitudinal contraction has a two components free wall as well as a septal axis. TAPSE measures only lateral or free wall component of longitudinal function. It is less influenced by septal long axis function.

*The long axis function of RV is influenced indirectly by the LV function also as both AV valves are attached to same ring.

*If we want to assess pure RV function the best index is RV free wall circumferential or radial contraction or strain.

*In various clinical situations like PH or acute pulmonary embolism the pressure distribution is non-uniform making the assessment of RV function difficult. Fractional shortening of area is a fair index.RV wall motion abnormality can be subtle yet a serious marker of RV dysfunction.

Final message

RV function assessment is complex and often incomplete. The habit of relying only on TAPSE, is not a high quality scientific practice.

Postamble : Apart from the contractile function, we don’t know at what RV pressure RV begins to dilate. This is different in acute vs chronic elevation. We also don’t know which patient will show RV hypertrophy, and which group prefers dilation. May be, all these are academic and has little significance at the bedside. However understanding this is essential to assess the response to RV inotropes and newer RV assist devices.

Reference

1.Nonaka H, Rätsep I, Obonyo NG, Suen JY, Fraser JF, Chan J. Current trends and latest developments in echocardiographic assessment of right ventricular function: load dependency perspective. Front Cardiovasc Med. 2024 Jul 1;11:1365798. doi: 10.3389/fcvm.2024.1365798. PMID: 39011493; PMCID: PMC11249019.

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Posted in Uncategorized | Tagged RV function, rv strain, TAPSE |

The tough task of reversing cardiac Amyloidosis : Classification of “Anti-Amyloid”drugs

July 11, 2026 by dr s venkatesan

Amyloidosis is a proteostatic disease , meaning a progressive disorder of extracellular deposition of insoluble protein fibrils in tissues.It affects , brain, kidney, nerves and almost any organ.Crucially, amyloid is an interstitial disease, accumulating strictly in the spaces between cells rather than inside them. This interstitial buildup exerts physical pressure, alters tissue architecture, and finally invading the cell and hence the organ function.

The primary culprit is a normal transport protein   transthyretin (TTR) (same as prealbumin) It is synthesized in the liver as a stable, four-part tetramer structure that safely circulates in the blood. Under stressful or aging conditions, this tetramer destabilizes unstable monomer pieces. These monomers undergo misfolding, polymerizing into rigid cross-beta-sheet amyloid fibrils. These abnormal ATTR fibrils escape cellular degradation.

Cardiac amyloidosis

Cardiac amyloidosis , presents as mainly as restrictive cardiomyopathy, but can be seen in any chronic heart failure associated with LVH, especially in Aortic stenosis, where it can involve both the valve and myocardium.There are multiple reasons why we diagnose amyloidosis more often than before. But , one thing is sure, it is not due to increasing incidence in the population , but more of a high awareness and availability of advanced cardiac imaging .

Image source : Agha AM,. Role of cardiovascular imaging for the diagnosis and prognosis of cardiac amyloidosis. Open Heart. 2018;5:

What is the confirmatory test for Amyloidosis ?

It was classically diagnosed by tissue biopsy with Congo red staining, showing “apple-green” birefringence under polarized light microscope. Mass Spectrometry, Immunofluorescence is then used to decode the protein composition. Currently , with typical patterns of cardiac imaging we can diagnose with confidence without biopsy. While echocardiography is good enough , MRI and technetium-99m pyrophosphate scans are crucial.

What are the specific treatment option for amyloidosis ?

Until recently, Amyloidosis, has been considered as irreversible degenerative disease .Now we have strategies to reduce progression or even regress the Amyloid deposition. Many drugs are still being studied with varying success.

Following table summarise the different pharmacological modalities to tackle Amyloidosis.

Final message

A limitation of currently approved anti-amyloid medication such as Tafamidis or Onpattro , is that it cannot be reversed and only be prevented.Emerging technologies like monoclonal antibody depleters hold promise to actively clear out existing deposits, potentially turning it to a truly reversible condition. Chronic fibrotic pathways from triggered fibroblasts are closely linked to Amyloidosis. Hence, antifibrotic drug research should go hand in hand with Amyloidosis.

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Posted in Uncategorized | Tagged acoramidia, amvuttra, amyloidosis, attr amyloid, best review article on amyloidosis, cardiac amyloidosis, classification of anti amyloid drugs, congored, coramitug, doxycycline for amyloidosis, onpatttro, pyrophosphate scan for amyloid, restrictive cardiomyopathy, tafamidis, tegsedi, ttr silencers, ttr stabilizers, wainua |

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