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Archive for August, 2026

What happens to CAC score after statin therapy ?

Posted in Uncategorized, tagged , , , , , , on August 20, 2026|

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 multiple analyses, we have seen the CAC score consistently increase up to 30 % . We 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 CAC 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  an 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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2026 AHA /ACC dyslipidemia guidelines : What is new ?

Posted in Uncategorized, tagged , , , , , , , on August 19, 2026|

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

Posted in Uncategorized, tagged , , , , , , , , , , , , , on August 11, 2026|

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

Posted in Uncategorized, tagged , , on August 9, 2026|

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 seamlessly . 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-revenue alternative for patients who just don’t feel like swallowing a pill every day.

Final message : LACC is clearly a useless device , still you can use, 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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Which one of the following is “least important” virtue to become great doctor ?

Posted in Ethics in Medicine, Medical ethics, tagged , , , , on August 5, 2026|

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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Welcome to one more “Naming- ceremony” in CAD

Posted in Uncategorized, tagged , , , , , , , , , , on August 1, 2026|

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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