In India , today 20th october 2026, is the festival of Vijyadashmi , the day goodness prevailed over evil .It is also celebrated as a process of searching the inner truth in all aspects of life .On this day I would like to share a enlightening lecture about our profession.
Ever since Hippocrates defined the principles of scientific medicine in the noble profession, along with the growth and development of technology, we have seen it all. Now we can treat any number of illnesses with much perfection. If an organ misbehaves, we can even dispose it out and implant an artificial or a new one from another person. Still, the health of mankind is on the edge. Why ? Millions of people with real disease continue to suffer from ill health due to a lack of basic care, mean while otherwise healthy people are facing a serious threat tothier well being from medical excess, making the growth of science almost irrelevant Today, an MD is a master of medicine, but they largely remain a slave to science and technology With AI sitting right under across our head, it is a matter of time before we lose the last bit of our thinking faculty
Through this lecture, Professor S.S. Kothari, the former HOD of Cardiology at AIIMS, provides an exemplary and brutally honest exposition of status of medical profession , accumulated over half a century.
Yes, it is a provocative study with important health data of 65,364 persons published in the American Journal of Preventive Medicine.It sort of, censures the traditional epidemiological paradigms suggesting a “wealth paradox” . High socioeconomic status in India comes with a hitherto unknown (but strongly suspected) downside and a possible new CVD risk factor.This is In contrast to Western nations where affluence tends to protect against CVD .
Glad this article went mainstream in India and appeared in today’s The Hindu, India’s national newspaper. It will definitely create greater awareness about the topic of wealth and CVD risk (Ref 1).
This longitudinal population based analysis revealed that 40% of participants maintained sustained wealth, while 19% remained poor, and 20% each documented either upward or downward mobility in wealth status. The study revealed a surprising fact. The sustained cohort faced a staggering 1.70 times higher odds of myocardial infarction and cardiac failure compared to the sustained poor.
What is not addressed in this study?
It seems highly plausible there could be a screening bias. In developing healthcare infrastructures, affluent populations possess superior healthcare literacy and financial access, leading to higher rates of clinical detection and self-reporting. (In India, it is called a “Master Health Check-up”—who the master is, we do not know!) Conversely, subclinical cardiovascular pathology among the poor often goes undiagnosed, or the first episode might present as a fatal ACS, skewing the relative risk data.
The new economic J-curve of CAD in India
It is clear , Indian CAD population represents a J-curve (or even a U-curve) of epidemiological transition . Past data from western economies told the same story. .CVD risks were concentrated among the wealthy who adopt sedentary lifestyles, physical inactivity, and hyper-caloric diets. As a country transitions into a mature economy, this curve flattens and ultimately reverses, as seen in Western populations. This happens because public health interventions reduce risks among the wealthy, while the commercialization of cheap, processed foods shifts the metabolic burden onto the poor (the dogma of “the rich are thin and healthy, and the poor are obese” seen in highly developed countries).
India currently sits at the peak of this curve. The irony in India is that the rich are flocking to McDonald’s and Burger King with pride. I am not sure when the aforementioned transition will fully happen. Managing the side effects of economic prosperity is no longer optional; it is a social compulsion.
Welcome wealth to your home, but allow wisdom to enter first
This epidemiological transition must not be mistaken as Health vs wealth vs poverty debate. The strong belief that the affluent people will emerge healthy as economies mature is a risky illusion.Meanwhike, both the wealthy and the poor should be aware of how our lives get spoiled by external forces in the name of life style. For a healthy life, remove “style” from your life.
We know , south Asians have unique lipid profile where most of them have normal LDL levels. In spite of the fact, LDL is our primary target. Why ?
So, this question is being asked .Does low LDL lowers the CAD risk consistently , in south asians ?
The simple answer is : NO. To justify this we don’t require any long explanation . Just few ounces of common sense is suffice. CAD is multifactorial , polygenic disorder. A high LDL per se may be harmless , unless it is whipped by BP spikes over a sugar coated endothelium. Also, it is widely accepted , like the traditional coronary risk factors , we must have many Invisible coronary protective factors ( Both geno & phenotypic protection eg empty shelled LDL etc )
Meanwhile, it is baffling , to note , up to 25 % of ACS patients do not have single traditional cardiac risk factor ? So, It is very clear, our current scientific data ( also thought process ) looks superficial. Still, we are happy to enforce dogmatic guidelines targeting LDL in isolation forgetting Apo-B and lip(a) etc.
Now let us enter the scientific Arena.
Does low LDL lowers the CAD risk consistently , in south Asians ?
The answer is a definite yes. (But it requires a long explanation )
South Asian populations ( India, Pakistan, Bangladesh, Sri Lanka, and Nepal) experience a disproportionate and premature burden of atherosclerotic cardiovascular disease (ASCVD). The landmark global INTERHEART Study demonstrated that dyslipidaemia is the single strongest population level risk factor for acute myocardial infarction in South Asians.The extensive clinical and pathophysiological evidence justifying aggressive lipid-lowering and the mandatory use of statins in this population is structured below.
1. The Pathophysiological Paradox
Standard lipid panels can be deceptive in South Asian individuals. A patient may present with what appears to be “normal” or only mildly elevated low-density lipoprotein cholesterol (LDL-C), yet remain at an incredibly high risk for a major adverse cardiovascular event (MACE).
Atherogenic Dyslipidaemia: Driven by systemic insulin resistance and visceral adiposity (the “thin-fat phenotype”), South Asians exhibit a triad of elevated triglycerides, profoundly low HDL-C, and high concentrations of Apolipoprotein B (ApoB).
Small, Dense LDL Particles: Even when total LDL-C numbers mimic a low-risk profile, South Asians possess a vastly higher concentration of small, dense LDL particles. These particles are highly atherogenic because they easily penetrate the arterial wall, have a prolonged circulation time, and oxidize rapidly, accelerate plaque formation.
Elevated Lipoprotein(a): South Asians have a genetically determined, elevated baseline of Lipoprotein(a) or Lp(a), a powerful independent risk factor for CAD. Because Lp(a) contains an LDL particle, lowering the background LDL-C as aggressively as possible is critical to tackle this non-modifiable risk.
2. Clinical Trial Evidence: Why “Lower is Better” even in South Asians
The principle of “lower is better” for LDL-C is universally proven by the Cholesterol Treatment Trialists’ (CTT) Collaboration, which established that every 1 mmol/L (38 mg/dL) reduction in LDL-C yields a consistent 22% reduction in major vascular events. However, for South Asians, this non-linear benefit applies even more due to their higher absolute baseline risk.
Absence of a Lower Limit Threshold: Large-scale data from international trials (ADA ) confirm that the cardiovascular benefit of reducing LDL-C continues linearly to very low levels , without a threshold where the benefit stops.(Zero LDL?)
The Power of Primary Prevention: Epidemiological registries consistently show that long-term statin therapy in South Asians reduces MACE, all-cause mortality, and coronary revascularization procedures across all risk groups including to those traditionally deemed as “low risk” by standard Western calculators.
3. Statin Mandates in International and Regional Guidelines
Because traditional risk calculators (like the US Pooled Cohort Equations or Europe’s SCORE) routinely underestimate ASCVD risk in South Asians, modern medical guidelines have adapted to mandate earlier and more aggressive statin implementation.
4. Maximizing Statin Safety and Pharmacokinetics
Equivalent Lipid-Modifying Efficacy: Head to head clinical evaluations show that standard doses of atorvastatin and simvastatin reduce LDL-C and optimize HDL-C fractions in South Asian patients just as effectively as the western popualtion.
Dosing: While east Asian populations possess clear genetic variations ( ABCG2 polymorphisms) that increase statin blood concentrations and require lower therapeutic doses, South Asians display different metabolic profiles. They safely achieve optimal target lipid goals using standard clinical guidelines.
Summary
For South Asians, lowering LDL cholesterol confers a direct protection against premature, aggressive coronary artery disease without doubt. Statins play a critical role in it.
Asymptomatic severe aortic stenosis remains a tricky and delicate decsion making process for the cardiologists. A fine balance of clinical assessment and indication as well as the academic and also peer prssure for an immedaute fix, that now includes non surgical TAVR.In fact with the arrival of TAVI , the decsion making has become much more complex .It is an invisible stastical abttle between succes , failure and complication rate vs sitting idle and watchfuly waiting.
Proponents of early surgery are on the edge, backed by the results of trials like RECOVERY and AVATAR .TAVI guys are smiling .Ofcourse , they can argue that timely intervention preempts irreversible myocardial fibrosis, sudden cardiac death, and failure.
The conservative* “wait-and-watch” approach cardiologists need not feel guilty or looked down upon. They rely on stringent clinical and echocardiographic surveillance. This strategy protects asymptomatic individuals from the immediate risks of perioperative mortality, prosthetic valve degeneration, and lifelong anticoagulation. *Conserves what ? (Valve, life , money ?)
Amidst this difficult debate, the landmark EVOLVED study from Scotland UK, stands out . By utilizing cardiac MRI to detect midwall fibrosis, EVOLVED demonstrated that routine early surgery based strictly on statistical thresholds does not universally superioritize outcomes over high-quality surveillance. Instead, it highlighted that meticulous clinical acumen and symptom tracking remain paramount.
Final message
Lack of data appear bad science , but datas can be deadly too. Some how , data will always push for early intervention . EVOLVED trial is unique .It proves that clinical acumen-based indications will prevail over technology . It sort of reminds us the principle of primum non nocere (first, do no harm), every patient should earn their procedure due to developing meaningful symptoms, rather than hospitals trying to earn out of patients.
Reference
RECOVERY Trial: Kang DH, Park SJ, Lee SA, Kim YJ, Kim DH, Kim HK, et al. Early surgery or conservative care for asymptomatic aortic stenosis. N Engl J Med. 2020 Jan 9;382(2):111-119. doi: 10.1056/NEJMoa1909883. PubMed PMID: 31733181.
AVATAR Trial: Banovic M, Putnik S, Penicka M, Doros G, Deja MA, Kockova R, et al. Aortic valve replacement versus conservative treatment in asymptomatic severe aortic stenosis: the AVATAR trial. Circulation. 2022 Mar 15;145(11):797-808. doi: 10.1161/CIRCULATIONAHA.121.057639. PubMed PMID: 34779220.
EARLY TAVR Trial: Généreux P, Piazza N, Alu MC, Nazif TM, Hahn RT, Pibarot P, et al. Transcatheter aortic-valve replacement for asymptomatic severe aortic stenosis. N Engl J Med. 2024 Oct 28;391(22):2111-2122. doi: 10.1056/NEJMoa2405880. PubMed PMID: 39466903.
EVOLVED Trial: Loganath K, Greenwood JP, Plein S, McCann GP, Berry C, McConnachie A, et al. Early intervention in patients with asymptomatic severe aortic stenosis and myocardial fibrosis: the EVOLVED randomized clinical trial. JAMA. 2024 Oct 28;332(20):1741-1750. doi: 10.1001/jama.2024.22557. PubMed PMID: 39466640.
Electrophysiology, we believe, is a field that contains a gamut of disorders of rate and rhythm defects, congenital or acquired, right from the SA node to the Purkinje fibers.The core principle of EP is interwined with LV function and preventing all preventable electrical SCD , should be be our primary aim. Unfortunately, nowadays if you open any EP journal, you will wonder whether electrophysiology is all about atrial fibrillation and pulmonary vein ablations.
Here is a table comparing the space allotted to AF and various ablation techniques in major EP journals between the years 2025 and 2026. It is clear that EP science is heavily biased towards AF. Meanwhile, PFA may be a genuine innovation in tissue ablation, but its overwhelming dominance in the EP literature is not acceptable and not in the best interest of patients.(Cryo and RF should not succumb to this inflated superiority of PFA) *The PACE journal should be appreciated as it seems to resist the peer pressure to promote pulsed field ablation (PFA).The editors deserve some complements.
Final message
Cardiac arrhythmias in ischemic structural heart disease are more critical than the more benign and nuisance arrhythmia of atrial fibrillation (AF), which can be effectively managed in 90% of the population with simple drugs and anti-arrhythmiclifestyle modifications.
An appeal to all stakeholders: Let us take a pause and bring back the original charm of electrophysiology (EP). Let us be inclusive.There are many more areas of crucial importance. Keep an upper limit for AF-related articles—maybe a maximum of 20% (even this appears liberal).
Bendopnea is a newer addition to the special forms of dyspnea, such as platypnea and trepnea.( Not exactly new .It was first reported by Jennifer T. Thibodeau from Texas in 2014 ) Though it initially appeared to be an inconsequential symptom, subsequent observations from many patients with heart failure have made this symptom highly significant. It seems to be a marker of high risk for decompensation. It occurs within 30 seconds of bending. In a patient with an already elevated left ventricular (LV) filling pressure, the act of sudden bending adds more stress by increasing the mean left atrial (LA) pressure further. A precise mechanical explanation for this phenomenon is not available.
The current literature attributes bendopnea to increased intra-abdominal pressure from bending forward, which pushes the diaphragm upward and forces congested splanchnic blood into the chest, causing a sudden surge in central venous return and pulmonary capillary wedge pressure. However, this fluid-shift mechanism does not explain why bendopnea correlates poorly with body mass index or abdominal girth.(Ref 1 the original paper do have BMI data)
The Mechanism of Bendopnea
The left atrium is the superior-most chamber of the heart in an erect posture, maintaining a strict superior-inferior relationship relative to the left ventricle.
Please realise a subtle relationship of LA to LV . LV may be the most crucial chamber of heart, but LV remains anatomically Inferior , that confers the humble LA, with some commanding powers over LV, especially in patients with LV compromised states.
In this upright position, LV filling is naturally assisted by gravity.When a patient bends forward more than 90 degrees, the LA-LV spatial relationship shifts from a vertical orientation to an almost horizontal one. Because of this shift, LA filling loses its gravitational advantage. The pressure must momentarily rise higher to compensate, resulting in acute stretch of the LA, pulmonary veins (PV), and J-receptors causes immediate dyspnea.
Clinical Implications
Though bendopnea is reproducible in many individuals, some patients can become accustomed to the sensation over time. Numerous papers also suggest that bendopnea serves as an excellent clinical marker for HFpEF, RV dysfunction, or pulmonary hypertension.
Final Message
Bendopnea is interesting new symptom . It is clear it can have multiple mechanisms. Posture-induced alteration in the LA-LV axis and the sudden elimination of gravity assistance can be an important factor in triggering dyspnea on bending. This can easily manifest in patients with advanced heart failure who have already exhausted all of their cardiac reserve mechanisms.
Reference
1.Thibodeau JT, Turer AT, Gualano SK, Ayers CR, Velez-Martinez M, Mishkin JD, Patel PC, Mammen PP, Markham DW, Levine BD, Drazner MH. Characterization of a novel symptom of advanced heart failure: bendopnea. JACC Heart Fail. 2014 Feb;2(1):24-31. doi: 10.1016/j.jchf.2013.07.009. Epub 2014 Jan 8. PMID: 24622115.
2.Karauzum K, Karauzum I, Kilic T, Sahin T, Baydemir C, Baris Argun S, Celikyurt U, Bildirici U, Agir A. Bendopnea and Its Clinical Importance in Outpatient Patients with Pulmonary Arterial Hypertension. Acta Cardiol Sin. 2018 Nov;34(6):518-525. doi: 10.6515/ACS.201811_34(6).20180528A. PMID: 30449993; PMCID: PMC6236562.
Postamble
Can bendopnea occur in a patient with a normal heart and normal LV function?
Yes, and here begins the problem. Many deconditioned, sedentary individuals do develop bendopnea. This is due to signals from the peripheral muscle spindle reflex. This condition is largely benign, but it implies that the person needs to improve their physical conditioning.
Today , September 29th is the World heart federation, backed official World Heart day.
Reclaiming the Soul of World Heart Day
Have you ever wondered why cardiologists, physicians, and big hospitals celebrate World Heart Day in a most sacred way as if it is festival of Diwali, Dussehra, or Onam? The scale of these celebrations and the accompanying mainstream media blitz have become truly overwhelming.
Originally, this day was meant to create genuine awareness about the rising global epidemic of heart disease. It was designed to propagate healthy lifestyle choices among the public and protect vulnerable hearts.
But it does not stop there. There is a concealed interest public rarely sees. Although we often emphasize that prevention is preferable to a cure , the explosive growth of high-tech diagnostics and aggressive therapeutic modalities has ironically become theenemy of true preventive care. World Heart Day has increasingly been hijacked as a marketing to drive hospital footfalls rather than to create true wellness.
The much glamourised , gadget based diagnostics , advanced screening packages, & biochemistry based “preventive heart checkups” have not yielded the desired results. In fact, by creating unnecessary anxiety and over diagnosing minor anomalies, they can have the exact opposite effect. As custodians of health, we must shift the focus away from lucrative diagnostic packages and return to the simple, low-cost fundamentals of diet, exercise and lifestyle modification.
I think, on this world heart day , We should make the public realise, it is absolutely possible they can prevent a heart attack in their life time, without fearing about their calcium scores, exotic lipid sub fractions or CT angiograms. Let us reclaim World Heart Day as a forum for genuine public health, not a corporate festival.
In the clinical practice of cardiology, some times, we are compelled to check our foundational concepts and refresh or reset the knowledge. Here is a two question challenge. The first question was in fact asked by one of my patients. Does negative TMT rule out CAD ? I thought it was a routine question, and told him no tests rule out CAD 100 % perfectly. It has only 70% accuracy. Some time later, after his consult , I was pondering over this 70 % accuracy . Very soon I realised , I was totally wrong with that answer as well. You can try to find the real truth about the validity of TMT in ruling out CAD.
1.Does negative TMT rule out CAD ?
A.No, It doesn’t
B.Yes, it rules out all significant CAD
C.Yes, it rules out obstructive CAD
D.No. It doesn’t rule out non-obstructive CAD .
Answer : To get the correct answer, go to the following question. (Response A,C,D are correct .B might appear right too , but it’s wrong.)
2.Which lesion often result in ACS in CAD population ?
A.Obstructive
B.Non obstructive
Answer : Both, (In fact, non obstructive CAD more often precipitates an ACS, because they are more in numbers)
So, what is the message from these two questions ?
TMT is in reality not useful to rule out ACS prone CAD. To include it in routine master health has little meaning , if that message is conveyed to our patients. (Of course a negative TMT rules out a severely obstructive lesion , that is really be a comforting news)
Read this Editorial from Dr Prem Pais for more insights.
Final message
What is significant CAD ? we can play with this word as long as we want. In the popular cardiology parlance , the word significance revolves around the flow limiting capacity only . So, be clear .The fact of the matter is, TMT can never rule out the presence of non flow limiting, ACS prone lesions at any level of exercise loads/METS . Hence the 70-80 % negative predictive value , we confer to it, is clearly misplaced in terms of ACS risk.
Wellens’ syndrome represents a unique pathophysiological subset in ACS. While typical ACS is characterized by dominant thrombotic luminal occlusion, Wellens’ syndrome is a prototype for a low-thrombus-load .Curiously it can even be termed as “Zero thrombus” ACS. This is not a new revelation. It was underscored by de Zwaan and Wellens in their original landmark 1989 angiographic study of about 180 patients. Notably, angiography performed days after stabilization revealed a ubiquitous absence of any visible, active thrombus burden. Instead, most of patients showed a severe, fixed mechanical stenosis ( 90-100 %) in LAD , some of them showing good collateral circulation.
However , the temporary total occlusions that cause the rest angina are either due to transient thrombus or dynamic epicardial vasospasm that make the occlusion complete , only to reopen later to maintain the UA/NSTEMI status.
*Quantifying the content of the lesion in ACS is tricky . STEMI we know there is definitely thrombus dominates. In NSTEMI it is combination of both . But in Wellens , it is pre-dominatly mechanical for sure.
Clinical implication of low thrombus load
While the original study by Wellen’s did not mention about thrombus at all, the OCT based study Arteaga et al from Mexico documents thrombus in only about 20%.
OCT image shows significant, eccentric, lipid-rich plaque in a patient with Wellens ( Ref 3)
This raises a highly provocative clinical question. If a meaningful thrombus burden is fundamentally absent during the stable phase of of Wellens , do these patients truly derive any clinical benefit from aggressive heparin infusions and dual antiplatelet therapy (DAPT)? It is still more concerning, many of text call Wellens as STEMI equivalent or occlusive myocardial infarction , suggesting a huge thrombus load which it rarely show.
Final message
Wellens’ syndrome demands better clinical , pathological and therapeutic reasoning.It probably demands an urgent PCI Some times, we have labelled them as refractory UA go on to receive given 2B -3A blockers* as well increasing the bleeding risk .The lesson learnt is , aggressive anti-thrombotic strategy is largely out of place and risky in Wellens.(Ironically, after the stenting the patient will require rigorous anti-platelet agents )
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