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 defaultstrategy 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.
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.)
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.
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,
CanI 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:
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.
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.
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.
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.
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)
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, Awould 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 ?
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 .
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 hatin various clinical situations.
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.
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
*Wemust 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.
A cath lab is an “optional accessory” in the management of Acute coronary syndrome (ACS).
True or False ?
Answer
“Without a CCU…you can never, treat any Acute coronary syndrome … while we can treat most ACSssuccessfully without a cath lab “ (If you still got the answer wrong …sorry, no comments)
Best comment
Accessory is ok , but it is “20% foolish” to state cath-lab is optional, it should be mandatory.
What will happen if you happen to thrombolyseWellen syndrome?
Will evolve into STEMI by prothrombotic trigger of lytic agent
ECG will get normalised with clinical stability in some
Nothing happens. ECG will remain same.
Worsen the situation in majority
Will be severely reprimanded by your consultant and peers.
Answer:
4 will be answer for most of us , while 2 and 3 is a lesser, but distinct possibility. I have never seen 1 happen .Whatever is the correct answer , response 5 will always be correct.
What is the criteria to diagnose Wellen syndrome ?
The criteria used to diagnose Wellen syndrome include symmetric and deeply inverted T waves or biphasic T waves in leads V2 and V3 in a pain-free state, plus isoelectric or minimally elevated (<1 mm) ST segment. In addition, the criteria require the absence of precordial Q waves, the presence of history of angina, and normal or slightly elevated cardiac serum markers.
Wellens is a glorified subset of ACS. It can be referred to as an ACS in a confused state of evolution. Most often a critical mechanical LAD lesion is noted. Thrombus, by no means is excluded. This is the reason some times lytics work. Spasm of epicardial coronary artery is also part of the problem. Since Wellens patients exhibit dynamic symptoms akin to their T waves (often in an inverse relation), it is natural that cardiologists are also tentative, especially if these patients have hypertension and LVH as well.
1.How to manage Wellen syndrome?
Majority of Wellens end up as NSTEMI, statistics tells us about 20% of them can be STEMI in incognito mode demanding lysis or emergency PCI. Since lysis is harmful in subtotal occlusion, it is safe to take all Wellens to cath lab and decide thereafter.
2.Is Wellens exclusive to LAD ?
No. RCA and LCX Wellens do occur, making this entity’s perceived unique importance less certain
3.How common is thrombosis in the culprit artery of Wellen syndrome ?
It is generally believed it is more of a mechanical plaque lesion. However by no means, we can say thrombosis do not occur. This is the reason lytics sometimes work , though we argue it as apparent contraindication.
4.Is there a benign face of Wellen syndrome ?
Yes, we believe so. If Wellen presents as evolved Non -Q-MI or as evolved NSTEMI, a term most cardiologist will not agree with existence of such a terminology .(Clinically, stabilised unstable angina also falls under this category)
Final message
It is curious truth, even fearsome STEMI can be effectively managed without knowing the coronary anatomy (with thrombolysis) ,while Wellen’s a lesser emergency demands more urgent knowledge of coronary anatomy .
15 % of body weight is fat. (10kg) Out of which just 250 mg of cholesterol is streaming in blood. We must understand fat, lipid and cholesterol are different entities. LDL is obviously a target against atherosclerosis. While the total body fat seems to do little in determining blood cholesterol levels, what is more scientifically shocking is the slope of curve between blood LDL levels and plaque burden is rarely linear. Mind you, LDL constitutes .000025% of total fat. We have many other targets in dyslipidemia like free cholesterol, harmful fatty acids, remnant cholesterol, TGLs, dysfunctional HDLs
LDL is not innocent
Cone electron microscopic Image : A macrophage after a diet full of LDL molecules
There are innumerable evidence for LDL, being the enemy number one in human atherosclerosis .It don’t know but, it fully deserve the name bad cholesterol.It looks like it may be counting its last few decades, as the whole pharma industry is activated to destroy this physiological molecule that carries some critical functions in our body. In one of the hyper-educated debate, I asked how low we can bring LDL down ? One leading professor of lipidology with a H index possibly crossing his LDL levels, said, we can go as low as possible , even to zero. He argued for possible eradication of this heinous molecule. No surprise, there was a thunderous applause from the industry benches.
How to go about lowering the LDL ?
Statins are the first line drugs. We have found it is not enough, it doesn’t bring down LDL below 70 in many , enhancing the residual risk .Now, we have found a God sent weapon. PCSK has got into our hands after some stunning collaborative research between geneticists, biochemist and pharma guys. Let us use it judiciously . This LDL receptor regulatory chaperone , prevents its recycling so blocking or reducing its function
This cartoon from the Dr. Libby’s article (Ref. 1) image depicts the potential pathways beyond Evolocumab (Repatha) and Alirocumab (Praluent). PCSK can either be blocked after its synthesis or paralyzed before it is synthesized (RNA manipulation therapy SiRNA). There is one hidden face for PCSK trials as exposed by BMJ report of FOURIER methodology that will argue some caution with this new target.
Bembidoic acid is a also can also join the death game of LDL .It just acts two step above the HMG-CoA axis blocking ATP citrate lyase, . BM-Acid is approved by FDA well before the CLEAR trial by Steven E. Nissen et al NEJM 2023Leqvio ® (Inclisiran) is also approved in 2023. Soon, we will get vaccines that will promote lipid catabolism.
Ok let us be practical : What does the current guidelines say about LDL target?
It depends upon the risk profile and the guidelines you follow. Numbers to remember are 70, 55, 40 mg
One of my suggestion is to try keep both LDL and HDL as narrow as possible. This would mean both LDL &HDL should hover around 55-60mg in high risk category
Can we allow the proposed free fall of LDL ? (Ref 2)
If we apply the 50% reduction from baseline criteria, if someone develops CAD at 50 mg, it would mean to reduce LDL to 25 mg, right? This is where the problem starts. LDL, apart from being a carrier of hormones, may have a role in the structural stability of every cell membrane. While, the relationship between LDL and atherosclerosis is so intimate, funnily we have heaps of data that show South Asian population with tons & tons of plaque with normal LDL. The lesson we haven’t learned from the Indian paradox is that there are more unknown and invisible culprits in promoting atherosclerosis and CAD.
*In fact, for the future generations, there is more exciting ignorance waiting to be decoded. CAD without standard modifiable risk factor SMURF is the new agenda (nearly 25% of CAD occurs in the absence of SMURF – Ref -3). In this scenario, whipping a single known culprit and playing the LDL number game among the public mind is not welcome.
Final message
The tendency to portray a physiological molecule LDL , as a sole villain for CAD is not correct. Further ,trying to eradicate it, Implies, inadequate understanding of human lipidology.
The contents of the this blog is being published as Kindle E book , as per the request of many of the readers. Every article will continue to be open source in this site. Again I shall reiterate the book format is not aimed at any commercial intent. It is only to facilitate learning in a single book format Here is the link to book https://amzn.in/d/euhL5vu
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Please Note
The author acknowledges all the queries posted by the readers and wishes to answer them .Due to logistic reasons only few could be responded. Inconvenience caused is regretted.
Dr.S.Venkatesan MD 