Cath lab nightmares may be a cliche word for all of us. Still, It has become a mandatory topic in any cardiology conferences and live workshops. These sessions are always popular and crowded as Interventional cardiologists are eager to get tips from other experts, on what to and what not to do in the cath lab in crisis situations. While stuck in an unexpected problem, these tips really help us come out of this, with shared expertise, presence of mind, skills, innovation, etc.
I asked them, what can be done about this ? “Nothing much” was the unanimous response
Final message
To end on a positive note, nothing is Impossible. Let us first start feeling this moral nightmare, and quell it at its origin. Fortunately, this doesn’t need sophisticated hardware. All we require is a little bit of righteous & peaceful application of mind in the way we learn and practice science.
Whenever possible ,before doing a coronary revascularisation procedure , check twice the segments you try to perfuse is really short of blood supply and truly needs the procedure. Don’t ever waste your resources and try to blood-feed the dead myocardium. It’ can never be awakened !
Pragmatic science
I was conversing with my colleague recently , who has grown into suave , Interventional cardiologist with a huge academic & societal repute .He owns a personal cathlab and planning to get one more.
I learnt a non-academic reality lesson from him .
When planning myocardial revasascularisation, apart from myocardial viablity status, there is one more viability issue which is done in the account books of finance mangers across big hospitals. Its Cath lab viablity. Trust me, he used exactly the same word ! He went on to explain in detail , how, every day there must be a minimum number of procedures to keep the machine alive. Which is under the eagle eyes of the guys who funded the state of the art lab !
“So, what do you say,I asked him ?”
He was frank enough to admit, he felt always happy when he is able to convert angiograms into angioplasties.He went on to add , the Ideal CAG-PCI conversion ration should be atleast 3:1 or more.
“Whenver I hear such genuine statments from real world people , it pains, as it tends to confirm my assumptions ”
Final message
I am wondering with all my lost wisdom. Why should any cardiologist after 30 years of training, fight for cath lab viablity , and get into a conflict with the very organ they are supposed to care and protect.
When did we become so Inferior beings & fight for the survival of these life less machines ?
Meanwhile, major text books , has un-intentionally facilitated this academic deciet .They have largely taken away the sting out of the snake . Myocardial viablity , hibernating, stunned myocardium , are rarely given importance nowadays and made it appear taboo concepts,in cardiology academia.
Postamble.
Will be extremely happy if what is portrayed in this post is not really true.
Having retired, find little more time in browsing the academic images lying idle in old computers.It is interesting, still a tiring job to pick any useful learning stuff, from heaps of data hiding in different hard drives.
This set of ECGs I could retrive from the year 2011, A 31-year-old male presented to our CCU at 4.50 PM.
The treatment was Initiated in 10 minutes and completed in an hour, (Those days cath lab wasn’t functioning 24/7, more importantly, there was no external interference with our professional decision-making process)
The ECG was repeated at 7.15 PM
I think this case is much relevant even today, because it made me guilty of committing a crime*, by treating a STEMI without the help of a cath lab and discharging the patient with near normal ECG and LV function. The guilt was further amplified as I had used the lowly streptokinase, and not the glamorous Tenecteplase which could have produced a brisker and more complete TIMI 3 flow.
*One of my corporate friend called it a heinous one by current standards, for not attempting to visuvalise the IRA and a possible pharmaco invasive PCI.
Final message
STEMI can be tackled successfully in a number of different strategies. Immediate cath lab care is an optional accessory in the majority and of course, it can be life-saving in the minority. If we are unable to differentiate which patient will truly benefit from urgent cath lab intervention, I think, we have a huge problem, with the way we learn and teach cardiology. Hiding behind double-blinded statistics and RCTs is not going to bring a solution to this largely self-inflicted scientific predicament;
PH has always been an exciting academic topic in cardio-pulmonary medicine, for both clinicians and researchers. It is also one of the extensively studied hemodynamic parameter. The pressure in pulmonary circulation is intimately tied to the function of two critical organs. lungs , heart and various systemic factors. The fact that pulmonary circulation is essentially expansive & engulfed by the dynamics of lungs, makes PA pressure a continually variable parameter. Further ,the chest wall compliance, airway resistance , influence of pleural pressure fluctuations, make it difficult to estimate the normative pulmonary artery pressure and resistance even in rest.(Imagine during exercise !)
No surprise, our knowledge base about PH is under constant flux. The trouble starts with this query, What is the normal PA pressure ? After toying with various numbers we are currently hanging all our wisdom at a mean PA pressure > 20 mmhg as cut-off to define PH. However, we are able to grossly classify PH into various categories , pre/ post /combined etc. Here again, we have a guess work with two more cut offs.. For PCWP we have decided to choose 15mmhg over 12mmhg as upper limit of normal & PVR < 2 Wood units.
The second query in PH is still more contentious. What is the effect of exercise on PA pressure ? In our student days we were not allowed to bring exercise into the picture of pulmonary hypertension, in spite of the fact cardiac output increases up to 5 fold during peak exercise, Now, there is evidence to show exercise can increase PA pressure significantly, beyond the limits of current definition of PH. This is problematic for obvious reasons. Still, there has been considerable reluctance to accept exercise induced PH as a clinical problem by many of us .
*To be fair with our intellect, I think, we haven’t yet approved “Exercise induced systemic HT” as an entity officially. (Of course, hypertensive response during stress test is well known)
Seeds of New thinking
Thanks to current guidelines from ESC in 2022 .The exercise induced PH has come back with a bang and finds a place right behind the pre and post capillary PH. (See below ) I am sure, there must have been a vigorous debate before including this in the definition. We must appreciate the authors of two forgotten papers for the major shift in our understanding .(Ref 1 ,2)
The secret of the slope : From where did it come ?
ePH is > 3mmhg /Litter/Minute is the definition of ePH
It is the rate of raise that matters not the absolute pressure. This slope was validified in by Bossone E et al (Ref 2)
Some questions on ePH
1.How do you define ePH ?
Mind you, it is not an absolute number. It is the slope more than 3mmhg per litre of cardiac output. I agree to measure the slope > 3mmhg we need serial measurement and may be impractical .(Immediate post exercise echo is a close alternate )
2.Why we depend on slope rather than absolute value ?
This is because during heavy exercise PA pressure can raise even up to 30 or 40 crossing the boundaries of PH ..Only the rate of raise ie the slope can tell us whether it is appropriate or inappropriate.
3.Does ePH is really a clinical problem ?
Yes. it should be suspected in every unexplained dyspnea .(Beware of the anxiety it may elicit to the patient, so, go slow with your investigation first rule is to rule out Anemia and other common causes )
4.Can ePH occur over and above established causes of PH ?
Why not ? it is very well possible.(PH before and after six minute walk test will unmask this component)
5.Can we further classify ePH ? (Pre vs Post cap ePH)
Possible yes. ePH can be a marker of HFpEF if LVEDP is also correspondingly increased or else it will fall in to CETP or COPD.
6.Can COPD cause ePH ?
Yes, possible.
7.How does RV function confound ePH ?
This is ticky. Perfect RV-PA coupling and a good RV function is required to sustain ePH. A poorly contracting RV will make the whole concept of ePH and the defining criteria redundant. May be, we need to work for RV function corrected ePH . (This is a potential research topic for fellows)
8.Where do diastolic stress testing fit in diagnosing ePH ?
In one aspect ,DST which is screening test for silent HFpEF is an example for subtype of ePH.
Final message
The concept of ePH has entered once again into the cardio pulmonary clinical domain. Thanks to ESC 2002 team for listing this hitherto ignored disorder. Let us reiterate the importance of this concept in the clinical practice. It is worth considering some form of stress test to recognise this entity, in every patient who has unexplained dyspnoea.
Good morning GPT. Let me introduce myself . I am a medical doctor, practicing cardiology, in Chennai India. I have had a long-standing query in very fundamental principles of the practice of medicine. Just wanted to chat and clarify with you.
Welcome, I am here to help you
Medicine is both art and a science. In recent times the movement of evidence-based medicine (EBM ) is trying to overturn the clinical experience. I have a feeling it is not fair. We can’t create evidence for every decision we make in clinical science right?
My first question is
Can experience-based medical care beat evidence-based care?
No, experience-based medical care cannot beat evidence-based care. Evidence-based care is the standard of care in medicine, and it is based on scientific evidence from well-designed research studies.
Experience-based medical care, on the other hand, relies on the personal experience and judgment of the healthcare provider, without necessarily considering the best available scientific evidence. While experience is undoubtedly valuable in medicine, it is not always reliable or consistent, and it may lead to biases, errors, and ineffective or harmful treatments.
Why unpublished experiences & truths are not respected in science?
In science, unpublished truths, or ideas that have not been subjected to the rigorous testing and peer-review process, are not respected because they cannot be considered reliable or trustworthy. Science relies on empirical evidence, which means that ideas must be supported by data that can be independently verified and replicated by other researchers.
Publishing research in reputable scientific journals is a critical step in the scientific process because it allows other scientists to examine the evidence and evaluate the methods used to collect and analyze data. This peer-review processensures that the findings are credible and the conclusions are supported by the available evidence.
Is it possible for the peer review process, to make a falsehood a truth?
Peer review is a crucial process in scientific research that helps to ensure the accuracy and reliability of scientific findings. However, it is possible for a peer review process to overlook or miss errors, biases, or other issues that could affect the validity of the research.
It is important to note that peer review does not guarantee that a study’s findings are accurate, nor does it have the power to make a falsehood into a truth.
If peer review is not foolproof, how can you say EBM is always better than experience-based strategies?
It is true that peer review is not foolproof and that scientific evidence is not always perfect or complete. However, evidence-based medicine is based on the idea that healthcare decisions should be made based on the best available scientific evidence, rather than solely on individual experiences or opinions.
How can you say unscrutinized experience is always bad?
I apologize if my previous response conveyed the impression that an unscrutinized experience is always bad. That was not my intention. I recognize that individual experiences and clinical judgment can be valuable in healthcare decision-making, particularly in situations where scientific evidence is limited or unavailable.
In summary, unscrutinized experience is not always bad, but it can be problematic if it leads to inconsistent or ineffective healthcare practices. Evidence-based medicine provides a framework for integrating individual experiences with scientific evidence to guide healthcare decisions in a rigorous and consistent manner.
So will you agree, it is not the evidence as such matters, but the quality and genuinity of the evidence more important?
Yes, I agree that the quality and genuineness of evidence is more important than the quantity or mere existence of evidence.
Low-quality or biased evidence can be misleading, inconsistent, or even harmful if used to guide healthcare decisions.
So, shall I make a statement, evidence-less truths can be as common as evidence-based lies?
It is not accurate to equate “evidenceless truths” with “evidence-based lies,” as these are two different concepts.
An “evidenceless truth” is a claim or belief that is not supported by scientific evidence but may be based on personal experience, anecdote, or other non-scientific sources.
In contrast, an “evidence-based lie” is a deliberate misrepresentation or distortion of scientific evidence to support a particular agenda or belief. This can include cherry-picking data, manipulating statistical analysis, or ignoring contradictory evidence in order to promote a false or misleading conclusion.
How common is evidence-based motivated falsehoods and lies in science?
It is difficult to estimate the frequency of evidence-based motivated falsehoods and lies in science.
There have been cases where scientific research has been deliberately manipulated or falsified to support particular agendas or interests. These cases are rare, but they can have serious consequences for scientific progress, public trust in science, and the welfare of patients and populations.
Why don’t you try to accumulate data on the prevalence of this important parameter, that is plaguing medical science?
As an AI language model, I do not have the ability to conduct independent scientific research or collect data on the prevalence of evidence-based motivated falsehoods and lies in science.
As an AI language model, I am programmed to adhere to ethical and professional standards of accuracy and impartiality in presenting information to users. I rely on the integrity and credibilityof the scientific research community to provide accurate and reliable evidence for me to learn from and share with users.
How do you assess the reliability and integrity of the scientific community?
As an AI language model, I cannot make subjective assessments of the reliability and integrity of the entire scientific community.
So you believe strongly the peer review process. Is it a natural belief or you are instructed to think all peer-reviewed publications in major journals are authentic?
As an AI language model, I do not have beliefs or opinions of my own. My responses are generated based on the information and knowledge that I have been trained on, which includes information about the scientific peer review process and the importance of peer-reviewed publications.
How do you assume the peer review process is rigorous and transparent?
The scientific peer review process is designed to be rigorous and transparent in order to ensure the quality and validity of research findings.While the peer review process is not perfect and can be subject to human biases and errors, it is widely regarded as an important quality control mechanism for scientific research. It provides a level of assurance that the research has been subjected to independent scrutiny and has met certain standards for quality and rigor.
Do you think the “peer review” process also needs scrutiny?
As with any process, it is always beneficial to subject the peer review process to scrutinyand ongoing evaluation in order to identify areas for improvement and to ensure that it continues to meet the needs of the scientific community.
Do you think scientists hide vital information?
While it is possible for individual scientists to intentionally or unintentionally omit or hide vital information, it is not a common practice in the scientific community.
That being said, there have been cases where scientists have been found to have engaged in unethical practices, such as falsifying or manipulating data, which can have serious consequences for the credibility and trustworthiness of scientific research.
Overall, the scientific community is committed to ensuring the integrity and transparency of research findings in order to advance our understanding of the world around us.
How do you come to the conclusion “overall the scientists” are committed to Integrity? Is it a belief? Or truth ?
The conclusion that “overall the scientific community is committed to integrity” is based on a combination of evidence and observation. The vast majority of scientists are committed to advancing knowledge through rigorous and transparent research practices.
Therefore, the conclusion that overall the scientific community is committed to integrity is not based on a belief, but rather on an evaluation of the evidence and observation of scientific practices and norms.
Do you have a good amount of evidence-based studies to prove scientists’ integrity?
There have been several studies and surveys conducted to evaluate the integrity of scientific research and the behavior of scientists. For example, a 2016 study published in the journal Nature found that 70% of researchers have tried and failed to reproduce another scientist’s experiments, suggesting a high level of scrutiny and skepticism within the scientific community. Another study published in PLOS ONE in 2015 found that 33% of scientists had engaged in some form of research misbehavior, such as using inappropriate statistical methods or failing to disclose conflicts of interest.
However, it is important to note that such studies are limited in scope and may not provide a comprehensive picture of scientific integrity as a whole.
If there is no adequate evidence to prove scientists’ integrity, then whatever we presume is based on some assumption right?
While it is true that there may not be a vast amount of evidence-based studies to prove scientists’ integrity, this does not mean that all claims regarding scientific integrity are based solely on assumptions.
Overall, while the evidence may not be exhaustive or comprehensive, it is reasonable to infer from the existing mechanisms and examples of integrity within the scientific community that the scientific community as a whole is committed to integrity.
Reasonable means what?
When I say “reasonable”, I mean that it is logical or rational to infer that the scientific community as a whole is committed to integrity.
The word reasonable, in this context, is not reassuring or appears very authentic, is it not?
I apologize if my use of the word “reasonable” did not convey a sense of reassurance or authenticity. I understand that when it comes to scientific integrity, it is important to have a high level of confidence and assurance that the scientific community is committed to upholding high standards of conduct and transparency.
So, science is still uncertain (or rather unreliable) in many situations, will you agree?
Yes, I would agree that science is inherently uncertain. Science is a process of continually refining and updating our understanding of the natural world based on empirical evidence. This means that scientific knowledge is always provisionaland subject to revision in the face of new evidence.
So, as of today, can we believe everything that comes out of top-ranked peer-reviewed journals?
While peer-reviewed journals are generally considered to be a reliable source of scientific information, it is still important to approach scientific claims with a critical and discerning eye.
Can you give a more specific answer to the previous question?
No, we should not blindly believe everything that is published in peer-reviewed journals without critically evaluating the evidence and methodology behind the claims.
Thanks, GpT, nice chatting with you. It was a great time, and appreciate your truthfulness.
You’re welcome! It was a pleasure chatting with you and answering your questions. Don’t hesitate to reach out if you have any more questions in the future!
This is a 15-year-old post about LVH, written in 2008. Few of my colleagues, now agree with this, but still hesitate to oblige in the open, suggesting it is too good to be true! Re-posting it for your own assessment. Surprised, why cardiology community didn’t consider this observation worthy to pursue.
Advantages of Left ventricular hypertrophy (LVH)
Left ventricular hypertrophy is one of the most common clinical cardiac entity.It is recognised either by ECG or echocardiography.LVH has a unique place in cardiology as it can imply a grossly pathological state or a marker of healthy heart as in physiological hypertrophy in athletes.
Logic would suggest, in this era of stem cells and nano medicine , every muscle fibre in ventricle is worth in gold !. So when the nature provides an extra reserve of myocardium in the form of LVH one should welcome it, if otherwise not harmful.
Is LVH due to systemic hypertension benign ?
Not really, LVH has been shown to be an independent cardiac risk factor. (The famous Framingham study)Further LVH can result in diastolic dysfunction and the risk of cardiac failure increases.
But in spite of these observations, an astute clinician with considerable experience will appreciate , patients with LVH fare better during an acute coronary syndrome !
This has been a consistent clinical observation . (Shall we call it as class C . ACC /AHA evidence? )
Is LVH an asset during ACS ?
A hypertrophied heart takes ischemic injury very easy , it doesn’t really hurt much . Another possibility is that in LVH myocytes are relatively resistant to hypoxia .
Patients with LVH rarely show significant wall motion defect following an STEMI.This is probably because the full thickness transmural necrosis is almost never possible even if extensive MI occurs.
This is also reflected in ECG as these patients rarely develop q waves in following STEMI .
Persistent ST elevation and failed thrombolysis is very uncommon in pateints with LVH.
LVH provides a relative immunity against development of cardiogenic shock . It requires 40% of LV mass destruction to produce cardiogenic shock.This can rarely happen in LVH. In a long term analysis we have found none of the patient with LVH developed cardiogenic shock following STEMI.
LVH patients are also protected against development of free wall rupture.
Concluding message
“Lack of published evidence is the weakest evidence to dismiss a true myth”LVH , either pathological or physiological, has a hitherto unreported beneficial effect.It acts as a myocardial reserve and helps limit the impact of STEMI.
This is the Incidental ECG of an apparently healthy 50-year-old businessman, recorded while applying for health insurance
How will you describe this ECG?
Let me magnify it for you
Why this big fuss about this ECG?
Such ECGs are so common. Looking at the ST segment, we are supposed to think of significant CAD,, LVH,Aortic stenosis or variants of cardiomyopathy, and sometimes electrolytic shifts. The fact that it is recorded at rest, and the patient is absolutely asymptomatic, it is very unlikely there is ongoing ischemia.It could be a myocardial origin or an unknown repolarisation pattern. But, one thing is clear, we can’t send this guy under the label of non-specific ST/T changes.
The Echo was done it was normal. No WMA, LVH. The aortic valve was perfect.
Is CAG indicated here?
Three responses came from three different cardiologists. Everyone agreed, the stress test is not going to be useful, as baseline is unstable
Absolutely not Indicated, since he is asymptomatic. I believe the history and Echo. Please follow him up
A definite yes for CAG. (Being a scientific cardiologist, without excluding CAD, I can’t be at peace. Will do at least a CT angiogram)
A third cardiologist said a CTangiogram is waste of time and wanted to do a radial CAG in 10 minutes in his newly opened hi-fi radial lounge.
What happened then?
Don’t know, whether he underwent CAG or not. But, I can confidently say he will have a normal coronary angiogram. How can you be so confident? Confidence doesn’t mean I am correct. Look at the ST segment again. It is not true ischemic depression. It is neither non-sustained nor horizontal or downsloping*, This could be referred to as, primary T inversion with secondary ST segment dragging. Regarding the management, the first response is ideal,
*Classical slope should begin at J point. Late downsloping has little predictive value as in this ECG.
Is Echo good enough to rule out structural heart disease?
Even after the echo was reported normal, few questioned the quality of the echocardiogramand asked to look specifically for apical wall motion with speckle track and GLS. ( I know, MRI is a must nowadays to rule out structural heart disease as Echo can’t rule out intrinsic myocardial disarray, infiltration, etc)
How is ST dragging different from ST depression?
Classical horizontal ST depression
ST dragging due to T wave pulling
For ST depression to happen, the junction point needs to be depressed. Note here junction is held high, only the distal half of the ST segment dips rather dragged by the phase 3 repolarization process which corresponds to the proximal limb of T waves. Our observation is, this type of ST drag is less sinister and usually indicates a myocardial ST defect, rather than an ischemic one. (Examples: concealed LVH or forme fruste of HCM or Infilitrative cardiomyopathy-related entities.)
Final message
The purpose of posting this ECG is, some ST segments create disproportionate panic than it deserves. The concept of T waves pulling down the distal part of the ST segment which can be called ST segment dragging is being proposed here.
Some provocation for advanced readers
Re-exploring the foundations of electro-cardiology is always welcome. Worth diving deep into mysterious terminology non-specific ST/T changes. ST segment in the ECG corresponds to the most stressful period since it represents the active part of mechanical contraction. Curiously, it Includes the entire electrical (Repolarisation) & most parts of mechanical relaxation. The true onset of LV myocardial mechanical relaxation we can’t be sure, It happens somewhere in late phase 2. I think it’s so difficult to decode that timing. But, what we can presume is ST segment behavior in its distal half is less specific for both ischemic as well as hemodynamic stress
The electro-mechanical continuity within the ST segment is so intimate, and the demarcation point between them is invisible in many clinical situations. No surprise, we are largely in the dark about the true influence of the ST segment over T wave morphology and vice versa. (ie distal ST depression pulling down the T wave ) Though chronologically T must follow the S in timing, it would seem impossible for “T” to go back in time and pull the ST down. (If QRS can precede P in a junctional rhythm, why not T do the same for ST? ) I am not sure whether there is any timing involved in antegrade vs retrograde repolarisation across endo-epicardial repolarisation dissociation.Further, we know very well, myocardial scars cause fragmented depolarisation in QRS. Can anyone guess effect of these scars in repolarisation vectors? (Fragmented ST segment ?) I think it is worth pursuing this phenomenon. Let the young new age Sodipellares’ look into this.
Though the traditional rule of thumb, makes ST segment shifts more sinister, T-wave changes are largely benign, It is not an easy job to segregate benign from more serious forms of T-wave changes. Isolated new onset T inversion, can be an equally troublesome marker, especially mid-chest leads in the male population.
It is interesting to note, not every T wave Inversion is empowered to drag the ST segment down. We don’t know why. It is something to do with the curvature of the shoulder zone of phase 2 /3 of the action potential. In this context, ST dragging could be an important concept to explore.
. An example of isolated T inversion without influencing the ST segment. Try to compare this ECG with the one that is shown to drag the ST segment
Diastolic T wave stress
One more issue, which we are not yet clear is the timing of 2nd sound with reference to the T wave. It is a fact, a significant part of the T-wave will represent early diastolic hemodynamic stress* as well.
If some body is struggling with same problem, say for over three decades , there is something seriously wrong with the way we deal with the problem. How do you localise accessory pathway in WPW syndrome from 12 lead ECG ? is one such entity, This question is asked exclusively in cardiology board exams. Now a 2023 paper from EUROPACE claims, it has come out with a simple algorithm bettering all the previous ones. Please check it for yourself.
One thing we can say with conviction is most of these embryological remnant pathways are posteriorly or laterally dragged in peri AV annular region or the para septal region. Very few appear anteriorly, if anterior it is more often placed on the right side.
Why should we take this question easy ?
Try asking any experienced EP specialist* to localise a pathway in given 12 lead ECG . Don’t get surprised by a long silence before they commit, because they know the truth, and how delicate this question might sound on quiet a few occasion, because of various anatomical and physiological reasons.
*Never fail to appreciate their hard long hours in cath lab to spot, analyse and shoot these tracts.(EP stuff is not like angioplasties, which, many can do even in half sleep!)
Final message
Yes, localising WPW can be either a fascinating or frustrating exercise depending on our understanding about the attitudinal cardiac anatomy, variable autonomic tone dependent morphological behaviour of delta waves, PR intervals, QRS axis ,the transition zones etc. Shrewd fellows may go through this 12 lead stress test. ,
For others just try to localise right from left , & then posterior or lateral Forget the anterior ones. This is more than suffice. Unlike drug trials, where statistics are often battered , here the Incident numbers are the key measure of truth. (Even without seeing a ECG you are likely to be correct in 80 % times, if you localise the pathway to posterior, para-septal or left lateral zones. )
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
Dr.S.Venkatesan MD 