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Lipidology

Feb 20 | 6:50 AM

Dr. Praveen Chandra: PCSK9 INHIBITORS ARE PROVEN and better strategy Dr. Rajeev Aggarwala: EZETEMIBE is much cheaper & Effective to IMPROVE-IT Dr. Ramesh Goyal: Saroglitazar has promising data in diabetic dyslipidaemia

[Music] [Music] regarding the diabetic dyslipidemia [Music] [Music] he has been awarded for success and achievement in the field of medicine with padmashree by the president of india all sir also served as a director of cardiac cath lab and acute mi service that [Music] he is distinguished faculty member in various international meetings he's organizing a director of ama ami course held in the daily from the year 2006 he has been published temple of articles reviews and abstracts in various prestigious national [Music] he works equally in preventive and invasive cardiology he has deep interest in the vascular biology his department it is bigger referral based in india he was awarded amber using national excellence award is inspiring dr fox india and health icon facility for lifestyle server by the times of india then he has a literally excellent honor by 2018 by bharat liman a private ngo since 1980 the third speaker is can i have the data of the third speaker please ah our senior consultant and hod department of endocrinology and diabetes at apple hospital is a faculty at so many places he's a former member of the national advisory board of indian journal of endocrinology and metabolism he was awarded his best laboratory in 2018 and best endocrine india thank you i want to share my screen if you allow this answer [Music] thank you dr kamal especially and all the organizers for taking me in on this very important aspect which is very close to my heart i think nature is kind i superseded praveen chandra because anthropologically speaking agitamide came earlier than pcsk9 so if you look at the evolution ajita my should be talked earlier than pcsk9 so i think everybody remembers the case there is this is a very interesting case i i think you have not shown the case can somebody put the case on the board because i have to build up the case rajiv i think i have the case on my slides like sure so praveen you can come in [Music] thank you thank you okay so here is the case okay now okay fine so uh thank you dr rajiv and thank you kamal and all the colleagues there in gujarat and for this very interesting program on discussions and debates on various day-to-day issues so here the issue which is in front of us today that this is a patient who is 57 years of age he is a diabetic he is has a ldl cholesterol of 112 on roosevelt's statin of 40 milligrams he had a previous pci about eight nine months back to rca and he has a strong family history of cad and now after the angioplasty of rca about eight nine months back he comes with a new acute condor syndrome and this time they find that the led is progressed and it is about 99 so of course he is undergoing going to undergo intervention which is without any uh delay but now we are going to discuss about his you know control of statins and protection for future events how do we do that okay so now let me take you through this case so now i think everybody will remember this case and the question here is what should be the target here for the ldl cholesterol whether you should blow it down how do we do it and when do we do it all these questions and so in this series what i'm going to share with you a little bit of you know why it is important because lipids are the most critical modifiable serious factors for acute macro infarction so this we have recognized for a very long time and here we have this data from many studies and also ldlc which is the building block of atherosclerosis has to be so this we have to really strike at the bottom of the whole pyramid otherwise we are not going to gain much benefit so the data from the ctt meta-analysis showed that the major vascular events versus absolute ldlc reduction here you see that there is a constant you know a slope which is there and this is from the five trials and this is like you know very very you know i must say pivotal to establish this concept of bringing it lower and lower but when we did that with the you know bigger more trials the ideal trial the tnt prove it everything and all of it showed that yes if you give high intensity statins it does reduce events but what happens what happens is that you still have some patients who will have events so it comes from 26 to 22 from 13 to 12 from 10 to 8 but it doesn't come to zero and what we require is that we want to bring it as low as possible and if you look at this data nearly one in five patients will have a recurrent cv event during the first year postmate so why are we delaying things we have to do things faster and here you look at the ischemic risk at 30 days it is greatest so post mi patient 30 days the risks are greatest and within one year the event rates are so high so the question here is very very important that of course we have to start doing something faster something earlier and this is the monotonic relationship between ldl cholesterol and major outcomes and you look at this ldlc less than 20 10 patients had ldlc less than 20 and it shows that there is no safety concern even if the allele goes below 45 50 or comes to 20. so based on all this information we had the new guidelines and here we have started looking at the new things which is the very high risk profile of this patient our patient which was given to us today falls into the very high risk category and beyond that there are additional risk factors in this case and if you look at this guideline that in this patient who is at a very high risk a combination of pcsk9 inhibitor therapy starts coming into the picture why because he has very high risk he has acute conditions and if you look at this information that this patient who was already on statins high dose statins was 40 milligram of rose was term or if the patient was 20 and that was the maximally tolerated dose for him even 20 is the highest dose for him and of course this patient is not on his dmi which will be discussed but estimate just becomes the second drug to be added in these patients but we will discuss more that why pac9 also becomes a natural you know second drug in this particular situation so pcsk9 has come to a very important you know stage where if the ldlc goals are still high despite maximum medical therapy and if this patient has you know come within one year of the first intervention is receiving the second intervention he starts coming into the picture of uh you know addition of pcsk9 therapy even if the sd has not been added we can start that and this all this house has to happen much faster than what we were thinking earlier so this is our indoor patient and if you look at the you know the research of the last 25 years 30 years what we see is progressively we found that high cholesterol was bad average is not good lower is better and even lower is even better and lowest is best so we have to bring down the cholesterol and why we should use pcsk9 because it reduces the cholesterol maximally if you look at the 140 milligram of biblical math if given twice a month it reduces cholesterol by 64 compared to astomy alone it just gave rise to 24 reduction and if you combine it with statins still it is lesser than pcsk9 combination so that is the most important agent and we have to start thinking of the most potent agent in this particular a very irish situation so pcsk9 as you all know i won't go into this that it just prepares the ldl receptors it stops the interaction of pcsk9 to ldl and the allele particles removal which happens through these receptors is enhanced and the ldl reduction happens starts very quickly within uh two to three doors we get a steady state so which means the action starts rather fast and the dose is you know as most of you know one forty twice a day or four twenty once a day and this is the average reduction of cholesterol when we combine high intensity statin with estermind it comes to about six intensity statin it comes to 75 and when we combine all the three it is 85 so this is the particular situation where i think this patient will require all three of them so it is not that i am saying pcsk9 alone is demand also should be added to this annumentarium for this medicaid for this patient so the evidence started from chronic coronary syndromes from the fourier trial which was the most important but that is not pertaining to us right now the most important thing is the subset of patients from fourier trial who were high risk and who get the maximum benefit and these are the patients who are high risk qualifying am i less than two years so our patient is in this category of less than two years you see the benefit is maximum so we have to use this more than two prior mis again this patient is the second mi falls into this category gets the maximum benefit so this patient has multi vessel disease again gets the maximum benefit although we are deriving all this information from the fourier trial but we can extrapolate all this information very easily onto this patient then the mason event in patients with with and without pid of course in pid if the patient also has a phd which we'll have to find out then this patient will definitely get benefit from this therapy and those patients who have previous prior pci will again have a better outcome compared to those patients who do not get every leukemia so you can imagine this patient is a very high respiration and all these patients who are previous bypass surgery complex pci and complex revascularization get more benefit when pcsk9 is added to this patient to this therapies and of course the safety of this therapy has been established quite well and the safety events has been also adjudicated and found to be much much if you know safe and there's no issues in terms of safety of adding this therapy to our patient then go to the acute condition syndrome subset of patients and if you look at the acute coronary syndrome subset of patients the first trial which comes in the picture is evopax in this study where you know these patients came with unstable angina less than 24 hours and here or less than 72 hours of still st elevation mi this was patients who were given a leukemia in the hospital and look at the change in ldl levels at 8 weeks it was substantially different p value was significant less than 0.001 then the reduction of ldl was very very consistent in the evac study another study for acute non st elevation mi given you know we look map in the first initial hospitalization ldl reduction was quite significant and rapid at day one day between day four and seven it was sixty percent and it did two percent so you can imagine how fast and how quick we are able to protect this patient from a second event or any other and you know untoward incidents so guidelines recommended ldlc targets applicable to acs can be achieved in most patients at hospital discharge and can can be continued and this is the level of you know small if you look at the uh with uh the difference is quite significant lpa levels reduction is also quite significant so basically adding pcsk9 becomes a reasonable strategy for patients coming with multiple events like our patient recurrent mi recurrent uh you know in interventions all this falls into this category then risk for non-culprit related recurrent mi was that twice that of culprit related different ami over a long period of time and here you see that it was actually the non-culprit vessel which has come and that is why it is important to treat these patients much more effectively and there are many studies intravascular ultrasound guided studies and then of course showing that lowering ldl and black regression is hand in hand so if you reduce ldl it really makes a difference even angiographically or intravascular ultrasound wise this is another study showing lipid core burden index going down in you know quite significantly if you give pcsk9 therapy to these patients and the oct trial also showed that the thin capped fibrous atroma which is the culprit is also treated well if you give them you know pcsk9 because in this study they showed that the cap becomes thicker at 12 week follow-up which means the chance of having mi is reduced and that is what we are interested in and many other studies like this in geographic study also showed that the vulnerable plaques can be stabilized after acs if they are given therapy with evolution initial period and then continue so we can modify this residual risk by adding this therapy and it has been shown so the three concepts of lipid lowering strategies to reduce events is start early treat more much much more aggressively and use combination therapy where tcsk9 and estimate both are to be added definitely in this pcsk9 definitely should not be missed out and based on the and all the evidence which we have ldlc should be lower the better and uh it should be less than 55 and in this patient it should be less than 40 and it should be then started in the hospital and one should not wait for four to six weeks in this patient and the effect on ldlc should be checked at photosys and also at four to six weeks as to how what is the situation and the lipid core burden index the fibrous cap everything improves and the five-year safety data of this therapy is available so one should not worry about giving this drug to our patients so this is the group of patients in my practice who will be benefited in by the last one minute giving a pcsk9 disease and multiple interventions like we see in the session so in to know just summarize pcsk inhibitors are proven and better strategy in recurrent mi reckoning you know quandary interventions and of course in patients who are having uncontrolled high cholesterol levels despite highest dose of statin therapy thank you very much now doctor rajiv also [Music] thank you dr praveen for presenting such crystal clear evidence for pcsk9 i think i have to move forward in a very simple mathematical way how i look at the case this reminds me of very famous quote from alvin roth disease is more expensive than health and you can imagine a patient having a repeat procedure is a bigger health burden and emotional burden i am very emotionally upset with the natural history of the disease and dissipation on account of social reasons an account of clinicians energia who had been who may be an interventionist or a clinician or a clinical cardiologist my take on this patient is there is a family history the patient was on high intensity statin and the consultant was not aware the difference between high intensity statin between a vis-a-vis high intensity lipid lowering therapy so i call it it is inertia versus ignorance i am not aware whether the lesion was existent in the artery before or it was it is a de novo led disease by no stretch of remedy imagination a patient who is post angioplasty should in follow-up have an ldl of 112. it is gross inertia versus ignorance the baseline ldl 257 reminds me of reduce it which was not practiced in the special there is a very famous table if you want to go through which is available from dutch lipid clinic network sport where you can calculate the current statin dose and a multiplication factor to decide the baseline ldl the baseline ldl with multiplication score of 2.3 into 40 milligram of bruised voice statin calculates the ldl of 257 which is alarmingly very high the lpa is 60 milligram repeat procedure in less than one year no mention of crp and bmi in a patient who has recurrence of disease hba1c is 7.4 my patient is diabetic and i'm not aware whether my patient is a part of polyvascular disease or a coronary artery disease with this background let me profile you the improved trial in brief general when used with symbol statin in improvement showed a mortality reduction of five percent absolute mortality reduction of five percent no intervention medical or surgical has shown absolute risk reduction of five percent in diabetics so let me say it is a dictate that agitamide should be used in every diabetic picture if you look at the polyvascular disease which has which is referred by dr praveen chandra also you find that as the ldl goes down as low as 55 first time in the history of led lowering there is a continuous reduction in events and mortality if you have polyvascular disease you do better the event rate is more in polyvascular disease only first event but multiple events when taken into consideration there is progressive protection so let us forget about the first event um there is a marked reduction in total evil music like we talked this phenomena in your heart failure trials as the disease burden increases within the heart from single vessel to multiple vessel or triple vessel the outcome improves so more the atherosclerotic burden inside the heart or outside the heart the outcome improves if you have a polyvascular disease with diabetes the absolute risk reduction of nine percent over a period of seven years giving an nd of 11 once again if you have patient like this there is no intervention which gives this kind of absolute risk reduction another which was very important outcome for this trial was there was no glucogenic signal so for the first time we learned that non-statin drug works and that the work with battery safety that means they are not glucogenic or diabetes i i must in the same breath continue to extend it to newer hope and this is a research study which shows that if you combine generic rose voice statin energy my unfortunately pcsk9 is not generic the two molecules which i am talking they are generic they are cost effective and improve the compliance then the ldl less than 70 is achieved in 80 percent of patient when combined with hdmi viscera is 30 percent so it almost doubles the patient population which brings down to significant level of ldl this is another way to look at it when oak acid is combined again there is 90 percent patient achieved less than 70 percent i'm taking it pcsk 9 versus oral therapy cost versus less cause and not only this newer drug they are this bambinoic acid is not diabetogenic so the two things which are very important with vampiric acid and agitamide is they're both non-diabetogenic they both decrease crp on top of each other so if the patient has got inflammation for the cause of recurrence i think they are the very good drugs like this patient has an event within one year so we have to achieve fifty percent or less than one millimolars per european diet this is our paper in clinical epidemiology we talked less than 30 which is a four-year data in extreme risk growth if the recurrence happens within a year so this qualifies for extreme risk group category b and if you look at guidelines agitamide on top of the statin is 2a because we have only one trial if you combine pcsk9 with the statin hdmi this is class 1a indication but if you combine statin or pcsk9 without having to uh without having hdmi the indication goes down to 2a so i'll say it is a mandate to combine high-dose statin and agit my then think of pcsk9 if you are not achieving the ideal ultra low level of ldl this is the latest guideline which has come from middle east to be very very visual and impressive to look at as the risk category goes down the values for ldlc non-hdlc goes down so another way to look it but it is very very visual to understand one thing which is very important and we should carry home that if you reduce the ideal 50 percent or more the residual risk is almost same irrespective of the baseline ldl level so we should know beforehand once we are starting a lipid lowering therapy that we have to achieve at least 50 percent and if you achieve 50 ldl reduction the residual risk is not much different in different classes that's why i say it is a mathematical equation that how much ldl you have to receive fifty percent or less than one milli mole whichever is lower should have been the target in this patient and that is why i feel there is a lot of inertia and ignorance on the part of clinician who are treating the patient i will think this patient because it's a very high risk a upcoming concept of zero ldl hypothesis how we achieve we know diamond approach in hypertension we know diamond approach in heart failure we know diamond approach in chronic stable indiana i think we should start thinking a diamond approach in lip lowering i am trying to make it simpler what dr praveen showed that high dose statin vis-a-vis with agitamide is always almost similar to pcsk9 alone so if you feel that 60 reduction of ldl in your patient will amount to 50 reduction of baseline ldl i think pcsk9 is out of picture to begin with if you feel that will fall short of your need then naturally pcsk9 should walk in and should walk in as early as possible that is how i can make it as very simple so once again if 60 reduction in ldl is the need to achieve 50 ldl reduction you should not think of tcsk9 if you feel you will fall short of that then pcsk9 should walk in on board as early as possible another very fascinating study which has come very recently that ultra low level of the high level of lk only make a difference when you have achieved ldl less than 70. if your ldl is more than 70 the lpa does not play that much of risk role the l because ldl is a bigger factor to challenge if lpa is less than 70 higher lpa translate into higher events and that is what i am trying to show ldl is achieved and your lpa is high then these patients are better off with lpa lowering therapy why i'm talking this will be clearer to you in the next slide let us imagine a patient who is achieved 70 milligram ldl with statin energy 5 is still falling short of ldl goal crp is high i'll probably choose vampire bambidoic acid in this patient if my patient is a statin agitamide is still 70 and lpa is still high i will choose pcsk9 because both the drug on the left side they are not lpa lowering and fortunately hdmi dampidoic acid and pcsk9 are not glucogenic so they are good jerks to use in diabetic as many of you must have seen there is a concept of hyper and hypo responders to statin we don't have snps to clearly define that but you will know that there are many patients with medium dosage drops down to 30 i call them hyper responders and there are some patients who do not respond that well so don't feel discouraged and try to see how the genetics play in these patients and many of your patients with moderate intensity studying and anita mike will drop down to 70 and they are hyper responders and i'll say it is good idea to wait for four to six weeks before starting statin pcsk9 to see whether your patient inherently is a hyper responder or not i am a strong believer in regression of atherosclerosis and i want to pass on this message to my colleague believe is this concept it is the best medication for your atherosclerotic patient and recurrence so early is a lot of inertia it must be embarrassment to the clinician that why my patient is coming so early in the natural history within within a year i did less than what i should have done i coined a new term that we need now metabolic interventionist who can tame lipids and diabetes with perfection because these are the patients who are benefited most by these intervention so i feel let us not feel belittled that i am an interventionist i am a mechanical cardiologist i don't understand metabolism i'll say you are not an atherosclerotic expert which you should have so i'm just showing you some images this is six weeks of aggressive lipid lowering i was images you can see in b2 image there is almost no lipid core and this is six weeks so believe in lipid lowering they still rises and this is a recent hidden study which showed that these drugs evolucomic pcsk9 can increase the fibrous cap thickness and make your plaque stable nobody dies of chronic stable indiana everybody dies of acute coronary syndrome so one of the aims of lipid lowering therapy is converting acs into ccs so shakespeare wrote long that what is in the name that which we call a rose by any other name would smell as sweet i'll modify his code by saying what is in the name it is statin my pcsk9 vampiric acid whatever it is it is all in the numbers and cost and compliance so let us not make it again about as you have named it i'll say we have to make a delicious choice of these molecules let us move ahead from boxing debates like we had cabg versus btca let us start combination therapy like hypertension and diabetes as early as possible in the natural history of the disease let us believe atherosclerosis is a metabolic disease not a mechanical disease and i feel we need newer generation of metabolic intervention cardiologists and we should not believe in artery cleaners of one hour job and this is what the master must have said today a good physician treat stenosis a great physician treats the atherosclerosis thank you very much now dr amish dr rameshwar [Music] good afternoon friends both the international cardiologists have debated with each other and in that process they forgot that this is a triangular contrast and dr rajiv has made my task very easy by saying that there is a need of a metabolic interventionist and yes metabolic interventionist is here to present his data on the diabetic dyslipidemia in a context of the patient which we are discussing so first of all when we talk about metabolic abnormality linking cardiovascular disease and type 2 diabetes there is a link between insulin resistance and various metabolic conditions we should not forget and the classic slide is the hypothesis the yy hypothesis says that at equivalent bmi uh the body fat content in asians is much higher than the body fat content in a occasion so here you can see uh professor eugene and professor yagni both are having same bmi of 22.3 but look at the body fat distribution in caucasian that is nine percent and it is more than normal in the indian person we asian indians have low insulin sensitivity compared to caucasians so here on the left we can see insulin sensitivity in this and on the y axis you can see the total body fat mass so at any total body fat mass the insulin sensitivity index for v asian indians is lower than the caucasians and similar relation is seen between insulin sensitivity index and some of trunkless in full thickness insulin resistance is a common link for various metabolic conditions so here you can see insulin resistance is a common pathogenetic mechanism for type 2 diabetes and we all know prevalence of type 2 diabetes in india it we have more than seven of diabetic patients in our country we have a unique atherogenic dyslipidemia profile and insulin resistance leads to high triglyceride which can cause cbd so the prevalence of hypertriglyceridinia in our cardiac patient is as high as 34.2 percent and unfortunately none of my cardiology colleagues even uh bothered to look at the trigger side value of our patient which was more than 300 and nfl the insulin resistance leads to diabetes and his major risk factor for nfld so i will focus more on ethereogenic diabetic dyslipidemia how does the atherogenic diabetic dyslipidemia influence various lipid parameters so insulin resistance is associated with elevated triglyceride and elevated triglyceride leads to increased uh free fatty acid levels in uh plasma leading to hypertriglyceridinia and ultimately it leads to low levels of hdl and high levels of small dense ldl and this is the pattern of dyslipidemia which is different in india compared to globally so here we can see most common dissipating my pattern we see are low hdl followed by high triglyceride now let me talk about hypertriglyceridine which my cardiology colleagues they conveniently ignore elevated triglyceride is a major risk factor for cardiovascular disease and residual cardiovascular disease risk remains in patients treated with statins and triglyceride is one of the risk factors which should be kept in mind so whether we are talking about the heart prevention study or the card study you can see that despite optimal statin therapy there was significant residual risk and residual risk was in tune of 70 to 80 percent now it could say body 2d study there is association between triglycerides and residual cardiovascular risk in patients with type 2 diabetes and established atherosclerotic cardiovascular disease so here in this 2000 plus patients with type 2 diabetes and cad with a mean baseline triglyceride of around 180 and the primary composite outcome was primed to cardiovascular death am i your stroke and secondary outcome was cardiovascular death and with mean follow-up of between 4.5 to 5.5 years so here we can see higher triglyceride is associated with the higher cardiovascular risk in diabetic patient so on the right side you can see every 50 milligram percent increase in triglyceride level was associated with the significant increase in the cardiovascular events i will quote another study the pre-diameter study where remnant cholesterol and triglyceride but not ldl cholesterol was associated with incident cardiovascular disease the trial population was around seven thousand highest patient for cardiovascular disease like a mean age of 67 years bmi of 30 and 50 percent of them with diabetes median follow-up was around five years and total miss incidents recorded were around 265 so these are the results and the results shows that the remnant cholesterol the triglycerides and the uh non-hdl uh cholesterol uh contributed significantly to the cardiovascular events as compared to the ldl cholesterol levels and here you can see if you categorize a patient with a triglyceride of more than 150 and hdl cholesterol of less than 40 in men and less than 50 in one then you can see the hazard ratio was one and half times higher for cardiovascular events so triglyceride non-hdl cholesterol remnant cholesterol and even ethiogenic dyslipidemia that is high triglyceride more than 150 and low hdl of less than 40 in men and less than 15 women were associated with the increased major adverse cardiovascular events but indian cholesterol was not associated with incidence cardiovascular disease the big study showed that 22 year mortality risk for patients with severe hypertriglycemia was increased by around 70 percent when compared with patients with low normal triglycerides so here you can see as the level of triglyceride starts moving beyond 150 there is increased risk of the cardiovascular disease now million dollar question does reduction in triglyceride reduce the cardiovascular risk or cardiovascular mortality so i will show some data the cardiovascular outcome data for triglyceride lowering drugs first was the field study 2005 baseline tg was 155 pheno 500 did not significantly reduce the risk of primary outcome of coronary events the second was awkward study 2008 baseline triglycerides slightly higher 162. after a mean follow-up of around 10 years phenotype rate did not show any cardiovascular mortality benefit was this flexible but in subgroup analysis pheno fibroid therapy effectively reduced cardiovascular disease in participants with the triglycerides of more than 204 and sdl of less than 34 and in reduced it in 2019 baseline triglyceride was still high around 216 and after follow-up of 5 years epa significantly reduced cardiovascular events compared to placebo so cardiovascular death was reduced by 20 mi 31 percent and stroke by 28 so if initial triglyceride is high lowering the triglyceride has shown to result in the cardiovascular mortality and morbidity benefit so critical importance of high triglyceride reduction is endorsed by esc 2019 and here they are quoted that in high risk patients with triglycerides between 135 499 despite statin therapy the and uh three profiles like ecosystem and ethereum should be considered in combination with statin and the american association of clinical endocrinologist 2020 says that patients with triglycerides between 135 to 499 treated with maximally treated statins who have cvd or dna so our patient has both our uh these uh this patient plus more than cardiovascular risk factors should receive ipe to prevent the ethical sclerotic cardiovascular disease what should be the ideal approach to manage diabetic dyslipidemia so here i am coating the anti-diabetic medications and the medication used for treatment of this lipidemia stretch of this are acting on insulin resistance the root cause of diabetic dyslipidemia so the answer is only metformin and the glytozone the second question is which drugs have dual action on both insulin resistance and high triglyceride for management of diabetic dyslipidemia and the answer is none i will talk about star obliter saro glitters is a new chemical entity from india and it is a dual paper gamma and paper alpha agonist and more action on the uh alpha so it has a primary effect on the people alpha and it improves the plasma lipid style by this biochemical processes and it is a secondary effect on the uh gamma it has a beneficial effect in ensuring the resistance reduction and glycemic control benefit so sarah glitters are improved glucose metabolism and insulin sensitivity index so here you can see it is insulin sensitizer and it improves the glucose metabolism and these are the various parameters which are improved by seroglitaza so here you can see it has a benefit on glycemic control fasting plasma glucose improved hb1c improved insulin sensitivity improved and the indices of the beta cell function and insulin resistance as measured by homa are also improved sarah glitters are effectively reduced high triglyceride and improves insulin sensitivity along with beta cell function and by reducing the glucose lipo toxicity uh it has a effect on the glycemic control and the lipid control so steroglitazar reduces elevated triglyceride hba1c and the raised liver enzymes in type 2 diabetic patients and this is the integrated review analysis of 18 clinical studies on more than 500 patients and seroglitaza effectively and safely reduced triglycerides by more than 50 percent non-hdl cholesterol by around 20 to 35 percent small dense ldl was reduced by 20 percent a1c was reduced by 0.7 to 1.6 percent and there were beneficial effects on liver enzyme also and before i conclude i will talk about the uniqueness of india and there is a word that means encirclement and this is a word which denotes a tactic used by labor activist and union leaders in india it is similar to picketing usually a group of people would surround a politician or a government building until their demands are met or answers are given and the oxford english dictionary could not find a english replacement name for this and they had to incorporate the word gera itself in their dictionary in 2004 point to the popularity of this world similar as the case of indian diabetic dyslipidemia the western guidelines they are focused on ldl but uh we should not ignore the fact that hypertriglycenia and low sbl are a common in indian population which is not seen in caucasian population and if we are trying and if we follow the western guidelines and keep on hammering the ldl cholesterol ignoring the triglyceride and low hdl then i don't think we are going to do justice to our patient to prevent recurrent cardiovascular events so to summarize insulin resistance is pathological hallmark for type 2 diabetes but it is also responsible for major cardiovascular risk factors like atherogenic diabetic dyslipidemia and liver disease like nash high triglyceride low hdl commonly observed in indian patients high triglyceride is responsible for increased risk of residual cbd saroglitazar is first nce from india which has shown promising effect on triglyceride non-hdl and hb1 reduction in world practice with least side effects and seroglit other is first and only drug involved which is approved by nfld in india by dcgi so thank you for patient listening i'll stop sharing my screen the house is open for discussion yeah you know all the speakers have nicely given a justification to their respective talks uh the one thing uh which uh i want clarification and uh more deliberation from the speakers is that uh one thing is very nicely predict uh depicted by dr coyle that unless we reduce triglycerides to below one feet once or 50 or 140 uh even though the ldl is at goal level the risk because of the atherogenic means small dense ldl is going to be to remain so for that triglyceride lowering therapy will is absolutely essential so as we can reduce the small density even at the same ldl level that is one thing and second thing anybody can comment about the itamas stated because pitamba stated is also as dr agarawala said that it is uh we should also consider that neo glucose i mean lean over diabetes should not occur with the stratus therapy so it was taken has got some data regarding that it does not produce any uh diabetes and its role on this yeah dr rajiv was trying to counter that yeah yeah please unmute please and dr granville muted for my strong comments the common sense medicine and evidence based medicine are there two different things there is a big jack review article anybody who wants can approach dr kamal i can send that there are two different things triglyceride is anthrogenic at the moment but there is no data to suggest that it reduces morbidity and mortality so let me make it very clear to my colleagues in endocrinology triangular side is a risk factor but modification of it does not translate into any kind of gains i call it cosmetic correction like seroglytazor is fine in correcting tgs but you don't get anything in terms of cv outcome so let us make it very very clear we are waiting for prominent trial which will be talking about pema fibrate this june 2 0 22 and then we will talk whether the tg interventions play any role or not like we have failed on hdl front and the last point i want to make it reduce it is not a triglyceride lowering trial reduce it use triglyceride as a walk-in criteria making it higher risk there is no outcome data and reduce it which is turtle related to tgs so don't make use it as a tg lowering trial so once again just to summarize triglyceride is atherogenic but like hdl tg lowering at the moment we don't have any evidence so that is the problem thank you and how long the benefit remains after giving that atherosclerosis never sleeps so it is lifelong intervention it is lifelong intervention a very costly upset this that is something that's a problem and i'll tell you inclusion is walking into the market and soon there will be price for between inclusion and pcsk9 and we'll be back thank you sir thank you i think uh what you were trying to bring out was the best tolerability is of course forbidden started but like this case where we are looking at a cv even production probably these three therapies will do come into play and yes you are very right as dr goel also pointed out the residual risk that exists with tg the dg risk is governed primarily reflective of hd tg by hdl being reflective of these small dense ldn if your pg hdl ratio is more than 3.5 what ldl you have actually reflects a smaller dense ldl which behaves like 30 milligram percent higher than what actually it is very so just don't be misled by the numbers of ldl alone and because we can't do electrophoresis or photochromatography for all for defining small dense or large dense ldl looking at tg is an important and that way i thought it was uh trying to pitch seraglitas although it does not have an evidence per say in a large clinical trial for an end point reduction mass reduction but it does have very sound robust evidence for reduction in the residual risk targeting therapy in terms of altering not only diabetes but also managing tg and residual risk that may exist so that way it's a novel therapy that's why it was pitched in but of course we are not countering it as a therapy of cb reduction but it does have a strong play when you have a dealing with a diabetic dislike again that's my comment high sensitivity with uh methods it has always served the purpose and it will be lesser costly than the pcs game tower starting is a moderate intensity stat and so it has got a very little role in day-to-day management of aggressive lipid lowering so that is the problem but if you have intolerance then today you can have pita over statin because the enzyme set is different to my bambidoic acid that kind of cocktail you can serve to the patient and a reasonably good ldl [Music] so thank you very much i enjoyed being on with you all i hope we had some insights into lipitor yeah yeah

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