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Approach to the case of Heart Failure

May 19 | 2:00 PM

Heart failure is a complex clinical syndrome in which the heart cannot pump enough blood to meet the body's requirements. It results from any disorder that impairs ventricular filling or ejection of blood to the systemic circulation. Patients usually present with fatigue and dyspnea, reduced exercise tolerance, and fluid retention (pulmonary and peripheral edema). Let's understand how to approach the case of heart failure and advances in the current line of management.

[Music] so basically the heart failure is defined by acc american heart association as a disorder or a clinical syndrome which is because of structure problem or a functional problem either of the two extremes where it's not either able to fill properly or empty properly that's a very baseline defining methodology of understanding what a heart failure would be if it's either a structural problem or it's a very important thing uh which is definition of heart failure so who do you call heart failure and there are various multiple of definitions that people have for heart failure people say very complex structural inability to commensurate with the capacity you know just forget it simple either a problem of structure or a function for two aspects either or both of them filling inability to fill properly or inability to pump it out or reject the blood properly that simple definition of heart failure now heart failure has been now categorized in the new definition into basically four i can say three that we all know and fourth i will add which is the new definition the first one is reduced ejection fraction so first and foremost for each of them patient must have either signs and symptoms or symptoms of heart failure that's number one and on top of that if ejection fraction is below 40 is called patient of f ref which is heart failure with reduced rejection fraction now you have the other extreme patient's ejection fraction is more more than 50 percent and he has got symptoms so then who are these patients these are patients whose heart is not able to fill properly what was previously called as diastolic heart failure now these patients will hence be called as fpf f means preserved heart failure preserved ejection fraction heart failure reduced ejection fraction so reduce is less than forty percent ef more than fifty percent but then how do you diagnose because everybody has got ef more than fifty percent so who do you call as heart failure those who have got a elevated bio net reutic peptide so if the bnp is elevated and at least you have relevant structural problem or a diastolic dysfunction now patients who are in between these values will be called as mid-range ejection fraction so less than 40 more than 50 and in the middle so mid range is 40 to 49 percent if you have diastolic dysfunction and structural abnormality now again once you have diagnosed so who is a patient one elevated biomarkers reduced ejection fraction or elevated rejection fraction but elevated biomarkers and more importantly symptoms so that is how you will categorize the patient into either of the three now i told you the fourth what is the fourth one improved ejection fraction so you had a patient whose previous ejection fraction was less than say 40 percent and now it has become say 50 so anybody who improves by 10 will now be called as improved ejection fraction so patient whose ef was say previously 35 now it is 45 he has a new category and this is called as patients of heart failure with improved ejection fraction now we are clear with these four definitions now what stage of heart failure you are so who's stage a b and c so this is very interesting anybody who's got any risk factor of heart failure is also stage a because we believe in preventing so what does it mean somebody who's got diabetes or hypertension is also stage a heart failure even though he does not have any structural problem but because he is at risk of developing heart failure hence he will be called as stage a of heart failure so a diabetic hypertensive patient or a coronary artery patient who's got normal ejection fraction has got no symptoms right now but he is still stage a so when you have these kind of patients you need to be very cautious about managing them that you are trying to do a preventive strategy in preventing heart failure in these patients because ultimately heart failure kills you by its manifestation so heart disease hypertension how does it because it's not the blood pressure 140 which kills you it translates into heart failure it translates into mi it translates into stroke and that's the reason you need to prevent it now what is stage b stage b is that the patient has got now structural problem but he still does not have symptoms so who are these patients suppose patient has an nmi acute mnt of all mi and with this anterior wall mi you have done an angioplasty his ejection fraction is now 45 percent there is a structural problem yes he doesn't have dystonia doesn't have dyspnea his ef is low he does not have symptoms there is a structural problem so asymptomatic structural problem is stage b who states c now this patient has started developing symptoms which kind of symptoms stable symptoms stable heart disease with symptoms of heart failure so he says i feel breathless when i climb two flights of cysts or that is uh disney or class two or he says i wake up from the middle of the night and i feel the snake sometimes but i can go back to sleep and i feel comfortable here something like paroxysmal lobster dystrophy stage c refractory heart failure patient who's got admitted you have given everything he's on so called four pillars and still coming back to you just take this take this that is stage d so once you know these classifications now i will be able to talk to you in various terminologies that are important for each therapy where they've been assessed improvised and assessed and proven to be started for each subgroup of this patient now this is the stages of heart failure and prevalence and stages now when you look at the functional class that is nyha class these are only patients because class a and b don't have symptoms so nyha is only for c and d a and b will not have any nyj understand now the most of the therapies for example mineralocorticoid antagonist spironolectome aldosterone antagonist or apliranone these have been studied in class 3 and 4. now some data emerging for class 2 and class 2 patients also nyh class i mean so these nyha class 3 4 is actually on the brink of c and d that's where so patient who's got class a you may not choose these therapies same way most of the therapies for sglt2 were evaluated again in patients in class c and d because the primal primary principle of management in medicine is you don't treat asymptomatics unless they are life threatening okay so asymptomatics you just do life risk stratification and risk factor modification you don't chase very aggressively so most of the trials are designed for class three four nyha class patients now the therapies when you look at in terms of staging the uh of 45 plus year population when you look the burden is so tremendous look at the refractory heart failure is 2 in thousand that's not that much but if you look at the other way round 2 in thousand means if you were to look in india what will happen in 45 plus this would translate into millions of patients millions of patients look at five million estimated population base for a 12 percent uh of estimation in stage c 8 to 10 million for 34 and 50 to 60 million patients who constitute 22 of patients who are at stage a of heart failure now once you are reached and suspected a patient of heart failure and you're trying to look as to how you're going to approach the case you can see that in a patient with heart failure if you can zoom into the slide uh you can pinch to zoom the slide at your end so when you look at the slide the approach is whether the patient has got peripheral perfusion which is adequate or not in a patient who's come with heart failure is the patient having acute heart failure or not so once the patient is diagnosed as acute heart failure if yes or no then when you see whether the patient is dry and warm and dry or cold dry and cold means he is hypoperfused volume depleted so when the adequate perfusion is not there when you look whether the patient is so you can have two four categories basically either the patient is dry or wet and patient is warm or cold so combinations of the two so patient is dry means he's dehydrated okay cold means sympathetic tone so dry and uh wet would differ in terms of volume status cold and warm would refer to the sympathetic tone so when the patient like like i discussed in my previous case on dyspnea approach to case of dyspnea when there is sympathetic tone there will be peripheral vasoconstriction hence the skin will become cold so when there is increased sympathetic tone patient is an acute heart failure that's cold well a patient who's warm means this peripheries are perfused well what is dry versus wet wet is somebody who's got edema whose volume overloaded while dry is somebody who's actually dehydrated who's been pushed lot of diuretics so once you can find these two things whether the patient is dry or wet you know the volume status cold or warm you know the sympathetic tone status so in a patient who's wet and warm you look at the vascular type of ideology you'll give vasodilator in diuretics if it's a cardiac etiology you'll give diuretics or you'll give vasodilator again if no then you look whether the patient is dry and warm whether it's compensated then you adjust the oral therapy if he is dry and cold which means there is an acute shock then then your case you'll have to continue the full fluid challenges to be given he's cold he's hypoperfused you have to give iv fluid to this patient so dry and cold means he's dehydrated and he's in failure maybe give him fluid he'll come out with his blood pressure improving and he'll do better so dry and cold you give fluid dry and warm it just the therapy if the patient is warm and wet then if it's cardiac then you give vasodilator in diuretic wet patients you always give diuretics and add vasodilator so based on this again you look at whether the patient's systolic blood pressure is hold on to not the systolic blood pressure should be at least more than 90 if it's below you'll have to give i know troops you'll have to give norepinephrine amongst the uh i know troops people a lot of times tend to give lot of dobutamine and dopamine this is not the best strategy you understand this is not the best strategy the best strategy which was evaluated amongst the patient or variety of shock especially septic shock though was that the best inotrope is nor adrenaline nor originally nor adrenaline will be causing less propensity of hypotension and arrhythmia while dopamine causes more arrhythmia ventricular tachycardia and cardiac arrest dobutamine will be also causing arrhythmia and cause fall in blood pressure because it is also a vasodilator so best inotrope in a patient with shock is nor adrenaline if the patient is having hypertension you can give hypertensive failure give nitroglycerin but if a patient is on top of nitrogen and then you think you need to adopt lubita then you may do that relative strength now once you've got a patient who's got you've seen a patient is in wet or dry shock or not shock in that state whether it's warm or cold or whether it's wet or dry based on that you suspect the patient to be heart failure what do you do next so diagnostic strength for non-invasive imaging for echo you can look at the structure you can look at function but you cannot very greatly look at the tissue or the myocardium and of course you very poorly can define metabolism what defines metabolism is the utility by either nuclear imaging or cardiac mri so in a patient who is previously stable does not require admission now you can send these patients to get a cardiac mr to evaluate which is good to catch up all the things morphology function tissue and metabolism when you look at the tissue again ct will not look at the tissue tissue means what what the myocardial cells are doing how good they are are they scarred or they are thick or they are viable or they are hibernating that is the thing that you can take by nuclear imaging or cardiac amount ct can look at coronary artery ct cannot again look at the muscle it cannot look whether the muscle is utilizing the substrate or not only cardiac mr and nuclear mr can look at the metabolism of the tissue eco can look at the function function can be picked by all of them but when you're looking at substrate levels these are the advantages and disadvantages in one slide that i thought i should cover now we will come to the various treatments now we all know the trials like what they say there are four pillars some say five pillars of heart failure what are the four pillars of the heart failure every patient of heart failure in a previous once he comes out from the acute failure should be on four important therapies one beta blocker two so card failure beta blockers are which bisoprolol metaprolol and carbonyl only three no other beta blocker has been proven or studied in heart field there are only three carbidinolol metaprolol and bisoprolol now between the three comparisons metoprolol fares the worst best studied is carbonyl but the problem with carbonyl is the dose is 25bd your starting door is 3.125 bd by the time you try to up titrate the patient either is lost to your follow-up or the benefits are lost metoprolol has got data which was actually compared between metropolitan and carbon was diox to carvedilol in heart failure bisoprol was started in serious trials and they found it to be good now that is about reduced ejection fraction patients who had ef low what about patients with preserved ejection fraction now there is a study with nabi bilol or which is called a senior's trial where they looked at nebulol in diastolic dysfunction or what is called as high f and they found out in an elderly patient with preserved ejection fraction seniors trial showed that nabi will all can be given in that subject so elderly hypertensive so extremes of the age is where you choose nabi belong second pillar is a vasodilator in form of either acini emitter or arb and now army what is rv well saturn plus succubutural what is cubital it is inhibitor of null present enzyme which is used to convert peptides and degrade them into vasoactive amine so when you give null present inhibitor what happens is the vasodilatory substances like bradykine in the substance p etc will also rise so you get double benefit not only you dilate the arteries but you also have the dilators like ready kind and substantially etcetera and present mediated compounds which will also add further vasodilatory property so that is arnie so army which is also available as well saturn's accumulator combination is preferred over ace or arb in the line of that so cardiologist how will he treat compared to a physician he will prescribe army compared to a c emitter or arb that's the difference again how will a cardiologist differ in treating a beta blocker he will choose either brazil prolonged or up titrated this uh carbide lol rather than metoprolol that's our cardiologist treats heart failure differently so that is second pillar third pillar is mra mra is basically nothing but mineralocorticoid receptor antagonist so which is aldosterone inhibitor so that you have either happilyron or you have patients treated with a spironolactone both of them have been started in trials like ephesus and ralph's that was done in patients with class three or four as i said so not for class one you can use it in acute my settings as a different subgroup study but in heart failure at least class three four was where it was studied and it also showed reduction in mortality now you had new data in preserved ejection interaction which is called topcat for again mra but for heart failure for preserved and reduced it is approved for both now you have one more therapy which you do is digitalis now whom to give digitalis you must give linoxin or digitalis to patient who has atrial fibrillation with lv systolic dysfunction class 3 class 3 af it's a drug of choice again a patient who's not in af if the class three patient is still refractory you can give that patient also a digitalis lennox again what is the dose previously people used to give one tablet five by seven five days they would give two days they will not give but now the dick trial analysis has shown the dose is not one tablet five by seven but half tablet five by seven because in if the digitalis level in serum goes more than one picogram per deciliter actually you have higher mortality so those of digital is also from a cardiologist has changed it's 0.25 half a tablet either 5x7 or if you have a drug like this caleptin or vera pamel you'll have to give alternate day because that's a drug interaction so if you're giving vera pamil or if you're giving carving amiodarone a lot of these patients may be on america you'll have to make it half tablet alternate day now you have some more therapies that we all know of in patients with heart failure which is sgl two inhibitor now sglt2 inhibitor is the fourth pillar what is the fourth pillar sglt2 we have two important trials people started it using in the empire egg in the empire flows in they found our patient who had an angioplasty they required lesser admission and they found it was primarily because it prevented heart failure admission and then they studied it in heart failure irrespective of diabetes irrespective of diabetes so irrespective of diabetes 50 patients in dhapa hf study were diabetic 50 for non-diabetic and then you give a clt what they found out that it reduces heart failure this was again found with emperor predator reduced and empire preserved trials and then people started realizing that empathy flows in and dapaging flows in which our sglt2 inhibitor can be given both for systolic as well as diastolic preserved as well as the reduced injection heart failure so that's the fourth pillar some people say iv iron in patients with low iron level may be the fifth pillar but we still don't have that strong data but now data is emerged for one new class of therapy and this therapy is now going to be available in india it's already available in west and that is very sigma very sick what is a cyclic amp analog basically it's nothing but it's it mimics the action of pd5 inhibitor so pd5 did not have much data a per se but like the nitric oxide donor for the pd5 was not beneficial but cyclic amp and cyclic gmp monologues like very sick word actually causes peripheral vasor riosig what you have in patients with pulmonary hypertension so riosig what everybody knows is already available in patients of pulmonary hypertension you can treat pulmonary hypertension by three therapies one endothelin intake one is two pd5 inhibitors alternate to pd5 you can use a selexi pack kind of a drug or you process cycling analog or instead of pdf you can use uh patients with that because the mechanism of action of nitric oxide is through the cyclic empty cyclic gmp pathways so instead of nitric oxide the pd5 you can directly give cyclic mpgmp analog and that therapy is very sigma is for heart failure studied in victoria trial patients who were admitted despite all the four therapy for heart failure when you added them with virus therapy and these patients in heart failure had reduced incident for readmission for heart failure so that's emerging as the new therapy hydrolyzine and a nitrate combination was started in african blacks in af trial and they found out this is a therapy that you use in patients with kidney failure because we all know that ac inhibitor arb and army in a patient whose creatinine is high you cannot give because they will have worsening in the law if their patients are already having secret attainment of three you will not be able to use asarb or rna with egfr below 30. so in that group of patients that are alternative vasodilator you can use hydrolyzine with nitrate this is available in market in various combinations and this therapy also has got a vasodilatory property nitrates will dilate veins hydrolyzing will direct arteries and they found out that the patients who cannot be given ace arb or rna if you give them hydrolyzine with nitrates these patients have reduced heart failure hospitalization and mortality especially in african blacks and hence this therapy was approved they studied this therapy neat hf but they did not find any benefit in preserved ejection fraction endothelial antagonist not proven in reduced ejection fractions zentang studied for preserved ejection fraction rna you have data both for reduced ejection fraction and there was a data called paramount and paragon which also had some benefit for preserved ejection fraction so that's when you treat hypertension crt and icd these are med therapies with devices so what is the problem in patients with heart failure if you have lbbd what will happen the heart like a fist instead of contracting like this you will have the septum contracting first and the posterior wall going away so this contracts this goes away this contracts this goes away so this is how the contraction is happening what you do is contract make them contract both together so you put two wires connect the posterior and the septal wall of the lv along with the atria synchronize between the two and make them contract together this is nothing but crt cardiac resynchronization therapy so hum patients what do we explain to our patients three wire walla pacemaker teen tarwala pacemaker so it's a pacemaker but explain to them that instead of increasing the heart rate it's going to make the heart contract like this rather than like this which was contracting when fingers contract thumb goes away thumb contracts finger goes away so this coordination is improved when you put a crt icds are sudden cardiac death preventers basically heart failure patients how do they die they die from etv here so you don't want vtv you have to be killing them when they were asleep or they were traveling and they were alone and they are not aware that they added so what the icd will do it's a diff automated implanted cardiac defibrillator it will sense the vt and it will deliver a dc shock and prevent death now what has happened is the vehicle now so when you've done these devices patient care white complex so there is no problem with synchrony so you can't put crt so what do you offer these kind of patients you can put a vehicle of stimulating device which i was part of the anthem study where i did the world's first implant or vehicle of stimulation device you use you you take help of your neurologist friend or a neurosurgeon friend or a vascular surgeon friend then dissect out the carotid artery and the carotid sheath of course it's done under ga around the vegas now view which is present in the carotid sheath you pull the vegas now out without of course resecting it you just make it separate from the carotid sheath around it you entwine the pacemaker lead and just like a pacemaker you connect that with the lead and the chest and this will give current to the vegas now which is supplying the nerve to the heart so this vehicle nerve stimulation has been studied now and is being emerging as a therapy in reduced ejection fraction is after barrow steam neo device which is now already a proven therapy in bhf trial that is baroreceptor it's already available exercise is proven as a good therapy for both uh on top of the current regime so these are the modalities now let's go to your so how do you treat stage a treat the risk factor so treat blood pressure treat diabetes treat hysteric heart disease what about stage b elbow dysfunction is developed patient is not got your symptoms you will have to give no diuretics but you'll give a centimeters beta blockers and also if required is gld but stage c and d you will have to now go back and step one so this is the algorithm for abc passed the patient out there this is when he comes to you he comes with this kind of a phenomena uh or symptomatology when he's coming with symptoms that's when he's already state c so state c the first step is the establish the diagnosis of the reduced rejection fraction and for that then you have to start guideline directed therapy the four pillars acrb or army army preferred beta blocker sglt2 inhibitor and mra aldosterone antagonist then if required you can give diuretics the patient is congested these don't diuretics otherwise don't reduce mortality these four therapies reduce mortality they prevent heart remodeling diuretics for symptom relief digitalis is for symptom relief same way very sick wise for symptom relief so these four reduce these four pillars reduce death so once you've diagnosed heart failure with class one to four you've started them on acrp or army beta blocker and mra or sglt2 is required next step is look at the functional class if the patient is class 2 to 4 look at this egfr if it's more than 30 then you will add step 3 a aldosterone antagonist if the patient is class two to three and adequate bp is still there and you've given good amount of asarb and it's no contraindication then if there is a contraindication you will discontinue and then switch between the two therapies if none and the patient is black as i said you can add hydrolyzine with nitrates if patient is class three to three with ef less than 35 and is expected to survive more than one month and he's post mi beyond 40 days so if you had a massive mi and the patient has got severe elbow dysfunction and his ef is said 20 don't put icd immediately you have to wait for 40 days c is remodeling sometimes the lbs which is stunned can improve if it still does not improve and beyond 40 days if ef is less than 4 35 that patient only you put an icd not icd is immediately posed by pass posting you have to allow 40 days for heart to recover if it does not improve then only icd again same way if ef is less than 35 and qrs is wide how wide lbbb and more than 120 milliseconds preferably more than 150 you have to put resynchronization crt as i said and class 2 to 4 sinus rhythm heart rate more than 70 and you already given beta blocker or you cannot give beta blocker one more therapy you can give which is ivab ready so iva protein was studied it reduces heart rate we all know but it does not reduce blood pressure and only if the patient cannot be given beta blocker or if you give beta blocker it's already full dose and still is heart rate is very high more than 70 if you give them they actually improve in survival and hospitalization you've done all this and patience is still in refractory heart failure same as symptoms what are the options left now so one is palliative and iv iron so artificial heart can also be given which is called as a heart mate so that therapies are emerging in west they are very costly india transplant may be cheaper than an elder device but people can actually end up getting those devices they can last for a couple of years and then you can change it or you can do a transplant while they are waiting for the donor so whatever is green is class one indication and whatever is yellow is class 2a so these are the therapies that you saw once you've got a patient of heart failure you've looked at bnp antiprobe enp those are good markers to diagnose heart failure but now what is new now let me take you to as i said i'll take you to recent advances so there are newer biomarkers there are markers of inflammation which is suggesting that the muscle is getting damaged there are markers of oxidative stress which is telling that there is a lot of oxidative damage happening to the myocardium and there is remodeling the muscle which is necrosis is getting replaced by certain fibrotic tissues and that is extra metrics remodeling so these all can be measured by various parameters inflammation by crp remember this is high sensitivity crp tnf alpha fast and interleukin 1 6 and 12. now this is important people why inflammation inflammation is emerging as the missing link in heart disease heart failure death and malignancy all of them there was a study called cantos trial where they looked at kinakinumab which is an interleukin antagonist which was injected to patients of mi after three months of acute mi what they found out that giving kanaki nub which is a inhibitor of inflammation led to 50 reduction of can you guess what malignancy surprising malignancy malignancy reduced in patients with acs when you treat inflammation of course it reduced death but this was driven by inflammation suppression of malignancy and now they are studying this link in malignancy prevention as a therapy so i think inflammation is the missing link between the whole spectrum oxidative stress by oxidized ldl myeloperoxidase urinary biopyramidines urinary plasma isoproteins and melinda d-aldehyde are other parameters which are of this category have help in pathogenesis of heart failure and targets of therapy in future extracellular metrics remodeling by metalloproteinases issue ebitdas of them collagen for epraptides pro peptide or pro collagen 1 or collagen type 3 they will be potential target therapies in future therapy again when you look at biomarkers is this is not complete you have some more for neuro hormones you have norepinephrine renin angiotensin aldosterone arginine in avp endothelin cardiac specific myocyte injury by proponents myocyte light chain kinase heart type of fatty acid protein cp kmb myosite stress by bnp and antipro bnp as we commonly do pro adreno methylene and st2 these are all again being used as diagnostic as well as therapeutic approach there are some more prognostic information which can be done with chromogranine galactin3 osteoprotegen adiponectine growth differentiated factor 15 gdf 15 soluble stf2 so these are all for those who are doing their residency and preparing for exams this is the list long list that you can write for your full questions but these are yet to become available above some of them which we already know now what are the new therapies as i was talking about so i've told you the four pillars to approach to heart failure and iv iron for those who have low serum iron and ferritin levels despite normal hemoglobin even those patients hemoglobin between 10 to 12 you give iv barium carboxy molecules it reduces heart failure hospitalization that again people say it may be because it inhibits the inflammation the drugs decreasing cardiac workload that are now available or getting available or being evaluated include carbi petrite nesiratide and ulratride these netri pep uretic peptides have not shown right now any benefit in terms of mortality reduction you have relaxin which is a vasodilator you have tolerapton which is used to treat heart failure with hyponatremia remember if you have low sodium especially if the patient is edimatous or euvonimic don't you treat hyponatremia with hypovolemia that's contraindication for tallwebton doloreptan should be given to edematous hyponatremia or normal volume hyponatremia that reduces also heart failure and prevents hyponatremia also you had l-scarring which actually failed in a trial called atmosphere aldosterone and antagonists are also being evaluated you have omnipretellate which is a vasopeptide inhibitor on top of that you have endothelin receptor antagonists like bozentan which are used to treat uh patients with pulmonary hypertension they are evaluating in heart failure and as i said a soluble cyclic guinea stimulator which is ceta sigma will soon be evaluated very sigo has already proven drugs increasing contractility will this is therapy is now already available om active mccarbil in us what it does cardiac myosin it activates chaotic myosin it forces myosin to contract more so that is used as omactive mccarbil it's available in u.s it will come in india maybe in a day in couple of years but you can use this theme of same principle the other way around in h o c m you have cardiac myosin inhibitor so that mama kempton is the name of the molecule it is used in hypertrophic cardiomyopathy you don't want heart to contract forcefully you inhibit cardiac myocyte so that is mawa kempton you want heart to contract forcefully you give cardiac myosin activator which is homo active mccarbil so also you have uh star exedone which is basically sodium potassium energy cation adps inhibitor you have rhinodine receptor stabilizers being evaluated and circa two activities also being evaluated livosimendan is available and oxymoron is also available livo cementite is commonly used it's a calcium sensitizer to increase contractility but it does not increase the uh the survival it just comes helps you to tide over acute phase another miscellaneous drug adenosine antagonist rolaphylene is being evaluated people are used are studying the carnitine also livocarnitine which is pulmonary toil transferase inhibitor also they have been studied also aiva breading which i told you and now you will have potassium absorbers they say it's again this patiroma was studied and published recently in acc american college of cardiology they found out that this potassium absorbers prevent hyperkalemia when you are giving patients with ace or arb or army so they prevent the arrhythmic deaths but they don't prevent any other survival benefit what people have been started on these oral patients in us and this therapy may also come in india soon so very sick as i said is the oral cylinder stimulator started in victoria trial class three four patients already on therapy recurrent hospitalization is prevented will be launched in india by bare pharma probably by this next two months uh basically the mechanism for this in cinesigo is similar it's like a nitrate it improves hemodynamic side effect is hypotension ionotropes as i said octave mccarbell which is basically for patients with increasing contractility initiates the power stroke by activating the myosin it increases systolic ejection time without altering the lv pressure dependency and increases hence the cardiac output in acute phase uh esteroxymone is a stimulator of membrane energy atpase and it enhances the circa 2 activity and this is very well known to you as glt-2 can ugly flows in 100 milligram empire 10 dapa 5 r25 all are once daily can be started actually dapper started in 10 most of the patients so don't give 5 i believe in 10 cut off for them now with dapa has come down to this slide is an old one it's come down to 30 and from empire it has come down to 20 egfr so up to 20 gfr you can give sglt2 initially the egfr will slightly go down but later on it improves and the long term it is a kidney protective agent it protects the kidney and produces a microalbumin media and need for dialysis so dapa heart failure trial was a very important trial which showed that it reduces the cardiovascular death by comparison with placebo by 18 and worsening of written function also with was 1.2 percent compared to 1.6 in placebo so patient with heart failure with reduced ejection fraction it was beneficial compared to placebo in preventing death and heart failure hospitalization there is another trial called champion trial which is basically a trial of sensors you have a hard sensor which allows to measure the pressures in the chambers of the heart which is inserted in a patient so wireless monitoring with daily available in a pa pressure you put a small sensor in addition to standard care and they found out that if you had that sensor that will alarm the patient and the doctor that the patient is getting congested and they will increase the dose of diuretics so it will go as a like a small pacemaker device which can be inserted into the pulmonary artery so over a six month period there is a significant fewer hospitalization and it's now led to the fda approval for implanted hemodynamic monitoring system and i believe in future you'll have variable hemodynamic monitoring system so molecular therapies for gene therapy is next people are targeting circa 2 sdf 1 adc 6 s100 a1 beta ark ct and even parva albumin which is nothing but alternate albumin barrow stream is the vehicle of stimulation as i told you you dissect the vehicle now connect it and then put it on and that's what a pulse generator also call it a bat therapy baroreceptor activation therapy you activate the baroreceptor by activating at the baroreceptor site and come out with improvement of the assessment of the adaption of the heart with the vehicle tone in improving heart failure so thank you very much i have started from zero and i've tried to take you to the gene therapy the other extreme i'll be pleased to take your questions thank you very much for slight sharing thank you yes thank you so much for that session for the audience i would request you to kindly put down your questions in the comments section you can also raise your hand if you want to ask the question directly to search for questions uh by dr sarjit khadev question what are the recommendations on high d dimer levels in adhd patients without vte yeah so re-dimer is not a strong predictor of heart failure it surely is a predictor of vascular event or thrombogenicity it also is a predictor of worsening of hospitalization related robotic milieu but if roughly in a patient with elevated d-dimer you should multiply it by 10 that's the rule i say for the age so 40 450 is 560 years 670 years 700 that's rough but anything above thousand you should be working out more as to what is the cause of elevated d-dimer so roughly you have multiplied by 10 for your age but uh thank you so much i have dr that answered your question we have a question by dr sushil a inotropic drug of choice in case of hf with reduced ef induced hypotension nor adrenaline i already shared that there is a big trial called for the comparison of the two and they've looked at primarily this had all kinds of shock coming in but uh very few cardiac shocks but again in our hemodynamics our own paper also has looked into it uh the best importance and that there is a study called diastasis study you will google it in our name you will find it we have published how uh norwegian lean actually fade much better compared to dopamine so non-adrenaline is the preferred choice only thing is you have to be very cautious give it with iv infusion and infusion pump and keep a close watch otherwise actually dopamine is more heterogeneity causes more vts and arrhythmia as compared to norwegian okay all right uh dr madison is asking how long you can continue noradrenaline good question because the tachyphylaxis with these iotropes is very common more so with patients with dopamine and vitamins so dopitamine has the biggest tachyphysis at 48 hours it stops working some say 24 hours not it really would work even up to six to eight days but again you can have a resetting of your sympathetic tone which can actually counter it so it's it's not something that they know not retrilling is better than adrenaline because of its slightly longer action but dopamine you can actually continue to give for a longer time but as soon as you get your good hemodynamics urine output patients stabilize you need to taper off moderately uh next question is by dr shirikan what would be the drug of choice when there is psvt with hypotension if you have a psvt of course you revert psp if you have a spt you need to revert the arrhythmia so anything which has got hypotension you treat it the patient has come with shock you shock that's what you do if the patient is an arrhythmia and is in shock you decision but if if you if you think that it's not the cause because a lot of these patients can mimic what is sweetie usually don't cause hemodynamic compromise but it's not a rule you can have vts where you can have normal blood pressure you can have acids which can have hypotension if in shock immunodynamic compromise shock is based otherwise triadino scene if it doesn't work maybe you dc what if it doesn't work you can of course use the tsm weird around is of course not much of value in patients all right asking a follow-up question that wouldn't it compromise the renal perfusion so theoretically it would cause renal impairment by causing constriction in the renal parenchymal vessel because of the property of noradrenaline but because that effect is negated by improvement in the central aortic blood pressure so that will actually negate and prevent but if your pressures are fine you have to just stop it whenever it's just to tide over the acute hypotension once you've done that you take it off and come out okay uh next question is if you could elaborate a bit about the surgeries for heart failure uh yeah so again a talk in a in itself uh but um just to summarize one device you can put is crt i told you indication class three four wide qrs lbb qrs more than 120 less than 35 admission class 3 or 4 crtd the second is aicd aicd is defibrillator ef less than 35 beyond 40 days of ischemic event patient class 3 4 prevents sudden cardiac death bat but simulate the whole vehicle now under evaluation and thumb study nectar hf study study they are evaluating it i mean data is out but ccm there is two current polarity chip kept into the heart current flows up and down not very poor therapy approved by usfd one more therapy is heart transplant and there is artificial art which is the lvad devices as you say left ventricular assist device in acute shock you can put ibp you can even put impella those are beyond so heart transplant is the next thing that you can have on top of this so those are the various surgeries of course do it list is incomplete you can have mitral clip you can have power in a s with elevators function so severe mr elvis function just keep so instead of the mitral leaflet like this you put a stitch in between and it becomes like this so instead of leaking from through two smaller mr will regress so that is mitra you cannot do mvr in these patients because function you can do it so lot of therapies of your words all right uh thank you so much uh dr singh has a question highest creatinine value to stop ac or arb acrb have different cutoffs april they said you can go up to 30 but the problem is not egfr problem is in these patients hyperkalemia these patients will actually start developing rise in potassium so if you have egfr up to 30 no harm in giving acrb but keep a watch on their potassium stop electron etc give them lassix rather than diet or semite give them full semi rather than dorsamide and that will actually check a good amount of it potentially if it starts going up you'll have to stop it so egfr 30 some people say 60 but 30 i think is now accepted bomb you can go up to 30 gfr as long as patient is not oligarchy and not hyperkilling okay thank you so much uh dr swamitra has a question what is the role of an anticoagulant in hf plus ef good question so anticoagulant if afib yes that becomes an afib indication atrial fibrillation indication lv clot that's another indication or ischemic revascularization then you can use vascular dose of rivaroxaban to prevent stroke otherwise giving warfarin to all aneurysms is not indicated so previously people used to give anticoagulation to every element is formed that's not the case because now you would not prefer to do that they can bleed fall have injuries which is not indicated doesn't prevent stroke only group is afib lv clot and patients with vascular disorder occipital and to prevent levels okay a similar question was asked by dr cardin that recommendations on anticoagulation in hf uh without af without af you would give an lb thrombus l a thrombus acute mi setups and vascular indication which is you have done a high risk angioplasty the pressure is beyond a year and you want to give it approximately which is not a problem for an hf patient what would be the indications to start dapagliflozin so i put the question this like this when i debate it in diabetologist forum and i tell them that you have to tell me a contraindication for giving sglt2 otherwise my every heart failure and every diabetic patient would receive sgld2 you're practically theoretically you're right because now we know in diastolic dysfunction systolic dysfunction every patient benefits from as long as his egfr is more than 30 and every patient of diabetes when you prescribe it unless you have say pylonephritis dehydration insulin dependent diabetes a patient who is not tolerating it who has got side effect to it recurrent urinary tract infection volume depleted frail fragile these group excluded i don't think a reason you have to tell me why you would not give hdlt otherwise every diabetic every heart failure should receive sglt2 because it's such a fantastic baseline therapy that it changes everything and one more interesting thing i thought because somebody has asked you you know what was the first sglt to discover the name was flourishing when was it discovered almost 150 years back where was it discovered from apple bark root apple so apple a day keeps the doctor away maybe it was that partly flows in orderly flows it that's how it kept it right true uh next question by dr paul of mishra is there any role of inter-arterial shunt device for heart failure management yeah so people have started actually decompensating heart and studies for fistula like appearances so what they do they put a graft in between artery and a vein so this is nothing but creating a large central autopulmonary fistula but this is not a proven therapy don't recommend it as a treatment of choice because it has its own complication it will unload the heart but at the cost of low cutting out so uh your perfusions may not be good patient will develop venous failure of venous encouragement and pulmonary hypertension and he will have the left heart failure left heart gets decompensated at the cost of right your question was answered dr vajragiri is asking is exercise contraindicated for pacemaker implanted patient absolutely not you must exercise exercise is the basic lifestyle modification forms the foundation in form of also cardiac rehab for every patient irrespective of what indication you put a pacemaker crt icd or even complete heart block all patients should get exercise there is no contraindication of exercise only thing they might be told not to do weightlifting because you don't want the stitches to break or you know something falling heavy on to it that's all otherwise exercise is absolutely uh recommended okay great uh dr anuj would like to ask when to start digoxin with relation to ejection fraction less than 35 class 3-4 patients already on four therapies or with atrial fibrillation these two group of patients you can start digitalis okay dr mithal has a question uh finer non and epirenone in patients with worsening chronic heart failure and diabetes medicals or kid chronic kidney disease which yeah so there are data emerging for the newer therapies uh in terms of the comparison between the two group of molecules that you mentioned but i think we don't have the availability right now of of the all of the alternatives so till that data becomes you know available i think we'll have to stick around with the capillary known bineron may not be still available as simplistically in our subgroup of patients but yes that's the subgroup there they are targeting ckd hyperkalemia but till that data emerges right now only april and spironolactone is recommended for patients with severe pah and right heart failure what you do is in a severe ph regard failure you create an asd so that the rad compensates to the left the problem again here is that you save patient from going into a recurrent heart failure but the shunt will be now from right to left because of right pressure being high and this patient will now present with cyanogens so it's a palliative procedure which is balloon atrial septostomy which you can do in patients with right heart failure to decompensate the right ventricle to the left some people do also pass for the left heart but it's not a very good strategy as i said but it may have some ground for a class 4 patient severe ph right heart failure to decompensate right to the left doing balloon atrial fibrosis all right we have one case based question that by asked by dr sushil mehta that he has a patient aged 55 male non-diabetic lvaf level is less than 20 percent can they go for a cabg cabg so this is a fantastic point of view that i always try to tell people bypass karnataka it does not depend on your ef it depends as i showed in your slide muscle improve is what you are are you pouring you know um i mean it's like it's like pouring gangajal in a dead man's mouth is not going to wake up so if the muscle is dead and your ef is 60 is not going to improve if the patient is ef is 20 but the muscle is viable is surely indicated so what determines revascularization is burden of ischemia not how much it is damaged right now more important is how much will it improve later on and to assess that you can do either a nuclear imaging as i showed in my slide or a or a cardiac mr or you can do even pet imaging without that your question has no value i mean if you have a artery which is totally occluded twenty percent has been there so for so it's a long long amount of time and you do a bypass he may not improve at all you will risk the surgery and ef may remain 20 only but you may have another patient whose eff is 20 all the muscle is hibernating and viable photographed if will become 45. so go by not the ef [Music] therapy for hf with mid-range ejection fraction i uh so i believe that mid-range should be treated just like the reduced rejection factor because in our subgroup of patients a lot of these mid-range actually have a heart failure symptoms and a lot of them can actually decompensate and become reduced ejection fraction so heart failure mid-range should be treated like reduced ejection traction dr anuj has a question how to calculate the salt and fluid intake fluid is easy 500 insensible loss compensate with 500 in sensible take and of course measure all the liquids that you ever take that's how insensible take is with the food that you may balance out with the uh insensible loss through the skin and through the perspiration and through the but for salt extra pinch of salt one pinch of salt is added five grams and if you do no salt added to any cooking you are still between 800 milligrams to one gram so that's that's the have to restrict salt to less than five grams to every patient of heart failure for sure and salt free diet as they say less than 0.5 is practically impossible less than 0.5 grams okay dr has a question a pileron versus spyron electron which is better or which is the best so spiral electron has their longest data for heart failure eplerino has got better data in acute mi heart failure so both can be done but now both have done reverse trial also so they have proven in both so you can choose either no problem but uh if you are more old-fashioned in that strategy that discuss purana data longest data so then maybe that's the real straw which showed us the way so stick to rails then spinal electron if you think patient has gynecomastia then i will switch to a polyurethane otherwise i go to i usually go doctor if there is a patient with severe mrtr with ef60 ph 45mm of hg what should i what should be advised for ph ph is secondary this means it has come from the left heart because of mr stevie tr we need to know because cbrtr why is it because of the ph or it's because of the secondary etiology i also be interested to know what is the cause of mr is it is chemical dysfunction or rheumatic depending on that cause you need to address both of them if the ph is because of the mr and secondary ph then repairing the mitral itself will be good enough you treat ph for the secondary ph if you don't have a ph only if you have a ph which is not primarily because of the tr itself and not overestimating it so of course the therapy would be either endothelin antagonist or a pd5 eliminator but then you have a lot of these patients can end up with hypotension and endothelial antagonist is my first choice over pd5 in such cases all right the last question for today is by dr anuj lvf30 mrtr ms la thrombus with pericardial infusion and ivc of 0.7 cm what can be done m s m r t r which means y e f is thirty have you ruled out carditis have you ruled out uh embolic phenomena the thrombus might have gone into coronaries cause there will be dysfunction ms will not amend up with lb dysfunction ms with cbrm mild msc mr mr lb dysfunctional or is it lb dysfunction or myocarditis or itself it is function of a coronary artery disease that is what you need to know you may have this thrombus thrown into coronaries causing mi and lb dysfunction you have carditis acute rheumatic fever causing elbow dysfunction you can have chronic mr leading to elbow dysfunction or it's it's ef which is dyschemic separated entity and this is separate ms you really should not come with elbow dysfunction if ms is with or tachycardia map you have af with fast ventricular rate and developing elbow dysfunction so why this lb dysfunction with ms mrtr can explain m elevators function ms does not explain so either ms is not tight enough or there is something else that's happening in that kind of a scenario of course you need to treat with the dilators you will have to treat heart failure the way you treat heart failure and more important read the cause keep the emboli treat the cardiac read the mr treat the ms treat the tachycardia myopathy and you will become coming out of the elbow okay great uh so so those were the questions we have some very positive good comments about it dr madison is excellent in depth discussion and you are very crisp and precise dr surya prakash says excellent oration and lecture in the last 50 years that he has heard and many more such positive comments so yes it was an amazing session so thank you so much i would like to thank you on behalf of netflix thank you so much and thank you sir thank you everyone hope to see you and catch you soon again on matters of the heart and always a pleasure to be working with netflix thank you everyone take care bye bye hope to catch you soon yes thank you so much

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Chief of Interventional Cardiology, SAL Hospi...

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