Dr.S.Venkatesan MD | Expressions in cardiology
Time 2020-10-19 19:03:26Web Name: Dr.S.Venkatesan MD | Expressions in cardiology
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Who is a doctor? Where are they made?I haven t clearly understood the true meaning of customary Dr tag, my name carries for more than 3 decades, till I saw this. Wish, this video is played to all young medical students on their graduation day. I am realizing with guilt, it requires a Holywood movie buff to remind us the true meaning of the famous WHO definition of Health, done in the most holistic fashion in the year 1948. Health is a state of complete physical, mental, and social well-being and not merely the absence of disease or infirmity.So, technically, whoever serves to improve these three components and alleviate human suffering becomes a doctor. Happy to share this on July 1st, the official Doctor s day in India in memory of the Bharat Ratna Dr.B.C.Roy of Bengal. ReferenceThe clip is from the movie Patch Adams, Directed by Tom Shadyac. A Hollywood celebrity movie maker, Virginian professor of communication turned philanthropist, now retired to a minimalist life. He is also known for his famous documentary I am that talks about the problems faced by the world. Though his works are much appreciated, I must say, they are underrated. Deserves more than an Oscar for communicating his thoughts on the medical profession perfectly and for social equality.Rate this: Posted in Uncategorized | Tagged ethics in medicine, hippocrates otth on medical education, Iam documentry Tom Shadyac, medical education, Patch adams, Tom Shadyac | Take Our PollI think it is an Invalid question. Whether you like it or not , medical science and philosophy are always bonded together and its relationship is eternal. It doesn t make sense to separate them. I think we have misunderstood the meaning of philosophy. While science is presumed truths, philosophy is trying to believe in unknown truths. Philosophical truths are built-into every decision a medical professional takes. Rudolf Carnap A German philosopher If the expected natural history of any disease is science, unexpected deviations are philosophy. (RT PCR testing for diagnosing Corona is science, why 90% of them are not infective and don t transform disease is philosophy) When something is not seen or quantifiable like human immunity, it is a perfect example of concealed science or manifest philosophy.Taking about what we think we know is science, Talking about what we really don t know is philosophy. The term Idiopathic syndrome finds a proud of the place in every specialty in medicine, Isn t? What will be your answer when your patient wants an assurance that a stent, you had just implanted will not get occluded in the next 6 months or so. I don t know, I cant assure you about that will be your most likely answer. (Though, we do it in style, hiding behind the scientific hyperbole decorated with numbers, also referred to as statistics) Please realize, this is the expression of medical philosophy in the finest form.Final message My Impression is, philosophical truths should be liberally used in a regular fashion right from the first-year medical school to advanced specialty teaching. This seems essential as science in the current times suffers from too much sanctity. This has spilled over to the doctor population as well, and make them appear invincible. If only we realize science often trails behind the philosophical truths at least by a few decades, our patients will not be injured inappropriately and prematurely. Mixing science with philosophy in the right composition ( a perfect academic cocktail ) will bring out the best from the noble profession. PostambleCan anyone guess, why scientists are given a doctorate in Philosophy degree (PhD ) ?Rate this: Posted in Uncategorized | Tagged ethics in medicine | A young man aged around 40 years, had a STEMI was promptly thrombolysed in a small hospital located about 40 KM away in the suburbs of my city Chennai. They did an awesome job of saving the patient life and salvaging the myocardium.Now begins the story . . . one of the non-medical person who is the owner of the hospital has an unfortunate working business relationship with a frighteningly big nearby hospital which had signed a memorandum of irresponsible understanding . It demanded any patient who arrives in the small hospital with MI should be transferred at earliest opportunity to them.So, an ambulance was arranged and the patient (with a fairly well reperfused heart ) was shifted in an emergency fashion . It reached desired destination after nicely chugging along the choked chaotic Chennai evening traffic for 45 minutes.The guy was taken directly to cath lab through the side doors to perform a second salvage procedure on a successfully opened IRA. Young cardiology consultants in designer cath suite welcomed the smiling ACS patient to their posh new lab .Did few rapid radial shots, mumbled among themselves for few minutes, decided to stent a minimal LAD lesion for a patient who was in zero distress with well-preserved LV function.*The relatives of the patients were curious when they were asked sign a fresh set of consent which elaborately mentioned about possible life risk during the procedure.The patient s wife was clearly amused and she pointed out to the superior cardiologists about the earlier briefing by the Inferior freelance cardiologist who treated him in the previous hospital. She recalled , I was told in confident terms that Initial thrombolysis has been spectacularly successful and bulk of the treatment is over and risk of complication has dramatically reduced .Then why is this distressing risk taking story again , she asked ?The doctors hurriedly explained , this procedure is different. We are sorry to say we have no other option but to add further risk to you ! but , its all for your good !Why should I ? If the initial lysis is very successful why do you want to meddle with it again ?No Madam , you are ill-informed , you can t talk like that .This is what modern science is all about. Leave the professional decision to us. We need to check immediately whether the lysis is really successful .We can t rely on the ECG.Further, true success lies in stenting the lesion as we fear the ill-fated site may close again.We are taught to practice protocols based on standard scientific guidelines. This hospital has highest rating in-terms of quality care. That s why we got updated ISO 2000 NABH accreditationThe women who is a soft ware engineer was smartly and scientifically silenced in 5 minutes flat !Post-amble :What happened to the patient then ? (When you fear something it happens is in t the Murphy s law ?)The apparently asymptotic and comfortable patient had uneventful PCI. A long drug eluting stent was implanted in recanalized lesion in LAD with around 30 % narrowing that ended with an innocuous looking diagonal pinch. The procedure was uneventful , however next day he developed some fresh ECG changes and chest pain . The worried team took him for another angio found stent was patent But , ultimately after a stressful 3 days of stay , some thing went wrong he ended up with new LV dysfunction.He got discharged fine with a caution that , his stent needs to intensively monitored for the next 1 year since technically he had recurrent ACS !Lessons we don t learn from such cases.When two procedures are done to accomplish the same aim (Reperfusion) , but with differing success rates, expertise, time ,and unpredictable hazards , the benefits from them may not add together. There is clear knowledge deficit here. Scientific data can never provide fair answers to these questions as all real life cofounders can never be recreated in study population.While we expect 1+1 to become two in pharmaco-Invasvie strategy ,one should realise it may end up with either zero or even 2 .1 -1 = 0-1 + (-1)= -2 ?Learning cardiology from lay persons The patient s shrewd wife threw this question ,After two modes of re-perfusion done sequentially in my husband s heart , at a total cost of Rs4.5Lakhs Why he is still left with significant LV dysfunction (Which was around 40% EF.)The query raised by the lady appeared much more crucial and logical than the ones discussed in many top-notch live interventional workshops we attend every few months!As usual , I started mulling over the issue. There is something wrong with the way , we understand the pharmaco invasive approach-PIA .You go with it only if initial pharmacological approach has failed.Of Course ,there is one more modality possible ie Pharmaco -Angio strategy where in, you look at the coronary anatomy and take a call ! This sounds good , the only issue is taking a right call ! My experience suggests wrong calls are the rule and exceptions are rare. Then a whole new issue erupts about all those non IRA lesionsFinal messageSo, til we have gain complete self-control over our evolved ignorance and evolving knowledge , it is better to follow this proposed funny new ACS algorithm called Pharmaco -non invasive approach (PNIA) in asymptomatic ACS patients who have had apparently successful lysis.*Please note, Incidentally PNIA actually refers to simple good old traditional stand alone thrombolysis.Counter pointNo one can deny Interventional cardiology carries a risk of untoward effects.Don t blow this out of proportion. Do you know, how many lives have been saved by routine Pharmaco -Invasive approach ?I am not sure , my experience may be limited.Let me ask the readers. Is routine PIA is warranted in all asymptomatic , successfully lysed STEMIs ?Rate this: Posted in Cardiology -Interventional -PCI, Cardiology -Therapeutic dilemma, Cardiology -unresolved questions, Primary -PCI | Tagged newer concepts in acute coronary syndrome, pharmaco non invasive approach, pharmaco-invasive approach, rescue pci | 8 Comments 100% occlusion of a coronary artery result in STEMI.This includes both thrombus and mechanical component .We are very much blinded till we touch , feel and see the lesion with a wire or IVUS to quantify the mechanical component s contribution in the genesis of STEMI.It is generally believed (True as well ) thrombus is the chief culprit .It can even be 100 % thrombotic STEMI with just a residual endothelial erosion and hencezero mechanical component .However , the point of contention that non flow limiting lesion is more likely to cause a thrombotic STEMI than a flow liminglesion seems to be biased and misunderstood scientific fact .What happens once 100 % occlusion take place ?Sudden occlusion , is expected to evoke a strong fire fighting response within the coronary artery.The immediate reaction is the activation of tissue plasminogen system. In this aftermath few succumb . ( Re-perfusion arrhythmia generated as VF ) .The TPA system activates and tries to lyse the clot.The volume , morphology, attachment, content of thrombus , and the elasticity of fibrin mesh , location of platelet core would determine the life and dissolvablity of thrombus. Even a trickle flow can keep the distal vessel patent .(Please note a timely TIMI 2 flow can be a greater achievement than a delayed TIMI 3 flow !)What happens to the natural history of thrombus in STEMI ?Thrombus formed over the culprit lesion can follow any of the following course Can remain static Get lysed by natural or pharmacological means Progress distally (By fragmentation or by moving en-mass ) Grow proximal and and involve more serious proximal side branch obstructionOrganise and become a CTOFactors determining thrombus migrationThe interaction between the hemodynamic forces that push a thrombus distally and hemo-rheological factors that promote fresh proximal thrombus formation are poorly understood. The altered intra-coronary milieu with a fissured plaque covered by platelet vs RBC / fibrin core, totally of obstruction, reperfusing forces , re-exposure of raw areas and the distal vessel integrity all matters.While, logic would tell us, thrombus more often migrates distally assisted by the direction of blood flow, an opposite concept also seeks attention , ie since the blood flow is sluggish in the proximal (to obstruction site )more thrombus forms in segments proximal to obstruction.(In fact, its presumed in any acute massive proximal LAD STEMI , it takes hardly few minutes for the thrombus to queue up proximaly and clog the bifurcation and spill over to LCX or even reach left main and result in instant mechanical death.)What is the significance of length and longitudinal resistance of the thrombotic segment in STEMI ?If thrombus is the culprit let us get rid of it , this concept looks nice on paper , but still we don t know why thrombus aspiration in STEMI is not consistently useful. We also know little about the length of the thrombotic segment .When a guide wire is passed over a STEMI ATO it may cross smoothly like cutting a slice of butter in some , while in few we struggle and end up with severe no-reflow inspite of great efforts .Why ?What is the Impact of distal collateral flow in flushing fresh thrombus ?The efficacy of collateral flow in salvaging myocardium is underestimated. Distal vessel flow if perfused partially by acute collaterals the thrombus load is not only less it s soft and fail to get organised early that would help cross the lesion easily.Rate this: Posted in acute coroanry syndrome, STEMI, STEMI -Managment | Tagged device migration, distal vs proxial migration of thrombus, FAILED THROMOLYSIS, primary pci total study, thrombus stemi | Leave a Comment Prosthetic valve implantation has revolutionized the management of valvular heart disease . The original concept valve was a ball in a cage valve , still considered as a fascinating discovery. It was conceived by the young Dr Starr and made by Engineer Edwards .This was followed by long hours of arguments, debates and experiments that ran into many months . The silent corridors of Oregon hospital Portland USA remain the only witness to their hard work and motivation. At last, it happened , the first human valve was implanted in the year 1960. Since then . . . for nearly 50 years these valves have done a seminal job for the mankind.With the advent of disc valve and bi-leaflet valve in the later decades of 20th century , we had to say a reluctant good-bye to this valve.There is a lingering question among many of the current generation cardiologists and surgeons why this valve became extinct ?Starr and Edwards with their child !We in India , are witnessing these old warrior inside the heart functioning for more than 30 years.From my institute of Madras medical college which probably has inserted more Starr Edwards valve than any other during the 1970s and 80s by Prof . Sadasivan , Solomon victor , and Vasudevan and others .It is still a mystery why this valve lost its popularity and ultimately died a premature death.The modern hemodynamic men working from a theoretical labs thought this valve was hemodynamically inferior. These Inferior valves worked like a power horse inside the hearts the poor Indian laborers for over 30 years.A Starr Edwards valve rocking inside the heart in mitral positionThe cage which gives a radial support* mimic sub valvular apparatus, which none of the other valves can provide.* Mitral apparatus has 5 major components. Annulus, leaflets, chordae, pap muscle, LV free wall.None of the artificial valves has all these components. Though , we would love to have all of them technically it is simply not possible. The metal cage of Starr Edwards valve partially satisfies this , as it acts as a virtual sub valvular apparatus.Even though the cage has no contact with LV free wall, the mechano hydrolic transduction of LV forces to the annulus is possible .Further , the good hemodyanmics of this valve indicate , the cage ensures co axial blood flow across the mitral inflow throughout diastole. .Unlike the bi-leaflet valve , where the direction of blood flow is determined by the quantum of leaflet excursion in every beat . In bileaflet valves each leaflet has independent determinants of valve motion . In Starr Edwards valve the ball is the leaflet . In contrast to bi-leaflet valve , the contact area of the ball and the blood in Starr Edwards is a smooth affair and ball makes sure the LV forces are equally transmitted to it s surface .The superiority of bi-leaflet valves and disc valves (Over ball and cage ) were never proven convincingly in a randomized fashion . The other factor which pulled down this valve s popularity was the supposedly high profile nature of this valve. LVOT tend to get narrowed in few undersized hearts. This can not be an excuse , as no consistent efforts were made to miniaturize this valve which is distinctly possible.Sudden deaths from Starr Edwards valve .Almost unheard in our population.The major reason for the long durability of this valve is due to the lack of any metallic moving points .Absence of hinge in this valve confers a huge mechanical advantage with no stress points.A globe / or a ball has the universal hemodynamic advantage. This shape makes it difficult for thrombotic focus to stick and grow.Final messageScience is considered as sacred as our religion . Patients believe in us. We believe in science. A good durable valve was dumped from this world for no good reason. If commerce is the the main issue ( as many still believe it to be ! ) history will never forgive those people who were behind the murder of this innocent device.Cardiologists and Cardio thoracic surgeons are equally culpable for the pre- mature exit of this valve from human domain. Why didn t they protest ? We can get some solace , if only we can impress upon the current valve manufacturers to give a fresh lease of life to this valve .http://www.heartlungcirc.org/article/S1443-9506%2810%2900076-4/abstractRate this: Posted in cardiac surgery, Cardiology - Clinical, cardiology -Therapeutics | Tagged ball valve, cardiommc, departemnt of cardiology, dr sadasivam madras medcial college, dr sadasivan, dr vasudevan, mitral starr edwards, portland hospital, prosthetic heart valve, solomon victor india chennai madras medical college, starr edwards valve, www.cardiommc.com, www.cardiommc.org | 5 Comments It is often said life is a cycle , time machine rolls without rest and reach the same point again and again . This is applicable for the knowledge cycle as well .We live a life , which is infact a fraction of a time ( 100years) when we consider the evolution of life in our planet for over 4 million years.Man has survived and succumbed to various natural and self inflicted diseases disasters. Currently, in this brief phase of life , CAD is the major epidemic , that confronts modern man.It determines the ultimate life expectancy . The fact that , CAD is a new age disease and it was not this rampant , in our ancestors is well known .The disease has evolved with man s pursuit for knowledge and wealth.A simple example of how the management of CAD over 50 years will help assess the importance of Time in medical therapeutics 1960s: Life style modification and Medical therapy is the standard of care in all stable chronic CAD The fact is medical and lifestyle management remained the only choice in this period as other options were not available. (Absence of choice was a blessing as we subsequently realised ! read further )The medical world started looking for options to manage CAD.1970s : CABG was a major innovation for limiting angina .1980s: Plain balloon angioplasty a revolution in the management of CAD.1990s: Stent scaffolding of the coronaries was a great add on .Stent was too dangerous for routine use was to be used only in bail out situationsMid 1990s : Stents reduced restenosis. Stents are the greatest revolution for CAD management.Avoiding stent in a PCI is unethical , stents should be liberally used. Every PCI should be followed by stent.Stents have potential complication so a good luminal dilatation with stent like result (SLR) was preferred so that we can avoid stent related complications.2000s: Simple bare metal stents are not enough .It also has significant restenosis.2002: BMS are too notorius for restenosis and may be dangerous to use2004 : Drug eluting stents are god s gift to mankind.It eliminates restenosis by 100% .2006: Drug eluting stents not only eliminates restenosis it eliminates many patients suddenly by subacute stent thrombosis2007 : The drug is not the culprit in DES it is the non bio erodable polymer that causes stent thrombosis. Polymer free DES or biodegradable stent , for temporary scaffolding of the coronary artery (Poly lactic acid ) are likely to be the standard of care .All stents are potentially dangerous for the simple reason any metal within the coronary artery has a potential for acute occlusion.In chronic CAD it is not at all necessary to open the occluded coronary arteries , unless CAD is severely symptomatic in spite of best medical therapy.2007: Medical management is superior to PCI in most of the situations in chronic CAD .(COURAGE study ) .Avoid PCI whenever possible.2009 :The fundamental principle of CAD management remain unaltered. Life style modification, regular exercise , risk factor reduction, optimal doses of anti anginal drug, statins and aspirin is the time tested recipe for effective management of CAD .So the CAD therapeutic journey found it s true destination , where it started in 1960s.Final message Every new option of therapy must be tested against every past option .There are other reverse cycles in cardiology that includes the role of diuretics in SHT , beta blockers in CHF etc. It is ironical , we are in the era of rediscovering common sense with sophisticated research methodology .What our ancestors know centuries ago , is perceived to be great scientific breakthroughs . It takes a pan continental , triple blinded randomised trial to prove physical activity is good for the heart .(INTERHEART , MONICA studies etc) .Medical profession is bound to experience hard times in the decades to come , unless we look back in time and constantly scrutinize the so called scientific breakthroughs and look for genuine treasures for a great future ! Common sense protects more humans than modern science and it comes free of cost too . . .Rate this: Posted in Uncategorized | Leave a Comment NSTEMI constitutes a very heterogeneous population .The cardiac risk can vary between very low to very high . In contrast , STEMI patients carry a high risk for electro mechanical complication including sudden death .They all need immediate treatment either with thrombolysis or PCI to open up the blood vessel and salvage the myocardium.The above concept , may be true in many situations , but what we fail to recognize is that , STEMI also is a heterogeneous clinico pathological with varying risks and outcome !Let us see briefly , why this is very important in the management of STEMIManagement of STEMI has undergone great change over the past 50 years and it is the standing example of evidence based coronary care in the modern era ! The mortality , in the early era was around 30-40% . The advent of coronary care units, defibrillators, reduced the mortality to around 10-15% in 1960 /70s . Early use of heparin , aspirin further improved the outcome .The inhospital mortality was greatly reduced to a level of 7-8% in the thrombolytic era. And , then came the interventional approach, namely primary PCI , which is now considered the best form of reperfusion when done early by an experienced team.Inspite of this wealth of evidence for the superiority of PCI , it is only a fraction of STEMI patients get primary PCI even in some of the well equipped centers ( Could be as low as 15 %)Why ? this paradoxPrimary PCI has struggled to establish itself as a global therapeutic concept for STEMI , even after 20 years of it s introduction (PAMI trial) . If we attribute , lack of infrastructure , expertise are responsible for this low utility of primary PCI , we are mistaken ! There are so many institutions , at least in developing world , reluctant to do primary PCI for varied reasons.( Affordability , support system , odd hours ,and finally perceived fear of untoward complication !)Primary PCI may be a great treatment modality , but it comes with a inherent risk related to the procedure.In fact the early hazard could exceed the potential benefit in many of the low risk STEMI patients !All STEMI s are not same , so all does not require same treatment !Common sense and logic would tell us any medical condition should be risk stratified before applying the management protocol. This will enable us to avoid applying high risk high benefit treatments in low risk patients . It is a great surprise, the cardiology community has extensively researched to risk stratify NSTEMI/UA , it has rarely considered risk stratification of STEMI before starting the treatment. In this context , it should be emphasized most of the clinical trails on primary PCI do not address the clinical relevance and the differential outcomes in various subsets of STEMI .Consider the following two cases.Two young men with STEMI , both present within 3 hours after onset of symptomsST elevation in V1 -V6 , 1 , AVL , Low blood pressure , with severe chest pain.ST elevation in 2 ,3, AVF , hemodynamically stable , with minimal or no discomfort .In the above example, a small inferior MI by a distal RCA occlusion , and a proximal LAD lesion jeopardising entire anterior wall , both are categorized as STEMI !Do you want to advocate same treatment for both ? or Will you risk stratify the STEMI and treat individually ? (As we do in NSTEMI !)Current guidelines , would suggest PCI for both situations. But , logistic , and real world experience would clearly favor thrombolysis for the second patient .Does that mean, the second patient is getting an inferior modality of treatment ?Not at all . In fact there is a strong case for PCI being inferior in these patients as the risk of the procedure may far outweigh the benefit especially if it is done on a random basis by not so well experienced cath lab team.(Note : Streptokinase or TPA does not vary it s action , whether given by an ambulance drive or a staff nurse or even a cardiologist ! .In contrast , the infrastructure and expertise have the greatest impact on the success and failure of PCI )Final messageSo , it is argued the world cardiology societies(ACC/ESC etc) need to risk stratify STEMI (Like we do in NSTEMI ) into low risk, intermediate risk and high risk categories and advice primary PCI only for high risk patients.Rate this: Posted in Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, Cardiology-Coronary artery disese | Tagged acc aha, acute coronary syndrome, angina, anterior mi, cardiogenic shock, coronary care unit, emergency triaging of chestpain, high risk nstemi, high risk stemi, inferior mi, is there a low risl stemi, jacc, LAD, left main, low risk nstemi, primary pci, RCA, stemi, thrombolysis, unstable angina, vulnerable plaque | 2 Comments Curiously, the management of VT is simple if the patient is unstable. Just, we need to shock. Cardiologists are troubled only with a hemodynamically stable patient with VT. Some of us still think Amiodarone is a universal antidote for any VT. Though It is effective in both ischemic and non -Ischemic VT, the success rate is not uniform.The mechanism of action of the Initial IV bolus is not a class 3 K + blocking action, instead, it is thought to be its beta-blocking action. If amiodarone fails, we may try Lignocaine, magnesium, Flecainide. .Many times it is the cumulative dose of amiodarone that reverts the VT. In some patients, it may reduce the ventricular rate instead of reverting to sinus rhythm. This is due to the prolongation of re-entrant circuit time. The question of amiodarone worsening polymorphic VT with a deleterious effect on the QT interval is still not clear yet.Why Amiodarone fails to revert VT in some ?(Up to 40 % ?)One of the factors we looked at some 15 years back was the relationship between IRA patency and amiodarone efficacy. Presented in CSI meet 2004.It was a simple conclusion. For Amiodarone to be effective IRA must be at least partially patent to enable the drug to reach the target tissue. I am not aware of any study on this issue. Request anyone to expand this study and publish it as a full paper. (Royalty-free research topic!) Please acknowledge the concept if you think it s original.Rate this: Posted in Uncategorized | Tagged brugada criteria for vt, efficacy of amiodarone, localisation of vt, magnesiusm for vt, research ideas in cardiology, research papers in cardiology | The field of cardiology is always at the forefront of any technological breakthrough. Cardiac pacing stands tall among all Innovations. While remote monitoring and pacemaker telemetry are well-known concepts. One would have wondered why Intracardiac leads couldn t communicate with each other wirelessly. Yes, It was just a matter of time, for that to happen. The leadless pacemaker Micra/Nanostim was Introduced recently but lacked the much needed physiological pacing as they were single chamber based pacing. Though mechanical sensing of atrial activity was possible with Micra TPS software patch (A VDD like mode) it wasn t providing perfect AV synchrony. (https://drsvenkatesan.com/2020/04/03/av-synchrony-in-lead-less-micra-av-pacemaker-how-does-it-sense-atria/)Now, technology has made it possible for dual-chamber leadless pacer. Here atrial and ventricular channels communicate in a wireless fashion, making it a truly wireless dual-chamber pacing. Interestingly the communication between them is not Bluetooth or NFC based but a concept called low-frequency Galvanic coupled intrabody communication. (Currently Implanted pig models.)Final message We have crossed new frontiers in the management of electrical cardiac disorders. While inadvertent cross-talk between atrial and ventricular lead was an issue in the past, now we are mastering the art of appropriate talk between these leads in a wireless fashion and use it for synchronized pacing. Rate this: Posted in Uncategorized | Tagged av micra tps, ddd vs dddr pacemaker, dual chamber wirless lead less pacemaker, micra nanostim paceaker, naspe cardiac rhythm society | If science is considered as a journey towards truth,.. knowledge, data, and statistics are the key companions in this infinite voyage to an unknown destination. While hundreds thousands of scientists do travel in this turbulent road daily, pursuing their mundane work, there are very few researchers worried about the true purpose of their journey, the quality of the road they travel, the dangerous fault lines they create. It has become a taboo topic to criticize medical science even after realizing the fact that we are compelled to follow and glorify some of the best nonsense.Dr. Jhon Loannidhis Professor of statistics and public health from Stanford University is of a different genre. He became so popular after his landmark paperHis lectures are so important to us. Physicians need to listen to his talks, infested with absolute truths, unpalatable though. RT-PCR: Real-time polymerase chain reaction, a sophisticated gene sequence-based biochemical test. Thanks to corona, this complex medical investigation has become a household name.Jones proposed his criteria to diagnose acute rheumatic fever in 1944, we still use it to diagnose with many modifications . Currently, AHA position statement 2015 by Gewitz et all is being followed. (Circulation 2015)From Braunwald textbook of cardiology. Apart from this, there is one catch . Even if the child fulfills Jone criteria, there needs to be evidence for preceding streptococcal sore throat, either by culture or antibody. Now, can we include an RT-PCR as a new parameter to diagnose streptococcal infection is the question?Why we Insist on evidence for preceding GAS?It is for a the simple reason, many entities other than rheumatic fever may fulfill Jones s criteria. (Still disease, HS purpura OR even simple viral arthritis etc) Some may even call it an essential criterion in the past. Practically it is not done is a different story.Tests for preceding streptococcal sore throat are ASO titer and anti-DNAase B. How about the now glamorous RT-pCR for streptococcus ? Though it was suggested as a useful test in the past ,the cost and logistics were prohibitive so it was never considered to be included in the Jones scheme of things.There could be three roles for RT-PCR testing in Rheumatic fever /RHD1.RT-PCR as evidence for recent streptococcal sore throat.(GAS organism) Which still not practically used often but has big scope.(Ref 1)2.To rule out co-viral (influenza-like) infections as a cause for fever and Joint pain (Used in population-based screening in a high endemic area (Ref 2)3.There could be one more indication (experimental though) Micro-RNA detection by RT-PCR to identify children who are prone for progression to RHD. (Ref 3)Final messageNow, we must introspect. While billions of dollars are going down the drain on RT-PCR for diagnosing a common cold pandemic which has no specific treatment. Will WHO and other cardiovascular preventive authorities consider to include RT-PCR as screening test for GAS in children. This will enable early start of primary prophylaxis and prevent RF/RHD a century-long scourge of the third world.Reference1.2 .Emmy Okello et all J Am Heart Assoc. 2020;9:e016053. DOI: 10.1161/JAHA.120.0160533.Lu, Q., Sun, Y., Duan, Y. et al. Comprehensive microRNA profiling reveals potential augmentation of the IL1 pathway in rheumatic heart valve disease. BMC Cardiovasc Disord 18, 53 (2018).Rate this: Posted in Uncategorized | Tagged acute rheumatic fever, aha rhd 2015 rhuematic fever, anti dnase streptococcus, group a beta hemolytic streptococci rtpcr, mirna rtpcr rhd, qpcr in rheumatic fever, revised jonec criteria 2015, RHD jones criteria, role of rtpcr fro rheumatic fever rhd | Heart failure has been classified in many ways, with prevailing levels of our knowledge and ignorance. It is based on a variety of factors like rapidity of onset, etiology, chambers involved, hemodynamics, etc. Forward vs backward failureAcute vs chronic failureRV/LV or Biventicular failure Systolic vs diastolic heart failureHigh output vs low out failureIschemic vs non-ischemic failure Reversible vs Refractory HF None of them have really helped at the bedside though it helped us understand the condition. Now, in the last decade, we have crash-landed on our favorite obsession to classify HF ie based on Ejection fraction. We believe we have found an exciting new classification. (HFrEF/HFpEF/HFmrEF).We embraced it, even after recognizing EF as a battered LV functional parameter due to its high load-dependence with a dubious reproducibility. Image courtesy : JACC: Cardiovascular Imaging volume 7, Issue 8, August 2014If we rely too much on echo, there can be a few more classifications for HF HF failure with preserved diastolic function(25% of all DCMs with HFrEF )HF with preserved mitral valve function HF with preserved Torsion and Twist.Finally, HF with normal Heart (Anemia/CKD etc) In anemia heart never fails in true sense. In fact, it works at peak capacity.(More of a Success than failure). Similarly isn t odd to put primary CKD/CRF in the CHF basket.Probably the most important and practical classification could bePrimary vs secondary HF (Primary means all muscle diseases under MOGES system ) Valvular vs non-valvular failure (Surgically correctable MVR/DVR/Mitral valve repair)Revascularisable or Non-revascularisable HF (STICH study responders)ICD/CRT eligible HF vs Non-eligible HF ( Rule out DANISH study non-responders)Refractory failure -Novel drugs/ Assist device/TAH/ Transplant suited Dr Thomas Lewis said over 100 years ago, the essence of the practice of cardiology is to recognize HF early. Looking back at the literature, there will be no dearth of classification for HF. It will come and go according to academic and Imaging whims. Of course, that may aid in ruling out primary cardiac conditions. But, we must always emphasize to the next-generation that HF is often due to systemic*(reversible too) conditions in substantial numbers. Here the heart is just a bystander watching helplessly, trying to adapt to a remote systemic comorbid problem. Such hearts don t require cowboy aggression but gentle care by concerned physicians.(One study reveals weight reduction and systematic exercise program adds more life to HF than drugs and devices. Will link the reference/ or try google)*Eg: Anemia is the commonest cause of HFpEF on a global scale. .CKD, undiagnosed autoimmune disorders, malignancy, are other classical examples. Let us be first a physician then a cardiologist, that will ensure our we don t miss important treatable conditions with our short-sighted definition of heart failure based on EF%. Is sudden, unaccustomed, physical exertion a trigger for plaque rupture and an ACS ?Yes, it is, but don t get apprehensive. The underlying risk factors, plaque burden, and its morphology matter much to result in a coronary event.What is the mechanism?Plaque morphology, the lipid core, the shoulder region s eccentricity, the crystallization of cholesterol lay the foundation. The Isometric component of stress surges Intra-coronary pressures and facilitate vascular injury. Endothelial dysfunction leading to erosion and subsequent acute total thrombotic occlusion is a well-known response to stress. Currently, spontaneous coronary dissection secondary to unaccustomed stress is increasingly recognized to be a culprit.Which is more dangerous? Mental or physical stress* ?No one can answer this query with certainty. The combination of both can prove deadly in vulnerable patients. The final common pathway for both physical and mental stress seems to be the same. Adrenergic toxicity at the cellular level.* Mental stress-induced primary electrical events (CPVT/ Inherited channelopathy ) are unrelated to plaque destabilization that is often confused with ACS in many SCDs.What are the natural protective factors to stress?Coronary autoregulation,stress-busting hormones like endorphins , natural anti-fibrinolytic systems do play a role. Human beings experience infinite episodes of mental stress in their lifetime. Only a fraction (of a fraction ) result in ACS. It is obvious , there must be some major invisible protective factors. One may call this as metaphysical force ( scientific equivalent to fate ?) operating on a particular plaque to destabilize it.Rate this: Posted in atherosclerosis, vulnerable plaque | Tagged physical and mental stress and vulnerable plaque, physical exertion and plaque fissure | Leave a Comment History is rarely kind to the original heroes in the scientific world.The classical Blalock-Taussig shunt,(BT shunt) the term we heard for the first time in the early clinical years of MBBS .We know, it as a dramatic surgery (Palliative though) connecting subclavian artery to the pulmonary artery for the commonest congenital cyanotic heart disease -Tetralogy of Fallot.Now, half a century later, came to know, there is a gripping story of an oppressed black hero behind this famous cardiac surgery. This post is all about the fascinating life of Vivien Thomas, a humble carpenter s son from Nashville. While he dreamed to become a doctor, circumstances and fate had some thing different to offer .He could join only as helper in the wards of John Hopkins, Baltimore . His extraordinary hand skills were recognised by then surgeon Alfred Blalock and made him as an assistant in the Hopkins animal lab.He was working on a project to resuscitate traumatic shock victims then. Dr Helen Taussig who was a pediatric cardiologist was wondering whether Dr Blalock could offer some surgical cure for the sick blue babies under her care.When Dr Blalock was brainstorming the problem , it was Thomas ,who created dog models of hypoxic circulation and helped create the concept and methodology of diverting blood from subclavian artery to pulmonary artery .He single handedly operated on nearly 200 dogs. He literally taught the chief surgeon Blalock the delicate vascular suture tricks .Come October 24th 1944 , the first blue baby was operated , with Blalock Insisting Thomas to stand beside. History was created -first heart surgery in USA. Which later on became the most famous concept that gave a fresh lease of life to thousands of children with TOF.It s painfully emotional to watch the Vivien Thomas standing right behind Dr Blalock,guiding his boss anxiously,with his hands tied just because he is not a qualified doctor. The others in the team included Dr Denton Cooley and Helen Taussig.No surprise, when this famous work was reported in the media, the entire cardiology community rejoiced as the news broke out over the globe .It was published in JAMA in 1945 (Blalock1945.pdf ) . Did you guess it , yes, the name Thomas was not to be found anywhere though. How can you expect it ? , after all , he is a black lab supervisor working with dogs !Thomas , work was never recognized for the next 30 years until a grand occasion (Lord made?) that happened in the Baltimore in 1971. His dream of becoming doctor became a moment of truth. Baltimore school,of medicine finally recognised his work and conferred a honorary doctor . Unfortunately Dr Blalock was no more by then to attend to his famous pupil.Its 2020 , 80 years after the monumental surgery , the BT shunt has since been renamed as Blalock, Thomas ,Taussig shunt . A new exclusive center for congenital heart surgery in Baltimore has come up in their name. What a great end to this black man s journey in troubled racial times.Thanks to Hollywood minds who thought this story deserved to be made as movie. Something Lord made directed by Joseph Sargent. It was a gripping scientific roller coaster .No surprise it got so many awards including three Emmys.Every physician,especially the cardiologists should watch this movie. I can vouch, the one and a half hours you are going to spend will enrich professionally and Intellectually. Lucky to find this movie free on you tube.The Remarkable Story of Vivien Thomas, the Black Man Who Helped Invent Heart SurgeryRate this: Posted in Uncategorized | Tagged baltimore john hopkins, BT shunt, dr blalock, dr helen b taussig, history of cardiology, modified bt shunt, something lord made, vivien thomas | It was April 15th 1912, Titanic, the Invincible, had just sunk into the dark waters of the Atlantic coast off Newfoundland. Exactly same time around, Dr. James Herrick, In Chicago, Illinois was busy documenting the first diagnosed case of acute coronary thrombosis. A new disease was born ie Myocardial Infarction. This was also the era of the Noble Prize-winning Invention of the ECG machine by Waller, Einthoven, and Thomas Lewis co that sow the seeds for the specialty of electro-cardiology.Though much was studied about MI with pathological specimens in the subsequent decades, there was a lull in the efforts to define the entity of myocardial Infarction till WHO defined in the early 1970s. It was dogmatic, still fair enough. (Clinical, Enzymes, ECG criteria, with any two feature, must be present to diagnose )Since then, the field of cardiology has seen unprecedented development in both the diagnosis and treatment of ACS. We now have a universal definition( EHJ 2019 Thygesen K ) that asks us to triage based on high sensitive troponin followed by clinical and other parameters. STEMI usually doesn t have much diagnostic confusion.Nomenclature Issues in NSTEMI/UAThe definition of NSTEMI refuses to settle, though we have come a long way since the times UA/NSTEMI were clubbed together as siblings. The term unstable angina was coined by one of the most revered cardiologists of our times Dr. Noble O Fowler in 1978. They are the same one hitherto referred to as Intermediate coronary syndrome/Pre Infarction angina. Later, if enzymes were raised it was labeled as non-transmural/Non-Q MI. This became the classical NSTEMI later changed to NSTEACS (Still it is valid)The semantics surrounding the NSTEMI is unlikely to end as long as we depend largely on ECG to diagnose and treat complex coronary obstructive syndromes. This, by no means, undermine the importance of ECG in this setting. It will remain the gold standard as far as, I can look into the future.Some observation about the new ESC 2020 NSTEMI guidelinesAnyway, ESC 2020 has addressed this issue. It suggests a new term ACS without persistent ST elevation for NSTEMI (Ideally they should have used this abbreviation NP-STEACS)(*I guess, the current ESC 2020 guidelines really wanted to get rid of both NSTEMI/NSTEACS for a very valid reason but still it was worried about the confusion it might create so retained the old term NSTEMI/NSTEACS )The categories included in the current NSTEMI scheme are1.Transient ST elevation (How transient ? Prinzmetal/ Non Prinzmetal ?)2.Persistent ST depression3.T inversion4.Flat (Absent ) T wave5.Pseudo normalization of TIt may include the following as well (Not in official ESC 20220 guidelines)6*.Hyperacute T (Very early STEMI ? or NSTEMI?7*.Wellen/Dewinter or its variantsI think ESC is to be appreciated for recognizing an off ignored observation that UA may have a transient ST elevation and end up later as NSTEMI/NSTACS. This group of ACS still poses a challenge for us to understand the overlap between total and subtotal coronary occlusion (Non-Prinzmetal ST elevation)Final message Does this nomenclature issue create problems in management? Yes, it does. The major implication is in the diagnosis ACS with dynamic ST segments ( ST-elevation / /depression or any combination)If a probable STEMI after spontaneous lysis presents as NSTEMI, Is it the baby STEMI or neo NSTEMI ? One may not rush such NSTEMI patients to cath labs.Of course, many of us are conditioned to follow a single point agenda that dictates all ACS shall reach the cath lab and managed thereafter based on coronary anatomy. If that is the case, I am sure the bulk of this 79-page new NSTEMI guideline appears redundant.(Ref 1)Reference1.Jean-Philippe Collet, ESC Scientific Document Group, 2020 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: The Task Force for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation of the European Society of Cardiology (ESC), European Heart Journal, , ehaa575, https://doi.org/10.1093/eurheartj/ehaa5752 Fourth Universal Definition of Myocardial Infarction (2018). Eur Heart J 2019;40:237-269. Rate this: Posted in acute coronary syndrome | Tagged herrick james stemi, nomenclature issues of acs, non q mi, NSTEACS, nstemi, NSTEMI new definition 2020, stemi | The incidence of stroke during TAVI up to 5 % (minimum ). Stroke risk reduction during TAVI is a critical requirement that can be a deterrent against this wonderful Intervention.Many devices are being consideredEmbolX (Edwards life science)EmrellaSentinel (Claret medical)TriGaurd (Keystone)TriGaurd 3just got the approval from CE and appear promising. (REFLECT trial) It is inserted through the transfemoral route , deflects embolic material to descending aorta since it covers all the three branches of Arch.What happens to these deflected particles? Any bodys guess.So , in my understanding it converts potential brain embolisation to peripheral microemboli , whA nice descriptive animation .https://player.vimeo.com/video/232995629While, these innovative aortic arch filters reduce the risk of periprocedural embolic stroke, please mind, TAVR patients continue to be at significant risk for stroke over a long period. This is due to other late causes like TAVR leaflet thrombosis, atrial fibrillation, arch atheromas, and bleeding due antiplatelet agents.Reference1.WienekeVlastra, JeroenVendrik, Karel T.Koch et al Cerebral protection devices during transcatheter aortic valve implantation Trends in Cardiovascular Medicine Volume 28, Issue 6, August 2018, Pages 412-4182.(REFLECT trial) Rate this: Posted in tavr tavi, Uncategorized | Tagged embolic protective device for tavi tavr, embolx, sentinel. triguard 3 | Older Posts October 2020(4) September 2020(7) August 2020(10) July 2020(6) June 2020(9) May 2020(9) April 2020(5) March 2020(7) February 2020(3) January 2020(4) December 2019(3) November 2019(6) October 2019(3) September 2019(6) August 2019(3) July 2019(1) June 2019(3) May 2019(2) April 2019(2) March 2019(2) February 2019(4) January 2019(2) December 2018(2) November 2018(2) October 2018(2) September 2018(1) August 2018(2) July 2018(3) June 2018(1) May 2018(3) April 2018(1) March 2018(3) February 2018(3) January 2018(1) December 2017(3) November 2017(3) October 2017(3) September 2017(2) August 2017(2) July 2017(2) June 2017(2) May 2017(4) April 2017(3) March 2017(3) February 2017(5) January 2017(3) December 2016(2) November 2016(5) October 2016(4) September 2016(3) August 2016(5) July 2016(3) June 2016(4) May 2016(3) April 2016(6) March 2016(4) February 2016(3) January 2016(5) December 2015(6) November 2015(5) October 2015(8) September 2015(2) August 2015(5) July 2015(7) June 2015(4) May 2015(6) April 2015(5) March 2015(7) February 2015(15) January 2015(8) December 2014(5) November 2014(8) October 2014(7) September 2014(9) August 2014(5) July 2014(11) June 2014(5) May 2014(4) April 2014(5) March 2014(8) February 2014(8) January 2014(5) December 2013(7) November 2013(7) October 2013(14) September 2013(11) August 2013(15) July 2013(15) June 2013(15) May 2013(15) April 2013(15) March 2013(15) February 2013(15) January 2013(15) December 2012(15) November 2012(15) October 2012(15) September 2012(15) August 2012(15) July 2012(15) June 2012(15) May 2012(15) April 2012(15) March 2012(15) February 2012(15) January 2012(15) December 2011(15) November 2011(17) October 2011(17) September 2011(17) August 2011(21) July 2011(20) June 2011(17) May 2011(15) April 2011(17) March 2011(25) February 2011(20) January 2011(20) December 2010(18) November 2010(21) October 2010(21) September 2010(25) August 2010(20) July 2010(10) June 2010(11) May 2010(19) April 2010(16) March 2010(14) February 2010(22) January 2010(18) December 2009(20) November 2009(20) October 2009(3) September 2009(21) August 2009(19) July 2009(12) June 2009(12) May 2009(11) April 2009(15) March 2009(21) February 2009(4) January 2009(12) December 2008(13) November 2008(9) October 2008(22) September 2008(20) August 2008(16) July 2008(14) June 2008(7) Please give your feed back . 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