This is a 15-year-old post about LVH, written in 2008. Few of my colleagues, now agree with this, but still hesitate to oblige in the open, suggesting it is too good to be true! Re-posting it for your own assessment. Surprised, why cardiology community didn’t consider this observation worthy to pursue.
Advantages of Left ventricular hypertrophy (LVH)
Left ventricular hypertrophy is one of the most common clinical cardiac entity.It is recognised either by ECG or echocardiography.LVH has a unique place in cardiology as it can imply a grossly pathological state or a marker of healthy heart as in physiological hypertrophy in athletes.
Logic would suggest, in this era of stem cells and nano medicine , every muscle fibre in ventricle is worth in gold !. So when the nature provides an extra reserve of myocardium in the form of LVH one should welcome it, if otherwise not harmful.
Is LVH due to systemic hypertension benign ?
Not really, LVH has been shown to be an independent cardiac risk factor. (The famous Framingham study)Further LVH can result in diastolic dysfunction and the risk of cardiac failure increases.
But in spite of these observations, an astute clinician with considerable experience will appreciate , patients with LVH fare better during an acute coronary syndrome !
This has been a consistent clinical observation . (Shall we call it as class C . ACC /AHA evidence? )
Is LVH an asset during ACS ?
A hypertrophied heart takes ischemic injury very easy , it doesn’t really hurt much . Another possibility is that in LVH myocytes are relatively resistant to hypoxia .
Patients with LVH rarely show significant wall motion defect following an STEMI.This is probably because the full thickness transmural necrosis is almost never possible even if extensive MI occurs.
This is also reflected in ECG as these patients rarely develop q waves in following STEMI .
Persistent ST elevation and failed thrombolysis is very uncommon in pateints with LVH.
LVH provides a relative immunity against development of cardiogenic shock . It requires 40% of LV mass destruction to produce cardiogenic shock.This can rarely happen in LVH. In a long term analysis we have found none of the patient with LVH developed cardiogenic shock following STEMI.
LVH patients are also protected against development of free wall rupture.
Concluding message
“Lack of published evidence is the weakest evidence to dismiss a true myth”LVH , either pathological or physiological, has a hitherto unreported beneficial effect.It acts as a myocardial reserve and helps limit the impact of STEMI.
Pardon ,this video is nothing to do with cardiology. It is from the archives of the United nations library .This can teach some important lessons in art of communication , sharing to all folks, especially medical students. It was recorded in 1959 in Newyork, UN head quarters.Four 17 year old school girls & boys were invited for a debate on a complex topic. Does God exist ? How do you pray ? and what is the purpose of different religions ?
I keep wondering , how these youngsters accumulated so much wisdom and express it in such a polite manner too. Mind you, this was recorded , when learning happened with out any digital aids.The word Internet was unheard off. No ego, no bluntness, no diatirbes that has become a norm in many debates now. I got a punching lesson from this clip, be gentle when taking extreme views in any topic.
I wish, every medical debate in class rooms should happen this way.The key to succesful debate is, to accumulate knowedge, willingness to question the convention, and respecting the oppositie point of view.
The high point of talk show, was, when the Brazilian girl(due respects, she should be nearing 80 years now) tell us casually some things are not meant to be understood in life .I tell the same when some patients ask too many questions about their illness which may not have an answer.
Wishing every one of you an Enlightening New year. As we begin a new journey around the sun, yet another time, let us re-dedicate ourself, to use science, for the welfare of our planet & people.
Thank you , for visiting this site and make all its worth.
Just one memory of 2022, lingers ! Retired and left Madras medical college,Chennai after 3 decades, which grew me up as a Cardiologist.
“I thought, he was not the right patient for the procedure. I believe, what I did was the correct decision. Why all this fuzz? after all, the patient is doing so well without that procedure,.. are you worried about that?
“No, I need an explanation, we have a fully functional cath lab in our center. The patient came in the right window period. Still, you haven’t offered the best mode of treatment”.
“I can reiterate it again sir. Just because a lab is available 24/7, it doesn’t make all patients eligible for a PCI. I think I didn’t commit a professional misdemeanor when I decided in favor of fibrinolysis. In fact, I would be guilty had I rushed him to the cath lab, just to satisfy the misplaced scientific position we have decided to adopt. If you think, I am culpable for successfully treating a patient without taking the patient to the cath lab, you may proceed with the penal action.
Before that, I would request you to please read the current edition of this book we all revere. (Which continues to mentor physicians all over the globe for the past 50 years)
The current edition of Harrison 2022 is just out. I thought, there is something great learning point in Cardiology chapter, specifically about the reperfusion strategies in STEMI
My hearty thanks to the editors of the chapter for the crystal clear expression about this much-debated procedure* and specifically choosing the word “PCI appears* to be more effective ” (even) if it is done in experienced persons in dedicated centers. The choice of the word used by the authors is Intentional and must be applauded. This message must be propagated to all our fellow physicians. What a way to convey an important truth pertaining to the management of the most common cardiac emergency, while many in the elite specialty are so dogmatic in their assertion without verifying the reality.
* The verdict is still under the jury even after 3 decades, since the PAMI days of the early 1990s. Thank you, Harrison. What a gentle, but a righteous way to express an opinion about a procedure that is apparently enjoying a larger-than-life image based on a handful of studies and a flawed meta-analysis.
Final message
Primary PCI is just an alternateform of treatment to fibrinolysis in STEMI. Both are equipoise in the majority of patients. Extreme care and diligence are required to harvest the small benefit the PCI seems to provide. There are lots of ” if and buts” that decide the success of this procedure. Get trained, and do it selectively for those who really need it.
Postamble
You may call yourself a super-specialist. But, please realize, If you have any doubt about key management strategies, never feel shy to take a cue from Internal medicine books. The greatness of these warrior books is that, it comes devoid of all those scientific clutters backed by premature evidence.
Dr.Richard Asher, a British physician from Sussex addressed a group of young passing out medical students way back in 1948 in London. The lecture was titled seven sins of medicine! We should thank the Lancet for having published this brief speech the subsequent year in its journal making it immortal medical teaching!
Though he was listing these sins among medical students, it is very relevant to every health professional.
1.Obscurity
Asher endorses the use of clear communication and plain language whether writing or speaking. Obscurity may be used to cloak one’s own ignorance, or due to an inability to communicate with those outside of the medical profession. “If you don’t know, don’t admit it. Instead, try to confuse your listeners.” is not uncommon. Regardless of the intention, whether to misdirect from incompetence or to foster a feeling of superiority, the patient and those surrounding them are often left confused and uncertainiy.
2. Cruelty
This sin is perhaps one of the most commonly committedby doctors and medical students. Whether it be the physical thoughtlessness of a half-dozen students palpating a painful tumor mass, or loudly taking (or presenting) a patient’s history in a crowded room, one of the first things that is unlearnt by a medical professional is to treat the patient as they themselves would like to be treated.
3.Bad Manners
Often overlooked, rudeness or poor taste in humour is condoned within the hospital setting. At the end of the day, many doctors and students are simply rude to patients that do not suit them. Whether it is a snapping at an uncooperative patient or making a cruel joke about them after leaving the room, the impact of these “coping mechanisms” (as they are considered to be by many) must be taken into account.
4. Over-Specialisation
In a growing trend by the medical establishment, over-specialization and under-generalization is a growing problem in the wider medical community. Ignoring aspects of one’s education in favor of more interesting aspects is a behavior that is pathological and outright negligent in a student. Failure to diagnose or to treat a patient because “their signs and differential fall outside of my field, let’s turf them to another service” ought to be a seriously considered Supervisory & Training issue.
5.Love of the Rare
(aka “If you hear hoof-beats, think horses. Not zebras”) The desire for rare and interesting diseases causes many medical students and young doctors to seek the bizarre rather than seeing a mundane diagnosis.
6. Common Stupidity
As well as the standard definition for this sin, the specific example of “using empirical procedures rather than tailoring for the patient” or the young doctor “flying on autopilot” must be mentioned. Ordering another test that is redundant, and for which the results may already be interpreted from the history, before starting treatment is such a situation. For example: requesting a hemoglobin count before beginning transfusion, despite the fact that the patient appears obviously anaemic.
7. Sloth
Laziness. Also includes ordering excessive numbers of tests, rather than simply taking the time to take an adequate history
Final message
It is astonishing, to note Dr.Asher made this observation in the very early days in the evolution of modern medicine,(No critical care units, no HMOs, No industry nexus with research, & commodification of medicine ) I wonder what Dr. Asher would have to write if he is alive in 2021.
Wish, every medical professional shall find their Asher score. Looking back on my career, I must confess my score would be 3 ( may be 3.5 !) out of 7. Now, desperately trying to get rid of them. Mind you, the 4th (Overspecailisation) and 6 th (common stupidity) is inherently built into the system. I think, very tough to avoid them.
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.
Reference
The 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 amthat 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.
I 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.
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 trailsbehind 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 ( aperfect academic cocktail ) will bring out the best from the noble profession.
Postamble
Can anyone guess, why scientists are given a doctorate in Philosophy degree (PhD ) ?
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 accreditation
The 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 strategywhere 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 lesions
Final message
So, 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 point
No 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 ?
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 hence
zero mechanical component .However , the point of contention that non flow limiting lesion is more likely to cause a thrombotic STEMI than a flow liming
lesion 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 obstruction
Organise and become a CTO
Factors determining thrombus migration
The 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.
Mohandas Karam Chand Gandhi , father of my country , India , made these observations in year 1925 about the fundamental constituents of violence in society . These words of monumental wisdom came when he was addressing young Indians in a country- side rally .
Note, his finger points to , what exactly is relevant to our profession ! He emphasized this nearly 100 years ago, when medical science was at its infancy .One can only guess what would be Mahatma’s comment about our profession in it’s current form !
Should we include moral, behavioral and ethical classes right from the first year of medical school along with Anatomy , physiology and bio chemistry.Medical council of India obviously need to burn more mid night oil , I wish it happens in my life time. !
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 position
The 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 message
Science 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 .
This was written originally in 2009 early days of this blog. Now, re-posting it in 2021 , wonder any one has new data on this!
We know diabetes, smoking, hyperlidemia, hypertension are major risk factors for progressive vascular disease. They damage the vascular endothelium either directly or indirectly , by aggravating the atheroscelortic process . Diabetes apart from affecting the medium sized arteries , also affect the microvasculature. Smoking has a direct effect on endothelial function .It depletes vascular nitric oxide. High levels of circulating lipids injures the sub endothelial structures and invades the media by entering macrophages .So , all these 4 risk factors either operate independently or interact with each other and result in progressive vascular disease.
While we believe , these risk factors do not have any bias in attacking the human vascular tree, in the real world it is observed they have their own behavior pattern and have unique predilection and a deadly alliance .
For example , in chronic smokers TAO is the commonest manifestation , thrombo angitis is far too less common to occur in the coronary arteries.
Similarly hypertension per se rarely results in an acute coronary syndrome while it is the single important cause for cerebro vascular disease. Diabetes especially in women has very strong predilection for CAD , while diabetic per se is a lesser risk for stroke. Hyperlipedimia may be the one which has fairly even risk throughout the vasculature. Similarly there is a difference in renal and carotid arterial involvement with reference to the conventional risk factors .
Why this apparent difference ?
We are unlikely to get an answer to this question in the near future . Left to the youngsters . . . of tomorrow !
* Note of clarification
The source for the above chart is collected from various studies and also a huge observational data from our hospital. There could be some geographical variation , a given individual may respond differently to these risk factor depending upon his genetic predisposition and susceptibility . So the above data can be applied to general population and not to a individual.
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 situations
Mid 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 use
2004 : 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 thrombosis
2007 : 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 . . .
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 STEMI
Management 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 paradox
Primary 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 symptoms
ST 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 message
So , 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.
This is a 15-year-old post about LVH, written in 2008. Few of my colleagues, now agree with this, still hesitate to oblige in the open, suggesting it is too good to be true! Re-posting it for your own assessment. Surprised, why cardiology community didn’t consider this observation worthy to pursue.
Advantages of Left ventricular hypertrophy (LVH)
Left ventricular hypertrophy is one of the most common clinical cardiac entity.It is recognised either by ECG or echocardiography.LVH has a unique place in cardiology as it can imply a grossly pathological state or a marker of healthy heart as in physiological hypertrophy in athletes.
Logic would suggest, in this era of stem cells and nano medicine , every muscle fibre in ventricle is worth in gold !. So when the nature provides an extra reserve of myocardium in the form of LVH one should welcome it , if otherwise not harmful.
Is LVH due to systemic hypertension benign ?
Not really, LVH has been shown to be an independent cardiac risk factor. (The famous Framingham study)Further LVH can result in diastolic dysfunction and the risk of cardiac failure increases.
But in spite of these observations, an astute clinician with considerable experience will appreciate , patients with LVH fare better during an acute coronary syndrome !
This has been a consistent clinical observation . (Shall we call it as class C . ACC /AHA evidence ? )
Is LVH an asset during ACS ?
A hypertrophied heart takes ischemic injury very easy , it doesn’t really hurt much . Another possibility is that in LVH myocytes are relatively resistant to hypoxia .
Patients with LVH rarely show significant wall motion defect following an STEMI.This is probably because the full thickness transmural necrosis is almost never possible even if extensive MI occurs.
This is also reflected in ECG as these patients rarely develop q waves in following STEMI .
Persistent ST elevation and failed thrombolysis is very uncommon in pateints with LVH.
LVH provides a relative immunity against development of cardiogenic shock . It requires 40% of LV mass destruction to produce cardiogenic shock.This can rarely happen in LVH. In a long term analysis we have found none of the patient with LVH developed cardiogenic shock following STEMI.
LVH patients are also protected against development of free wall rupture.
Concluding message
“Lack of published evidence is the weakest evidence to dismiss a true myth”
LVH , either pathological or physiological, has a hitherto unreported beneficial effect.It acts as a myocardial reserve and helps limit the impact of STEMI.
Having retired, find little more time in browsing the academic images lying idle in old computers.It is interesting, still a tiring job to pick any useful learning stuff, from heaps of data hiding in different hard drives.
This set of ECGs I could retrive from the year 2011, A 31-year-old male presented to our CCU at 4.50 PM.
The treatment was Initiated in 10 minutes and completed in an hour, (Those days cath lab wasn’t functioning 24/7, more importantly, there was no external interference with our professional decision-making process)
The ECG was repeated at 7.15 PM
I think this case is much relevant even today, because it made me guilty of committing a crime*, by treating a STEMI without the help of a cath lab and discharging the patient with near normal ECG and LV function. The guilt was further amplified as I had used the lowly streptokinase, and not the glamorous Tenecteplase which could have produced a brisker and more complete TIMI 3 flow.
*One of my corporate friend called it a heinous one by current standards, for not attempting to visuvalise the IRA and a possible pharmaco invasive PCI.
Final message
STEMI can be tackled successfully in a number of different strategies. Immediate cath lab care is an optional accessory in the majority and of course, it can be life-saving in the minority. If we are unable to differentiate which patient will truly benefit from urgent cath lab intervention, I think, we have a huge problem, with the way we learn and teach cardiology. Hiding behind double-blinded statistics and RCTs is not going to bring a solution to this largely self-inflicted scientific predicament;
PH has always been an exciting academic topic in cardio-pulmonary medicine, for both clinicians and researchers. It is also one of the extensively studied hemodynamic parameter. The pressure in pulmonary circulation is intimately tied to the function of two critical organs. lungs , heart and various systemic factors. The fact that pulmonary circulation is essentially expansive & engulfed by the dynamics of lungs, makes PA pressure a continually variable parameter. Further ,the chest wall compliance, airway resistance , influence of pleural pressure fluctuations, make it difficult to estimate the normative pulmonary artery pressure and resistance even in rest.(Imagine during exercise !)
No surprise, our knowledge base about PH is under constant flux. The trouble starts with this query, What is the normal PA pressure ? After toying with various numbers we are currently hanging all our wisdom at a mean PA pressure > 20 mmhg as cut-off to define PH. However, we are able to grossly classify PH into various categories , pre/ post /combined etc. Here again, we have a guess work with two more cut offs.. For PCWP we have decided to choose 15mmhg over 12mmhg as upper limit of normal & PVR < 2 Wood units.
The second query in PH is still more contentious. What is the effect of exercise on PA pressure ? In our student days we were not allowed to bring exercise into the picture of pulmonary hypertension, in spite of the fact cardiac output increases up to 5 fold during peak exercise, Now, there is evidence to show exercise can increase PA pressure significantly, beyond the limits of current definition of PH. This is problematic for obvious reasons. Still, there has been considerable reluctance to accept exercise induced PH as a clinical problem by many of us .
*To be fair with our intellect, I think, we haven’t yet approved “Exercise induced systemic HT” as an entity officially. (Of course, hypertensive response during stress test is well known)
Seeds of New thinking
Thanks to current guidelines from ESC in 2022 .The exercise induced PH has come back with a bang and finds a place right behind the pre and post capillary PH. (See below ) I am sure, there must have been a vigorous debate before including this in the definition. We must appreciate the authors of two forgotten papers for the major shift in our understanding .(Ref 1 ,2)
The secret of the slope : From where did it come ?
ePH is > 3mmhg /Litter/Minute is the definition of ePH
It is the rate of raise that matters not the absolute pressure. This slope was validified in by Bossone E et al (Ref 2)
Some questions on ePH
1.How do you define ePH ?
Mind you, it is not an absolute number. It is the slope more than 3mmhg per litre of cardiac output. I agree to measure the slope > 3mmhg we need serial measurement and may be impractical .(Immediate post exercise echo is a close alternate )
2.Why we depend on slope rather than absolute value ?
This is because during heavy exercise PA pressure can raise even up to 30 or 40 crossing the boundaries of PH ..Only the rate of raise ie the slope can tell us whether it is appropriate or inappropriate.
3.Does ePH is really a clinical problem ?
Yes. it should be suspected in every unexplained dyspnea .(Beware of the anxiety it may elicit to the patient, so, go slow with your investigation first rule is to rule out Anemia and other common causes )
4.Can ePH occur over and above established causes of PH ?
Why not ? it is very well possible.(PH before and after six minute walk test will unmask this component)
5.Can we further classify ePH ? (Pre vs Post cap ePH)
Possible yes. ePH can be a marker of HFpEF if LVEDP is also correspondingly increased or else it will fall in to CETP or COPD.
6.Can COPD cause ePH ?
Yes, possible.
7.How does RV function confound ePH ?
This is ticky. Perfect RV-PA coupling and a good RV function is required to sustain ePH. A poorly contracting RV will make the whole concept of ePH and the defining criteria redundant. May be, we need to work for RV function corrected ePH . (This is a potential research topic for fellows)
8.Where do diastolic stress testing fit in diagnosing ePH ?
In one aspect ,DST which is screening test for silent HFpEF is an example for subtype of ePH.
Final message
The concept of ePH has entered once again into the cardio pulmonary clinical domain. Thanks to ESC 2002 team for listing this hitherto ignored disorder. Let us reiterate the importance of this concept in the clinical practice. It is worth considering some form of stress test to recognise this entity, in every patient who has unexplained dyspnoea.
Good morning GPT. Let me introduce myself . I am a medical doctor, practicing cardiology, in Chennai India. I have had a long-standing query in very fundamental principles of the practice of medicine. Just wanted to chat and clarify with you.
Welcome, I am here to help you
Medicine is both art and a science. In recent times the movement of evidence-based medicine (EBM ) is trying to overturn the clinical experience. I have a feeling it is not fair. We can’t create evidence for every decision we make in clinical science right?
My first question is
Can experience-based medical care beat evidence-based care?
No, experience-based medical care cannot beat evidence-based care. Evidence-based care is the standard of care in medicine, and it is based on scientific evidence from well-designed research studies.
Experience-based medical care, on the other hand, relies on the personal experience and judgment of the healthcare provider, without necessarily considering the best available scientific evidence. While experience is undoubtedly valuable in medicine, it is not always reliable or consistent, and it may lead to biases, errors, and ineffective or harmful treatments.
Why unpublished experiences & truths are not respected in science?
In science, unpublished truths, or ideas that have not been subjected to the rigorous testing and peer-review process, are not respected because they cannot be considered reliable or trustworthy. Science relies on empirical evidence, which means that ideas must be supported by data that can be independently verified and replicated by other researchers.
Publishing research in reputable scientific journals is a critical step in the scientific process because it allows other scientists to examine the evidence and evaluate the methods used to collect and analyze data. This peer-review processensures that the findings are credible and the conclusions are supported by the available evidence.
Is it possible for the peer review process, to make a falsehood a truth?
Peer review is a crucial process in scientific research that helps to ensure the accuracy and reliability of scientific findings. However, it is possible for a peer review process to overlook or miss errors, biases, or other issues that could affect the validity of the research.
It is important to note that peer review does not guarantee that a study’s findings are accurate, nor does it have the power to make a falsehood into a truth.
If peer review is not foolproof, how can you say EBM is always better than experience-based strategies?
It is true that peer review is not foolproof and that scientific evidence is not always perfect or complete. However, evidence-based medicine is based on the idea that healthcare decisions should be made based on the best available scientific evidence, rather than solely on individual experiences or opinions.
How can you say unscrutinized experience is always bad?
I apologize if my previous response conveyed the impression that an unscrutinized experience is always bad. That was not my intention. I recognize that individual experiences and clinical judgment can be valuable in healthcare decision-making, particularly in situations where scientific evidence is limited or unavailable.
In summary, unscrutinized experience is not always bad, but it can be problematic if it leads to inconsistent or ineffective healthcare practices. Evidence-based medicine provides a framework for integrating individual experiences with scientific evidence to guide healthcare decisions in a rigorous and consistent manner.
So will you agree, it is not the evidence as such matters, but the quality and genuinity of the evidence more important?
Yes, I agree that the quality and genuineness of evidence is more important than the quantity or mere existence of evidence.
Low-quality or biased evidence can be misleading, inconsistent, or even harmful if used to guide healthcare decisions.
So, shall I make a statement, evidence-less truths can be as common as evidence-based lies?
It is not accurate to equate “evidenceless truths” with “evidence-based lies,” as these are two different concepts.
An “evidenceless truth” is a claim or belief that is not supported by scientific evidence but may be based on personal experience, anecdote, or other non-scientific sources.
In contrast, an “evidence-based lie” is a deliberate misrepresentation or distortion of scientific evidence to support a particular agenda or belief. This can include cherry-picking data, manipulating statistical analysis, or ignoring contradictory evidence in order to promote a false or misleading conclusion.
How common is evidence-based motivated falsehoods and lies in science?
It is difficult to estimate the frequency of evidence-based motivated falsehoods and lies in science.
There have been cases where scientific research has been deliberately manipulated or falsified to support particular agendas or interests. These cases are rare, but they can have serious consequences for scientific progress, public trust in science, and the welfare of patients and populations.
Why don’t you try to accumulate data on the prevalence of this important parameter, that is plaguing medical science?
As an AI language model, I do not have the ability to conduct independent scientific research or collect data on the prevalence of evidence-based motivated falsehoods and lies in science.
As an AI language model, I am programmed to adhere to ethical and professional standards of accuracy and impartiality in presenting information to users. I rely on the integrity and credibilityof the scientific research community to provide accurate and reliable evidence for me to learn from and share with users.
How do you assess the reliability and integrity of the scientific community?
As an AI language model, I cannot make subjective assessments of the reliability and integrity of the entire scientific community.
So you believe strongly the peer review process. Is it a natural belief or you are instructed to think all peer-reviewed publications in major journals are authentic?
As an AI language model, I do not have beliefs or opinions of my own. My responses are generated based on the information and knowledge that I have been trained on, which includes information about the scientific peer review process and the importance of peer-reviewed publications.
How do you assume the peer review process is rigorous and transparent?
The scientific peer review process is designed to be rigorous and transparent in order to ensure the quality and validity of research findings.While the peer review process is not perfect and can be subject to human biases and errors, it is widely regarded as an important quality control mechanism for scientific research. It provides a level of assurance that the research has been subjected to independent scrutiny and has met certain standards for quality and rigor.
Do you think the “peer review” process also needs scrutiny?
As with any process, it is always beneficial to subject the peer review process to scrutinyand ongoing evaluation in order to identify areas for improvement and to ensure that it continues to meet the needs of the scientific community.
Do you think scientists hide vital information?
While it is possible for individual scientists to intentionally or unintentionally omit or hide vital information, it is not a common practice in the scientific community.
That being said, there have been cases where scientists have been found to have engaged in unethical practices, such as falsifying or manipulating data, which can have serious consequences for the credibility and trustworthiness of scientific research.
Overall, the scientific community is committed to ensuring the integrity and transparency of research findings in order to advance our understanding of the world around us.
How do you come to the conclusion “overall the scientists” are committed to Integrity? Is it a belief? Or truth ?
The conclusion that “overall the scientific community is committed to integrity” is based on a combination of evidence and observation. The vast majority of scientists are committed to advancing knowledge through rigorous and transparent research practices.
Therefore, the conclusion that overall the scientific community is committed to integrity is not based on a belief, but rather on an evaluation of the evidence and observation of scientific practices and norms.
Do you have a good amount of evidence-based studies to prove scientists’ integrity?
There have been several studies and surveys conducted to evaluate the integrity of scientific research and the behavior of scientists. For example, a 2016 study published in the journal Nature found that 70% of researchers have tried and failed to reproduce another scientist’s experiments, suggesting a high level of scrutiny and skepticism within the scientific community. Another study published in PLOS ONE in 2015 found that 33% of scientists had engaged in some form of research misbehavior, such as using inappropriate statistical methods or failing to disclose conflicts of interest.
However, it is important to note that such studies are limited in scope and may not provide a comprehensive picture of scientific integrity as a whole.
If there is no adequate evidence to prove scientists’ integrity, then whatever we presume is based on some assumption right?
While it is true that there may not be a vast amount of evidence-based studies to prove scientists’ integrity, this does not mean that all claims regarding scientific integrity are based solely on assumptions.
Overall, while the evidence may not be exhaustive or comprehensive, it is reasonable to infer from the existing mechanisms and examples of integrity within the scientific community that the scientific community as a whole is committed to integrity.
Reasonable means what?
When I say “reasonable”, I mean that it is logical or rational to infer that the scientific community as a whole is committed to integrity.
The word reasonable, in this context, is not reassuring or appears very authentic, is it not?
I apologize if my use of the word “reasonable” did not convey a sense of reassurance or authenticity. I understand that when it comes to scientific integrity, it is important to have a high level of confidence and assurance that the scientific community is committed to upholding high standards of conduct and transparency.
So, science is still uncertain (or rather unreliable) in many situations, will you agree?
Yes, I would agree that science is inherently uncertain. Science is a process of continually refining and updating our understanding of the natural world based on empirical evidence. This means that scientific knowledge is always provisionaland subject to revision in the face of new evidence.
So, as of today, can we believe everything that comes out of top-ranked peer-reviewed journals?
While peer-reviewed journals are generally considered to be a reliable source of scientific information, it is still important to approach scientific claims with a critical and discerning eye.
Can you give a more specific answer to the previous question?
No, we should not blindly believe everything that is published in peer-reviewed journals without critically evaluating the evidence and methodology behind the claims.
Thanks, GpT, nice chatting with you. It was a great time, and appreciate your truthfulness.
You’re welcome! It was a pleasure chatting with you and answering your questions. Don’t hesitate to reach out if you have any more questions in the future!
This is the Incidental ECG of an apparently healthy 50-year-old businessman, recorded while applying for health insurance
How will you describe this ECG?
Let me magnify it for you
Why this big fuss about this ECG?
Such ECGs are so common. Looking at the ST segment, we are supposed to think of significant CAD,, LVH,Aortic stenosis or variants of cardiomyopathy, and sometimes electrolytic shifts. The fact that it is recorded at rest, and the patient is absolutely asymptomatic, it is very unlikely there is ongoing ischemia.It could be a myocardial origin or an unknown repolarisation pattern. But, one thing is clear, we can’t send this guy under the label of non-specific ST/T changes.
The Echo was done it was normal. No WMA, LVH. The aortic valve was perfect.
Is CAG indicated here?
Three responses came from three different cardiologists. Everyone agreed, the stress test is not going to be useful, as baseline is unstable
Absolutely not Indicated, since he is asymptomatic. I believe the history and Echo. Please follow him up
A definite yes for CAG. (Being a scientific cardiologist, without excluding CAD, I can’t be at peace. Will do at least a CT angiogram)
A third cardiologist said a CTangiogram is waste of time and wanted to do a radial CAG in 10 minutes in his newly opened hi-fi radial lounge.
What happened then?
Don’t know, whether he underwent CAG or not. But, I can confidently say he will have a normal coronary angiogram. How can you be so confident? Confidence doesn’t mean I am correct. Look at the ST segment again. It is not true ischemic depression. It is neither non-sustained nor horizontal or downsloping*, This could be referred to as, primary T inversion with secondary ST segment dragging. Regarding the management, the first response is ideal,
*Classical slope should begin at J point. Late downsloping has little predictive value as in this ECG.
Is Echo good enough to rule out structural heart disease?
Even after the echo was reported normal, few questioned the quality of the echocardiogramand asked to look specifically for apical wall motion with speckle track and GLS. ( I know, MRI is a must nowadays to rule out structural heart disease as Echo can’t rule out intrinsic myocardial disarray, infiltration, etc)
How is ST dragging different from ST depression?
Classical horizontal ST depression
ST dragging due to T wave pulling
For ST depression to happen, the junction point needs to be depressed. Note here junction is held high, only the distal half of the ST segment dips rather dragged by the phase 3 repolarization process which corresponds to the proximal limb of T waves. Our observation is, this type of ST drag is less sinister and usually indicates a myocardial ST defect, rather than an ischemic one. (Examples: concealed LVH or forme fruste of HCM or Infilitrative cardiomyopathy-related entities.)
Final message
The purpose of posting this ECG is, some ST segments create disproportionate panic than it deserves. The concept of T waves pulling down the distal part of the ST segment which can be called ST segment dragging is being proposed here.
Some provocation for advanced readers
Re-exploring the foundations of electro-cardiology is always welcome. Worth diving deep into mysterious terminology non-specific ST/T changes. ST segment in the ECG corresponds to the most stressful period since it represents the active part of mechanical contraction. Curiously, it Includes the entire electrical (Repolarisation) & most parts of mechanical relaxation. The true onset of LV myocardial mechanical relaxation we can’t be sure, It happens somewhere in late phase 2. I think it’s so difficult to decode that timing. But, what we can presume is ST segment behavior in its distal half is less specific for both ischemic as well as hemodynamic stress
The electro-mechanical continuity within the ST segment is so intimate, and the demarcation point between them is invisible in many clinical situations. No surprise, we are largely in the dark about the true influence of the ST segment over T wave morphology and vice versa. (ie distal ST depression pulling down the T wave ) Though chronologically T must follow the S in timing, it would seem impossible for “T” to go back in time and pull the ST down. (If QRS can precede P in a junctional rhythm, why not T do the same for ST? ) I am not sure whether there is any timing involved in antegrade vs retrograde repolarisation across endo-epicardial repolarisation dissociation.Further, we know very well, myocardial scars cause fragmented depolarisation in QRS. Can anyone guess effect of these scars in repolarisation vectors? (Fragmented ST segment ?) I think it is worth pursuing this phenomenon. Let the young new age Sodipellares’ look into this.
Though the traditional rule of thumb, makes ST segment shifts more sinister, T-wave changes are largely benign, It is not an easy job to segregate benign from more serious forms of T-wave changes. Isolated new onset T inversion, can be an equally troublesome marker, especially mid-chest leads in the male population.
It is interesting to note, not every T wave Inversion is empowered to drag the ST segment down. We don’t know why. It is something to do with the curvature of the shoulder zone of phase 2 /3 of the action potential. In this context, ST dragging could be an important concept to explore.
. An example of isolated T inversion without influencing the ST segment. Try to compare this ECG with the one that is shown to drag the ST segment
Diastolic T wave stress
One more issue, which we are not yet clear is the timing of 2nd sound with reference to the T wave. It is a fact, a significant part of the T-wave will represent early diastolic hemodynamic stress* as well.
If some body is struggling with same problem, say for over three decades , there is something seriously wrong with the way we deal with the problem. How do you localise accessory pathway in WPW syndrome from 12 lead ECG ? is one such entity, This question is asked exclusively in cardiology board exams. Now a 2023 paper from EUROPACE claims, it has come out with a simple algorithm bettering all the previous ones. Please check it for yourself.
One thing we can say with conviction is most of these embryological remnant pathways are posteriorly or laterally dragged in peri AV annular region or the para septal region. Very few appear anteriorly, if anterior it is more often placed on the right side.
Why should we take this question easy ?
Try asking any experienced EP specialist* to localise a pathway in given 12 lead ECG . Don’t get surprised by a long silence before they commit, because they know the truth, and how delicate this question might sound on quiet a few occasion, because of various anatomical and physiological reasons.
*Never fail to appreciate their hard long hours in cath lab to spot, analyse and shoot these tracts.(EP stuff is not like angioplasties, which, many can do even in half sleep!)
Final message
Yes, localising WPW can be either a fascinating or frustrating exercise depending on our understanding about the attitudinal cardiac anatomy, variable autonomic tone dependent morphological behaviour of delta waves, PR intervals, QRS axis ,the transition zones etc. Shrewd fellows may go through this 12 lead stress test. ,
For others just try to localise right from left , & then posterior or lateral Forget the anterior ones. This is more than suffice. Unlike drug trials, where statistics are often battered , here the Incident numbers are the key measure of truth. (Even without seeing a ECG you are likely to be correct in 80 % times, if you localise the pathway to posterior, para-septal or left lateral zones. )
A 62-year-old man who is being scheduled for prostate surgery with no cardiac risk factors or comorbid status came for surgical clearance. I examined him and took an ECG, everything was fine and gave him clearance for surgery.
I was surprised to spot him the very next day, waiting in the lounge of my office. He said, his anesthetist was not happy with my pre-op-cardiac assessment report, suggested it was incomplete, and sent me back for echocardiography to know the LV ejection fraction.
I wanted to clarify with the patient, what exactly happened when he met his anesthesiologist.
“I am not sure doctor, the moment he saw your report, he called my urologist. I overheard his call, they were discussing the need for an echocardiogram and they were also wondering, how could a cardiologist give a surgical clearance without even an echocardiography”.
I wasn’t really surprised by the turn of events and told the patient.
“I am experienced enough to say, your heart is 100 % normal without an echocardiogram”.
“I understand doctor, but sorry to bother you. Can you please take it for the sake of my anesthetist and urologist, after all, right now I am worried about their peace of mind”
“You are absolutely right. This is a topsy-turvy world. Investigations are dictated to me in my own field of expertise. Anyway, I am not a fool, to expect a patient’s help to guard my principles of practice. Please check in, let me do the echocardiogram as they wish”
“Thank you so much, Doctor“.
I showed him, the vigorously contracting ventricle and taught the student trainee who was nearby, a simple clinical tip ie, a loud first heart sound on auscultation is good enough to tell you, the EF is beyond 60% in most situations. (A forceful AML movement is a direct auditory marker of EF %)
Final message
It is getting more & more clear, physicians will face huge hurdles in applying their clinical skills to practice. They may even be unauthorized to do so. It seems, in our misplaced quest for perfection, we have fallen into a scientific trap, that every clinical decision must be authenticated by some objective lab-made obsession. The word clinical acumen could soon become a laughing stock, as AI-powered medical zombies are waiting to join our consultation suits.
(Meanwhile, the guidelines are very clear. (Read below) Do echo only in high-risk surgery, if patients’ functional capacity is poor. But, let me confess, at least in our part of the world, we are happy to violate standard guidelines without any degree of guilt )
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Dr .S.Venkatesan MD
Dr.S.Venkatesan MD 