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The “World anti-platelet” boxing championship 2019 !

September 20, 2019 by dr s venkatesan

Caution : Non-Academic stuff

Anti hypertensives, lipid-lowering drugs along with antiplatelet drugs always find a proud place in most cardiac prescriptions. The toxic rivalry between various drugs and their creators is a well-known secret. However, the current fight among the antiplatelet agents is reaching comical proportions. The punches and reverse punchs on and off the podium is there for everybody to see.

It all started with clopidogrel two decades ago which was crowned after conquering then-popular Ticlopidine. It was followed by Prasugrel and Ticagrelor. Ticagrelor seems to taste its own medicine from Prasugrel, which brought back memories of the same knock out punches both of them gave to clopidogrel in the past. I guess the ISAR bruised Ticagrelor is just taking a time out, expected to REACT with fresh vigor in the next bout vs Prasugrel.

While these financial heavyweights struggle to keep the bull run, in the multi-billion-dollar stent maintenance market . Aspirin, the aged warrior is enjoying the theatrics silently. While Aspirin is repeatedly shown ( shown literally means shown: Mind you, It is not a synonym for a proven fact ) that it is inferior in stented patients.For stable CAD Aspirin still in the very much in the reckoning. Let the Twilight shine soon. Don’t get a shock of your life, if Aspirin regains the championship one day.

 

Final message

Let us hope the fight gets over till another Grelor  crash lands from nowhere. Meanwhile, we shall strive hard as professional physicians to increase the per-capita antiplatelet drug consumption in  every acute and chronic coronary syndrome (with or without PCI). This will help keep Homosapien’s coronary artery eternally patent.

 

For pure Academics  (Conclusions in science is a misnomer . . . )

 

 

 

Posted in anti platelet drug | Tagged , , , , , , , , , , |

Who is the “Real master” in Master health check up clinics ?

September 17, 2019 by dr s venkatesan

Master health checks* , superficially look like a perfect modality to practice the greatest medical concept ie “Prevention is better then cure” .Let us detect all human diseases early , prevent its progression, regress it or completely cure it . Absolute bliss is it not?

Why then articles such as this one should ever get published, that too in one of the prestigious journal of medicine?

*Master health check .( Also referred to as annual General health checks.)

Master health check up geenral cochrane bmj editorial

While the title itself is provocative, it adds a tag line which is still more a shocker.

There are specific well-researched reasons for this preventive health check fiasco.The masters, who were originally the guardians of health soon became disease mongers.In the process, the primary aim of propagating the doctrine of “prevention is better than cure”, could not reach its desired goals. Instead of ignoring and reassuring the minor deviation of biological data and Imagery generated, they became a perfect feed for the hunters who are after the trivial and non-existing illness.

Final message

Good intentioned health checks are always welcome in selected high-risk population say pregnant women/children of developing a world (As in endemic countries of rheumatic fever) Also cancer , CAD , screening in people with a positive family history can be critical.

However, when these masters of health deviated and started making a living out of apparently healthy people. ( The side effects reached monstrous proportions hiking global health cost in a meaningless way).People, especially in counties with poor resources, are the ultimate sufferers, as the cost and efforts are diverted, to fix the health of healthy, while people with true illness continue to struggle.

Will the WHO* wake up and intervene against this skewed practice of routine master health checks in healthy, that are rampant in both rich and poor countries. Ideally, doctors should order preventive health assessment for those who may need it.

There are enough grounds for public Initiated periodic walk-in health checks to be banned (or at least restricted)

*WHO is world health organization

Posted in Uncategorized | Tagged , |

Digoxin in Heart failure: Foxglove blossoms again, please don’t crush it this time!

September 14, 2019 by dr s venkatesan

William Withering the British Botanist of 18th century now laid to rest in the St Barthomlew Churchyard ,Edgbaston is known for his astonishing isolation of the wonder moelcule Digoxin from Foxglove. (Of course, let us not forget original old lady Ms. Hutton from Shropshire who was treating epidemic dropsy with a concoction of herbal Tea ) He reported this in the seminal paper “An account of Foxglove’ in the year 1750 and subsequently became a fellow of Royal college of science.

(The story of Withering and Digoxin is extensively researched and written by Dr Dennis M, Krikler in a classic review article of 1985 JACC )

Near-death experience of Digoxin

After 250 years , saving millions of life, modern science has killed this warrior (inadvertently ?) by a minuscule study with serious flaws called DIG trial *published in NEJM 1997. It exposed the truth that science in flimsy forms can misrepresent fact. Actually many wouldn’t agree its a bad study. But , everyone realised , the conclusion was misinterpreted and disproportionately given weight to one aspect.The conclusion was worded in such a fashion, which sort of implied a negative bias.

*Yes , flaws were discussed in one of our detailed journal club meeting .

DIG trial

This one study was good enough to smear this drug with a knockout punch as if we are administering poison to a patient with heart failure.Thus a grand old drug became an object of ridicule in academic forums. Subsequent offline real-world scrutiny clearly indicated reduced hospital rate admissions and preventing worsening of HF was directly improving the mortality for which there were no takers. At least occasionally we need to realize there is foolish face for statistics. Now we are beginning to restore some lost sense.

What’s happening in 2019

The same scientific methodology finds Digoxin to have great value . JACC. Awais Malik from Veterans Affairs Medical Center, Washington DC and others try to dig out a truth.

screenshot_2019-08-24-23-37-54-789_com1423849373.png

Whoever is blaming this as a withdrawal study are requested to go through the basics of how adding a drug doesn’t help but stopping it worsens. Another group has a different issue. There is a tendency among the scientific community, to look down on studies done in VA hospitals as if they have lesser academic value. I strongly object to that if it’s true. Never have preformed opinion about a study by its source.

How does Digoxin act?

Mind you, Digoxin was working all alone in CHF in the past without the help of all-powerful loop diuretics which was discovered 200 years later, This adds more credit to Digoxin since it has a combined the action of diuretic, anti sympathetic and vagal modulating action, and AV nodal regulation. The only issue with Digoxin could be its safety profile, which if carefully taken care can be overcome. (Afterall, we are trained for this job ) One may call it a most comprehensive drug amongst others in cardiac failure.

Final message

Ignore the greatness of old drugs at your own peril. Foxglove blossoms again, after a gap of 30 years. Please don’t crush it this time! Let Willaim Withering smile from deep inside his resting place at Barthomlew Church along with millions of heart failure patients.

ESC 2020 Update

RATE-AF study reinforces value of Digoxin in AF rate control.

https://www.acc.org/latest-in-cardiology/clinical-trials/2020/08/28/15/59/rate-af

Reference

1.

2.History of William Withering

3.Ahmed A, Rich MW, Love TE, et al. Digoxin and reduction in mortality and hospitalization in heart failure: A comprehensive post hoc analysis of the DIG trial. Eur Heart J. 2006;27(2):178-186

Postamble

A funny business Idea

I guess Parke Davis those days had wholesome rights for Digoxin. May I suggest few tips for the industry how to capitalise this newly generated enthusiasm. Please ensure this drug sounds anything other than Digoxin which seems to have a stigma attached for the modern guys.

Try renaming this drug , a sodium-potassium ATPase blocker, as DiNaKatban and patent it as a unique weekly depot Injection with an attractive 499$ price tag. Another option is to add Digoxin ,Neprilysin and Frusemide, possibly an ARB ( Dinephrimab) and project it as polypill for HFrEF . Publish it in NEJM with a huge non Inferiority trial,break it in ESC or ACC .Consider selling it on all heart failure clinics with a special launch. I am sure, the same guys who ridiculed this drug for so long, will ask their patients to stand first in the queue. Call me, if this new generation Digoxin doesn’t vanish like hot cakes from these pharma malls.

Posted in cardiac failure, history of cardiology | Tagged , |

Evidence based errors in cardiology . . . urgent need for special cognitive skills !

September 13, 2019 by dr s venkatesan

Preamble

Hey dudes, will you stent this 76 year old  fragile man’s Aortic valve ?  It looks shaggy and it seems to be leaking as well.Iam not sure its really tricuspid or not .It is so distorted . By the way , he also has a left main lesion with no protection.What shall we do ? Will the Jena valve do the trick ? My experienced collegue threw this question to a flock of freshly hatched senior residents of a upscale cardiac center. 

After rapidly feeding the necessary risk predicting numericals, clinical and hybrid imagery data , they dug deep into the iOS-powered gadget, loaded with latest TAVR app fused with SYNTAX 2 and FAME 2 overlay for few minutes and started responding one by one.

Yes sir , no Issues, we can comfortably stent it , Its class 2 A / with level B evidence according to JACC intervention article, but, I must say , it was class 2B just a month ago. Another fellow interfered, no sir, ESC says it’s still class 3 but the evidence is C so I am  not sure how to interpret it. The third fellow who usually is a quiet guy, came up with this, but sir, It seems TCT and EURO-PCR  has just released an update, the indication is currently upgraded to class 1 backed by level A evidence . 

Are you talking about TAVR or Left main? the confused consultant quipped… that’s EBM at its best !

Evidence-based errors in cardiology 

Evidence is the most sacred word in current medical practice. How much of our practice is evidence-based ? It is considered as a quality check. But, today we harshly understand, the evidence to which our conviction clings has a very short expiry date. Apart from expiry , the evidence thing comes with serious invisible manufacturing  defects as well. It may become null and void  even before its fully disseminated into the patient domain.(Please mind, your patient’s life is tied to this clueless evidence !)

So, how to tackle this dangerous dissemination of premature wrong evidence from injuring the patient ?

We don’t have a definite answer  . . . except to say, use the available evidence carefully and cautiously. If necessary (it will often be) throw it to the nearest dustbin by your own evaluation assisted by intuition, and a liberal dose of learned empiricism. Mind you, to do this you must be blessed with enough knowledge, wisdom, and courage as you need to overcome strong pressure to do the opposite.

My prediction is, bulk of the future problems in medicine would come from failure to dispose evidence based errors in medicine.

Posted in Uncategorized | Tagged , |

DM cardiology course suffers from a 50% entry block… A NEET angioplasty done.

September 8, 2019 by dr s venkatesan

The most premier course in medicine, DM cardiology just got an entry makeover.

The qualifying mark was lowered to 20% from the current 50th percentile The reason is many private medical college seats went vacant after the Initial counselling in NEET superspeciality exams.

Becoming a cardiologist was a dream come true for those days for us. “You have to read the red covered 3rd edition Brunwald and all clinical chapters from Hurst for two full years” before even to think of writing DM entrance, my senior used to tell me in late 1980s.Yes, life may still be tough in post graduate entrance but, there is an exclusive fast lane for privileged few where the “Goal posts”start coming towards you.Thanks to the explosion of private medical institutes.

Nothing wrong, it’s not a medical calamity. If the entry is made easy. It doesn’t mean all students are below par.Just 80 % below par.

One big consolation

Medicine is an art to be learned. Unfortunately (or fortunately) students of medicine requires more of sincerity, hardwork, motivation, honesty and Intention to learn. Intelligence and knowledge is there in the list but definitely not in the top.

While mediocrity is a menace in medical education, three decades into medical profession, my conscience tells me even merit, expertise, competence end up as double edged swords if they land up in wrong place with a dubious motive. So, ultimately academic guarding of all these so called entry and exit points to DM courses doesn’t really matter much.

Get ready for grand future

Let’s welcome all the new generation cardiologists in whatever form and this country needs more of them to tame the raising cardiovascular disease burden.

Posted in Uncategorized |

Whenever my ego bloats up . . . I see this video, to get it deflated !

August 17, 2019 by dr s venkatesan

Whenever we have difficulty in accepting our mistakes or unable to forgive other’s mistake,or when we make big fuss about trivial events in life, I was advised to ask these three questions and Introspect.

1. Who you are?

2.From where did you come ?

3.What for, you are present in this world?

It was a really tough ask , until I saw this video. It not only stuns but also humbles us and whatever little knowledge we acquired over the years looks nothing.Yes, whenever my ego tend to bloat up… this 3-minute video never fails to get it deflated.

Just one requisite , you need to Imagine it’s you lying there instead of that girl.

Post ample

It’s good to realise, how this world suffers by actions and inactions of apparently smart people, who spend some transitory moments in this universe, sharing space with millions of non-human lives and lifeless things (Mind you, the later don’t suffer from death since they have no life!)

Thanks to Google, the technology company for stimulating us to think and find the true meaning of life.

Posted in Uncategorized | Tagged , , , |

FAQs in STEMI : Why is the 3 hour gap recommended before pharmaco Invasive strategy?

August 14, 2019 by dr s venkatesan

Background STEMI knowledge check : Evidence-based Ignorance

I think , It is unfortunate, In the management of STEMI , the two popular strategies of myocardial reperfusion is made to fight with each other as if they are perennial enemies for over two decades. Suddenly, someone with a rare coronary insight thought, why fight each other , they can have a friendly hug and work together. That brought the concept of pharmco -Invasive approach or strategy(PIA) backed up by STREAM, FAST-MI, and TRANSFER AMI studies.Yes, it appears to work well and devoid of all the early adverse events of pPCI. (Much to the dismay of ardent fans of Primary PCI )

*May I add one more shocker of a fact . Deep subset data mining from the above trials did show very early lysis may even act as a perfect stand-alone therapy negating the need for acutely one pharmaco Invasive PCI altogether.(Which was never published) Don’t get alarmed the concept is nothing but , the good old lysis , followed by leisure & elective Ischemia guided PCI in all uncomplicated STEMI.

Now coming to the FAQ in Cardiology Boards: Why is the time window for PIA is 3 to 24 hrs ?

The simple answer for an uncomplicated fellow is “published studies have shown benefit only in this time window. If you do PCI early (,<3h) after lysis paradoxically both bleeding and pro-thrombotic complication over the stented lesions are more common. The upper limit is 24 hrs , since by that time we lose all the potential for myocardial salvage”

– End-

Larger version of the answer

(Advanced readers who are willing to get confused, may read further)

1. Lysis and immediate PCI doesn’t go well at least in trial world. (FINESSE study, by Ellis et all NEJM 2008) Though cardiologists tend to blame lysis (effect of) to Interfere with their hand skills, it can very well be the opposite. The PCI undo the true benefit of lysis. For cardiologists to accrue maximum benefit in the early time window, they need to be too fast, in the process, they accelerate and fuse adverse events of both modalities.

2. The time window 3 to 24h could simply be evidence-based empiricism. In the major STREAM trial, invasive limb happened between 6 and 16 hours only. We stretched both in the top and bottom in the time clock and made it 3 to 24 hours with other trial data.

3. One realistic reason could be this. It requires a minimum of three hours for a patient to reach a place of coronary Invasion after lysis. So one may argue its time allowance for transport .It comes in handy at times.

4 .If the patient reaches earlier, we need to delay the PCI intentionally to please the evidence based medicine. Mind you, every minute delay increases the chance of no reflow as the microvasculature goes for edematous and porous death.

5. Please note, the time window for pharmaco Invasive strategy will go for a tail spin if the initial lysis is failed. Here, we have to rush I guess. Mind you, In this situation, the evidence based blaming that early PCI increases the adverse events immediately following lysis goes topsy turvy . This is where , we should recall old studies of routine rescue PCI (without clinical criteria) rarely succeeded to correct failed thrombolysis (SWIFT trial)

6.Now, why not PCI after 24hrs? The game can be played reversed if you document ongoing Ischemia in IRA or Non IRA, one may do it . The problem arises when the flawed thought process of a cardiologist could legally justify all PCI beyond 24 h /class 3 Indication after STEMI.The argument goes like this. I think this patient has residual silent Ischemia in- spite of severe LV dysfunction (Suspicion is the justification, to which ,unfortunately no one can dispute) It only suggests open artery hypothesis is still trying to raise from the graveyard more than a decade after its near burial.

Final message

To all those energetic, evidence-based cardiac physicians, we all know coronary care is all about time. In fact, we need to be blessed much more than a sense of time. There is something called medically( or spontaneously )stabilized ACS.  Please realise , “timely and safe intervention” for your patients could simply mean either playing the time button slow/ fast / slow or fast forward / pause or simply shutdown the cath lab, reach home early and enjoy some music or movie in your favorite streaming player.

Reference

1.Ellis SG, Tendera M, De Belder MA, FINESSE Investigators Facilitated PCI in patients with ST-elevation myocardial infarction. N Engl J Med. 2008;358(21):2205–2217. [PubMed]

2. Armstrong PW, Gershlick AH, Goldstein STREAM Investigative Team Fibrinolysis or primary PCI in ST-segment elevation myocardial infarction. N Engl J Med. 2013;368(15):1379–1387. [PubMed]

3. Danchin N, Puymirat E, Steg PG, T, on behalf of the FAST-MI 2005 investigators Five-year survival in patients with ST-segment-elevation myocardial infarction according to modalities of reperfusion therapy: the French Registry on Acute ST-Elevation and Non-ST-Elevation Myocardial Infarction (FAST-MI) 2005 Circulation. 2014;129(16):1629–1636. [PubMed]

4. Cantor WJ, Fitchett D, Borgundvaag B, TRANSFER-AMI Trial Investigators Routine early angioplasty after fibrinolysis for acute myocardial infarction. N Engl J Med. 2009;360(26):2705–2718.. [PubMed]
5.. Bonnefoy E, Steg PG, Boutitie F, , CAPTIM Investigators Comparison of primary angioplasty and pre-hospital fibrinolysis in acute myocardial infarction (CAPTIM) trial: a 5-year follow-up. Eur Heart J. 2009;30(13):1598–1606. . [PubMed]

Posted in acute coronary syndrome, Cardiology - Animations, Cardiology -Interventional -PCI, Cardiology -unresolved questions, cath lab tips and tricks, Infrequently asked questions in cardiology (iFAQs), open artery hypothesis, STEMI, STEMI -Managment, STEMI-Primary PCI, Thrombolysis | Tagged , , , , |

Localising “Angina related artery”( ARA ) in UA/NSTEMI : Can we differentiate culprit artery from lesion ?

August 11, 2019 by dr s venkatesan

Identifying the culprit after a criminal event may be easy for the police.For cadiologists investigating the crime scene after a coronary event, it is a different story. (Of course, localization of IRA after a STEMI may not be really difficult.) But , when a patient is having UA  and coronary artery shows multiple lesions, we do have real diagnostic issue. The general dictum could be, tightest lesion or the complex eccentric ones with thrombus is likely to be the culprit. This has important therapeutic Implication,  as we are argued to address the active lesions first. The following study was done in 2009 trying to find the ARA solely by ECG features.

The conclusion was

The following ECG findings were helpful in localizing Angina related artery . ST depression in V3- V5 correlated  with  LAD  angina .Global ST depression was highly correlated with proximal LAD or Left main disease ( 6/6 patients). ST depression in V1 –V3 was associated more commonly with dominant LCX/OM disease. ST depression in 2 ,3 , AVF , or I, AVL  had  no significant correlation with either RCA or LAD  system.However multiple culprit lesions or diffuse inflammatory CAD should always be thought off. One more possibility is , its simply a demand ischemia or micro vascular angina were there is no true epicardial culprit lesion. 

A revisit to my 2009 IHJ article.

http://indianheartjournal.com/ihj09/nov_dec_09/509-523.html

 

IDENTIFYING ANGINA RELATED ARTERY (ARA) IN UNSTABLE 
ANGINA /NSTEMI BY ADMISSION ECG AND ECHOCARDIOGRAPHY
S.Venkatesan C.Krishnakumar .G.Gnanavelu .R.Subramanian.Geetha Subramanian B.Ramamurthy.P.Arunachalam.M.Somsundram.V.E.Thandapani.M.A.Rajasekaran.
S.Murugan , Madupraphu doss ,P.Pachiappan.
Madras Medical College. Chennai

Unstable angina( UA /NSTEMI ) constitute a  heterogeneous  group of  patients with  lesions ranging from  normal coronary  artery  to severe multi vessel  disease. Even  though  multiple active plaques are documented ,  one  critical  lesion  would be   responsible  for  the  index  episode  of  angina..  Contrary to STEMI  there is no standard methodology   to identify  the  Angina  related artery.(ARA) in UA .We under took this  analysis  to find  whether  admission  ECG  with the help of echocardiography   could  predict  the ARA  in patients with UA

26  patients with  UA  admitted in  our  CCU  were  the  subjects of  study. Patients with   post  infarction angina,  CABG ,  PCI , old  MI , left ventricular  dysfunction  were  excluded. All patients  were treated  as per institutional protocol. Echocardiogrphic analysis   of  wall motion defects (WMD)  were  documented  between  2hrs  and  24hours of admission  .CAG  was  done  between  24 hrs and  7  days. The  coronary  lesion was considered angina related  if  the  WMD  detected   by  echocardiography matched with  the  myocardial  segments supplied by the  arterial territory  containing the lesion . After locating the ARA , the patient’s  admission ECG   was  compared  retrospectively   with  CAG  finding  to study  whether  it has  any  predictive  value  for identifying  ARA.  6 patients  who  had single vessel disease the ARA  localization  was straight forward. (LAD -4 , LCX -1 RCA-1 ). In 2  patients  there was  obvious  eccentric thrombus containing plaque indicating the culprit lesion . 18 had DVD or TVD with no clearcut culprit lesion.

The following ECG findings were helpful in localizing ARA.ST depression in V3- V5 correlated  with  LAD  angina .Global ST depression was highly correlated with proximal LAD or Left main disease ( 6/6 patients). ST depression in V1 –V3 was associated more commonly with dominant LCX/OM disease. ST depression in 2 ,3 , AVF , or I, AVL  had  no significant correlation with either RCA or LAD  system.

It  is  concluded  ARA  can be  identified  with  fair  degree  of accuracy   by admission  ST segment  profile. This  observation  differs with  the existing literature which  suggest little role for ECG to localize arterial lesion in UA. In patients with multivessel CAD  with  more than one  critical lesion  a  combination of ECG  and echo features  help  us to  fix the angina related artery and possibly the lesion. This has  important  therapeutic implication.

Keywords: Angina Related Artery, Unstable Angina/NSTEMI, ECG, Echocardiography.

Postample

I am reposting this abstract again because the same paper has been plagiarised in at least two occasions and got published in predatory journals. Now, we realise Journal article shopping and trading has become a scientific scam .

Reference

This paper  from Japan analysed this ARA concept in 1996 itself with SPECT Imaging

 Oka T, Kobayashi H, [Detection of angina-related coronary artery in patients with unstable angina pectoris by using 123I-BMIPP myocardial scintigraphy]. Kaku Igaku. 1996 Mar;33(3):279-84.

 

Posted in Uncategorized |

Understanding Ischemic mitral regurgitation

July 16, 2019 by dr s venkatesan

The mechanism of MR in ischemic /Functional is complex. Technically, pure ischemic MR should have a structurally normal leaflet and the subvalvular mechanism dominates But,the combination of the two is also prevalent. In fact, a degenerative component is added to this in many elderly patients.

Mechanism of Ischemic mitral regurgitation

Any of the following may contribute either alone or in in different combinations.

  • Global LV dilatation with or without annular dilatation
  • Spherical left ventricle
  • Altered inter papillary muscle distance (Degree and direction of  posterior vs apical displacement of pap muscle)
  • Chordal shortening /Lengthening/Abnormal tethering
  • Leaflet tenting distance and volume
  • Basal LV dysfunction and Local LV (Sub-mitral) remodeling

We have come a long way ,  since the days of  Carpentier and Duran who did pioneering work .It involved partial or complete mitral annular stabilization with surgical ring technology that  helped us to change the shape of the annulus. Advanced imaging, with 3 D printing will enable us to procure perfectly matched designer valve rings and (may be leaflets also) in the near future. Percutaneous mitral valve Interventions, with clips , valve, are going to dominate the mitral valve therapeutics.

Still, we are largely ignorant about Individual contribution from various components in the genesis of  ischemic /functional MR. This becomes important because the preservation of native valve is better on any day than replacing.  One thing is very clear, even though left ventricle forms part of mitral valve apparatus, the degree of LV dysfunction has no linear correlation with the severity of MR . Its a well-known fact, even severe LV dysfunction (Say < 25 % )may enjoy the company of a perfectly competent mitral valve. It’s interesting to note uniform global LV dysfunction cause more of central MR , while dispropotinate basalLV dysfunction especially the posteroinferior pap muscle cause eccentric jet. One more curiosity is mitral regurgitation improving with worsening disease as contractile force weakens.(Functional MR depends on LV function you know !)

We have witnessed at least two patients who had a significant MR following an inferior posterior MI which was managed medically, showed dramatic regression in the degree of MR  when he had anterior MI later*.The pleasant irony was apparently due balanced dysfunction of anterolateral pap muscle that happened in countering the original postero-medial pap muscle dysfunction.(*Allowing second MI to happen is of course a treatment failure !)

Image source -Christos G. Mihos  Journal of Thoracic disease Vol 8, No 1 (January 2016)

Mitral valve is essentially avascular structure, Still, ischemia affects this valve not by valve necrosis but by other sub valvular mechanisms .Note the MR here is due to poor motion of PML due to ischemic LV dysfunction.

 

Ischemic MR in early hours following STEMI (also NSTEMI) is still a nightmare. We realized in a harsh way, it’s rarely corrected fully even with a successful IRA plasty. (Especially LCX and posteromedial pap muscle that is in extreme distress) In fact , many of the mechanical complications that lead to flash pulmonary edema would need emergency CABG rather than primary PCI. (What to do for Ischemic MR ? An excellent review article( Elsayed Elmistekawy Curr Opin Cardiol 2013, 28:661–665) 

Mitral valve, though looks like an obedient, innocuous structure that  silently does its job , only in special times, it makes us realize, its the most critical part in the entire heart.(Guarding the lung against flooding when the left ventricle experiences turbulent ischemic times during ACS.) Note -Acute MR often kills , not the ACS as such.ischemic mitral regurgitation functional carpentier drsvenkatesan venkatesan madras medcial college 002The  mechanism of MR in various pathologies is comparable to the behavior of a cow grazing in an arc tethered to a poll. Normally its expected to follow a set pattern. If it behaves wayward, one may need to tighten the rope(Chordae), or loosen it, strengthen or move the poll(Pap muscle) . . . still more options like whipping (clipping ) the cow(Leaflet) may be tried. Of course ,ultimately one may need to replace the cow (MVR). EP guys do  have an electrical solution to tame this cow , called CRT to regress Ischemic MR .

 

Reference

1.Yiu S.F.,Enriquez-Sarano M.,Tribouilloy C.,Seward J.B.,Tajik A.J.Determinants of the degree of functional mitral regurgitation in patients with systolic left ventricular dysfunction: a quantitative clinical study. Circulation 2000;102:1400–1406

2.Mitral valve repair over five decades  Ann Cardiothorac Surg. 2015 Jul; 4(4): 322–334 

Posted in Mitral annulus -Functional mitral regurgitation, Mitral regurgitation | Tagged , , , , , , , | Leave a Comment »

Was the past perfect ? I don’t know, but the future looks tense… welcome on-board, to automated ACS management.

June 23, 2019 by dr s venkatesan

GettyImages-865142952-5b5eef884cedfd0050112fa6

Charles river esplanade ,Boston* : A healthy middle-aged man who was jogging quietly, while his heart was under intense scrutiny by the bionic eyes of Apple i-watch’s smart patch electrode. Suddenly, it detected some bizarre ST segment fragmentation (Seems it can predict in advance , Ischemic signals 10 minutes prior to onset of ACS ) The built-in cosmos direct GPS instantly alerted & summoned a titanium powered Space X drone that pulled the patient from the riverside to the nearest human wellness port .

EHANG 184

It dropped him through a remotely accessed split glass roof right inside the hybrid heart lab, to find , men and women chatting with flattish Artificial intelligence panels who readily allowed the robotic arms to hug the patient which engaged the coronary artery pushing radiation free magnetic gas found nothing inside and what would become a perfectly normal human coronary artery .

An amused resident robot gently plucked the patient from the cath table with sheepish laughter and called for another drone to drop the patient exactly in the same place from where he was picked up.The healthy hearted patient thanked the doctors profusely and continued his routine evening jog across the Charles of course with a 16-minute delay!

Next day . . .

Event auditing firm medi-logic mind congratulated the entire cardiac team and its digital health hub for the quality of the network and completing this daring coronary rescue mission in 16 minutes. While the drone to hospital roof time was 3 minutes, the coronary artery visualisation time was perfect.The auditing team had a special mention about the astonishing capability of Apple time watch algorithm that made sure that the patient’s evening routine was unaffected in spite of this life-threatening non cardiac pseudo-emergency. The crowning glory was, the entire expenses amounting to 250000 dollors (after a special money back discount coupon for the first false alarm) were taken care by the patient’s virtual insurance blockchain payment gateway.

*You have just read the news that wasn’t – January 2030 AD

Now, back to reality,

Stumbled on this news clip from pages of Times of India, (20-6-2019) months after I wrote the above piece. I wondered the chase between fact and fiction is becoming  really a close race.

Posted in acute coroanry syndrome, Clinical cardiology, Ethics in Medicine, Hippocratic oath, history of cardiology, Histroy of medicine, Left main disease, Medical ethics, Primary PCI |

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