Here is a video recipe !
Posted in dr s venkatesan -Personal, general medicine | Tagged best cardiologist india, cardiologist, cardiology fellows training, crash course on cardiology, dr s venkatesan, drsvenkatesan, ethical cardiologist, good cardiologist, madras medical college, teaching video in cardiology, venkatesan sangareddi | 5 Comments »
Is reciprocal ST segment changes occur only in STEMI ? Can it occur in UA/NSTEMI ?
Even after 100 years of electro cardiology the electrophysiological mechanism of ST elevation in STEMI and ST depression in Unstable angina is still in the hypothetical stages. One popular theory says that the current of injury as we see as ST segment elevation in surface ECG is actually an illusion. It’s apparently due to constant negative current pushing down the rest of ECG segments. Ironically the concept of reciprocal ST depression in patients who have ST elevation is well debated for over 3 decades and is considered a settled issue. It probably represents , a purely electrical phenomenon where the tail end of the lead picks up the opposite vector. Even as conflicts continue to confront the basic electro physiological concepts management strategies of acute coronary syndromes is witnessing great strides.
We hypothesized if ST depression occurs as response to ST elevation it’s logic to expect strong ST depressive forces should possibly elevate The ST segments in the reciprocal leads .
In fact we have seen this phenomenon in three distinct clinical situations.
1) ST elevation in posterior leads: Patients who present with isolated ST depression in V1, V2 , V3 and ST elevation in posterior chest leads V7, V8 .These patients were initially thought to have isolated posterior MI. But later the cardiac enzymes were found to be normal indicating no myocardial necrosis echo evaluation revealed wall motion defects in anterior segments rather than in posterior segments. CAG revealed critical LAD disease . This we believe a pure reciprocal ST elevation in the posterior leads to a ST depressive forces in anterior leads.
2) Inferior ST elevation with ST depression in V4- V6 : Few patients who present with infero lateral STEMI later do not evolve into Q MI but as a NSTEMI .The initial ST elevation was found be transient and disappeared much earlier, while the ST depression lateral leads persisted.
3) ST elevation in AVR in high risk unstable angina :As already reported in the literature, we have seen ST elevation in AVR in patients with high risk unstable angina. This was more often observed when there is > 3mm ST depression in V4-V6. The AVR ST elevation possibly represents the reciprocal vector.
ST elevation in certain specific leads in some of the patients with ACS, could be a pure reciprocal electrical phenomenon to dominant ST depressive forces in Opposite leads . And hence ST elevation in the surface ECG during early hours of ACS should be interpreted more cautiously. The sanctity assocociated with ST segment elevation could be opened for debate.
To down load full PPT click on the slide
Posted in Cardiology - Electrophysiology -Pacemaker, cardiology -ECG, Uncategorized | Tagged ECG, electro physiology, myocardial infarction, nstemi, reciprocal changes, reciprocal st depression, stemi, unstable angina | Leave a Comment »
Oral anticoagulant usage has been steadily increasing for variety of indications.Dengue fever is also appearing in different avatars with low platelet counts and bleeding being a primary risk.
I was recently contacted by a physician , regarding a therapeutic dilemma .A young lady with mitral prosthetic valve and a febrile illness diagnosed as dengue . She has a platelet count of 100,000 .She is on regular warfarin and aspirin .The physician wanted to know , should he stop the OAC and aspirin ?
What are the options ?
- Confirm if it is really dengue.
- Look for clinical bleeding.INR, platelet function tests are not helpful.
- Continue OAC.You can do that in most situations.
- Stop OAC only if there is clinical bleeding episode.
- Anti-platelet drug usage is more tricky .One may stop it if the trend of falling platelet is steep by at least two serial measurement.(or 50% fall from baseline)
- Fresh blood and platelet infusions should be ready .
- Finally and most importantly , Inform the patient and family about the difficult decision we are making.
*Is OAC safer than aspirin and clopidogrel in dengue ?
It is believed OAC has no major Impact on platelet function .It may not pose a threat of excess bleeding in the setting of falling platelet levels .(*Evidence base -nil )
Another potential situation : DES and dengue
The number of DES in developing countries are increasing where Dengue is endemic . It is not a surprising to expect both to occur together.
Anti-platelet agents can be problematic .It is better to withhold it during the active phase of dengue.(If the stent has recently been deployed you have no option !)
1. Prosthetic valve , Warfarin Dengue .
2. DES, Dual antiplatelet agents ,Dengue.
They extraordinary events throw a complex therapeutic task .There are only two options .Continue or discontinue ! Whichever way you do , you explain to your clients (patients!) the (un)reality games we play.
My personal option would be , with hold all hematological drugs during the active phase of dengue .
It is better to believe in the natural thrombus fighting force . Leave the job of anti-platelet action to the dengue virus for a week or two and give oral anticoagulants and dual anti-platelet agents a holiday
It may be foolish to rely on the dengue virus to guard against prosthetic valve and DES thrombus , In reality we have to do that !
No reference exists.It is a statistical mind game.Individual assessment should prevail. Either way, if something adverse happens court of law should protect us !
Posted in Cardiology -guidelines, Cardiology -Mechnisms of disease, Cardiology -Therapeutic dilemma, cardiology -Therapeutics, Cardiology -unresolved questions, Cardiology-Statistics | Tagged dengue and coronary stent, des and dengue, falling platlets and coroanry stent thrombosis, how to manage fever, thromocytopenia and dengue | Leave a Comment »
In one of my meetings , I told a small gathering , that regular exercise can shrink atherosclerotic plaques and regress CAD. I also quoted , a recent large study which has proven this fact convincingly !
I concluded, simple exercise and other life style changes,risk factor correction may convert a 90% lesion to 70 or even 50 % . I stressed the importance of this study and asked my colleagues to avoid misuse of Angioplasties .
When many seemed to agree with me , one angry Interventional cardiologist questioned me, and asked the name of the study, and in which journal it came , What was quality of the paper ?
I told him , It is an Imaginary study done in my back yard . It never got published in print. You may call it as E-journal* , not exactly though.It is not available in any websites , but located in the biological servers, and neuronal circuits as digital imprints in learned brains !
*Journal of experience
You may call it , a scientific forgery , to quote a non-existent study,
“But this study benefits whole lot of my patients”.
He was amused , and became agitated !
He told over the mike , “You are making foolish statement. . . don’t corrupt young minds” !
May be , he is true !
I asked him to be calm and requested to listen to another study which I was about to quote . . .
He couldn’t sit any more and rushed out of the hall !
We are ready to believe all those rubbish stories about a fourth generation self disappearing BVS that is able to scaffold a coronary artery and maintain a MLD by 2.5mm and TVR by 20 % and prevent near MAZE at 30 days by 9 % and improve long term survival by 6 months at the cost of 100, 000 Rs per month .Only to realise, it may be a farce . . . 5 years down the lane !
How to cleanse the darkened face of science ?
When falsehoods come with evidence and harm people , Good deeds can be preached without evidence to save our fellow human beings !
Posted in bio ethics, cardiology-ethics, Land mark articles in cardiology, medical quotes | Tagged cad prevention, cardiology practice, cleansing medical literature, commerce based medicine, courage study, emprical medicine, evidence based medicine, ignorance based medicine, lifestyle modification in cad, principles of practice of medicine, randomised controlled trials, rct | Leave a Comment »
Every pacemaker has a metallic “Reed switch” . Putting this switch on and off is possible with an external magnet .The circuitry is such that , switching on makes sensing function null and void.It functions as asynchronous mode.In other words pacemaker converts to a mandatory pacing mode .All sensing related issues are immediately removed.
When a magnet is applied the pacemakers changes the mode in the following way.
- VVI to VOO (Paces only ventricle without sensing)
- AAI to AOO (Paces only Atria)
- DDD to DOO (Paces both ventricle and atrial with a fixed AV interval )
Purpose of magnet application .
Essentially it may be called as a safety mechanism to prevent external sensing in strong electrical fields in case the need arises.
Indirectly , it may aid us in detecting end of life of battery as well
During elctrocautery and related procedures application of magnet will help.
What is magnet rate* ?
- The moment you apply the magnet the pacing rate changes
- This is variable with each make and preset.
- End of life magnet rate will be different . It can be 65 to 85 fixed depend upon the make.
- Some pace makers fire initial magnet rates with 3-6 beat fast run and later revert to steady baseline rate.(One should not be confused )
* Always check with the pacemaker manual for the exact response.
When I put a magnet over nothing happened .What is the inference ?
- Magnet is not placed properly
- Pacemaker battery is totally dead.
- Very rarely some pacemakers have magnet function turned off
What happens during magnet application in ICD ?
- There is no change in ICD mode.
- All anti tachycardia functions are immediately suspended. (A major use in an unusual runaway inappropriate ICD shock situation )
Is there any risk of applying magnet ?
Since magnet removes the sensing function , interfering a cardiac rhythm which is dependent on sensing can be problematic.Similar situation arises in MRI scans and other magnetic fields.
Hence , application of magnet in a patient as a part of pacemaker trouble shooting who has no pacing spikes is rarely a problem While one should not do it without supervision of a learned cardiologist.
What is smart magnet ?
Each pacemaker and ICD is interrogated with the respective programmer.As such , there is no cross brand programmer available.This makes it difficult for patient( as well as physicians) to call for help in case of malfunction.
The solution is to make standard universal analyser and programmer .This requires cooperation between various stake holders.Meanwhile as temporary relief a magnet which can community two way with basic functional switches can be developed .
There is a need for universal smart magnet with constant interaction between device and magnet ..
Since , the generation next generation human heart is going to be wired and deviced in a complex manner, we need to know the basics about these issues.
Magnet application is akin to novice’s pacemaker analyzer. Every cardiac care unit must have one in their shelf. It aids us to diagnose over-sensing as a cause for pacemaker malfunction.(* please note , it has little role in all other pacemaker issues !) .In an emergency it can help stop inappropriate ICD shocks.(More importatnly It gives time to call an expert ! )
Posted in Cardiology - Electrophysiology -Pacemaker | Tagged asynchronous mode, magnet rate, pacemaker issue, problem of over sensing, use of magnet in pacemaker evaluation, vvi pacemker | Leave a Comment »
Distribution of Left main disease.
- Ostio-proximal (Within 1 cm of origin )
- Shaft -Discrete mid left main
- Shaft -Diffuse
- Isolated distal shaft( 1.0.0)
- Bifurcation ( Medina 1.1.0 -LAD)*
- Bifurcation (Median 1.1.0-LCX)
- Bifurcation ( Median 1.1.1)*
- Trifurcation ( With ramus )
* These three locations account for nearly 75% of all left main lesions.
We know atherosclerosis is a branch point disease .Normal left main measures 1 mm to 20mm.The shorter the left main lesser is the the incidence of LMD. Short left main can not engage the atherosclerosis much (No left main = No left main disease ) However ,very short left mains may increase ostial lesions .
- The commonest left main lesion is distal left main with one of the branch involvement (1.1.0.LAD is more common )
- Least common entity is discrete mid shaft lesion.
First dictum : All complex looking LMDs should be referred to a good surgeon.
Final dictum : Remember medical management for left main disease is still an accepted strategy in stable , non flow limiting situations .
Interventional Cardiologists feel they have the exclusive rights to indulge between these two spectrum of LMD .May be true! But extreme caution is required as we are playing our game in the most critical coronary high way .
Some suggestions and thoughts.
- 50 % diameter stenosis is significant. But significance does not mean we should tackle the lesion by aggression.
- Symptomatic flow limiting lesion only to be intervened . (Flow limiting means both angiographic and a stress test .FFR <.8 is also an index for flow limiting .Symptom means Angina on exertion )
- IVUS, OCT, FFR,NIR ,SYNTAX are not path breaking tools .They essentially add more glamor to left main disease than anything .
- Most bifurcation LMDs are managed by single stent with stent jailing the major side branch (Yes side branch can be LCX !)
- However ,two stent strategies is not banished .It can be vastly superior in some selected cases .(Especially with huge plaque load at carina )But needs expertise .
- In very small vessels two stent strategies are risky .
Reference (2012 update)
Posted in Cardiology -Interventional -PCI, Cardiology -unresolved questions, Left main disease | Tagged classification of left main disease, left main artery imaging, left main disease, medina classification, short vs long left main | Leave a Comment »
We know Nitroglycerine(NTG) as a most powerful epicardial coronary dilator . We use it for instant relief during episodes of coronary arterial spasm in cath lab.
What will happen if we administer NTG over a stented segment ?
Does it dilate it with same vigor ? What will be the consequence ?
A perfect setting for stent migration isn’t ?
Let us bust the myth around NTG . NTG rarely show visible coronary dilating effect except in the setting of coronary spasm .
Does a LAD with 3 mm diameter become 3.1 or 3.2 and so on with NTG ?
No .It won’t .It is my belief. It is well known , NTG’s action varies significantly in normal and diseased endothelium . Again , there is an irony .It seems , it can act only in normal endothelium , but we need require it’s therapeutic action only in pathological segments.Further any stented segment would contain clusters of both normal and abnormal endothelium .
One more inference is that, stented segment exerts constant pressure on intima making any pharmacological vasodilatation irrelevant .
Importance of radial strength of a stent
This issue of vaso-dilator induced stent migration may not arise in self expanding wall stent with high radial force.But we do not know how long these metals will carry this metallic property .Balloon delivered stents ( currently used 99% of times ) do not have permanent radial strength .
I am yet to comprehend what nitrates are expected to do (and what it really does ?) in a patient post PCI ? (By the way . . . why we need to prescribe Nitrates it in the first place ? but In real world most continue to take this for many reasons .)
We need to analyse the micro-vasomotion at the stent -coronary intimal interface.The dynamism in this narrow space can be critical , and may make the difference between life and death !
After thought .
In the hind sight, this post appears quixotic for myself . But some one , some where , may generate a great idea out of it , that will help our patients.
Posted in Cardiology -Mechnisms of disease, Cardiology -unresolved questions, Cardiology research topics, Infrequently asked questions in cardiology (iFAQs) | Tagged coronary spasm and ntg, epicardial coronary vasodilation, factors determining stent migration, nitrate action in normal and diseased endothelium, nitrate action in stented segment, nitric oxide and ntg action, nitroglycerine, stent coronary artery interface, stent dislodgement by ntg ?, stent migration | Leave a Comment »
Today , November 2nd 2013 is Deepawali , Nearly 1 billion people celebrate it
Deepawali is an ancient festival of lights , millions of Hindus celebrate It with sanctity.
It is a war on darkness and ignorance .On this day goodness prevailed over evil (Asura)
Unfortunately , In the current versions , it would seem Asura’s also join Deepawali celebrations and enjoy it with more vigor ! which is supposed to eliminate them !
Please ensure , that doesn’t happen . . . at least in your domain !
God is supreme . . . he will never allow the evil to take over the world ! Be a soldier to God’s Army !*For more about this great Hindu festival click on the Link here Deepawali