Cheers to duke university for sharing ! www.echoincontext.com
Posted in echocardiography | Tagged 2d echocardiography, best site for echocardiography, drsvenkatesan, echo video, echocardiography, echoincontext, jase, madras medcial college | Leave a Comment »
Vasovagal syncope is the commonest cause for syncope in our population.It is also referred to as simple syncope .The mechanism is thought to be an abnormal overshoot response by the vagus in response to a sudden surge of adrenegic activity usually occurring in erect posture following , often an emotional or physically stress full situation .The receptors for this reflex pathway is thought to be located left ventricular myocardium .
There are two components for the VV syncope
The quantum of contribution by each component in a given episode of syncope varies. Pure vasodepressive or cardioinhibitory forms can occur .
Diagnostic issue
Before labeling a patient as simple vasovagal syncope all potentially serious , cardiac causes must be ruled out. this may require a fairly extensive investigation in some
Read the related blog : Why syncope is rarely fatal ?
https://drsvenkatesan.wordpress.com/2008/09/30/why-syncope-is-rarely-fatal/
Management of vasovagal syncope.
Some will benefit from beta blockers, fludro cortisone(Increase the intra and extra cellular fluid space )
Since these are simple , cheap treatments , we worked over time to innovate & find some interventional solutions for this life threatening condition !!!. Thus , the indication for cardiac pacing for vasovagal syncope came into vogue .
DDDR pacemaker was implanted worldwide for thousands of patients with vasovagal syncope .
It took many years for our intellectual brains to realise , there are two limbs to vasovagal syncope Pacemakers , at no stretch of imagination is expected to counter vasodepresssive component of the syncope.
And then this article came !
Water , (Simple H2O ! ) administered at right time in right quantity can prevent most episodes of vaso vagal syncope . When a tumbler of water can be substituted for a 10000 $ misadventure (DDD pacing) , and further we have hundreds of similar examples in modern day health care , no surprise why our health care system is sinking along with our economy !
Epilogue :
In this 21st century medical “AVATAR ” , we need to realise in a strong manner, low cost medicines often provide high quality cure ” while ,” many of the high cost therapies may end up in low quality treatment !
It took 50 years of intense research of medical comunity to realise , a good diet , physical activity and quitting smoking has the greatest way to control and reverse the cardiovascular epidemic . Please , note all of them come at free of cost .
Posted in Cardiology - Clinical, cardiology -ECG, Cardiology-Arrhythmias | Tagged ddd pacing for vasovagal syncope, fludrocortisone, neuro cardiogenic syncope, syncope, vaso vagal, water for syncope | Leave a Comment »
Many times , human coronary arteries are the sacred sites upon which mankind’s history and destiny is written.We now have an pandemic of CAD in our hands. It has a great impact not only on the cardiovascular health but also the productivity of this world .
- We , work hard , day and night in cath labs , to remove the blocks from the suffering CAD patients
- Some treat it medically.
- Few others work in preventing CAD
- Not even a handful work on the anatomy of the problem !
How and why the human coronary arterial system behave so bizarrely ?
- From where does coronary artery originates ?
- What determines the coronary collateral seeding and genesis ?
- Why some have only anatomical collateral without functional use ?
- Why artificial neoangiogenesis has not helped much in CAD ?
- Why , one human being lives comfortably with a totally occluded coronary artery , while others suffer with severe angina even with a 70% occlusion ?
- Why the COURAGE and OAT study had the surprising conclusion ?
Answers to all these lingering questions may be clarified soon !
Read this gem of an article from Brazil in a less fancied “Journal of morphology “
International Journal of Morphology – Origen y Desarrollo de las Arterias Coronarias
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ECG of an athlete is many times difficult to interpret. The influence of autonomic tone in athlete’s heart is an complex one.Contrary to our expectations the parasympathetic tone is higher in well trained athletes. The resting heart rate can be as low as 30/mt which is 99.9 times pathological in non athletes.This happens due to a concept called accentuated antagonism.The athletes who have episodic surge of high catecholamines keep stimulating the para sympathetic neurones in a constant fashion.
LVH is the most common feature.Here there is simple myocyte hypertrophy, without pathological fibrosis.This differentiates athlete’s, heart from HOCM .
Many ECG abnormalities are reported in athletes.
Excerpts from the ACC recommendation
1. Electrocardiographic findings that are common and training-related and that do not require additional evaluation are sinus bradycardia, 1° atrioventricular block (AVB), incomplete right bundle branch block (BBB), early repolarization, and isolated voltage criteria for left ventricular hypertrophy (LVH).
2. Uncommon and training unrelated electrocardiographic findings that mandate further evaluation include T-wave inversion, ST-segment depression, pathological Q waves, atrial enlargement, a hemiblock, right ventricular hypertrophy, a BBB, or a Brugada-pattern of ST-segment elevation.
3. Training-related electrocardiographic findings are more common in men than women, athletes of African descent, and high-endurance athletes such as cyclists.
4. Sinus rates <30 bpm and sinus pauses >2 seconds are common in highly trained athletes, particularly during sleep.
5. A normal chronotropic response to exertion and the absence of bradycardia-related symptoms distinguishes training-related sinus bradycardia from sinus node dysfunction.
6. 1° AVB and Mobitz I 2° AVB are common, but Mobitz II 2° AVB or 3° AVB should not be assumed to be training-related and require evaluation.
7. Early repolarization in Caucasian athletes most commonly consists of upwardly concave ST-segments and tall and peaked T waves; in black athletes, there often is convex ST-segment elevation and negative T waves, mimicking a Brugada pattern.
8. In the presence of voltage criteria for LVH, pathological hypertrophy should be suspected if there is left atrial enlargement, left-axis deviation, repolarization abnormalities, or pathological Q waves.
9. T-wave inversion ≥2 mm in ≥2 adjacent leads should prompt evaluation for structural heart disease.
10. Electrophysiological testing for risk stratification with possible catheter ablation is appropriate in athletes with ventricular pre-excitation.
Source : Fred Morady, M.D., F.A.C.C.
http://www.ncbi.nlm.nih.gov/pubmed/19933514?dopt=Abstract
For an excellent article on the topic click here
Posted in Cardiology - Clinical, cardiology -ECG | Tagged athelete heart, athlete's heart, concentric lvh, ECG, echocardiography, pathological lvh, resting heart rate, sinus bradycardia, vagal tone | Leave a Comment »
” This is post is 5 years old , Newer developments should be given considerations”
STEMI is the “Numero Uno” of cardiovascular emergency .The treatment has evolved over decades, right from the primitive arm chair approach to the air dropping of patients over the cath lab roofs for primary PCI ! We realise by now ,both are extreme forms of treatment and may have unique hazards. What we forget is the , the natural history of STEMI is too much dependent on the degree of initial damage to the myocardium , and it is very difficult to alter this, however good is the therapeutic strategy . We are yet to find an answer regarding the mechanism of primary VF and modes of preventing it. We also have no answer for , why some develop myocardial damage very fast and the cardiogenic shock occur in an accelerated fashion. (Fate ?)
Many would consider ” non availability of infrastructure and expertise ” is the major issue for primary PCI . But the real problem is much more than that .When an illusion of knowledge is created by constant bombardment of data , it is natural for human beings to believe whatever is told or printed in books and journals. We cardiologists are made to believe thrombolysis is a far . . . far inferior treatment than primary PCI in STEMI . It is not so in any stretch of imagination !
The fact that,there is no entity called ” Failed primary PCI ” in cardiology literature , would suggest how biased we are against thrombolysis. Every cardiology resident will recognise thrombolysis fails at least 40% of time .Yes , it is a fact , but the irony is , this is often used to convey a surrogate meaning , that is , primary PCI is near 100% successful !
How do you assess success of primary PCI ?
Unlike elective PCI where the criteria is too liberal, we can not afford to adopt the same in an emergency PCI. Here the aim of the procedure is entirely different (Salvaging dying myocardium vs pain relief ).
It’s still a mystery , while thrombolysis is vigorously assessed for it’s effectiveness primary PCI is rarely subjected to the same scrutiny . A check angiogram after the procedure , is all that is done . . . and every one leaves the cath lab happily. The effect of primary PCI on ST segment ECG resolution must be documented immediately after PCI. While , It is mandatory to take ECG after 60 -90 mts after thrombolysis , this sort of protocol is rarely followed after PCI.
If the ST segment fails to retract > 50% immediately following PCI the procedure should be deemed to have failed . Further , unlike thrombolysis in primary PCI , the ST segment has to regress within 10 mts , as IRA patency occur instantly .If we apply this criteria , the success rate of primary PCI would be far less than what we believe*
* Not withstanding the official lesion , hardware, related failure. If we encounter a severe triple vessel disease , with a bifurcation lesion and thrombus it’s a tough exercise as we are racing against time .
Primary PCI Camouflaging in semantics
Why is it important to recognise failed primary PCI ?
For failed thrombolysis we have a strategy . Unfortunately , even in this modern era we have no useful strategy for failed primary PCI . Handing over a patient to a surgeon in a such a situation is considered by many as a great rescue strategy but in real world it does no good in most of the patient.
Doing an emergency CABG in a sinking patient with a battered coronary artery is no easy job /Many times it only rescues the cardiologists from the embarrassing situation of facing the relatives who ask for explanation.
So , what can be done at best , in failed primary PCI ?
Final message
Coming soon
Surgeon’s real time experience of operating on a failed primary PCI. To our surprise , only a handful of surgeons have this experience
Posted in Cardiology-Coronary artery disese | Tagged primary pci | Leave a Comment »
Persistent ST elevation is the general technical term for failed thrombolysis.Regression of 50% of admission ST elevation is the required criteria for susccesful thrombolysis .
Thrmobolysis fails in about 40-50% .
Main determinant is the timing of thrombolysis – not the thrombolytic agent ! do not get carried away with all those curent hoopla about Tenecteplase stuff
If we take 100 patients with persistent ST elavation 90-95 will be in anterior LAD territory .
This is a stunning a cardiology secret no book of cardiology address . . . Implication of which could be very significant . Primary PCI will always struggle to prove it’s superiority over thrombolysis in the right coronary artery .(Note LCX STEMI is different , infact it is more tricky than even even LAD .This issue will be addressed seperately in my blog.)
Read the following link for answer to the title question .
How common is persistent ST elevation in inferior leads following STEMI ? https://drsvenkatesan.wordpress.com/2008/09/22/why-thrombolysis-rarely-fails-in-right-coronary-artery/
Posted in cardiology- coronary care, Infrequently asked questions in cardiology (iFAQs) | Tagged failed thrombolysis, LAD, lcx, nstemi, primary pci, RCA, stemi, successful thrombolysis, thrombolysis | Leave a Comment »
It is a well known fact , CABG and PCI provides immediate relief for patients with angina , which is refractory to medical therapy. Of course , this happens only if a critical occlusion of at least one epicardial coronary artery is opened . It need to be realised , angina due to microvascular disease can not be cured by maintaining epicardial patency .
While angina relief is prompt , dyspnea is not ! . If we believe, opening up a coronary artery in a patient with LV dysfunction will restore the LV function , it is grossly mistaken !
Why is it so ?
Angina relief requires simple restoration of oxygen supply and correction of local ischemia . This happens without any issue as the blood seeps in to the ischemic cells and soothes the ischemic nerve fibres that trigger the pain signals . While , for LV function to improve , the blood flow has to be converted to mechanical activity in the form of myocyte actin/myosin interaction. For this, there need to be an intact cellular contractile mechanism . The myocyte architecture should be appropriate .In post MI ventricles we know there is zig zag orientation of myofibrils due to myocyte slippage that interfere with mechanical recruitment . Further , integrity of extracellular matrix namely the collagen frame work is also vital . Note , angina relief is not concerned with any of the above .
And now , we also realise dyspnea in failing ventricles is vitally dependent on diastolic function , which is also very much impaired in ischemic DCM .There is little proof for PCI/CABG to correct the molecular mysteries in diastolic dysfunction !
Dysfunctional LV means what ? (read the link )
It is a collection of variety of myocardial tissues . Viz : Fully necrosed , partially necrosed , ischemic viable, non ischemic viable, ischemic non viable, non ischemic non viable , Apart from this patchy necrosis, patchy ischemic, areas are common. Finally , necrosed segments may also be perfused normally by spontaneous reopening of an IRA.
One can imagine the complexity of events in these segments once we do the PCI /CABG . The response is highly variable and unpredictable. The major concept we , the physicians believe or ( to be precise made to believe !) is the sanctity devoted to the viable myocardium .For many us , it is considered a holy exercise to identify viable myocardium in patients following MI and then revascularise them if found to have significant viable myocardium (Atleast 20% of infarcted area )
A full 2 decades were lost or (shall we say wasted on this futile exercise !) as we have since realised most of the cardiologists do not follow this rule .
Now , even a scarred myocardium is revascularised in the hope of recovery .As such , we have reached a stage where there is no contradiction for not doing a PCI /CABG with reference to LV dysfunction.
Now every patient with post MI LV dysfunction is considered to have some amount of viable myocardium that is fit enough for revascularization
Are we justified in doing this ?
Many clinical trials have revealed , the recovery of LV function in these segments has not been consistent at all .
The most surprising discovery is a viable myocardium need not be ischemic .It might get adequate blood supply either from invisible collaterals or trickle of antegrade flow . Hence an adequately perfused myocardial segment can still be non contractile . This shatters the myth that revascularisation must have a dramatic effect on the recovery of contractility in all viable segments.
The other major finding is , even ischemic viable myocardium ( documented by metabolic activities PET etc) need not regain it’s original contractility after the ischemia is fully corrected .
*reference for both the above statements are available from variety of sources including real life experiences .(Type C evidence )
Final message
Counter point
If the above statements are really true , How does PCI/CABG help relieving dyspnea and functional class what is your answer for thousands of patients with CAD and ischemic DCM who have greatly benefited from CABG ?
The answer could be simple , The revascularization piggybacks over the medical management (which , these patients pursue vigorously) like ACEI, statins, salt restriction, betablockers , optimal diuretics and tend to hijack the credits from the poor drugs !
Read a related blog
Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, cardiology- coronary care, Infrequently asked questions in cardiology (iFAQs) | Tagged angina relief, cabg, canadian cardiovascualr, cardiomyopathy, courage study, diastolic dysfunction, dilated cardiomyopathy, dyspnea, functional class, ischemic dcm, lv dysfunction, lv fucntion, nyha class 3, nyha class 4, oat study, pci, ptca, stable angina, toat study, unstable angina | Leave a Comment »
Acute MI is a major medical emergency encountered in ER . Prompt adminstration of thrombolytic agents or rapid triaging for a primary PCI may be required . The whole concept of management of STEMI revolves around time as a therapeutic target .Every minute counts . The beneficial effects of reperfusion and the resultant myocardial salvage rapidly declines over time . Hence , the symptom to door time remains the ultimate determinant of outcome in most situations.
So , estimating the time window of “Symptom to door time ” becomes an all important parameter. This is often done by paramedics .
The apparently simple job measurement of time window can be misleading at times especially in elderly, diabetic and alcohol abusers .
When a patient says he has chest pain since yesterday straightaway he is excluded from reperfusion strategies as 12 hours would have elapsed
When a patient describes chest pain since two days , but more intense only since today morning what does it imply ?
So , calculating the time window when a patient has recurrent episodes of angina prior to an MI is a real difficult issue.For the benefit of doubt, we have to take the last episode of chest pain which was continuous and more severe as the infarct pain.
How does ECG help to time STEMI ?
When it is difficult , to differentiate pre infarction angina from infarct pain, the ECG may give useful clues to time the STEMI.
Among the above three ,T wave inversion is most useful to time an infarct. If T wave begins to invert, it can generally assumed the acute infarct process is almost complete . Q waves are less reliable to time a acute MI as ischemic stunning can in the very early phase of STEMI inscribe a q wave over the infarct territory.
How will you time a STEMI in silent MI ?
There is no symptom to door time in patients with silent MI . Many do not even reach the door , for the simple reason there is no symptom that drives them to hospital. Those who are refered have vague non cardiac symptoms and incidental ECG which shows STEMI like changes. Here , the decision to thrombolyse is taken entirely on the basis of ECG *finding .
Note : Cardiac enzymes are can also be used to diagnose to estimate the time window .
Posted in Cardiology - Clinical, cardiology -ECG, Cardiology-Arrhythmias, Cardiology-Coronary artery disese, Infrequently asked questions in cardiology (iFAQs) | Tagged pre infarction angina, preinfarction angina vs acute MI, stemi, time window in stemi | Leave a Comment »
When we get contaminated with excess knowledge , we lose our ability to think ! & Common sense is the casuality . . .
Human beings differ from other forms of life by their sixth sense . Our planet is few billion years old . Life came into existence over a million years ago .Our life has evolved over many thousands of years .The average life span of human race is 75 years . We need to realise , our life constitutes only a fraction of our planet’s life (<.0000001% ) . A may fly , which lives a life of less than a day , does it in style , looking for the light throughout the night , says good bye , to earth by morning leaving it unharmed . Actually , in terms of time , the life of the fly is just a fraction less than human life span , when compared to our planet’s life !
When these children are longing for food , some of earthly humans go to spend millions for obesity surgery ! That is the progress of knowledge driven society . . .
It is extremely common to experience the following scenario in any corporate hospitals of both developing and developed country .A uninsured or half insured ! person is refused entry into a hospital even for an emergency care while a wealthy person is lying comfortably watching TV in a five star suit of the same hospital after an inappropriate coronary angioplasty for an innocuous lesion of his heart !
The irony is , in this short span of earthly life , we want to prevail over the nature and conquer the planet . God is watching this human behavior silently . And he is smiling . . .
With all our knowledge base , modern science have done the maximum possible damage to our planet .We have made many lives extinct. If we tend to think , with the help of 6th sense we can become immortal , it would be the ultimate foolishness. When every one of us , is obsessed with our own health , we are deaf to the silent cries of our beloved planet earth .
Now , all of a sudden we realise all the accumulated knowledge & development has actually worked against us. We find our knowledge is dissociating our thoughts and now , we are fighting vigorously over acquiring the rights to damage our planet .
So it seems , the more we learn, less wisdom we have ! We may need to learn important lessons of living from all those species which do not boast to have the 6th sense !
Read a related article , excellent one published in British medical journal nearly 2 decades ago
Knowledge disease BMJ. 1993 December 18; 307(6919): 1578.
Posted in bio ethics, Cardiology - Clinical | Tagged african children, bmj, cardiology, climate summit, evidence based medicine, green house effect, health outcome analysis, hunger, knowledge disease, lancet, logic in medicine, malnourished, nejm, obesity, poverty, rich vs poor, unequal world, unlearning in medicine | Leave a Comment »
Can modern technology bring back the life from a dead person ?
Yes it is possible , not in the near future ! but in the present era . . .
This revolutionary new portable heart lung machine may just do that .
Imagine this scenerio : A cardiac arrest victim – failed resuscitation with ACLS , the patient needs to be taken for an emergency cardiac surgery or intervention .You need time at least , few hours .Till that time this simple device takes over the role of GOD i e sustaining life by pumping and oxygenating 6 liters of blood !
Learn more about this award winning wonder machine from lifebridge .Germany
Posted in Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology-Coronary artery disese, Great websites in cardiology, Hemodynamics | Tagged acls, artifitial heart, bls, cardiac arrest, cpr, femor femoral bypass, heart lung machine, lifebridge, portable heart lung | Leave a Comment »
Dr.S.Venkatesan MD 