August 31, 2008 by drsvenkatesan
Coronary angiogram is a video graphic snap shot of coronary arterial lumen which is filled with radio opaque dye. This is some times called as coronary luminogram . It is a paradox , when we say normal coronary angiogram we can only mean normal coronary lumen. But generally, this can provide sufficient information regarding the status of coronary blood flow.There are three structured layers in coronary artery wall . Coronary angiogram can not give any information about the status of the intima, media or adventia .

Lesions A to F may be totally missed by conventional coronary angiogram
A patient with normal coronay angiogram can have diffuse atheroscelrosis or localised atherosclerosis within the media of coronary artery .Many times these atherosclerotic plaques grow outward into the adventia and fail to encroach upon the lumen to be detected by coronary angiogram. These plaques , even though has an hemodynamic advantage, in that it doesn’t block blood flow , has a serious risk for sudden rupture and result in an acute coronary syndrome.
So what is the message?
A normal coronary angiogram can never convey a meaning of normal coronary arteries.

A person who has a normal coronary angiogram has no guarantee that he won’t develop a coronary event in the near future.(But the the chances are very low)
If coronary angiogram has serious limitations what is the next alternative ?
Intra vascular ultra sound imaging(IVUS) can give us an idea of the coronary arterial wall anatomy. This investigation , though available for clinical application is too complex for regular use.So , you can’t subject every patient with normal CAG to an IVUS (Intra vascualar ultra sound) to confirm the normality. The best option is what we follow every day in our practice .Tell your patients with normal coronary angiogram , that they are likely to have normal coronary arteries ! don’t add up to their anxiety by saying, in spite of normal CAG still they can carry gross atherosclerosis in their arteries. Anxiety can precipitate an coronary event. Too much technical information to the patients can be counter productive. Instead advice regular life style modification, blood pressure ,diabetes, lipid control etc .
Posted in Cardiology - Clinical, Cardiology -Interventional -PCI | Tagged cad, cardiology, cleveland, coronary angiogram, coronary artery, intra vascualr ultrasound, ivus, mayo clinic, pci, ptca | 1 Comment »
September 22, 2008 by drsvenkatesan
Differential response of thrombolysis between left and right coronary system
- Thrombolysis is the specific treatment for acute myocardial infarction. ( Privileged few , get primary PCI))
- Failed thrombolysis occurs in significant number of patients ( 30-40%).
- Persistent ST elevation 120 minutes after thrombolysis is best indicator of failed thrombolysis.
- It has been a consistent observation failed thromolysis almost always occur in anterior or LAD myocardial infarction.
In a simple study we have documented patients with inferior MI rarely had persistent ST elevation and thrombolysis has been almost always successful ( Except in few patients associated lateral MI)

The mechanism of better thrombolysis in right coronary artery is simple.The success of thrombolysis , apart from early time window , is directly correlated with pressure head and the duration of contact between the thrombolytic agent and the thrombus. In right coronary circulation the blood flow is continuous , occurs both in systole and diastole that facilitates the maximum delivery of the thrombolytic agent . Further there is a favorable pressure gradient across RV myocardium as the transmural occluding pressure across RV is considerably less then LV myocardium.

This paper was presented in the “Annual cardiological society of India scientific sessions”
at Chennai, Tamil Nadu.India December 2000
Click to down load PPT full presentation
Posted in Cardiology -Interventional -PCI, Infrequently asked questions in cardiology (iFAQs), cardiology- coronary care | Tagged acs, acute myocardial infarction, angiogram, bmj, cardiology, ccu, circulation, coronary, coronary circulation, failed thrombolysis, lancet, left anterior descending, nejm, nstemi, persistent st elevation, stemi, streptokinase, successful thrombolysis, thrombolysis, tissue plasminogen activator, tpa | 1 Comment »
September 24, 2008 by drsvenkatesan
No reflow is the terminology used primarily in cath labs where, even after a successful opening and stenting of a coronary artery the coronary blood flow is not restored to myocardium . The point to be emphazised here is blood do cross successfully the site of the obstruction but fails to enter the muscle segment to which the coronary artery is supplying. So the paradoxical situation of artery being open but the myocardium is closed to receive blood flow happens . This is termed as no -reflow. Actually it is a misnomer , and ideally it should be called “no flow” because normal distal flow does not occur (After PCI) in the first instance to get interuppted later on and be labeled as no re-flow. .The only positive effect of PCI in these situation is blood flow would have improved by few centimeters ie till it reaches but falls short of myocardium . In fact no reflow , can be termed as glorified and concealed terminology for PCI failure . It needs urgent action . No reflow is also called as myocardial epicardial dissociation.
Mechanism of no reflow.

Curious case of open coronary artery and closed myocardium !


Coronary microvascualr plugging is mainl due to thrombus and atheromatous debri , myocardial edema , microvascualr spasm may also contribute.
Where can it occur ?
- First described in cath lab, especially following primary angioplasty.
- It can very well happen following thrombolysis in STEMI.
-
Can occur in venous grafts.
How do you recognise no reflow?
In cath lab it will be self evident from the check angiogram. Some times it is less obvious and may require, myocardail blush score, TIMI frame count, contrast echocardiography, PET scan etc. In post MI a very simple method to recognise this entity could be the observation of persistent ST elevation in ECG .
Treatment.
Extremely difficult. Almost every coronary vasodilator has been tried.(Nitrates, nicorandil, calcium blockers, etc).Success is less than 30%. High pressure flushing with saline inside the coronary artery is advocated by some.Others believe it’s dangerous to do it. So prevention is the key. Avoid doing PCI in complex, thrombotic lesions. Use thrombus suction device like export catheter(Medtronic). Distal protective devices are double edged devices , useful only in experienced hands.
Unanswered question
What is the size of the particle (thrombotic and atheromatous debri) the coronary microcirculation safely handle and push it into the coronary venous circulation and the coronary sinus for disposal ?
If we can lyse the thrombus into micro particles by some mechanism and make it traverse the coronary circulation this complication of microvascuar plugging can be treated and prevented .
What is the final message ?
- No reflow is relatively common condition during emergency PCI done for ACS patients
- More common in complex thrombotic lesions.
- Can also occur in STEMI
- Treatment is often vexing . In fact the treatment of this condition is so difficult , it can be termed almost synonymously with “Failed PCI” if flow is not restored.
- Suceesful treatment of no reflow means not momentry restoration of myocardial flow by mechanical and pharmacological modalities ,but to maintain sustained myocardail perfusion. This we realise, as patients who have had a no reflow during a PCI, do not perform as well in the follow up .
- So prevention is the key.
Posted in Cardiology -Interventional -PCI, Infrequently asked questions in cardiology (iFAQs), cardiology- coronary care | Tagged acs, cath lab, ccu, complications in cath lab, distal protection device, drsvenkatesan. cardiology, epicardial myocardial dissciation, europcr, export catheter, failed primary pci, failed thrombolysis, jacc, lancet, medtronic export, micro vascular plugging, myocardial edema, nicorandil, no reflow, nstemi, pci, primary angioplasty, primary pci, scai, slow flow, stemi, tct md, thrombus aspiration, timi 3 flow | Leave a Comment »
February 9, 2010 by drsvenkatesan
As the name suggests dilated cardiomyopathy would imply cardiac chambers will dilate , at least some time in the course of the disease .It can be minimal, mild or massive. A new entity called non dilated cardiomyopathy is also gaining wider acceptance . (That will be dealt seperately )
Logic would suggest , the first chamber to dilate in DCM should be the left ventricle because it is facing the direct load of systemic blood. But we also know , whenever LV is stressed , left atrium comes to it’s assistance .
Left atrium does this by total self sacrifice ( by all means!) increases it’s force of contraction, elevating it’s mean pressure or even increasing it’s rate (AF) .
Like most other critical questions in cardiology , the factors that determine LV dilatation in DCM , is also poorly understood !
- Is it the after load ?
- Is it the muscle mass ? or it’s turgid or flabbiness ?
- Is it the interstitial integrity?
- Is it the blood volume ?(LVEDV , LV residual volume )
When the issue is complex , it is usual to make the the unknown genetic defects , the scapegoat !
As of now the most important determinant of LV dilatation could be the behavior of the desmins, the gap junctions and myosins the titins etc
If the LV of a DCM patient refuses or resists dilatation what might happen ? Is it good or bad for the patient ?
Here is a catch . A LV that does not dilate obviously should be be good for the patient is in’t ? Medicine is not that simple.
When LV fails to dilate it means it has become too stiff and rigid and pass on the burden to to LA which faces the music. And in the process it dilates.This is the reason , we observe diastolic dysfunction in vast number of DCM patients.( Currently it is estimated > 75% DCM will have significant diastolic dysfunction )
So , now we can imagine how complex the sequence of hemodynamic stress in DCM that determine the chamber enlargement.( RA, RV dimension in DCM is a separate issue !)
So now answer this question : Which chamber dilates first in DCM ?
- Left ventricle
- Left Atrium
- Any of the above
- Both of the above dilate simultaneously
The answer must be 3 .
Why recognising this sequence of chamber enlargement in DCM is important ?
- It gives us an opportunity to assess the dominant mechanism of LV dysfunction.There are reports , where some DCMs have more diastolic dysfunction than systolic dysfunction .This will have important therapeutic implication.Further , many of the infiltrative disorders of LV can have features of both DCM & RCM .
- When a RCM begins to dilate it is usually a harbinger of terminal heart failure. But, it need not be always true . A small restrictive LV , when dilates , may acquire a slightly improved diastolic properties , as the LV becomes more placid . And , if it happens the LA size may regress.
- The role of LV restriction devices like, Acron mesh, Dor procedure, plication in refractory DCM is not well defined. All these modalities actually adds a small dose of diastolic dysfunction in these patients who have grossly dilated ventricles. This fact is very important , as presence of any preexisting significant diastolic dysfunction in DCM makes the role of LV restrictive devices and surgery a big question mark !
Posted in Cardiology -unresolved questions, Cardiology-Coronary artery disese, Infrequently asked questions in cardiology (iFAQs), cardiology -Therapeutics, echocardiography | Tagged cardiac failure, cardiology, DCM, dilated cardiomyopathy | Leave a Comment »
February 9, 2010 by drsvenkatesan
Imaging coroanry artery is generally in the domain of interventional cardiologists. MDCT has helped us to change that.
The humble echocardiography can identify the origin* of coronary arteries in most persons. The resolution power of modern day echocardiography is 2mm and the left main ostium is >3.5mm in 99% of population . If some body says one can’t visualise the coronary artery by echo , it can only reflect their ignorance or lack of patience to get an optimal image. Of course technological limitations are there.
* To be emphasised again , only the origin can be identified.
Can we identify ostial leftmain or proximal left main disease by echocardiography ?
It should be possible in few .

Can we place a doppler sample volume within the left main and measure coronary flow velocity ?
When obsterticians are able to assess the uterine artery flow in a bulky uterus , it should be possible to do the same in a coronary artery . Motion artifacts is the issue in the heart. Micro sample voulme (<1mm) are expected in the future that will make a non invasive coronary flow assesment a distinct possibility.
Posted in Cardiology - Clinical, Tutorial in clinical cardiology, cardiology -Therapeutics, echocardiography | Tagged aortic cusps, coroanry ostium, coroanry sinus, coronary, coronary artery, coronary artery origin, echocardiography, lcc, left main coroanry artery, left main disease, lmd, ncc, non coronary cusp, rcc, right coroanry cusp, short axis in echocardiography | Leave a Comment »
February 6, 2010 by drsvenkatesan
Hypotension is one of the dreaded complication of acute STEMI.
- It can be due to either a mechanical complication or hypovolemia.
- The hypotension in inferoposterior MI is often related to enhanced vagal tone and easily correctable with atropine and fluid administration.
- RVMI is the classical example of hypotension that may improve with fluid resuscitation
- Hypotension, if not reversible within 12 hours , is more likely to represent a more sinister mechanism like pump failure, MR or ventricular septal tear etc .
A new mechanism for persistent hypotension is increasingly recognised.
This is due to the
1.Loss of LVOT dynamic activity.
2.Excessive dynamism of LVOT.
LVOT contractile and ejectile falure
Even though LV outflow tract contain less contractile myocytes , it has an important mechanical job to do. We know , it’s primary job is that of a conduit but it also has to eject the blood into aorta with sufficient force. In fact, it is thought much of the acceleration of blood velocity occur in LVOT . So, LVOT plays a key role in maintaining the cardiac index. An excessively dynamic LVOT will impede the forward blood flow as in HCOM. Similarly less dynamic contraction of LVOT results in low velocity propulsion , that interferes with proper delivery of blood from LV cavity into the aorta .
These factors get amplified in acute MI , as it is a compromised situation with fluctuating HR and contractility. So a properly functioning LVOT conduit is absolutely mandatory.
STEMI due to a proximal LAD obstruction located can involve the septal .If the first septal branch happens to be a major one, there will be definite impact on the LVOT function.
Excessive dynamism , LVOT desynchrony LVOT collapse .
LVOT has a medial border formed by IVS , an anterior surface and a posterior surface .The lateral border is relatively boundary less , except it is guarded by the anterior mitral leaflet.
But one should recall , the AML comes towards the LVOT only in diastole . When it comes in systole it becomes a pathological event called SAM (Systolic anterior motion )
The LVOT wall desynchrony can occur in both anterior and posterior MI.In a mulivessel CAD this can happen when there is disproportionate inferior to anterior wall motion defect.
Management.
- There is no specific management strategies aimed at restoring LVOT function.
- Emergency revascularisation will attenuate the mechanical dysfunction
- Dosage of powerful inotropic agents should be moderated in dynamic LVOT obstruction.
- Spontaneous recovery may occur in few
http://circ.ahajournals.org/cgi/reprint/116/5/e110.pdf
Haley et all Mayoclinciproceedings 1999

Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, Cardiology -unresolved questions, cardiology -Therapeutics | Tagged dynamic lvot obstruction, hcm, hocm, hypotension in stemi, lvot collapse, lvot stemi, refractory hypotension, RVMI, sam | Leave a Comment »
February 5, 2010 by drsvenkatesan
- It is only rarely a journal of International caliber is published from India . IJEP is one such journal.
- Cutting edge articles on Electrophysiological science break here !
- This is an online journal . No print issues . Enjoy, it is free !
Here is the Link

Just sample an article : A great review about cardiac arrhythmias in congenital heart diseases , Must read by all cardiologists http://www.ipej.org/0906/khairy.htm


Posted in cardiology journals | Tagged cardaic pacing, cardiac arrhythmias in children, carto, ddr, drsvenkatesan, ECG, electrophysiology, endosense, ep study, heart rhythm society, IJEP, india, pace, pediatric cardaic arrhythmias, pediatric cardiology, vvi | Leave a Comment »
February 4, 2010 by drsvenkatesan
- It is going to be the era of non invasive imaging in cardiovascular diseases .Future looks very exciting
- We have now ability to slice the heart 356 times a second !
- Image resolutions are getting sharper .
- The only worry ( Of course a major one !) would be the radiation , that has to be addressed .
Now we have a dedicated journal for cardiovascular CT scan .
Does it surprise you ? For me . . . It is !
Link to the current journal page . Get updated !

http://www.journalofcardiovascularct.com/current
Posted in Cardiology - Clinical | Tagged 64 slice ct, cardiology, cardiology journals, ct coroanry calcium, ct scan, drsvenkatesan, mdct | Leave a Comment »
February 4, 2010 by drsvenkatesan
There are millions of articles in cardiology . Some simply occupy valuable spaces without any purpose . Some give us knowledge . Some enlighten us. While few are so vital , it is almost a crime if we do not read such articles and apply it in day to day practice .
This an article written by Henri Justino that has a immense importance for the patients as well as the physicians .
Do not think the article which came in pediatric radiology is not applicable in adults !


Posted in Cardiology - Clinical, Cardiology -Interventional -PCI | Tagged 64 slice ct, alara, angiocardiography, cardiac catheterisation, cath lab, drsvenkatesan, hazards of ct scan, mdct scan, physician safety, radiation badge, radiation dose, radiation hazard, radiation safety | Leave a Comment »
February 4, 2010 by drsvenkatesan
- Here is a site which has dedicated resources for learning echocardiogrtaphy .
- The site has collection of various work shop and coference highlights
- The basic echocardiography with classical line diagrams would be very much useful for the beginers,
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 »
February 3, 2010 by drsvenkatesan
STEMI is the major cardiac emergency .The acute mortality is about 20% (Both prehospital and in CCU ) STEMI occurs whenever a coronary artery is occluded suddenly in toto .We traditionally believe that STEMI occurs only in the major epicardial vessels. (LAD/LCX/RCA .)

The total length of coronary tree is much longer than the length of the three vessels put together.The diagonals , the ramus, the OMs ,the septals run for varied distances. The caliber of these vessels can be quite large.It is estimated the diameter of first diagonal , the first OM or the ramus can be as big as LAD proper in 30% of CAD population . Law of statistics tells us sudden occlusion can occur any where in the coronary tree in ACS prone patients.
What is the real incidence of side branch STEMI ?
The dogmatic answer is ” We do not know”
Will we ever know ?
How will a Diagonal / OM /Ramus or PDA STEMI behave ?
It is surprising this question is not addressed by us for so long . Some may even question the existence of such an entity(Side branch STEMI ). This is most likely , reflect our ignorance on the issue . We know bifurcation lesions at the side branch origin is very common . Further , thrombus can migrate from a main stem to a side branch immediately after formation .

Clinical presentation of side branch STEMI
- Acute presentation is identical to that of a major main branch STEMI . The pain can be severe , the primary arrhythmic threat is real . Ischemic VF , once initiated does not modify it’s character according to the quantum of insult .
- ECG is the major variable. You , don’t expect gross , ST elevation in many leads as one would see in LAD MI /RCA MI.
- The age old teaching that an ECG can be entirely normal in acute MI , could actually imply the side branch STEMIs . When a small D2 or D3 gets occluded the ECG may not pick up the ST shifts .
- The commonest site of atherosclerosis apart from proximal LAD is the bifurcation of PDA in RCA. STEMI due to PDA occlusion is the most difficult thing to recognise. Many of them have very subtle ECG and clinical findings.
- There has been reports of acute complete heart blocks with isolated AV nodal infarcts. Here sudden cardiac deaths are reported
It is very much possible , many of the side branch MIs may be wrongly diagnosed as unstable angina by us , for the simple reason the myocardial necrosis is not large enough to produce ST elevation .They may actually respond to thrombolysis , as there is total occlusion in the coronary artery. Since, they do not manifest ST elevation there is a lost opportunity here . This , probably is the population in TIMI 3B trial that showed some ( statistically insignificant ) benefit for thrombolysis in NSTEMI.
Is primary PCI justified in side branch STEMI ?
May not be . The chances of side branch STEMI to result in LV dysfunction and progressive adverse remodeling is considerably less . The hazards of primary PCI for exceeds the risks of MI due to a septal or diagonal branch lesion .
Final message
- STEMI due to branch coronary artery occlusion is a less recognised entity among ACS.
- Cardiologists , need to look into this issue with little more seriousness as it could represent a new intermediate risk category among the much flaunted classification of acute coronary syndrome. Triaging and risk stratification of ACS needs a revamp.
- It is possible many of the UA patients , may in fact represent total occlusion of side branches.
- There is a definite case for showing less aggression in these patient subsets , provided we are sure about the location of lesion.
Counter point
* Identifying a side branch STEMI with confidence may be very difficult at bed side in an emergency . Implication of wrongly calling a STEMI as benign can be dangerous . So it will be argued , one need not do this exercise of traiging STEMI into main branch or side branch .
Image courtesey
Coronary tree : http://www.southcharlestoncardiology.com/64cta.html
Posted in Uncategorized | Tagged cardiology | Leave a Comment »
February 2, 2010 by drsvenkatesan

Modern medicine promises healthy new lives to millions. We all , enjoy the fruits of great scientific discoveries. But do we realise , medical science is nothing but experiments done on live human beings . All treatment modalities are under constant scrutiny. A great drug becomes the most harmful drug over a short time.
A drug or a device which is banned in one country is freely used in other country , marketed by the same parent company . How on earth this can happen ? A device ( Eg : A stent ) which is found inferior can still can be used legally elsewhere , hiding the information .
- Do we divulge all vital information to our patients ?
- Do we reveal all our conflicts of interest to our faithful patients ?
Informed consent is the “greatest invention” in medicine . That is democracy in medicine . Doctor patient conversation is supposed to be most noble of all communication !
But . . . this is under genuine threat . In this ” New medical AVATAR ” truths remain only as thoughts , they rarely come out as words or action !
One such situation a physician often faces in his office , as he is compelled to act against his conscience
If only we have an ability to read his silence it will go something like this . . .
For the sake of Science & Commerce , I have to implant this device in your heart , and my gut feeling says , you will do much better without this device as well ! But , I am sorry . . . I can’t avoid it .
Doctors are not be blamed . . . rather , we can’t blame any body
Patients believe in doctors , and doctors believe in science And the irony is , doctors have no other option as they are coerced to believe , in whatever is published as science even if it is half baked , unproved, unapproved or even dangerous science .
Let us prey for the genuine science to prevail at least in human health and the mankind reap the maximum benefits !
Let us recall Mahatma Gandhi’s “Seven Social sins” That included one advice for the scientific world nearly a century ago when it was at it’s infancy !
Seven Social Sins By Mahatma Gandhi
- Politics without Principle
- Wealth Without Work
- Pleasure Without Conscience
- Knowledge without Character
- Commerce without Morality
- Science without Humanity
- Worship without Sacrifice
– Young India, 22-10-1925
Posted in Uncategorized | Tagged ethics in cardiology | Leave a Comment »
January 31, 2010 by drsvenkatesan
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
- Cardio inhibitory
- Vaso depressive.
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 ?
http://drsvenkatesan.wordpress.com/2008/09/30/why-syncope-is-rarely-fatal/

Management of vasovagal syncope.
- Reassurance is the mainstay . By this we mean , V V syncope may never kill . . .
- Prevention – Involves identifying syncope prone situations & taking precaution
- Emotional support
- Pharmacological approach
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 !

http://circ.ahajournals.org/cgi/content/full/108/21/2660?ijkey=ba86da897c167581c498c81743c32afe14fc9393
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-Arrhythmias, cardiology -ECG | Tagged ddd pacing for vasovagal syncope, fludrocortisone, neuro cardiogenic syncope, syncope, vaso vagal, water for syncope | Leave a Comment »
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