Distribution of Left main disease.
- Ostial
- 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.
Simple strategy.
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 .
Final message
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 | 1 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
Posted in Quotes, Science and Religion, Venkat quotes | Tagged Deepawali, ethics in medicine, festival of lights, hippocrates | 1 Comment »
CAD is growing as an epidemic in most parts of the globe. It is a major determinant of health status of any country .Great strides in diagnostic, treatment modalities of CAD have been made in the last few decades. Still , the core principle of management of CAD resides in simple things like risk factor reduction / optimization , life style changes and few essential cardio-protective medications Aspirin, beta blockers and statins.
However , modern scientists have made a firm statement that knowing the coronary anatomy before starting the treatment is the only scientific approach . It is a huge assumption !
Is it practical ? or is it really required ?
CAD can be managed by means of medicines , interventions or surgery. Revascularisation is required only for those , who have critical , symptomatic lesions.
It is estimated , in only a fraction of CAD patients , we would require to know the anatomy . We have set criteria to choose patients for CAG , who are likely to have critical lesions.Physicians are trained for that elusive wisdom to choose such patients .Standard text books do mention clear-cut Indications for doing CAGs. Unfortunately , it is least respected and followed .
Cardiac physicians who would boast they can’t treat a CAD without knowing the coronary anatomy are clinically handicapped or poorly trained.
I am afraid such a class of cardiologists are rapidly breeding in the country side. They are encouraged to attend CME on clinical cardiology and basic principles of clinical decision-making .
We can’t keep on doing CAGs like ECG for every episode of angina . In fact treating CAD without knowing the anatomy remains (And it should be ) the dominant theme contemporary clinical practice . CAG is multi -edged sword
The most important side effect of routine coronary angiogram is , it ends up in infinite number of inappropriate interventions !
I think , we should pray in Hippocratic temples for sufficient wisdom to choose our patients. We can also learn it from Neurologists , they somehow manage most forms of cerebrovascular diseases (scientifically too ! ) without asking for angiogram of circle of Willis ! Mind you. . . brain is equally a vital organ !
Final message
It needn’t be a crime to treat CAD* without knowing the coronary anatomy. Rather . . . it would be so , to ask for CAG indiscriminately , in every episode of chest pain , without applying clinical sense !
* Emergencies included.
Posted in Cardiology -Interventional -PCI, cath lab tips and tricks, Infrequently asked questions in cardiology (iFAQs), Venkat quotes | Tagged acc/aha criteria for coronary angiogram, appropriate coronary angiogram, can we manage cad without coronary angiogram ?, cardiologist behaviour, coronary angiogram in chronic stable angina, ethics in cardiology, hippocrtes, inappropriate coronary angiogram, Indication for coronary angiogram, indications for coronary angiogram, waht is the indication for coronary angiogram ?, what is inappropriate coronary angiogram ?, when do you do coronary angiogram ? | Leave a Comment »
We know LVH and SHT go together . Mind you , this is not an Intimate relationship.
Widespread utilisation of echocardiography has revealed , definite LVH occurs only in about 20% (A guess !) of HT . (Do you know in the Famingham study the incidence of LVH after 12 year follow up was a paltry 3 % .Will you agree with that ? Mind you , It was in 1969 when Echo was not there )
What determines LVH ? The clear answer is elusive. It is easy to escape from the issue by calling it multi factorial !
Why don’t you try this question .
My guess would be , magnitude ( or even duration of HT !) is less important than genetic predisposition or associated diabetes , renal involvement.Our analysis from hypertension clinic reveals LVH is many fold common in secondary HT when compared to primary HT !
I often used to provoke the students by saying if the LVH is gross in HT it can not be primary , 9/10 times ! Invariably we find some other association or reason for the HT !
Link to related topic in this site
Why-lvh-does-not-occur-in-all-patients-with-systemic-hypertension ?
How-diabetes-modifies-lvh-due-to-hypertension ?
Next . . .
How does LVH regress with treatment ?
Posted in Cardiology -Mechnisms of disease, Cardiology -unresolved questions, Clinical cardiology, Hypertension, Infrequently asked questions in cardiology (iFAQs) | Tagged determinants of lvh in hypertension, genetic factors in LVH, left ventricular hypertrophy, lvh, mechanism of lvh in hypertension, sht, systemic hypertension | Leave a Comment »
The current fad called EBM has lots of lacunae. Though evidence based approach is considered the ultimate journey towards truth ,lot of non academic factors contaminate it .In it’s current form , it is difficult to comprehend it.
This is an attempt to decode the mystery of EBM expressed in a simplified lay person’s term .They are the ones from whom we learn medicine. They are our teachers in the true sense.
By the way ,it is also my approach to EBM .Sorry , if this post sounds arrogant ! It is not the intention .Truths often times appear brutal .
And . . . the Genius approach to EBM for comparison
Posted in bio ethics, cardiology journal club, Cardiology quotes | Tagged ethics in cardiology, ethics in medicine, evidence based cardiology, guidelines in cardiology, guidelines in medicine, principles of medicine | Leave a Comment »
In one of my classes , this ECG was presented . Controversy erupted.It was about the basics .
What is the QRS axis of this ECG ?
Not surprisingly there were handful of answers .
- North west Axis
- Indeterminate QRS
- +150
- +180
- 0 degrees
- Extreme Right axis
Which is correct ? My guess is , it should be closer to + 180 . Lead 2 is equiphasic and perpendicular lead is negative limb of AVL ie + 150 .If you plot Lead 1 and AVF in graph and calculate we get + 135 . (In the strict sense , we are not supposed to take one standard lead and an augmented lead for plotting ). Finally, the strongest argument was , since AVR shows only positive forces it would make north west axis more likely .
Causes of North west QRS axis
- Denova North west axis
- Extreme Left becoming NWA*
- Extreme Right becoming NWA
*Left becoming NWA is much more common than other types.
Chamber enlargement alone is not sufficient to shift the axis to NW corridor. There must be anatomical distortion of his bundle and it’s branches to shift the axis dramatically .This usually occur in complex congenital heart disease. In acquired heart disease the an apical VT is probably an important cause for NWA.
One word about indeterminate qrs axis .
By the way , Indeterminate QRS axis is not synonymous with north west axis. This term should ideally be used if qrs complex is equiphasic in all limb leads , when qrs axis can not be truly determined .This situation commonly occurs when we encounter very very low voltage qrs as in cardiac tamponade and severe hypothyroidism , constrictive pericardits, etc
If the QRS is in north west corrodor , How to differentiate , whether it came from extreme left axis or right axis ?
I am yet to find a correct answer for this.
- Pre-cardial pattern will help.
- A q in V5/V6 would suggest extreme left axis.
- May be we have to look the initial qrs vector in AVR lead for more clues
Traditionally , we talk about net qrs axis . We should realise net qrs axis is a combination of initial and late vectors .It can be dramatically different in different leads . QRS axis is a two dimensional representation of three or more (omni) dimensional electrical forces .That is the source for confusion. So, do not unduly worry about the complexity .Blame it on the limitations of surface ECG !
Expecting some comments .
Posted in cardiology -ECG, Infrequently asked questions in cardiology (iFAQs) | Tagged ecg in pulmoanry atresia, extreme left and right axis, indeterminate qrs axis north west axis, what is north west qrs axis ? | 1 Comment »
It is estimated nearly half a million PCIs are done all over the globe every year .Evaluating diagnostic angiogram is a critical vital step, but often times it is given less time and left to fellows .This is done mostly offline by Image processing software. Curiously , lesion assessment becomes a causality to the visual acuity .It ends up with lot of whims , intuition and bloated egos of senior cardiologists !
Technical issues
The fundamental flaw in the lesion assessment is ,there is a dissociation in choosing the “best view” for lesion morphology and length . Size need not be well assessed in the same view as morphology . For example , LAD is fore shortened in LAO caudal view , length measurement would be erroneous , still morphology may be well delineated .(Vice versa in RAO caudal view )
Other source of errors
Reference catheter may be far away in the Aorta , and confer a magnification error . This becomes important especially in ostial lesions and associated major branch lesions. The computer uses the edge detection algorithm which carries an inherent error .
Advantage of guide wire as a scale
- Instant online measurement
- Always on . Repeatedly used in multiple views .
- You can’t ask for more accuracy .The scale is within the coronary artery hugging the lesion
- The end on view is effectively nullified .
- Magnification factor do not operate.
- Finally , and most importantly in complex tortuous , tandem lesions few mm errors can be disastrous .These calibrated guide wires will make our life lot easier.
Final message
Measuring a coronary lesion remains a delicate issue . If only we have radio opaque rings every 1mm or so in the distal end of the guide wire , we can measure the lesion instantly and most accurately.
This will definitely make our life not only simple but help our patients with accurate stent sizing and avoid costly geographical miss (or inappropriately long stent that increase metal load .)
After thought
I do not know whether any of the existing guide wires have this facility .(I guess it is not . . .then , let this idea be patented in my name !) After all , It is a mean task for all those mighty coronary hardware companies to add few radio opaque rings to all PTCA guide wires!
Medtronic, Abbot, Boston are you listening ?
And . . . your opinion please !
Posted in Cardiology -Interventional -PCI, carotid interventions | Tagged calibrated guidewires, coronary stenting, lesion length assessment, morphology of lesion in ptca | Leave a Comment »














