Coronary collateral circulation is the God’s gift to mankind.It has potential benefits ( and of course real benefit !) both during acute and chronic coronary syndrome.
Collaterals in CCS
The classical role of coronary collateral is in patients with chronic stable angina.It is quiet common to see patients with totally occluded LAD or RCA with normal LV function maintained by extensive collaterals .
Collaterals during ACS.
An intact and functional collateral circulation can prevent an NSTEMI from converting into STEMI.In fact many of the patients with unstable angina patients carry on with viable myocardium just because thaey have good collaterals.It gives us a time window to intervene .Some times the col laterals are good enough and help us avoid a revascularisation in toto.
Collateral’s in STEMI.
This is not well understood. Some researchers reported opening up of collateral channels very early after a STEMI. Logic would suggest , anatomically patent functionally closed collateral channels are always available at time of crisis. But not every one is blessed with such rescue mechanism.
What determines the native collateral channel development in human cor0nary circulation ?
When the answer is unknown , it moves to the genetic domain also called – God’s domain .
Our ignorance in decoding coronary collaterals is vast.
The chief cause of this ignorance is we always tend , not believe things which we don’t see.
Coronary collaterals channels need to atleast 1mm to be visualised by CAG.There could be a vast network of micro collaterals out there within the myocardium invisible to current imaging methods. (In fact , this has a link with outcome of the COURAGE study )
Is coronary collaterals have all the three layers of an artery ?
Yes .But the media lacks muscle.
Is coronary collateral less prone for spasm ?
May be.
The drugs we give , Calcium blockers , betablockers, and nitrates have same hemodyanmic effects as in native coronary circulation ?
We don,t know as yet. Nitrates are supposed to improve collateralisation
How common is atherosclerosis to involve the coronary collaterals ?
How often is an ACS precipitated by an collateral occlusion ?
May be more common than we think.
Can we stent a 2mm wide collateral to maintain the patency in case of a CTO ?
A question need to be answered by current generation interventional cardiologists.
Is coronary collateral gives protection against primary VF ?
In one sense , the number one killer of mankind is in fact not STEMI but the VF that follows it .
Why only a few develop a VF following an MI ? What determines the arrhythmic response to ischemia ?
Some anecdotal observation of suggest a role for early coronary collateral opening in the prevention of VF .

