When LV fails the  lung gets congested and flooded with blood . Similarly when coronary sinus  ,  the major draining outlet of coronary  circulation resists  the incoming blood  flow . . .  myocardium  will  get congested !

This is  the concept  of  retrograde perfusion  in treating refractory CAD with angina . It is a double-edged concept. If the coronary  sinus  pressure is  excessive it may interrupt even  the normal  flow .It should be optimal so that it prolongs coronary micro-circulation time without compromising ante-grade flow. .

Picture courtesy : http://www.dartmouth.edu

Clinical example

We know cardiac failure patients rarely complain of  angina .

Why ? . . The myocardial congestion due to coronary sinus pressure is the most likely explanation.This goes well with the back flow concept in treating refractory angina.

While surgeons tried to link artery to vein  , Interventional cardiologists were smart enough to occlude the coronary sinus partially , that will result in stasis of blood in coronary micro-circulation and hence facilitates oxygen extraction .

Final message

God is a master craftsman. Do not think  there is only  one access to coronary micro circulation.Apart form LCA and RCA there is  a vast network of coronary  veins  traversing  the delicate surfaces and grooves of the heart .

Remember ,they also reach the same micro vascular  bed but in a different direction !

If we  can exploit  them  for myocardial arterial  perfusion we have a real breakthrough   in our hands. . After all , why should we take a vein  from a far way from legs (saphenous veins )  for by-pass surgery  when venous channels are  simply there beside  every branch of a  coronary  artery !

Let us be quixotic , we shall attempt to   congest the myocardium with blood for refractory angina by whatever means ! Mean while let us also remember  what happened to  TMR (Trans myocardial laser  revascularisation ) the biggest technology failure in cardiology in recent times !


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                                          CRT , cardiac resynchronisation therapy  is being  projected  as a revolutionary treatment for cardiac failure , where a failing heart is rewired electrically through multiple leads and make it contract  more effectively.The success rate of CRT was highly variable.The basic question here  is,  there should be a  significant  documentation of desynchronisation  prior to CRT , for resynchronisation to be effective. Further , the sites of  myocardial  stimulation ( Coronary sinus/LV epicardial) , dose of electricity and the sequence of stimulation and the  electrical delay  are very  critical. Achieving this into perfection  is not a simple job and is  real rocket science ! ( If we can achieve 5 % of what  the normal purkinje network do within the LV we can term it a huge success.) Let us hope we catch up with nature . Finally , it is ironical  the sites of LV pacing ,  electrophysiologists  select currently  is infact not selected by them but pre selected by the patients coronary venous anatomy ! .So as on date ,  one can imagine how scientific this treatment could be !

                                         Initially it was adviced for patients with only wide qrs later for even normal qrs patients.When people started using it indiscriminately  insurance companies started to rethink and thus came the   RETHINQ study in NEJM  and brought a full stop to CRT in normal qrs CHF.

How to identify who will benefit from  the costly CRT  ?

It is a million dollar question. So millions of dollars were spent to identify the correct tool to identify the true responders to CRT.Echo cardiography with sophisticated methods tissue doppler, tissue tracking and , 3 D echo ,velocity vector imaging were done .These methods are not only costly but also time consuming and  hugely expertise driven.

Does all this  efforts with  advanced echo techniques worthwhile ?

This simple question was addressed in PROSPECT study in circulation

Click to read the article

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                                               The superior aspect of   coronary sinus and a portion of the left atrium share a common wall .Embryological defects in this area result in a communication between left atrium and coronary sinus. This defect  descriptively called as unroofed coronary sinus .This entity is most commonly associated with persistent left SVC. Extreme form of unroofing is some times termed as absent coronary sinus.

How to diagnose it ?

A high degree of anticipation is necessary in all patients with ASD or LSVC. A dilated coronary sinus in routine echocardiography warrants full investigation. A contrast echocardiography with agitated saline injection in left cubital vein will clinch the diagnosis as contrast enters LA after opacifying the dilated coronary sinus. During  right heart catheterisation catheter course entering coronary sinus and  advancing into LA through the fenestrations (Unroofing)  will confirm the defect.

How do you classify unroofed coronary sinus ?

The morphologic type of URCS was classified as Kirklin and Barratt-Boyes

 Type   I, completely unroofed with LSVC;

 Type II, completely unroofed without LSVC;

 Type III, partially unroofed midportion;

 Type IV, partially unroofed terminal portion

What is the clinical relevance of this entity ?

This entity should be suspected in every patient with persistent LSVC, ( and LSVC should be suspected in every patient with ASD). The hemodynamics is that of an ASD but if sufficient mixing of LSVC blood and LA blood takes place the child will have mild cyanosis.Some times when the coronary sinus is totally absent it will present as a typical dusky ASD picture which can closely mimic a TAPVC clinically.

Surgeons have a greater role in recognising and treating this entity. A typical repair will be done like this


Links to some of interesting articles on this topic

Raghib circulation 1965

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