Dr.S.Venkatesan MD

Coronary artery and veins are married life long . . . with a purpose !

September 9, 2018 by dr s venkatesan

Cardiologist are always worried about the supply side of coronary blood flow. It’s fair enough, we can condone our brain for this one way thinking , afterall arterial supply remain the life-line for the heart. Some of us could (should) realise the importance of these  humble coronary veins which are anatomically and physiologically tied together.Its existence is as unique as their arterial counterpart.Coronary blood flow of about 250 ml traverses both the arms every minute.Imagine the scenario if the veins refuse to clear the blood from previous cardiac cycle . . . total hemodynamic chaos right ? Luckily such situations are rare !

See how the the two coronary arteries and its branches interwine with the 4 major coronary veins.

J. M. Bourgery from Atlas of Human Anatomy and Surgery / Atlas d’antomie Humaine et de Chirurgie by Jean Marc Bourgery (1797-1849) Los Angeles: Taschen, 2005. Atlas Case QM 25 .B67 2005

Is the LAD flow coupled with Great cardiac venous flow ?

It is curious to see the LAD  hugging its spouse great cardiac vein within the anterior Inter-ventricular groove , but directing the flow exactly in the opposite direction . One should  wonder is it the same stream of blood from LAD ?(Near 100% So2) goes out into myocardial tissue comes back with 30 % *saturation in GCV ? If this is true , one can measure the “LAD micro-circulatory bed” integrity by computing the arrival time of levo phase blood in GCV.

J. M. Bourgery from Atlas of Human Anatomy and Surgery / Atlas d’antomie Humaine et de Chirurgie by Jean Marc Bourgery (1797-1849) Los Angeles: Taschen, 2005. Atlas Case QM 25 .B67 2005

* Its an important physiological fact the most desaturated blood(30%) in the body is from coronary veins as the aerobic organ extracts maximum oxygen .(For comparison IVS/SVC saturation is around 75% )

What happens to GCV flow in LAD  STEMI ? or CTO ?

In  ATOs of LAD there is temporary collapse of GCV. If it prolongs it may end up in complete thrombotic occlusion of GCV which has implication in slow flow , no reflow and poor myocardial salvage.

What happens when there is  acute  coronary venous occlusion ?

Nothing alarming happens. God’s masterly protection  ? Yes it is .Still its a mystery , sudden death is not the rule if we clip the coronary sinus as  thebesian venous system take over which drain direct to chambers.The fact that obstruction of  these veins may not result in acute coronary syndrome brings  less attention to this circulation , in spite of vital hemo dynamic role . Acute venous infarct due to coronary sinus infarction is still  possible.

Is there chronic coronary veno occlusive disorder ?

We know ,venous system is Intrinsically prone for thrombosis  in susceptible individual as the flow velocity is sluggish . Almost every venous system right from portal, hepatic pulmonary , renal cortical venous , experience this pathology. It’s surprising to note coronary venous system is largely devoid of this.(or at least it’s not recognised as often !)

Some of the patients with chronic CAD with syndrome X /Y show extreme slow flow with normal epicardial coronary arteries.We need to study them for sluggish coronary venous flow syndromes.

Assessment of coronary venous hemodynamics 

Coronary venous circulation integrity is critical component of  coronary micro -circulation.We have done original studies in the timing of filling of coronary sinus that reflects integrity  coronary micro circulation.( Sangareddi V, Alagesan R. Coronary sinus filling and emptying time: A new parameter to assess coronary microcirculation by a simple angiographic frame count. 59th Annual Conference of the Cardiological Society of India December 7–10, 2008. (Abstract).)

Microscopic analysis of coronary venous debris following PCI is our future area of study to assess the mechanisms of no reflow.

Clinical utility of  coronary venous circulation 

• Coronary veins are popular with  electrophysiologist.The typical CS catheter is used to record intracardiac ECG around the AV groove .
• They also provide an alternate site for ventricular pacing and cardiac resynchronisation therapy. However the efficacy of CRT is related directly to the coronary venous finger print .Unless it matches with the scar free areas of ischemic cardiomyopathies the response is likely to be less. So essentially EPs are at the mercy of these veins and scars.
• Coronary veins can be used for retrograde perfusion of myocardium in diffuse obstructive  coronary arterial CAD where CABG is not possible with some success.
• There is one trial (COSIRA) which suggested increased microvascular perfusion if we narrow the CS diameter with a device .This is hemodynamically Ironical though as coronary  perfusion gradient is increased still because of stagnation suggest some improvement in perfusion( Verheye S ,NEJM 2015)

Reference

Coronary venous circulation has an Integral link with micro circulatory bed .It will be of huge importance to understand the highly unpredictable response of PCI with reference to myocardial salvage in STEMI and revascularisation in chronic CAD.Youngsters are encouraged to dwell deeper into the mystery of coronary microcircualtion .

This one from Dr. Muller ,Florida  is a perfect review to start with.

A good review about the venous anatomy with reference to electrophysiology

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Posted in cardaic physiology, cardiology-Anatomy, coronary sinus anatomy and physiology, coronary sinus filling and emptying time drsvenkatesan, coronary veno occlusive disorder, coronary venous circulation | Tagged acute coronary sinus syndrome, coroanry vein, CORONARY SINUS, coronary sinus occlusion, coronary venous anatomy, venous infarct of heart | Leave a Comment »

This Innocuous looking ECG made me scratch the basics of EP without an answer !

August 11, 2018 by dr s venkatesan

This 70 year old man in routine check up showed up this ECG.

What is it ? a  quick debate ensued !

Is this

1. RVH
2. RBBB
3. Or Both ?
4. Neither RBBB nor RVH
5. Wrong lead placement
6. Is it a normal ECG after all ?

Incidentally the ECG shows a Wenkebach AV block in the bottom strip lead 2.

I thought it was RVH. (do considered RBBB) but since lead V 2 showed tall R , I was more than sure RVH was likely . Many voted for RBBB. .Some others said RBBB can never occur in monophasic form.I said it’s possible.

Some body challenged me without Echo Imaging a  monophasic RBBB can never be differentiated from RVH. After a mini argument I reluctantly agreed.Yes, it seemed there is no way to differentiate the two.

What do you think ?

Curious to know the Echo finding in the above patient  ? Yes , your guess was right /wrong. There was no RVH.He had normal Echocardiogram.

How to diagnose RVH in RBBB ?

1. Look at the r’ wave if its taller than initial r by more than 5mm suggest RVH (Not absolute evidence though)
2. Look for other evidence like Right axis , RV strain etc.

How to diagnose RBBB in RVH ?

Sorry.I don’t know the exact answer.It could be masked within Qrs complex of RVH.RVH could convert biphasic  RBBB into monophasic RBBB.

Some more about this RVH/RBBB duo

• The term incomplete RBBB is liberally used with minor rsr’ pattern.It is not advisable to do so.
• RBBB is classically multiphasic (To be precise RBBB can be complete to incomplete  rsr’ with various combinations of small r and big s big R or big S).
• But more than the morphology of Qrs in V1 the S wave in lead V 6 or Lead 1 could be Important.It should be delayed slurred.
• QRS width has no great use to diagnose RBBB as it can be narrow or wide.

Final message 

To diagnose monophasic RBBB( in V1 ) by itself requires some guts.However ,the entity do exist.

Finally , please recall there is a traditional list for  tall R in V1 other than RVH.

• Wrong lead placement
• RBBB
• Some cardiomyopathy(RV myopathy)
• Systemic Duchenne’s muscular dystrophy
• Pre-excitation
• Posterior MI
• Normal variant*

*Why should normal guys grow a tall R in V1 , it mystifies ! but true.

What is the rarest cause of tall R in V1 ?

Localised cardaic tumors over RVOT. Cagli K , Tok D, Basar FN   .An unusual cause of tall R wave in lead V1: cardiac lipoma.Heart Asia. 2013 Mar 7;5(1):33. 

 

Annexure : Further questions in RBBB

 

1.How does AV bundle penetrate to become bundle of HIS and branches ?

Note AV node is fully Intra atrial structure , while part of His bundle is atrial , after crossing the membranous septum second part lies within the ventricle at the crest of muscular septum .Then the bundle of His goes for the famous division. Left fans out  tow streams, while right descends on right side of IVS. Note : Applied anatomy 1.Its this small portion of HIS we are trying to physiologically pace the ventricle 2.In proximal LAD lesions both RBBB and LBBB is common still LBBB can’t be used to localise but RBBB can be.Guess why ? Read the next question and find the answer..

 

2.What is the blood supply of bundle branches ?

Image source Clinical Cardiovascular Physiology April, 1976 by Herbert J. Levine

 

3.What is the mechanism of RBBB in ASD ?

Is it true RBBB or Right bundle delay ? Students should know there need not be conduction system pathology to cause RBBB. Simple delayed conduction in RVOT can cause a RBBB. (The concept of central RBBB vs Peripheral RBBB) This is what happens in ASD.

In fact , true pathological damage due to right bundle branch due to necrosis, Ischemia, Infiltration is much rarer than pathological LBBB.

4. What are the  structural , histological  difference between right and left bundle branches that has electrophysiological Importance ?

Wait . . . I am trying to collect info for this .Meanwhile ,Why don’t one of the energetic young  fellows in cardiology find the answer and post here !

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Posted in cardiology -ECG, RBBB vs RVH | Tagged how to diagnose RBBB in RVH and vice versa, rbbb in rvh, rvh in rbbb, tall r in v1 differential diagnosis |

Friendly Infarcts in ACS : Ischemic mitral regurgitation and the Papillary muscle paradox !

July 18, 2018 by dr s venkatesan

Ischemic MR is a critical entity in determining the long-term survival in post MI patients as well as dilated cardiomyopathy. (Originally described  by J. H. Philips Ann Intern Med. 1963;59(4):508-520)

The mechanism of MR  can really be complex .We know mitral apparatus consists of  six components.The sub valvular apparatus plays a key role. LV  free wall especially the inferior and lateral segments which subtends the two papillary muscle has a critical role in maintaining the mitral valve competency .

There seems to me a complex mechano -anatomical behavior of subvalvular structures in progressive LV dysfunction especially so in ischemic cardiomyopathy. The LV size, shape eccentricity in attachment of leaflets to papillary muscle is (Simply called altered geometry ) .The intraventricular desynchrony ,disproportionate  LV dysfunction also make MR more likely .

Beware of a striking  physiological irony in ischemic MR.

While infero basal free wall dysfunction occurs commonly with  LCX/RCA Infarct and  is commonly associated with Ischemic of MR .There is something unique happens . . . when the infarct is larger and involves the head of the papillary muscle .Yes, it attenuates the severity of MR.(Friendly Infarct extension!) The mechanism is , papillary muscle dysfunction  tends to prevent apical tensor effect leading to   improved tethering of leaflets .This may appear a blessing in terms of  prevention of acute pulmonary edema. This also explains why some patients are as cool as cucumbers and lie flat comfortably with silent lungs in spite of severe LV dysfunction .The LV is too weak it doesn’t  have contractile energy to generate acute  severe MR.

Here is an illustration  from circulation .Note: The Infarct extends to pap muscle head, the MR is arrested.

Image courtesy : Emmanuel Messas J. Luis Guerrero, Mark D. Handschumacher, et all  Paradoxic Decrease in Ischemic Mitral Regurgitation With Papillary Muscle Dysfunction Insights From Three-Dimensional and Contrast Echocardiography With Strain Rate Measurement Circulation. 2001; 104: 1952-1957

Further debates 

Papillary muscle dysfunction may be protective against progressive MR.Still ,sudden papillary muscle rupture result in flash pulmonary edema and death is imminent . How ? Complete rupture  causes flail free-floating leaflet that prolapse into LA and result in free MR.While simple dysfunction without flail leaflet is less likely to cause MR . The key determinant seems to be the net force that keeps the alignment of mitral,leaflet at annular level.

In this context , we also realise the impact of primary PCI on the  regression of  Ischemic MR is not uniformly positive.Reasons not clear.

Final message

Ischemic MR  due to LV free wall infarct is a near knockout punch , that may determine the ultimate ACS  outcome. However , a simultaneous lesser punch ( by a friendly devil ! ) on the adjacent head of papillary muscle neutralises the effect of Initial Injury. While such non academic scripts are enjoyable , we are still a long way away to understand this anatomical ,hemodynamic conundrum.

Reference

1.

2.Leaflet remodelling in functional mitral valve regurgitation: characteristics, determinants, and relation to regurgitation severity Philippe Debonnaire , Ibtihal Al Amri , Darryl P./ehjci/jeu216 290-299 First published online: 3 November 2014

3.Fang Zhu, Yutaka Otsuji, Goichi Yotsumoto Mechanism of Persistent Ischemic Mitral Regurgitation After AnnuloplastyImportance of Augmented Posterior Mitral Leaflet Tethering , Circulation. 2005; 112: I-396-I-401

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Posted in Dilated cardiomyopathy, Mitral regurgitation | Tagged mechanism of ischemic mitral regurgitation, papillary muscle dysfunction | Leave a Comment »

What is the blood supply for the coronary artery ?

July 10, 2018 by dr s venkatesan

One may recall some stunningly simple facts from our high school biology classes that every living cell needs energy on a moment to moment basis.

Blood vessels which take care of the vital organ’s energy supply also need the same blood (Nutrients /Oxygen) for its own survival.

Coronary arteries carry about 250 ml of blood every minute , 24/7 supplying ATP enriched fuel to the heart.

Who is feeding these delicate vessels which carry on this life-sustaining work ?

It is easier to assume the three layers of the blood vessels which are bathed with blood would never suffer from Ischemia. Reality is different .Blood vessels do suffer from Ischemia.We do have evidence medial necrosis, plaque instablity , fibrous cap disruptions may be due to a vascular insult or vessel wall energy deficit.

The much debated entities like endothelial erosion and dysfunction are often atributed to mechanical stress , sympathetic spike , or smoke . This may be a virtual guess as no one knows what causes these. It could well be a patchy Ischemia due to endothelial perfusion defect from within or a vasavasoral dysfunction from outside. Coronary ulcers some times mimic gastric ones and guess the cause ! yes it is mucosal ischemia !) *Ischemic ulcers in GI tracts can be common (Schweiz Rundsch Med Prax. 1993 Jun 15;82(24):709-13)

Image source http://www.wikidoc.com

How does coronary artery gets it blood supply ?

Busy cardiologists have no time to worry about nourishment of the coronary arteries . . . even as they play inside with unlimited arms and ammunition.We leave it to our basic scientists.

So , how does coronary artery gets its blood supply ?

The easiest answer is, blood supply to coronary artery is taken care by a vast network of micro vessels called vasa vasorum(VV) . Of course, the inner layers of Intima and media do get some nourishment by the flowing blood as mentioned earlier.No one really knows the quantum of blood flow that perfuse within the planes of coronary artery.

*By the way , does the vasa -vasorum comes from extra-coronary source or from the same parent vessel ? (I think the answer is both ! will try to find out!)

It should be noted Vasa vasorum is well developed only in large arteries. VV has one more important function ie to drain the metabolic excreta from the walls of blood vessels. This function could never be taken lightly as failure to do so will result in vascular wall edema in acute setting or thickening In chronic setting.

Does coronary arterial tree goes for necrosis in STEMI ?

There is some evidence , when acute total occlusion happens in an epicardial vessel , not only the myocardium is ischemic , the entire distal coronary vascular tree becomes vulnerable. The ischemic time and resistance of coronary macro vs micro vasculature is currently not known. It is expected to show significant variation . We know ,one of the important mechanism of no re-flow following PCI is due to microvascular damage(Non thrombotic)

Many times we fail to realise myocardial viablity and micro-vasculature integirty are two different things. ! This questions the concept of reperfusion based on the status of viable myocardium alone.This we have experienced in many patients as myocardial viability doesn’t guarantee you full recovery from LV dysfunction as microvasculature may recovery may lag behind or never restored (Permanent vasa-vasoral damage ?)

What is our knowledge base about exclusive pathology of coronary vasa vasorum ?

Do you know, ectasia, arteritis, aneurysms and external band like compression of coronary artery all are related to some sort of vasa vasoral dysfunction ? We are not yet clear whether atherosclerosis really involves the vasa vasorum.(Takayasu does it for sure ! )

What is the relationship between vasa vasorum and coronary collaterals ?

It seems to me , many of bridging collaterals are nothing but extension of vasa vasorum and ultimately arise from epicardial coronary collaterals. (Some youngster’s take up this topics for research)

Why is high pressure post dilatation a double-edged sword ?

It’s often thought , larger the lumen its better. Need not be. These are all some questions which we don’t have an answer.

What is the radial pressure exerted by coronary stents on coronary trans -arterial perfusion ?

Does coronary artery go for Ischemic necrosis with high pressure Inflations ? As such there is no published evidence . By the time we wait for published evidence enough number of coronary arteries might get damaged. So try to use common sense .

Relationship between delayed Mal-apposition & vasa vasoral damage

It is very likely ,the so-called endo-leak which is quiet prevalent in aortic interventions is could be seen in coronary arteries. We are not recognising it. It could be same as Intramural hematoma in certain subsets.

Meanwhile, self expanding stents with good radial strength has made a come back .While it may prevent a mal-apposition ,has a potential to stress the vessel wall (Radially) and in the process interfering with perfusion.

 

Does Vasa vasorum promotes Atherosclerosis or negates it ?

hehttps://www.hindawi.com/journals/bmri/2014/701571

 

The irony is, while de-novo vasa vasorum is the life line for coronary arterial nutrition, neo-vascularisation is problematic .Then how to selectively promote good vasa vasoral growth and avoid the pathological network that promotes adventitial nodular degeneration ? This is were the curious basic scientists and casual cath lab guys need to interact.What is positive remodelling ? (Often referred to the famous concept of Glagov ) How can we promote it to maintain good luminal diameter inspite of large burden of atherosclerosis by manipulating the vasavasorum.

 

Final message

Cardiologists are ahead of others in many cutting edge technology. There is no two opinions about it. Who can repair a live beating heart without stoping it for a moment ? Still, there is a whole lot of coronary Ignorance waiting to be explored. Blood supply to coronary artery is one such area to be decoded.This will have larger implications as Vascular healing , plaque survival and growth depends upon vasa vasoral integrity as well as neo vascularisation.

While , metallic management of CAD seems to be the order of the day as it tends to give an instant fix .My guess would be medical sense would ultimately prevail one day with controlled vascular aging and natural ,pharmacological ,biological repair of cells will prevail over temporary patch work in cath labs.

Reference

What is the role of newer Imaging and OCT in visualising Vasa vasorum ?

It is going to open up new avenues in our coronary vision.

Vasavasorum review article

(Kensuke Nishimiya European Cardiology Review 2017;12(2):121–3)

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Posted in Uncategorized |

Side branch sacrifice : Smart cardiologists shall do it scientifically !

June 2, 2018 by dr s venkatesan

This seems to be good side branch sir, … a resident was mumbling as he was reviewing the RAO caudal test shot .Forget that diagonal man , focus your mind on main vessel , If you keep pitying these small twigs , you can never become a glorified Interventionist .I heard one of the senior consultant  was telling (rather yelling) at his assistant !

I used to wonder ,why should the fate of side branches be decided by the mercy of semi cardiac Intellectuals ?

What determines the hemodynamics after side branch jailing ?

• Size
• Territory
• Myocardial viability
• Alternate source
• Collaterals

How do you classify side branch jailing ?

Okamura et all (Ref 3)offered a new OCT based classification based on the shape of the jail grills.

JACC Cardiovascualr Interventions 2010 : Okamura  types V, T , and H jails. Implications are many both during short term as you cross , recross /rewire etc.Long term implications are largely unknown.

Does Jailing Implies flow is Interrupted  ?

This is the most critical question, We got the answer from University of Southampton in 2007 a rare and vital contribution to the knowledge base of coronary physiology. It said the struts won’t block the flow, it simply bumps on the path of blood.

You know , if the side branch ostial diameter is 2.5 mm the luminal area will be around 6sqmm. At least 1 or two struts is likely  occupy and criss cross the ostium. The issue is more than  simple compromise of side branch flow .The major concern is  the ostial jail should not be a nidus for future thrombosis that can spill over to main branch.Unfortunately there is no single meaningful study that addresses this issue of long-term patency of main vessel  in which  small side branches were jailed.(We in our department  have just started to analyse this aspect of coronary Intelligence )

Markers of significant side branch compromise.

For most of us it is not a big deal .I think there is none .There are little discussion  on new onset angina or troponin elevation after side branch jailing.

Can we Jail LCX ostium (or even LAD ostium ) during Left main PCI ?

• Jailing a side branch can be casual or even a fashionable act , but can you do the same for left main bifurcation ?
• It’s all about what you mean by side branch ? and the reaction time , and the useful muscle mass the branch would supply etc.
• In emergency situations , there has been occasions one even put a stent across left main to LCX.Tackle the jailed LAD later if required.

FFR analysis of side branch jailing

Image courtesy from Bellenger 2007 Heart

Doing a FFR to assess the significance of side branch is simply a obsessive academic exercise .It is not warranted in most clinical situations. This study has taught us most side branches retain good FFR give us more confidence to sacrifice the sibling branches of main stem arteries.

Final message

Practicing cardiology in a truly professional way in cath lab can be tricky.We need to disrespect most of the side branches .Believe in your gut feeling (or your consultant’s.) If you are a sensitive scientific cardiologist do FFR pre / post procedure to the side branch .If compromised physiologically try probing the jailed struts and dilate one of them in absolute blindness , of course with a strong conviction of doing good for the science’s  sake.

A Research concept  

Long term sequelae of side branch jailing on the main branch ostia  (Please acknowledge  if some one take up this study )

References

1.

2. Bon-KwonKooMD, Hyun-JaiKang,Tae-JinYoun Physiologic Assessment of Jailed Side Branch Lesions Using Fractional Flow Reserve Journal of the American College of Cardiology Volume 46, Issue 4, 16 August 2005, Pages 633-637

3. Okamura T¹, Onuma Y, García-García HM, Regar E3-Dimensional optical coherence tomography assessment of jailed side branches by bioresorbable vascular scaffolds: a proposal for classification. JACC Cardiovasc Interv. 2010 Aug;3(8):836-44

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Posted in Cardiology-Coronary artery disese, cath lab tips and tricks, side branch jailing | Tagged ffr in side branch jailing, side branch jailing, what is the significance of side branch compromise, what is the significant side branch |

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