Feeds:
Posts
Comments

Archive for the ‘cardiology-Anatomy’ Category

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

Read Full Post »

Answer  is question is wrong : RAA clot do occur in AF and severe right heart failure.It is less often recognised , since echo views are difficult and clinical events are silent.

RAA right atrial appendage clot tee echocardiographyBrief account of RAA clot formation

  • RAA is broad flat ,thin ,  chamber comparable to elephant’s ear.The ostium is not that distinct as the body as it  blends  with crista  terminalis .
  • Rough pectinate muscles  should make it prone for thrombus.Further , RAA has more sluggish flow than LAA  increasing the propensity for thrombus.However , the flat nature of the chamber , absence of tortuous tracts , constant  SVC flow which is abutting the  RAA can counteract this.
  • RAA clots are  less recognised as echo views are difficult .TEE is often required.
  • Overall RAA clot is 50% less common than LAA.
  • RAA clot should be specifically looked  for  in chronic AF and any severe right heart failure. (Unlike MR jet TR jet has less efficiency in flushing the  Right atrium )
  • Finally,clinical events from RAA clot are less conspicuous as the emboli reaches the pulmonary  bed silently.Unlike its colleague on the left side it  neither triggers TIA nor a stroke !

Reference

right atrial appendage clot raa clot in af atrial fibrillation

1. Buğan B, Baysan O, Demirkol S, Güngör M, Yokuşoğlu M. Right atrial appendage thrombus in a heart failure patient with sinus rhythm. Gulhane Med J. 2011; 53(3): 214-215.

 

2.Subramaniam B, Riley MF, Panzica PJ, Manning WJ. Transesophageal echocardiographic assessment of right atrial appendage anatomy and function: comparison with the left atrial appendage and implications for local thrombus formation. J Am Soc Echocardiogr.; 2006; 19(4):429-33.

3.Sahin T, Ural D, Kilic T, Bildirici U, Kozdag G, Agacdiken A, Ural E. Right atrial appendage function in different etiologies of permanent atrial fibrillation: a transesophageal echocardiography and tissue Doppler imaging study. Echocardiography;2010; 27(4):384-93

4 .Ozer O, Sari I, Davutoglu V. Right atrial appendage: forgotten part of the heart in atrial fibrillation. Clin Appl Thromb Hemost; 2010; 16(2): 218-20

 

Read Full Post »

We do know about left main equivalent . Do we have a proximal LAD  equivalent ?

Proximal LAD lesions deserve a special attention and probably urgent intervention. Medical management is not an option in most  patients. (Proximal alone is not suffice , it should be critical as well )

But we have another issue on hand .What really is proximal LAD ? .

  1. First 5 Cm of LAD ? (LAD normally measure about  15cm so 1/3rd becomes proximal .How logical it looks  isn’t ?  )
  2. Before any  S1 or D1 ?
  3. Before any major S1 or D1 ?
  4. Septal branch is not considered at all  . A lesion is said to be proximal if it is before a major D1
  5. Some others may argue if there are  three major branch  distal to lesion it should be considered proximal.

Proximal LAD equivalents .

LAD first or second   bifurcation  lesions ( Medina1 1 1 , 1 1 0 , 1 0 1)

Mid LAD lesion with major D1 ostial  lesions

For  a super-dominant LAD  even  mid segment  lesion  can  be a   proximal equivalent (By area at jeopardy )

If LAD is giving collaterals  to LCX /OM  /  due to  associated  lesions ,   LAD lesion at any level  becomes  a left main equivalent .

Read the related article in this site

Read Full Post »

Any structure which has a foundation on which it  stands is generally called base or basement. By tradition   base is  synonymous  with bottom .Ironically , for  heart this rule does not apply. This is the core area of confusion. The heart is a complex shaped  3D organ with multiple surfaces with  4 chambers connected  each connected to its own  great vessel .

shape of the heart base and apex of heart

We know  heart is  simply suspended by these vessels inside the middle mediastinum and  anchored  with ligamentous attachment to chest wall, diaphragm  through pericardium .

Now, traditionally the heart was thought to  be cone like stricture with  apex located near the left mid clavicular line .

base of heart apex  waht is the shape of the heart

If there is  an apex there must be a base  .So ,  we  reasoned the highest and farthest part of the  heart  must be  the base .  Paradoxically , this base is at the top ,  and  not in the  traditional sense  of bottom .

Like wise ,  during auscultation  the  events  in the base represent the great vessel  and semilunar activity  (Anteriorly )

Baseless  base

Clinical base is not the anatomical base . When a patient lies  on his back  essentially  the atria and posterior aspect of ventricles form the  base . In  erect posture the  diaphragmatic surface becomes  the true anatomical  base  of the heart .

Further confusion during  Echocardiography

It is well known , basal LV function is a critical determinant of LV function .But we should be very clear  what area we are talking about ! Basal  aspect   can  lie   either  superior , inferior , anterior  even  posterior surface  of left ventricle .(It took me years to realise this simple fact !)

Similarly   basal septum  can mean either a LAD zone or even RCA zone one has to specify basal  anterior septum to define LAD zone ischemia .

(Please note , this is contrast to clinical cardiology where  the  base of the heart refers only to anterior aspect of heart ! )

FInal message

Calling  a  particular portion of the heart as base  would be an  anatomical misnomer . This  nomenclature is based ,  more  by  tradition and  our faulty  perception .(As visualized   by anatomists and pathologists )

We have come a long way  from the Da Vinci  days. Modern cardiologists  with  sophisticated imaging techniques would like to  call  the basement of heart  differently  in the future and correct the nomenclature issues.

Read Full Post »

Anatomically ventricles are separated by a single muscular wall namely inter ventricular septum.But physiologically it has to contribute to both ventricular function.

How does IVS  is able to achieve this ?

For the naked eye both ventricles appear to contract almost simultaneously , but there is an intrinsic delay , first the LV contracts , followed by about 70 milliseconds right ventricle generates the peak pressure. So the IVS is able to help in a sequential, & coordinated contractions.This is called ventricular interdependence. Please note pericardium also contributes to this  .

Final message

The mechanical function of  IVS is effectively  and intelligently shared by both chambers. The electrical  delay even in milliseconds is enough to facilitate this sharing .Such is the power of nature. From this concept it is obvious LV dysfunction can have an adverse effect on RV function & vice versa.Similarly any electrical delay( LBBB, RBBB  ) can impact the septal function. Fortunately the myocardium has much reserve function , bundle branch blocks in isolation rarely result in serious consequences unless there is loss of associated muscle mass.

Read Full Post »

Dual LAD is an interesting coronary artery anomaly proposed  originaly  by Spindola in 1983 .He classified it into 4 types. In recent years the  dual LAD has increased from 4 to 6 types.

The essential criteria to diagnose  could be summarised.

  1. Two LADs should be identified.
  2. One would be  large and another small
  3. Both should give a  diagonal  branch .

* Ramus is virtually unknown  if there is dual LAD .

The origin  of second LAD can be from

  • LMCA
  • RCA
  • Direct from Right coronary sinus

Course

  • Can be epicardial
  • Intra -myocardial
  • Or both

Branches

  • Diagonal
  • Septal
  • or Both

Drainage area

  • Highly variable

Implication for intervention

  1. Apart  from  the surprise element , the second LAD   has  little impact on the interventional protocol.
  2. However , it may confer a  ischemic protection  as the critical anterior wall has a twin blood supply.
  3. Whether  they are protected from primary  VT or VF is to be studied  because of better electrical stability
  4. Second LAD may act as an additional collateral channel.

Spindola’s  classification of Dual LAD (Types 1 to 4  was called sometimes A,B,C,D )

classification of dual LAD

Source : Lee et al. BMC Cardiovascular Disorders 2012, 12 :101

Spindola type 1 to 4 classification of dual LAD

An illustration of  first 4 types  of Dual LAD .Note  the type 4 originates from RCA. Image courtesy : Prachi P. Agarwal Ella A. Kazeroon . AJR:191, December 2008

Surgical issues ( This is  excellent data  from India . I convey  my   greetings to one  the authors Dr D.B Baruah,  my friend  from  CMC Vellore !)

dual lad classification Spindola-Franco H, Grose R, Solomon

Reference

Spindola-Franco H, Grose R, Solomon N. Dual left anterior descending coronary artery: angiographic description of important variants and surgical implications. Am Heart J 1983:105;445-55

Dual Left AnteriorDescending CoronaryArterySurgical Revascularization in 4 Patients Tex Heart Inst J 2000;27:292-6

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3509398/pdf/1471-2261-12-101.pdf

Dual LAD  CT  Angiogram : http://www.ajronline.org/doi/pdf/10.2214/AJR.08.1193

Read Full Post »

If only  . . . we get  an  image like this , echo can help rule out most  left main disease with conviction .

Have a close look  at it ! One can get a good image of  coronary ostia in short axis view . But , here it is well visualized  in long axis .

left main

I tried to put color flow within left  main .

left  main color flow

What about pulsed  Doppler across left main ?

After all it needs 2mm sample volume and this left main was near 4.5mm . So keep trying !

Read Full Post »

Older Posts »