What is a normal coronary angiogram & What is a normal coronary artery ? Do they mean the same ?

Coronary angiogram is a video graphic  snap shot of coronary arterial lumen which is filled with radio opaque dye. This is some times called as coronary luminogram . It is a paradox , when we say normal coronary angiogram we can only mean  normal coronary lumen. But  generally, this can provide sufficient  information regarding the status of  coronary blood flow.There are three structured layers in coronary artery wall . Coronary angiogram  can not give any information about the status of the intima, media or adventia .

Lesions A to F may be totally missed by conventional coronary angiogram

A patient with normal coronay angiogram can have diffuse  atheroscelrosis or  localised atherosclerosis within the media of coronary artery .Many times these atherosclerotic plaques grow outward into the adventia and fail to encroach upon the lumen to be detected by coronary angiogram. These plaques , even though has an hemodynamic advantage, in that it doesn’t block blood flow , has a serious risk for sudden rupture and result in an acute coronary syndrome.

So what is the message?

A normal coronary angiogram can never convey a meaning of normal coronary arteries.

A person who has a normal coronary angiogram has no guarantee that he won’t develop a coronary event in the near future.(But the the chances are very low)

If coronary angiogram has serious limitations  what is the next alternative ?

Intra vascular ultra sound imaging(IVUS) can give us an idea of the coronary arterial wall anatomy. This investigation , though available for clinical application is too complex for regular use.So , you  can’t subject every patient with normal CAG  to an IVUS  (Intra vascualar ultra sound) to confirm the normality. The best option is what we follow every day in our practice  .Tell your patients   with normal coronary angiogram , that they are likely to  have  normal coronary arteries  ! don’t add up to their anxiety by saying,  in spite of normal CAG  still they  can carry  gross atherosclerosis in their  arteries. Anxiety can precipitate an coronary event. Too much technical information to the patients  can be counter productive. Instead  advice regular life style modification,  blood pressure ,diabetes, lipid  control  etc .

Why thrombolysis rarely fails in right coronary artery ?

Differential response of thrombolysis between left and right coronary system

• Thrombolysis is the specific treatment for acute myocardial infarction. ( Privileged few , get primary PCI))
• Failed thrombolysis occurs in significant number of patients ( 30-40%).
• Persistent ST elevation  120 minutes after thrombolysis is best indicator of failed thrombolysis.
• It has been a consistent observation  failed  thromolysis almost always occur in anterior or LAD myocardial infarction. 

In a simple study we have documented  patients  with inferior MI  rarely had persistent ST elevation and thrombolysis  has been  almost always successful ( Except in few patients associated lateral MI)

 

The mechanism of better thrombolysis in right coronary artery  is simple.The success of thrombolysis , apart from early time window , is directly correlated with pressure head  and the duration of contact between the thrombolytic agent and the thrombus. In right coronary circulation the  blood flow is continuous ,  occurs  both in systole and diastole that facilitates the maximum delivery of the thrombolytic agent . Further there is a favorable  pressure gradient  across RV myocardium  as the transmural occluding pressure across RV is considerably less then LV myocardium. 

 

 

This paper was presented in the  “Annual cardiological society of India scientific sessions”

at Chennai, Tamil Nadu.India December 2000

Click to down load PPT full presentation

What is no reflow ? What is the mechanism of no reflow ?

No reflow is the terminology used primarily in cath labs where, even  after a successful opening and stenting  of a coronary artery the coronary blood flow is not  restored to myocardium . The point to be emphazised here is blood do cross  successfully the site of  the obstruction but fails to enter the muscle segment  to which the coronary artery is supplying. So the paradoxical situation of artery  being open but the  myocardium is closed to receive  blood flow  happens . This is termed as no -reflow.  Actually it is a  misnomer , and  ideally it should be called “no flow” because  normal distal flow  does not  occur (After PCI)  in the first instance  to get interuppted  later on  and be labeled as  no re-flow.  .The only positive effect of PCI in these situation is blood flow would have improved by few centimeters ie till it reaches  but falls short of myocardium . In fact no reflow , can be termed as  glorified and concealed  terminology  for  PCI failure . It needs urgent action . No reflow is also called as myocardial epicardial dissociation.

Mechanism of no reflow.

Curious case of open coronary artery and closed myocardium !

Coronary  microvascualr plugging  is mainl  due to thrombus and atheromatous debri , myocardial  edema , microvascualr spasm may also contribute.

Where can it occur ?

• First described in cath lab, especially following primary angioplasty.
• It can very  well happen following thrombolysis in STEMI.

• Can occur in venous grafts.

How do you recognise no reflow?

In cath lab it will be self evident from the check angiogram. Some times it is less obvious and may  require, myocardail blush score, TIMI frame  count, contrast echocardiography, PET scan etc. In post MI a very simple method to recognise this entity could be the observation of persistent ST elevation in ECG .

Treatment.

Extremely difficult. Almost every coronary vasodilator has been tried.(Nitrates, nicorandil, calcium blockers, etc).Success is less than 30%.  High pressure flushing with saline inside the coronary artery is advocated by some.Others believe it’s dangerous to do it. So prevention is the key. Avoid doing PCI in complex, thrombotic lesions. Use thrombus suction device like export catheter(Medtronic). Distal protective devices are double edged devices , useful only in experienced hands.

Unanswered question

What is the size of the particle (thrombotic and atheromatous  debri)  the   coronary microcirculation safely handle and push it into the coronary venous circulation and the coronary sinus for disposal ?

If we can lyse the thrombus into micro particles by some mechanism and make it traverse the coronary circulation this complication of microvascuar plugging can be treated and prevented .

What is the final message ?

• No reflow is relatively common condition during emergency PCI done for ACS patients
• More common in complex thrombotic lesions.
• Can also  occur in STEMI
• Treatment is often vexing . In fact the treatment of this condition is so difficult , it can be termed  almost synonymously with “Failed PCI” if flow is not restored.
• Suceesful treatment of no reflow  means not momentry restoration of  myocardial flow  by mechanical and pharmacological modalities ,but to maintain sustained myocardail  perfusion. This  we realise, as patients who have had a no reflow during  a PCI, do not perform as well in the follow up  .
• So prevention is the key.

In dilated cardiomyopathy which chamber dilates first ?

As the name suggests   dilated cardiomyopathy  would imply  cardiac chambers will dilate , at least some time in the course of the disease .It can be minimal, mild or massive. A new entity called  non dilated cardiomyopathy is also gaining wider acceptance . (That will be dealt seperately )

Logic would suggest , the first chamber to dilate in DCM  should be the left ventricle because it is  facing the direct load of systemic blood. But we also know , whenever  LV is stressed , left atrium comes to it’s assistance .

Left atrium does this    by total self sacrifice ( by all  means!)  increases  it’s  force of contraction, elevating it’s  mean pressure or even increasing it’s rate (AF) .

Like most  other critical questions in cardiology  ,  the factors that determine LV dilatation in DCM ,  is  also poorly understood !

1. Is it the after load ?
2. Is it the  muscle mass ? or it’s turgid  or flabbiness ?
3. Is it the interstitial integrity?
4. Is it the blood volume ?(LVEDV ,  LV residual volume )

When the issue is complex , it is  usual  to  make the   the unknown  genetic defects  ,  the scapegoat !

As of now the most important determinant of LV dilatation  could be  the behavior of the desmins, the gap junctions and myosins the titins etc

If  the LV of a DCM patient  refuses  or  resists  dilatation what  might happen ? Is it good or bad for the patient ?

Here is a catch .  A  LV  that does not dilate  obviously should be  be good for the patient  is in’t ? Medicine is not that simple.

When   LV  fails to  dilate  it means it has become  too  stiff and rigid    and pass on the  burden to  to LA which  faces the music. And in the process it dilates.This is the reason , we  observe  diastolic dysfunction in vast number of DCM patients.( Currently it is estimated > 75% DCM will have significant diastolic dysfunction )

So , now we can imagine how complex the sequence of hemodynamic stress in DCM that determine the chamber enlargement.( RA, RV  dimension in DCM is a separate issue !)

So now answer this question :  Which chamber dilates first in DCM ?

1. Left ventricle
2. Left Atrium
3. Any of the above
4. Both of the above dilate simultaneously

The answer must be 3 .

Why  recognising this sequence of  chamber enlargement  in DCM   is important ?

• It gives us an opportunity to assess the dominant mechanism of LV dysfunction.There are reports , where some  DCMs  have more diastolic dysfunction than systolic dysfunction  .This will have important therapeutic implication.Further , many of the infiltrative   disorders of LV can have features of both DCM & RCM .
• When a RCM begins to dilate it is usually  a harbinger of terminal heart failure. But,  it need not be always true .  A small restrictive LV  , when  dilates ,   may acquire a  slightly improved diastolic properties , as the  LV becomes more placid . And ,  if it happens the LA size may regress.
• The role of LV restriction devices like, Acron mesh, Dor procedure, plication  in refractory  DCM is not well defined. All these   modalities actually  adds  a small dose of diastolic dysfunction in these patients who have grossly dilated ventricles. This fact is  very important  , as presence of any preexisting  significant diastolic dysfunction in DCM makes  the role of LV restrictive devices and surgery a big question mark !

Simple tips in echocardiography : Where to look for coronary artery origin in short axis view ?

Imaging  coroanry artery is  generally  in the   domain of interventional cardiologists. MDCT has helped us to change that.

The  humble echocardiography can   identify the origin* of   coronary arteries   in  most   persons. The resolution power of modern day echocardiography is  2mm and the left main  ostium is >3.5mm in 99%  of population . If some body says one can’t  visualise the coronary artery by echo ,   it can only reflect their ignorance or lack of patience to get an optimal image. Of course technological limitations are there.

*  To be emphasised again , only the origin can be identified.

Can we identify ostial leftmain or proximal  left main disease  by echocardiography ?

It should be possible in  few .

Can we place  a doppler sample volume  within  the left main and measure coronary flow velocity ?

When obsterticians are able to  assess the  uterine artery flow  in a bulky uterus ,  it should be possible to do the same in  a coronary artery . Motion artifacts is the issue in the heart.  Micro sample voulme (<1mm) are expected in the future  that will make a non invasive coronary flow assesment a distinct possibility.

Acute myocardial infarction of LVOT : An unrecognised cause for refractory hypotension

Hypotension is one of the dreaded complication of acute STEMI.

• It can be due to either a  mechanical complication or hypovolemia.
• The hypotension in inferoposterior MI is  often related to enhanced vagal tone and easily correctable with atropine  and fluid  administration.
• RVMI is the classical example of hypotension that may improve with fluid resuscitation
• Hypotension,  if  not reversible within 12  hours  ,  is more likely to  represent a more sinister mechanism like pump failure, MR or ventricular  septal tear etc .

A new mechanism for persistent  hypotension is increasingly recognised.

This is due to the

1.Loss of LVOT dynamic activity.

2.Excessive  dynamism of LVOT.

LVOT contractile and ejectile falure

Even though LV  outflow tract  contain  less  contractile myocytes  , it has an important mechanical  job to do. We know , it’s  primary job is that of a  conduit  but  it also  has to  eject the blood into aorta with sufficient force.  In fact, it is thought much of the acceleration of blood velocity occur in LVOT . So, LVOT  plays a key role in maintaining the cardiac index.  An excessively dynamic LVOT will impede the forward blood flow as in HCOM.  Similarly  less dynamic contraction  of LVOT  results in  low velocity propulsion , that interferes with   proper delivery of blood from LV cavity into the aorta .

These factors get amplified in  acute MI , as it is a compromised situation with fluctuating HR and contractility. So a properly functioning  LVOT conduit is  absolutely mandatory.

STEMI due to a proximal LAD obstruction   located can involve the septal .If the first septal branch  happens to be a major one,  there will be  definite impact on the LVOT function.

Excessive dynamism  , LVOT   desynchrony  LVOT collapse .

LVOT has a medial border formed  by IVS , an  anterior surface and  a posterior surface .The lateral border is relatively boundary less , except it is guarded by  the anterior mitral leaflet.

But one should recall , the AML comes towards the LVOT only in diastole . When it comes in systole it becomes a pathological event  called  SAM  (Systolic anterior motion )

The LVOT wall desynchrony can occur in both anterior and posterior MI.In a mulivessel CAD  this can happen when there is disproportionate inferior to anterior wall motion defect.

Management.

• There is no specific management strategies aimed at restoring LVOT function.
• Emergency revascularisation will attenuate the mechanical dysfunction
• Dosage of powerful inotropic agents should be moderated in dynamic LVOT obstruction.
• Spontaneous recovery  may occur in few

http://circ.ahajournals.org/cgi/reprint/116/5/e110.pdf

Haley et all Mayoclinciproceedings 1999

A leading Indian journal on pacing and electrophysiology

• It is only rarely a journal of International caliber is published from India . IJEP is one such journal.
• Cutting edge articles on Electrophysiological science  break here !
• This is an online journal . No print issues . Enjoy, it is free !

Here is the  Link

Just sample an article  : A great review about cardiac arrhythmias in congenital heart diseases , Must read by  all cardiologists    http://www.ipej.org/0906/khairy.htm

And now , a journal exclusively for cardiovascular CT scans !

• It is going to be the era of non invasive imaging  in  cardiovascular  diseases .Future looks very exciting
• We have now ability to slice the heart 356 times a second !
• Image resolutions are getting sharper .
• The only worry ( Of course a major one !)  would be the radiation , that has to be addressed .

Now we have a dedicated journal for cardiovascular CT scan .

Does it surprise you  ?   For me  . . . It  is  !

Link to the current journal page . Get updated  !

http://www.journalofcardiovascularct.com/current

How to minmise radiation injury in cath lab ? The importance of less appreciated “ALARA”concept .

There are millions of  articles in cardiology . Some  simply  occupy   valuable spaces without any purpose  . Some give us knowledge . Some enlighten  us. While few are  so vital , it is almost a crime  if we do not read such articles and apply  it in day to day  practice .

This an article  written by Henri Justino that has a immense importance for the patients as well as the physicians .

Do not think  the article which came in pediatric radiology  is not applicable in adults !

A great website for learning Echocardiography : A gift from Duke university

• Here is a site which has dedicated  resources for learning echocardiogrtaphy .
• The site has collection of various work shop and coference highlights
• The basic echocardiography with classical line diagrams  would be very much useful for the beginers,

Cheers to duke university for sharing ! www.echoincontext.com

What is branch vessel STEMI ? How common it is , among STEMI population ? Can you afford to manage it less aggressively ?

STEMI is the major cardiac emergency .The acute mortality is about 20% (Both prehospital and in CCU )  STEMI occurs whenever a coronary artery is occluded  suddenly in toto .We traditionally believe that STEMI occurs only in the major  epicardial vessels. (LAD/LCX/RCA .)

The total length of   coronary tree is much  longer than the length of the three vessels put together.The diagonals , the ramus, the OMs ,the septals  run for varied  distances. The caliber of these vessels can be quite large.It is estimated the diameter  of   first diagonal ,   the first OM  or the   ramus can be as big as LAD proper in 30% of CAD population . Law of statistics tells us sudden occlusion can occur any where in the coronary tree in  ACS prone patients.

What is the real incidence of side branch STEMI ?

The  dogmatic answer is   ” We do not know”

Will we ever know ?

How will a  Diagonal / OM /Ramus   or PDA   STEMI  behave ?

It is surprising this question is not addressed by us  for  so long . Some may even question  the existence of  such an entity(Side branch STEMI ). This is most likely ,  reflect our ignorance on the issue . We know  bifurcation lesions at  the   side branch  origin is very common . Further , thrombus can migrate from a main stem to a side  branch  immediately after formation .

Clinical presentation of side branch STEMI

• Acute presentation is identical  to  that of a major main branch STEMI . The  pain  can be severe , the primary arrhythmic threat is real . Ischemic VF , once initiated does not  modify it’s  character  according to the  quantum of insult .

• ECG is the major variable.  You ,  don’t expect gross , ST elevation in many leads as one would see in LAD MI /RCA MI.

• The  age old teaching that  an ECG can be entirely normal in acute MI ,  could actually imply the side branch STEMIs . When a small D2 or D3  gets occluded the ECG may not pick up the ST shifts .

• The commonest site of atherosclerosis apart from proximal LAD is the bifurcation of PDA in RCA.  STEMI due to PDA occlusion is  the most  difficult thing to recognise. Many of them have very subtle ECG and clinical findings.
• There has been reports of acute complete heart blocks with isolated AV nodal infarcts. Here sudden cardiac deaths are reported

It is very much possible ,  many of the  side branch  MIs   may be wrongly diagnosed as unstable angina by us , for the simple reason the myocardial necrosis is not large enough to produce ST elevation .They may actually respond to thrombolysis ,  as there is total occlusion in the coronary artery.  Since, they do not manifest ST elevation there is a lost opportunity here  . This ,   probably  is the population in TIMI 3B  trial that showed some ( statistically   insignificant ) benefit for   thrombolysis in NSTEMI.

Is primary PCI justified in side branch STEMI ?

May not be . The chances of side branch STEMI   to result in LV dysfunction and progressive adverse remodeling is considerably less . The hazards of primary PCI for exceeds the risks of  MI  due to a   septal  or diagonal branch lesion .

Final message

• STEMI due to   branch coronary artery  occlusion is a less recognised entity among ACS.
• Cardiologists ,  need to  look into this  issue with little more seriousness as it could represent a new  intermediate risk  category   among the much  flaunted  classification  of  acute coronary syndrome. Triaging and risk stratification of  ACS  needs  a revamp.
• It is possible  many of the UA  patients  ,  may in fact represent total occlusion of side branches.
• There is a  definite  case  for showing less aggression in these patient  subsets  ,  provided we are sure  about  the location of lesion.

Counter point

* Identifying  a side branch STEMI with confidence  may be very difficult at bed side in an emergency . Implication of wrongly  calling a STEMI  as benign  can be  dangerous . So it will be argued ,  one need not do this exercise of traiging STEMI into main branch or side branch .

Image courtesey

Coronary tree : http://www.southcharlestoncardiology.com/64cta.html

Ethics in cardiology : Truths , when silent are not heard in the consultation rooms !

Modern medicine promises   healthy new lives  to millions. We all , enjoy  the   fruits of  great scientific discoveries.  But do we  realise , medical science is nothing but experiments done on live  human beings . All  treatment modalities   are under constant scrutiny.  A great drug becomes the most harmful drug over a short time.

A drug or a device which is banned in one country is freely used in other country , marketed by the same parent company . How on earth this can happen ?  A device  ( Eg : A stent )  which is found  inferior  can  still can  be used legally elsewhere ,  hiding the information .

• Do we divulge all vital information to our patients ?
• Do we reveal all our conflicts of interest to our faithful patients ?

Informed consent is  the  “greatest  invention” in medicine . That is democracy in medicine . Doctor  patient conversation is   supposed to be  most noble of all communication !

But . . . this is under  genuine threat .  In this ” New medical AVATAR ” truths  remain only as thoughts , they  rarely  come out as words or action !

One such  situation a  physician  often  faces  in his office ,   as he is compelled  to act against his  conscience

If only we  have an ability to  read  his silence it will go something like this  . . .

For the sake of  Science &  Commerce , I have to implant this device  in your heart , and  my gut feeling says  ,  you will do much better without this device as well !   But ,  I am sorry . . .  I can’t avoid it .

Doctors are not be blamed  . . . rather  , we can’t blame  any body

Patients believe in doctors , and doctors believe in science  And the irony is ,  doctors have no other option as they are  coerced to  believe ,  in whatever is published  as science even if it is  half baked , unproved,  unapproved or  even dangerous science .

Let us prey for the genuine science to prevail  at least in human health  and the mankind  reap the maximum  benefits !

Let us  recall  Mahatma Gandhi’s    “Seven Social sins”   That included one  advice for the scientific world  nearly a century ago when it  was at it’s infancy !

Seven Social Sins By Mahatma Gandhi

---

• Politics without Principle
• Wealth Without Work
• Pleasure Without Conscience
• Knowledge without Character
• Commerce without Morality
• Science without Humanity
• Worship without Sacrifice

– Young India, 22-10-1925

Common sense based cardiology: A simple and effective way to prevent an episode of vasovagal syncope !

Vasovagal syncope is the commonest cause for syncope in our population.It is also referred to as simple syncope .The mechanism is thought to be  an abnormal overshoot  response  by the vagus  in response to a  sudden surge of  adrenegic activity  usually occurring  in erect posture following   , often an emotional or physically stress full situation .The  receptors for  this  reflex pathway is thought to be located  left ventricular myocardium .

There are  two components  for  the VV syncope

• Cardio inhibitory
• Vaso depressive.

The quantum of contribution  by each component in a given episode of syncope varies. Pure vasodepressive or cardioinhibitory forms can occur .

Diagnostic issue

Before labeling  a patient as simple vasovagal syncope all potentially serious , cardiac causes must be ruled out. this may require a fairly extensive investigation in some

Read the related blog  : Why syncope is rarely  fatal ?

http://drsvenkatesan.wordpress.com/2008/09/30/why-syncope-is-rarely-fatal/

Management of vasovagal syncope.

• Reassurance is the mainstay . By this we mean , V V syncope may never kill . . .
• Prevention  – Involves  identifying syncope prone situations  & taking precaution
• Emotional support
• Pharmacological approach

Some will benefit from beta blockers, fludro cortisone(Increase the intra and extra cellular  fluid space )

Since  these are   simple ,   cheap  treatments ,  we worked over time to innovate  &   find some interventional solutions for this life threatening condition !!!.  Thus ,  the indication for cardiac pacing for vasovagal syncope came into vogue .

DDDR pacemaker was implanted worldwide for thousands of patients with vasovagal syncope .

It took  many years  for our  intellectual brains  to realise ,  there are  two limbs to vasovagal syncope Pacemakers ,  at  no stretch of imagination  is expected to counter vasodepresssive component of the syncope.

And then this article came !

http://circ.ahajournals.org/cgi/content/full/108/21/2660?ijkey=ba86da897c167581c498c81743c32afe14fc9393

Water ,  (Simple  H2O ! ) administered at right time in right quantity can prevent most  episodes of vaso vagal syncope . When a tumbler of water can be substituted for a  10000 $ misadventure  (DDD pacing)  , and  further  we have  hundreds  of similar examples in modern  day health care  ,   no surprise  why our health care system is  sinking  along  with our economy !

Epilogue :

In this  21st century   medical “AVATAR “  , we need to realise   in a strong manner,   low cost  medicines  often   provide   high  quality  cure  ” while ,”   many of the  high cost  therapies  may  end up in  low quality  treatment !

It took 50 years of intense research of  medical comunity to realise ,  a good diet , physical activity and quitting smoking has the greatest way to control  and reverse  the cardiovascular epidemic . Please , note all of them come at free of cost .