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coronary-artery1

                                                      Coronary arterial circulation is the life line for  the human heart  and it’s survival.Typically it is supplied by two coronary arteries,  left and right coronary artery.Both, together carry about  250ml of blood every minute.( Approxinately  equal to a  cup of  coke !  ).These coronary arteries  generally divide in a predetermined  fashion , and have multiple branches . It is a  mystery , what  decides this  branching pattern

Is it like a our palmar crease  ? or the cerebral gyri ?

However , it does follow a certain rule,  one major coronary artery  will follow the  four  important grooves of heart. In the left side ,  left main coronary artery (LM) originates in the left coronary sinus (Size varying between 1mm -20mm)  and usually bifurcates into LAD and LCX. The left anterior descending artery (LAD) runs in anterior interventricular  groove while ,  the right atrio ventriculo groove carries the right coronary artery(RCA) .Left  circumflex artery (LCX) traverses the  left atrio ventricular groove.The most inconstant branch is the posterior descending artery (PDA) which runs in the posterior interventricular  groove.PDA  can arise from either RCA, LCX or both or even from LAD.

The major branches of LAD are called diagonal and septal  while the branches of LCX are called obtuse marginal(OM).There can be two to three diagonal and OMs. 

What is ramus intermedius coronary artery ? What is the incidence of Ramus ?

The left main coronary artery  instead of bifurcating into two ,  it trifurcates into three vessels.(LAD, LCX, Ramus)

The real incidence could vary betweenn (10% to 30%) depending upon the series.

ramus

What course it takes ?

It generally goes in the angle between the LAD and the LCX.It may either behave like a large OM or a diagonal branch.It supplies the lateral free wall of the LV many times.The peculiarity of this vessel is it does not run in a anatomical groove .It simply slides over the free surface of LV.Rarely, a  very abnormal course of ramus,  criss cross the aorta and pulmonary artery .

How common is atherosclerosis within  Ramus ?

We don’t know yet. But it is very likely since it is an early branch from left main, it  might  have a  predilection for atherosclerosis  as like LAD or LCX ostium.In fact now we recognise more of  trifurcation lesions involving  three branches of left main .

What would be the ECG finding if a large ramus is the culpirit vessel during STEMI ?

This scenario could be rare.

ACS in ramus could  present as ST elevation in 1/Avl /V5,V6

  • Lateral MI
  • Apical MI
  • High lateral MI

But it is realised , whenever the ECG changes are not fitting with typical ASMI or a lateral MI one should suspect a ramus lesion

 What is the significance of ramus for an interventional cardiologist ?

ramus-2

                                                   PCI in ramus is a rare opportunity for a cardiologist .The issue here  is,  if ramus is involved  adjacent LAD and LCX is also likely to be involved .So it would logically be a multivessel , complex angioplasty.Isolated ramus lesion could be tackled easily.Another issue here could  be ,since this vessel is not within  any anatomical groove  stent deployment would have a poor  support and prone for mobilisation and migration .

Stents are mechanical  devices like  a  spring ,  used to  keep an artery open after a PTCA or PCI.

des-why4

                                Bare metal stents(BMS) were found to have restenois rate of about 25%.  So it was perceived a stent should have it’s own protective coat , so that it won’t get restenosed.For this the researchers thought  anti cancer drugs are ideal as they block cell proliferation and thus neovascualrisation and restenosis.Alas, they were found dismally wrong ,  after all , neointiaml proliferation is only a part of the problem of restenosis  and simple blocking of cell growth is insufficient . The issue doesn’t stop with that, the anti cancer drugs incorporated within the stent simply can not differentiate normal from abnormal cells and

DES effectively blocks the normal endothelisation over the stents and make this highly vulnerable for acute stent thrombosis .

This complication is unique to DES and can result in SCD.Further ,during the last 6 years of DES , we recognised the restenosis rate has increased form the much hyped O % to almost 15% and it’s still growing . These  complications  has made a huge question mark over the future of drug eluting stents !

des-coverage

The concept of DES may not die , but which drug it should elute should be answered ! This  again is  going to be a long battle. So it is currently   adviced,  based  on common sense ( With due respects to  those RCTs  funded by industry )

Whenever you encounter a block within the coronary artery* Ask the following  questions in sequence  ,

  • Whether we can leave it alone  with medical therapy  ,  if the answer is no , proceed  to the next step !
  • Is there a possibility for plain balloon angioplasty in a given vessel (POBA, Yes !  the concept is not dead yet !)
  • If you decide a stent is required , Will  the  bare metal  do the job ?
  • In multivessel CAD  , Did the issue of increased metal load on the  long term outcome was considered ?
  • If lesions appear complex,  should we  not strongly consider CABG as an option ?

However  if we  have the habit of  ask ing the following  question  you are likely to deviate from scientific approach  

Is it possible to put a stent  across  the block ?

Yes , will be the answer most of the time ,and the patient will invariably get one or more stents  and carry a life long  stent related problems.

*The rule does not apply in Acute coronary syndromes

Also read this letter  posted by the author published in  British medical journal

                                      One of the important principles of  post PCI care is,   we need  to be very careful  till the metal struts are fully endothelialised . This is of vital importance as improper endothelialisation  is a powerful trigger and nidus for a  imminent thrombosis and  acute coronary syndrome.

stent

It is a billion dollor irony , the much hyped DES does exactly what we don’t want ! and still it’s  usage is  increasing world wide .  The drugs (Anti cancer agents)  which coat the DES   are the villains as it  prevents  the  metal struts  from being endothelialised  and  keep the metal surface  raw and vulnerable , while the  much maligned  bare metal stents allow  this natural endothelialisation  process  without any interruption ! So right now it is mandatory  to administer dual antiplatelet agents  life long( life of the stent !)   for the patients with DES.

 Just look , at the following image of  a stent in vitro at  30 days follow up

des

des-2

Let us not forget the basics !

  • HT management has been made  easier with the availability of  many  good drugs , at the same time it has become a complex  issue with as many classification and guidelines.
  • The management of HT has evolved over the decades. Now we have realised  HT  is not a simple number game . Reducing the blood pressure to target levels is not  sufficient and is not the primary aim !.
  • In fact we now know controlling the numbers alone is never going to work  , combined risk factor reduction is of paramount importance.
  • HT per se is less lethal but when it combines with hyperlipidemia and diabetes or smoking  it becomes  aggressive.The blood lipids  especially the LDL molecule  enjoy the high pressure environment  ,   penetrate and invade the vascular endothelium.
  • ASCOT  LLA  study has taught us,   for blood pressure reduction to  be effective and reduce CAD  events one has to reduce thier  lipid levels also.So , for every patient with HT there is not only a target BP but also a target LDL level .

picture1

 

Final message

The tip for better vascular  health is  , all  hypertensive patients should keep their lipids to optimal levels and all hyperlipidemia patients should keep their BP as low as possible .

“Keep your LDL  as low as  your diastolic blood pressure  and  let us  keep it around 70 -80

sinus-node

 

Sinus node  as the pacemaker , orchestrates the rhythm of life . It has  to fire for the entire life time of  a person.It  can not afford to take any rest ! But it can pause a little bit , of course that pause  could  be less  than 15% of it’s basic sinus length. This variation of sinus  cycle length is called sinus arrhythmia.This is physiological. When it exceeds 15 % of the previous sinus cycle it is referred to as sinus pause.

 Have a look at this ECG

sinus-pause-2

 

What follows a long pause ?

By strict terms  of definition a sinus   pause should be followed by  a delayed , next sinus  beat only. A  sinus pause  , many times  is followed  by   JPD – Junctional escape beat.This situation should be ideally  referred to sinus arrest as the sinus node is taking too much of rest and it is not able to wake up from the slumber and it needs assistance form the junctional pace maker.

So even though sinus pause and sinus arrest is used many times interchangeably, it should be avoided. 

What are the electrophysiological mechanisms of sinus pause ?

  • Simple sinus bradycardia . The commonest  mechanism is  the  increased vagal tone. This occurs more often in young athletes. Eventhough increased vagal tone  conveys   a innocuous meaning , at times  this can also be symptomatic  and require intervention.
  • Sinus node exit block.
  • First degree, second degree, complete SA block can occur as in AV node.

First degree SA block can not be diagnosed by surface ECG. Third degree SA block is same as sinus arrest and subsidiary pacemaker will function in these patients.  Second degree SA block is usually diagnosed when the sinus pause is in the multiples of resting sinus cycles. If the pauses are not in exact multiples  sinus arrest is diagnosed. All these arrhythmia’s are collectively called sinus node dysfunction(SND)

How do you manage these patients?

Sinus node disorders can occur in number of systemic diseases*. It  needs to be  ruled out.

  • Infiltrating diseases like amyloidosis, hypothyroid states can result in SND.
  • Drug induced SND like beta blocker and calcium blockers are fairly common and should be excluded
  • Some congenital heart disease (SVC ASD) can involve sinus node.
  • Ischemic SA node disease is rare but can occur  following  infero posterior  myocardial infarction
  • Sinus node disorders are  very often related to degenerative atrial diseases associated with HT, cardiomyopathy etc

*The list is not exhaustive

A very important association is noted  with atrial fibrillation as  a part of tachy brady syndrome .The link between SND and AF  is obvious as   atrial pathology is the common denominator in both ! This will be discussed later.

When is a  pause  significant ?

Any pause that is producing significant symptoms is significant.This depends upon the overall  hemodynamic compensation of the patient.Young, and fit can even tolerate three second pause without symptoms.Underlying heart disease makes even a smaller pause symptomatic.But generally a 3  second or more  pause is almost always pathological .Pauses can be up to  5  seconds (  a 5 second pause actually means a  heart rate of 12/mt , obviously it can not go on for a minute, a patient will develop a syncope). A 3 second pause  corresponds to 20/minute.

How will you evaluate a patient with sinus pause ?

There are sophisticated electrophysiological studies (EP) available like sinus node ECG ,sinus node function studies like sinus node recovery time, activation time etc. But these are generally of  academic interest.

If a patient is symptomatic  (syncope) because of bradycardia  he requires a pacemaker and  EP study is redundant . Similarly , if  he is totally asymptomatic in spite of pauses , again  EP study is  not  indicated.

Only for patients  in the  grey zone,   further studies are indicated .This would include a extended holter, loop recorders, event monitors etc.

Another important issue to consider  is , before putting a pacemaker   patient”s   symptom  must be correlated  with their arrhythmia.

What is  the overlap  between sinus node dysfunction and neuro cardiogenic syncope ?

SND  can occur as an overlapping syndrome with neurocardiogenic syncope.(NCS ).NCS is also a very common cause of syncope .In NCS  there are two limbs .Cardio inhibitory and vasodepressive. The cardio inhibitory form can exactly mimic an SND. In a given patient  it is very difficult to pinpoint which of this limb is dominant.Head up tilt test(HUT)  might help in few.  If a patent’s symptoms are due to inappropriate vasodilatation pace maker may not reduce the symptom of dizziness or syncope.

Management

  • There is no ideal  medical therapy* available as on date
  • Withholding all drugs which might aggravate bradycardia is of paramount importance.
  • Pace maker is the specific treatment in all symptomatic patients.

*Aminophyline tablet may be useful in some patients .It acts by antagonising adnosine receptors in SA node.Other drugs which can incrase the heart rate in the short term include  Orcipranaline(Beta 2 stimulant /Alupent ) Probantheline(M 1 blocker)

The key issue is to avoid unnecessary pacemaker implants in patients who have insignificant pause.

 Which pacemaker is ideal in SND ?

pacemaker

                                                              The need for dual or single chamber pacemker will be taken by the electrophysiologist .Atrial based pacemaker (AAI)  is preferred as it gives physiological pacing .But a simple ventricle based VVI pace maker is good enough in vast majority of patients. This takes care of   future risk of AV block also. DDD pace maker is the most physiological pacemaker and it is supposed to provide better quality of life. But it has an issue of insertion and  maintenance of  two leads, multi parameters to be programmed.It should switch to appropriate modes  at different times.(Like VVI mode during atrial fibrillation etc).Trouble shooting needs expertise , while  VVI is simple,  safe , and just effective as well .(In this turbulent world, quality of life is a  too trivial an issue  to be determined by a DDD  maker)

                                                 It is now mandatory for all  journals  to declare the  conflict  of interest by the authors  who are involved in medical research .The purpose apparently is to make all transactions or links  between the researchers and their funding agencies transparent .Even major journals  do not go beyond this . Some ensure it , to appear in the first page of  the article.

 What does the the journals tend to  convey to the reader by publishing the conflicts of interest ?

  •  Does it  mean the article in question  may have a bias or indeed have a bias  ?  and readers are warned  hereby !
  •  Do they send across a message  that the  article may not be really a genuine one and the judgement is left to the the consumers of the articles ?

How often a journal article is rejected purely on the basis of  conflicts of interest ?

Most of  journal articles are rejected  for poor methodology, statistical analysis and so forth .We don’t know how often a paper is rejected  due to a conflict issue per se.If this could happen ,bulk  of drug trials would face a torrid time from the editors.

Why , even the leading scientific  journals never indulge in grading the significance of the conflict ?

Here is an example .

accomplish

nejm1

The much hyped drug trial on Hypertension “ACCOMPLISH”  was published in the  world’s most prestigious medical journal recently .It  left  it to the readers to  have their  own assessment  on the conflict issue.

  The consequence of not , grading and investigating  about the conflicts could have  serious  global health  implications both financially and academically .

This study was designed, formulated, completed and published  with a single hidden aim of neutralising the land mark trial  of ALLHAT which recommended diuretics as a first line drug in HT.Apparently diuretics are very  cheap  , effective  generic drugs.

 Is it a scientific rule  that  the  latest evidence  ,  should always prevail over the older evidence ?

No. Science can never have such a rule ! The question is how good and genuine is the evidence.
Just because an evidence is current , it does not  attain a scientific sanctity !

One of the important principles of medicine  is  “Diagnosis should  always precede treatment”

This quote , though appear reasonable , can not be practiced always especially in emergencies,  where we  have to first stabilise the patient   without a  prior diagnosis  .(Like administering IV fluids in hypotension , acetaminophen for fever , etc)

Modern medicine  considers treating a patient without a diagnosis as unscientific.

But,  it is a well recognised fact ,  millions  of decision in everyday medical practice is not based on scientific diagnosis  but on clinical acumen and empirical therapy . There are many  instances  wherein , we are never near the  diagnosis  even after exhaustive investigations. 

prescription3

                       Ironically , in this era of evidence based medicine , when  we are  unable to  conclude ,  we are forced  to do the most  funniest  thing , namely converting patient’s symptom itself as disease entity and  be happy  in labelling them. Like , Motion sickness ,  poly-arthritis, , chronic fatigue syndrome, adult respiratory distress syndrome ,  pre mature ejaculation, fever of unknown origin  , attention deficit disorder , etc (The list is endless . . .)

               This happens because physicians always feel guilty if they are unable to label a patient with a disease entity.

Is the guilt  justified ?  Not necessarily so !  Symptomatic treatment without  diagnosis  is the most dominant theme even today (Fever, pain etc ).So don’t feel unduly negative* when one is not able to fit a patent’s  symptom into a disease entity  but ensure  he  gets relief from his symptom.

 *Except of course , one has to rule out a serious disorder.

 Comments welcome

                                Hypertension is the most common clinical  cardiovascular entity.Left ventricular hypertrophy (LVH) is  an important consequence of  HT.In fact, it is considered as a end organ effect or damage. Others being brain, kidney, and peripheral vascular disease.Knowing about LVH is important because it has been linked to increased cardiovascular events.

lvh-4

                              Though LVH is considered  as a close companion of  HT  it is  surprising  only a minority (15-30%)  show evidence of LVH .Some  experienced clinicians (Level C evidence)  quote even lower < 10 %  .Traditionally LVH was detected by ECG and now it is replaced by echocardiography.

What determines the LVH ?

It will be suprising to note , answer to this question  is  still not  clear .

  • Is it the duration of elevated blood pressure ?
  •  Is it the absolute level of blood pressure ?
  • If so , is it  the systolic BP  , diastolic BP or the mean BP ?
  • Or is it related to the etiology of HT ?
  • There has been no significant correlation between the above parameters

When we don’t know  the answer to a question in medicine , the answer will  generally will be inside the genes !

So in HT also the major determinant of LVH is in the genes that determine the myosin heavy chain  response .

and also ACE gene polymorphism.ACE genes are involved in the expression of growth factors within the myocardium.

An excellent study  on the issue http://www.nature.com/jhh/journal/v17/n3/full/1001523a.html#tbl1

It implicates , gender, age, race etc in the genesis of LVH

Final message

So , the  myocardium does not respond with LVH   in all patients with HT.It happens only in a minority* .Duration of HT can be an important determinant , but  the major factor is  the alteration of genetic switches  within the myocytes How this switches are going to  behave ,  is largely inherited .Regression of LVH is also not uniform again implying lesser role for hemodynamics. (Some studies revealed ACEI have maximum regression  of LVH , later disputed )

*LVH is more consistently seen  in hypertension due to reno vascular  or parenchymal disorders .It is also an observed fact , a  combination of diabetes and HT is more likely to result in  LVH.

The other major issue  that needs explanation in HT/LVH  is   , how much of LVH is due to  myocyte hypertrophy perse  and how much is contributed by interstitial cell hypertrophy(Non myocytic hypertrophy)

This issue will be discussed soon

This paper was presented in the just concluded 60th Annual scientific sessions of cardiological society of India , Chennai.India

POSITIVE  ALLEN’S  TEST  FOLLOWING RADIAL CORONARY ANGIOGRAM

Venkatesan  sangareddi , G.Gnanavelu, R.Alagesan,V.Jaganathan.

Department of cardiology, Madras Medical College, Chennai.

 

                          Radial  artery  has become the  major access  site for the interventional cardiologist in recent years. Radial approach has provided increased patient comfort and  less access site complication. Many  of  the   complications  are  unique to radial approach mostly due to  anomalies of origin, and course while others are  hardware related .Unlike femoral arterial access ,  compromise of blood supply to hand is never considered a  threat because of dual blood supply to hand  .But the fact  is that,  it  could be sub-clinical  and the hand is rarely assessed for vascular insufficiency after a radial procedure.

             The aim of the study is to assess the  impact of   radial  procedures  on the  blood flow  to  hand . 20 patients who had undergone routine  radial coronary  angiogram  formed the study population. All patients had negative Allen’s test prior to the procedure. The mean procedure time was   25mts (18-45) .Standard  hardwares were used. Difficulty in crossing at forearm and   subclavian   was observed in  4  patients. Extravasation of dye  in forearm was observed in two. Allen test  was  done 24 hours  after sheath removal and  repeated 48 hours after the procedure .  4 patients   showed positive Allen test  at 24hrs. One  patient   regained  Allen negativity at  48hours. The incidence of positive Allen test at  24 hours is 20%. The compromised blood flow was correlated with the  procedure time, and a difficult catheter course .

                 We propose,  radial procedures especially , when prolonged has a potential to compromise palmar arch flow .This phenomenon  is  either  permanent  or transient  and  may be attributable to enhanced  endothelial tone and sheath related injury. Irreversible  compromise  of blood flow to  palmar arch  may  also occur  in radial dominant hands. Further enhanced  sympathetic tone can  spill over to ulnar artery as well . 

             It is concluded, interventions through radial route has hitherto unreported adverse effect  of  “Post procedural  positive  Allen test”  . It  implies , radial  procedures  could  convert  a dual blood supply  pattern of the  hand to ulnar dependent  uni-modal  blood flow  in a significant  subset of patients. This is important   to recognise, as it   precludes further radial procedures in the same patient.

 

Final message

Hand function could be as vital as our heart’s ,   please handle with care to avoid this complication

 

Click on the slide to download PPT presentation

radial2

                                            The science of medicine has evolved over 2000 years since the stone age days.It has  currently reached  a glorious era with  cutting edge  scientifc  technology .Today  one can map the entire human genetic blue print and intervene in the  disease  even before they manifest .One can   keep dying people alive for years with multi organ transplantation. Modern medicine has taught us  how human sufferings can be prevented and life can be prolonged (with or without purpose !)

The term conservative management  conveys two different

meanings for medical professionals.

conservativ-3

For other group of physicians

 

conservative-4

                         

                             Ever since the days of  application of leech over the  head for treating migraine and a crude knife abdominotomy for emergency exit of babies from  pregnant mothers in distress  , healer’s   mind has always  perceived “something  has to be done  urgently when some body suffers”  this sort of  reaction is probably  inherited  and is related to  the primitive flight or fight response .

This may be true in  some of the emergencies but it is untrue in many of the non emergencies.

                                          Unfortunately ,  our mind  finds it difficult   to differentiate  between these  situations . With constant exposure to dramatic medical breakthroughs , modern day physician is made to believe   “Some thing  is always  better than nothing  when illness strikes. Human body is a wonderful machine which has it’s own service station ! in the form autoregulation  and the meticulous  homeostatic mechanisms. Only if the disease process overwhelms,  it needs intervention.( Typical example:In the routine viral fever , you don’t adminster Acyclovir or other antiviral  for all of them !

                                        The problem with early aggressive approach is,  it fails to give an oppurtunity  for the body’s natural defence forces  to respond. Further , we will  never ever know how the administered treatment is going to fare vis a viz the natural response.( With due respects to RCTs).   While the field of medicine   has  so much  evolved , our thought process,  especially  the  aspect of clinical  reasoning  has always been lagging behind .It is now considered  as inferior or even unscientific  treatment  if  some one follows a conservative approach to a problem even if  it  provides   same outcome of that of an invasive or aggressive approach ( The classical example is PCI for chronic stable angina The COURAGE study).

The other major issue is the hazards of unwarrnted  invesitigations , drugs and procedures

Classical example:No one knows how much morbidity or mortality the routine Swan ganz catheter  caused when it was rampantly used for over two decades to monitor central venous pressure .It is estimated  that in modern medicine  there are at least  few  drugs or devices  in each speciality waiting  for the same fate  as that of  the swan ganz catheter.

No body knows when it will be exposed .Our EBM will take it’s own time . . .Till that time humanity need to suffer.

This thinking is not new  The concept  “First do no harm is over 2000 years old”

hippocrates-primum-non-nocere

Questions in search of answers

 Does law of conservation of energy applicable to human body and medicine  ? 

 Can we defy death with modern medicine ?

Final message

  • Conservative management is still  a great medical concept  in many situations  and one should not allow it to die  by the whims and fancies of the modern scientific forces.
  • Whatever you do on the patent’s body  do it ,  only if it is going to helpful for him /her. If you are unsure  Whether a given  treatment  is going to help or not ask this question to an expert .
  • The widely prevailing  dogma  of aggression is always better than  non aggression  has absolutely no evidence.
  • So approach a clinical issue disease by disease ,  individual by individual.
  • Now , in this era  high tech  medicine  ,  It is lot more tougher to choose a conservative path as the pressure to do more and more  looms  larger ! It is easier to follow the crowd  than a path of your own .
  • Always remember it needs a  stronger  mind to  act according to our conscience !