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Archive for the ‘Cardiology-Coronary artery disese’ Category

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

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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)

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                                   ACS   is the  most common cardiac emergency .  Management of STEMI is relatively straight forward.  The  only decision that to be taken is the  modality of reperfusion. (Primary PCI   or thrombolysis.) There is no need to risk stratify  STEMI on arrival. All STEMI patients are considered high risk on admission. Whereas  NSTEMI consists of  a heterogeneous  population. They need to be   triaged into low intermediate  or high risk categorizes on arrival.There is two management  approaches for unstable angina .All high risk UA should enter early invasive strategy . And low risk and intermediate risk group will get early conservative management. 

                                       The principle of management of  UA differ from STEMI in a fundamental way , as there is no issue of myocardial salvage in UA .The primary aim is to provide relief from pain and prevent an MI. So in the strict sense there is no time window in unstable angina /NSTEMI.

 

                                       But it is generally considered 48 hours is the time limit for an early invasive approach.If the patient has crossed this time there is apparently no great difference in outcome for conservative and invasive approach. 

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