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Posts Tagged ‘coronary’

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.

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STEMI is the most common cardiac emergency . It  removes  more human lives out of this planet than any other illness. Fortunately  modern medicine has an answer to this deadly disease  . Of course ,  we are far  . . . far away  from conquering it. Only  if a  patient with STEMI reach the hospital  one   can   make a significant  impact on it.

This , unfortunately does not happen in about 30 % of  patients . They  never reach the   hospital . It does not imply all those   who do not reach hospital die . Current  understanding is that the incidence of  out of hospital  STEMI  deaths have been overestimated. The classical teaching of  50% die before reaching the hospital is based on data from old community observations  when the awareness , transport, modalities were grossly inadequate.

Now most of the  patients has access to emergency  care  like  911 /108 etc .

It is  the era of coronary care in the streets . The concept is  , If the patient is not reaching the hospital , let the coronary care reach the patient ! In spite of all these there  are  major “time pockets” which stand between the patient and his /her  ailing heart .

There has been  lot of  analysis of the  various components  of  delay in  STEMI. Of course  ,this is directly dependent upon the  economic and health  status of a country .  For example   in country like  Sweden emergency cardiac services  can reach the  patient  within 10 mts ,  while a person suffering from an MI in a remote Indian village can reach the hospital only after  most of the  myocardium undergoes complete necrosis !

Even in urban areas  where there is  excellent emergency  services  are available the following factors have a great role  in determining  the  time window  and outcome .

  1. Symptom   recognition by self
  2. Early Reactions -(Example : Spouse response time )
  3. Calling for help -Role of Close relatives and family members.
  4. Transport delays ( vehicle personal/public/Traffic jams )
  5. Hospital entry /ER woos . . .
  6. Door to ECG time
  7. ECG interpretation time
  8. Reperfusion decision time
  9. Door to Needle ( Hospital door ? CCU door ?)
  10. Door to Balloon (Cath lab door ?)

Among the above  10  time pockets can you guess which  has the greatest potential to make a deep impact on the outcome of STEMI ?

Yes , you are right The first two !Patient misinterpretation of symptoms is the key obstacle for effective care of STEMI .What drives a patient from home or office to a hospital .It is the symptom .If it is  severe  there is acceleration of every aspect of patient  transport to the hospital .The spouse response time is also critical.The problem with STEMI is many times it can occur less dramatically so the patient is likely to miss it!So cognitive response to symptom becomes vital .An intelligent patient or spouse shortens this time window .

Whether to call emergency service or use personal transport ?

This is some times difficult decision especially in country like India. One has to make a rapid assessment , what is the chances of getting   a 911/108  services within 15 mts. Developed countries have improved upon ER response time. The issue here is the  destination of the patient should be a place where there is a facility  to manage a primary VF . In short the ultimate aim of STEMI management in the early hours  is to narrow the physical distance between the patient and a defibrillator . This requires availability of  health care personnel , equipment , simple physical  presence of medical  personnel is not sufficient .They should be able to recognise  the VF and shock  when needed . Next come the method of reperfusion . Shifting to a tertiary hospital for primary PCI or to the nearest hospital for thrombolysis is a separate issue that needs elaborate discussion.

Where should the victim go ?

  • To  the  tertiary care hospital
  • A nearest nursing home
  • His  family physician
  • Nearest General practitioner

The answer is not a simple one . There  will always be a  trade off between optimal STEMI care and  the common  panic reaction  &  false alarm  and  wastage of ER resources .

Since the first  hour is very crucial  , the outcome  depends lot  on the patient response pattern .Health education and awareness become vital .Emergency medcation , self adminstred aspirin may be an answer in the future.

What ails emergency cardiac care in our country ?

Every citizen of a country should be made aware of the nearest   cardiac medical  facility  ie  . Coronary care unit (CCUs)  . It is an  unfortuante fact , many of our country people have it  in their finger tips  , the  movie house that is showing the current hit & restaurant that  serves best cuisine , have zero knowledge about the  nearest  coronary care unit in their  vicinity . Many  lives have been lost because of this ignorance  . More important than this  , is lives are lost   on transit to many ill-equipped ambulances and some times even  hospitals .

In the modern era  STEMI patient should not  die  due to an  electrical death (Venticular fibrillation)  within a ambulance or a hospital .An ambulance that do not have a defibrillator is not an ambulance at all .It is a sorry state of affairs  some hospitals do have such ambulances .

There are  numerous instances of patients dying in the ER due to poor response time of para medics  in defibrillating a VF.  It should be made a cognisable offence* to allow a patient die for lack of  proper defibrillation within the hospital premises

There has also been instances of good intentional deaths , as a patient is shifted for a better place for  catheter  reperfusion strategies  . If these centres are located  in the other end of   city ,  the door ( In fact it is  the   second door  to balloon time )  to balloon time is directly related to the degree of traffic jam ! and has a great potential to accelerate the death of myocardium and some time the patient as well

*Deaths due to pump failure , cardiogenic shock is an allowed mode of death in STEMI as the natural history demands it ! Some body has to die for the sake of statistics

How to recognise the ACS early : Read  the link elsewhere in my blog.


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Atherosclerosis   remains the number one cause for all vascular disease of human beings. It probably  kills more  patients than all other causes put together .

Modern medicine has never conquered the disease. How  the vascular system ages and why some develop premature atherosclerosis remains largely speculative. While it is true , we have identified some major risk factor for development and progression of the atherosclerosis  , patients with out any of those risk factors do develop severe atherosclerosis !So researchers sought to look for some other risk factors . There lies the difficulty  and irony .

We always tend to the research with the affected population .When we know millions of people with the so called risk factors live comfortably , there lies an opportunity  to  analyse why they are protected against the onslaught of atherosclerosis .It is always convenient to blame it or bless it on the genetic predisposition .But we need to look beyond that .Of course  . every genetic expression has to  manifest phenotypically .

While the search for all those hidden secrets has to continue , we should also realize in pursuit of breakthrough we some times waste our energy in false targets  for too many decades !

The reality as on today is ,  there is no reliable  &  undisputed drug available to arrest atherosclerosis  (Some would love to call statin so . . . )

While  our basic science colleagues struggle  in molecular  factories and biological models in pursuit of answer against  atherosclerosis , our elite  cardiac physicians   carry on with the cosmetic touches over this   progressive disease  in  sophisticated cath labs.

Let us hope  man prevails over nature . . .

A cartoon , Just for laughs . . .

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Which is  the most important factor that determines thrombolysis failure in STEMI  ?

  1. Thrombus load .
  2. Drug efficiency
  3. Time delay
  4. Presence of a mechanical lesion
  5. Hemodynamic instability

Answer : 3 .(Though all 5 factors operate )

Failed thrmbolysis occur in about 40-50% after streptokinase and slightly less with TPA   and TNK-TPA . Delayed arrival and late thrombolysis are  most common cause of failed thrombolysis. As the time flies , the  myocardium gets damaged and the intra coronary  thrombus gets organised .Both these processes make delayed thrombolysis a futile exercise.

               Not all STEMI patients have large thrombus burden. There need to be a critical load of thrombus for thrombolytic to be effective

Some may have a major mechanical lesion in the form of plaque fissure, prolapse and it simply blocks the coronary artery mechanically like a boulder on the road  . The poor  streptokinse  or the rich Tenekteplace !  nothing can move this boulder .The only option here is emergency PCI .

How will you know when the patient  arrives in ER with STEMI whether his/ her coronary artery is blocked with soft thrombus or hard mechanical boulder ?

It is impossible to know.That’s why primary PCI has a huge advantage.  But still thrombolysis is useful as some amount of thrombus will be there in all patients with STEMI.Lysing this will provide at least a  trickle of  blood flow that will jeep the myocardium viable and enable us to take for early PCI.

Final message

The commonest cause for thrombolytic failure is the time of administration and the degree of underlying mechanical lesion  . So  it does not make sense  to blame  streptokinase always !

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During acute  ischemia the most immediate requirement for the heart is

A.Blood

B.Oxygen

C.Glucose

D.High energy ATPs

E.Free fatty acid

Answer : A  will be considered  by most , as  correct answer .  A can provide B to E . But it is also a fact heart can survive without  A.  

Myocardium requires energy first  ! it does not in fact bother about from where it is coming at the time of crises.It may be right if you restore the coronary blood flow all other components (B-E) are made available to the heart .

The heart can survive off  the coronary circulation with only chemical support during cardiac surgery and also a during  heart transplantation  explanted  donor heart survives on a ice box during transit and till it is transplanted into the recipient heart

But ironically we spend much of our energy and efforts in restoring blood flow.One need to spare a thought about the quality of blood also . This is especially important  in the setting of ischmia  where a  metabolic centric approach will add further benefit.

Energy based approach to ischemia : Is it relevent ?

Heart is a fascinating  mechano biological organ  pumping   millions of  gallons of blood  .Fuel for this is self generated  on a continuous basis  from the circulation blood .So  the key to human survival is the coronary blood flow that supplies the fuel and nutrients to the heart. When this key supply line is under threat  during  acute coronary syndrome cardiologist have  the only option of restoring the compromised blood supply by any means . But during chronic ischemia there is  no  urgency. There has always been an option of enriching the  blood with energisers like ATPs,  glucose,  hemoglobin etc .Providing energy support to the failing heart has never captured the imagination of cardiac physicians until recently.Still most are skeptical about  the concept of biochemical ischemia.

Click to download full PPT presentation

Metabolic manipulation of  CAD( Will be available shortly)

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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  is more frequent in anterior   or LAD myocardial infarction.

In a simple study we have documented  patients  with inferior MI  rarely had persistent ST elevation and thrombolysis  was   successful in vast majority  of  patients  ( 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

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                              Cardioversion with DC shock  offers immediate cure in many of the dangerous ventricular and atrial tachycardias.  It is often  taught ,  any hemodynamically unstable tachycardia  refractory to  medical therapy respond to electrical cardioversion.  One should also  remember electricity is in fact be called  as a drug !  and it should be delivered in proper form and dose. Here it is the paddle size, paddle position and the axis of current flow all are important. Now we have bi phasic currents for better efficacy.

                             While it is true, most of cardiac arrhythmias respond to shock,  there are few which do not respond or respond very transiently.There are few arrhythmias  in which ,DC shock is not only ineffective but may precipitate a ventricular  fibrillation.

                            Generally arrhythmias of reentrant etiology respond well to DC shock were interuption of  electrical circuit by external current is easily possible. In arrhythmia’s of enhanced automaticity ,  and ectopic tachycardia  it is difficult  to extinguish  the tachycardia focus with DC shock .

Arrhythmias where DC shock is not going to work are

A. Mutifocal atrial tachycardia(MAT)

B. Digoxin induced arrhythmias.Patients who are on digoxin,  has  enhanced ventricular  automaticity.These patients if they  get a DC shock will unmask the  ectopic foci.

C. In elderly with atrial fibrillation and sinus node dysfunction it may be dangerous to shock them with out temporary pacing support as sinus node goes for prolonged sleep mode.

D.In electrical storm with VT ,  if more than three shocks are required within a minute,  the VT will most often going to be permanent and the  electrical therapy can be termed as a failure. These patients will require intensive pharmacological management( Including magnesium, bretyllium etc)

E. And finally , sinus tachycardia (whatever the rate)  is an absolute contraindication for DC shock.

 Verapmil is often effective in MAT  but correction of hypoxia and acidosis may be critical.For digoxin induced arrhythmias phenytoin may be tried.

What to do when the DC shock fails?

  • It will be a  tricky situation and one wonder what to do next when the so called  universal antidote for cardiac arrhythmia fails !
  • Cellular internal millieu  is altered  by hypoxia and acidosis .It may prevent the  effectiveness of cardioversion.So try to correct them .
  • Over dirve atrial  pacing  is one option for automatic tachycardia.
  • And now ablation of arrhythmic focus is possible with radio frequency waves  in some of these patients.( Diffiuclt as an emergency procedure)

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