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Archive for the ‘cardiology- coronary care’ Category

What determines hemodynamic stability in ventricular tachycardia ?

Posted in Cardiology - Electrophysiology -Pacemaker, cardiology- coronary care, Infrequently asked questions in cardiology (iFAQs), tagged , , , , , , , , , , , , on October 3, 2008| Leave a Comment »

Ventricular tachycardia is considered as one of the most  dangerous  cardiac arrhythmia .Rather , it is the label  VT  that spreads more  fear than the arrhythmia itself. It is a fact many patients with VT walk into hospital , still  VT will always be a sinister arrhythmia as long as it carries a risk of degenerating into ventricular fibrillation.

What determines hemodynamic stability in VT ?

  • Origin and location of VT
  • The ventricular rate
  • Presence or absence of AV dissociation
  • Impact on mitral inflow pattern
  • Associated left ventricular dysfunction or valvular heart disease.
  • VT in the setting of acute coronary syndrome.(Ischemic VT)
  • Inappropriate drug selection

Origin and location

VTs originating high up in the ventricle( High septal VT,Proximal VTs) have more organised ventricular contraction  and they are more stable.Distal VT  originating  in the myocardium away from the conducting system has chaotic myocyte to myocyte conduction.These are very unstable.

The term fascicular VT is nothing but VTs originating  in the His bundle and it’s branches( Can also be termed Septal VT ).These VTs are also stable and some of them respond well to calcium blockers indicating that they are very close to the AV junction and carry the properties of junctional tachycardia. QRS width gives  a rough estimate about the location of VT. Narrower the VT higher it’s origin.( But remember even in VT ,  qrs can further widen on it’s way downhill !)

LV dysfunction.

This is probably the most important determinant of the outcome in VT. Patients with severe LV dysfunction (EF <30%) fare badly .Hence the land mark concepts from MADIT 1& 2 demanded ICDs in these patients.The most common clinical setting is  dilated cardiomyopathy.SomE of them have bundle branch re entry(BBR).This particular  VT can be stable for many  hours.

Ventricular rate.

Usually VT has a rate between 120-200.Higher the rate of VT more the chances of instability .This rule is also not always true as fascicular VT can be well tolerated at high rates.So location of VT focus  and LV dysfunction usually over rides the impact  of ventricular rate.

Mitral inflow pattern

Proper left ventricular filling is the key to hemodynamic stability in VT. In proximal, septal,fascicular, LVOT VTs doppler studies  suggest (ACC /AHA Type C evidence : Personal observations in CCU during VT) near normal preservation of  bi modal filling of mitral valve inflow.In ischemic myocardial VT  the mitral inflow profile is critically affected . There is no distinctive forward filling was observed .In fact  at rapid rates a short pulsatile MR jets are noted instead.

Associated valvular diseases

It is obvious,  aortic  and mitral valve disorders can aggravate the hemodyanmic instability.

Final message

The clinical behavior of  ventricular tachycardia is widely variable and dependent on multiple factors.

Associated LV dysfunction and  structural heart disease ultimately determine the outcome.

 

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

Posted in Cardiology -Interventional -PCI, cardiology- coronary care, Infrequently asked questions in cardiology (iFAQs), tagged , , , , , , , , , , , , , , , , , , , , , , , , , , , on September 24, 2008| Leave a Comment »

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 interrupted  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  microvascular plugging  is mainly  due to thrombus and atheromatous debri , myocardial  edema , microvascular 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, myocardial  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 microvascular  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.
  • Successful treatment of no- reflow  means not momentry restoration of  myocardial flow  by mechanical and pharmacological modalities ,but to maintain sustained myocardial   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.

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Why thrombolysis rarely fails in right coronary artery ?

Posted in Cardiology -Interventional -PCI, cardiology- coronary care, Infrequently asked questions in cardiology (iFAQs), tagged , , , , , , , , , , , , , , , , , , , , on September 22, 2008| 7 Comments »

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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What is myocardial ventricular tachycardia ? and non myocardial ventricular tachycardia?

Posted in cardiology- coronary care, Infrequently asked questions in cardiology (iFAQs), tagged , , , , , , , , , , on September 21, 2008| Leave a Comment »

The cell of origin of ventricular tachycardia is rarely discussed at bedside. It is still in research labs !

                                    Ventricles are not made up off entirely myocytes. Apart from myocytes it contains specialised  purkinje cells , fibrocytes, interstitial cells and  some times primitive mesenchymal cells. Ventricular tachycardia can arise either in purkinje cells, the myocytes  or even the fibrocytes. The myocyte  VT  classically occur during ACS or post infarct VTs.They are  more often hemodynamically unstable and quickly degenerate into ventricular fibrillation. Myocardial VT is likely to be pulseless and require DC cardiversion frequently. Purkinje VTs are relatively less unstable. If VT arise proximally in the septum near the distal his, or in bundle branches (BBR) the VT is more stable.They  are likely to respond to be medical management.

What is the therapeutic implication of knowing  myocardial VT ?

                               In fact  ,simply knowing the cell of origin of VT is not suffice .The ionic currents inside the cell that trigger and sustain the VT is more important. There are few ionic circuits responsible for VT. Sodium , Intra cellular calcium, potassium , beta receptor mediated calcium current.If we know the individual ionic culpirit we can block that specifically  . Now we have multi purpose ion blockers  like amiodarone which acts like a broad spectrum antibiotic and terminates a VT.

                              So as of now there is no real purpose of breaking our head  in locating the cell  of origin  and the ions responsible for VT  at  the bed side ,( Researchers will do that for us !).  We have only few  antiarrhythmic drugs available in our crash cart  .Our job is to choose the optimal  drug  which will fit in for our patient. In electro physiology labs, radio frequency ablation is done .This is  nothing but shooting down the abnormal electrical  focus (Cluster of cells or a samll segment of myocardium).  In future,  a single abnormal  cell could be selectively neutralised with cell based therapy assisted by  nanopore robots !

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In which tachycardias electrical cardioversion is ineffective or rather contraindicated ?

Posted in Cardiology - Clinical, cardiology- coronary care, Infrequently asked questions in cardiology (iFAQs), tagged , , , , , , , , , , , , , , , , on September 20, 2008| 4 Comments »

                              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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What will happen if you accidentally thromobolyse early repolarisation syndrome ?

Posted in cardiology- coronary care, Infrequently asked questions in cardiology (iFAQs), tagged , , , , , , , , , , , , , , , , , , , on September 19, 2008| 2 Comments »

                                  Indication for thrombolysis in ST elevation MI  is mainly determined by clinical and ECG features. ST elevation of more than 1mm in two consecutive leads with a clinical suspicion of acute coronary event demands immediate thrombolysis.

                                 Early repolarisation syndrome(ERS) is a  is typical mimicker of STEMI . In ERS , ST segment elevation occurs in many leads especially precardial .This entity is estimated to occur in nearly 3-5% of population where a genetic variation in the potassium channel activation is reported.

                              If they  land in ER with some sort of chest pain , chances are high for labelling  them as ACS . It is not uncommon for  CCU physicians  to  witness  an  ERS being lysed . Even in many of the land mark trials (ISIS ) there has been many inappropriate thrombolysis , recognised later on.

What can really happen if you thromolyse them inadvertently ?

Generally nothing happens . But they are exposed to the risk of thromolysis. The ECG changes persist. And troponin will be negative and  echocardiogram will not reveal any wall motion defect.

Are we legally liable if a patient  with ERS was thrombolysed and he ends up with a bleeding complication like stroke ?

                        While the physician may feel guilty , there is no reasons for him to feel so.The guidelines are kept little lineant  for  the indication for thromolysis. When we are promoting  a strategy of early  thrombolyis  on a population based approach  in STEMI ,  there is bound to have a overlap with normality .The benefits out of early thrombolysis for eligible  patients for outweigh the few inappropriate thromolysis.

When you want to catch  a   real criminal  it is unavoidable,  one gets hold of all suspected criminals before letting them free . Unfortunately  in this exercise , some of the innocent  might experience   intimidation or even a injury  at the hands of law enforcers.

                               Similarly if a patient with ERS develop a severe esophageal spasm and typical  angina like chest pain he is absolutely certain to receive thrombolysis. (Troponin, CPK come later , and the results never veto the clinical and ECG criteria ,except probably in LBBB) .Many times critical  time dependent decisions are prone for errors in CCU.   So it may be  unscientific to ask why an ERS was  thrombolysed !

 How can one prevent inadvertent thrombolysis in ERS ?

                            Always ask for the previously recorded ECGs .If it is available and  look exactly similar to the current ECG  chances are unlikely  for ACS. In ERS ST segment is generally concavity upwards . ACC/AHA  guideline for STEMI  ,is  aware of this fact , but still  advices thrombolysis for all ST elevation irrespective of the morphology of ST segment elevation. This is propably intentional,   not  to incorporate morphology cirteria of ST elevation  for thromolysis .It would potentially  make many true STEMIs  diagnosed falsely  as ERS and deny thrombolysis.

 

What is the latest news about ERS ?

                       Now data are coming up, ERS is not entirely benign condition.Some of them ( Even a fraction of ERS population could be a significant number) can have a overlap between Brugada syndrome and they  could be prone for dangerous ventricular arrhythmia when challanged with ischemic or other stress.

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Advantages of Left ventricular hypertrophy (LVH)

Posted in Cardiology - Clinical, cardiology- coronary care, Infrequently asked questions in cardiology (iFAQs), tagged , , , , , , , , , , , , , , , on September 10, 2008| 1 Comment »

This is a 15-year-old post about LVH, written in 2008. Few of my colleagues, now agree with this, still hesitate to oblige in the open, suggesting it is too good to be true! Re-posting it for your own assessment. Surprised, why cardiology community didn’t consider this observation worthy to pursue.

Advantages of Left ventricular hypertrophy (LVH)

Left ventricular hypertrophy is one of the most common clinical cardiac entity.It is recognised either by ECG or echocardiography.LVH has a unique place in cardiology as it can imply a  grossly pathological state or  a marker of healthy heart as in physiological hypertrophy in athletes.

Logic would suggest, in this era of  stem cells and  nano medicine ,  every muscle fibre in ventricle is worth in gold !. So when the nature provides an  extra reserve of myocardium in the form of LVH one should welcome it , if otherwise not harmful.

Is LVH due to systemic hypertension benign ?

Not really, LVH has been shown to be an independent cardiac risk factor. (The famous Framingham study)Further LVH can result in diastolic dysfunction and the risk of cardiac failure increases.

But in spite of these observations, an  astute clinician with considerable experience will appreciate , patients with LVH fare better during an acute coronary syndrome !

This has been a consistent clinical observation . (Shall we call it as class C . ACC /AHA evidence ? )

Is LVH  an asset during ACS ?

  • A hypertrophied heart takes ischemic injury very easy , it doesn’t really hurt much . Another possibility is that in  LVH myocytes are relatively resistant to hypoxia .
  • Patients with LVH rarely show  significant wall motion defect following an STEMI.This is probably because the full thickness transmural necrosis is almost never possible even if extensive MI occurs.
  • This is also reflected in ECG  as these patients   rarely develop q waves in  following STEMI .
  • Persistent ST elevation and failed thrombolysis is very uncommon in pateints with LVH.
  • LVH provides  a relative immunity against development of cardiogenic shock . It requires 40% of LV mass destruction to produce cardiogenic shock.This can rarely happen in LVH. In a  long term analysis we have found none of the patient with LVH developed cardiogenic shock following STEMI.
  • LVH patients  are also protected against development of free wall rupture.

 Concluding message

                   “Lack of published evidence is the weakest evidence to dismiss a true myth”

LVH , either pathological or physiological, has a hitherto unreported beneficial effect.It acts as a myocardial reserve and helps limit the impact of STEMI.

 

 

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Why thrombolysis is contraindicated in unstable angina ?

Posted in Cardiology - Clinical, cardiology- coronary care, Infrequently asked questions in cardiology (iFAQs), tagged , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , on September 10, 2008| 9 Comments »

              Intra coronary thrombosis is the sine qua non of acute coronary syndrome ( Both STEMI and NSTEMI.) But thrombolysis is the specific therapy in STEMI and is contraindicated in NSTEMI/UA.

Why is this apparent paradox ? What is basic differnce between UA and AMI ?

In STEMI there is a sudden & total occlusion of a coronary artery usually by a thrombus with or without a plaque .The immediate aim is to open up the blood vessel . Every minute is important as myocardium undergoes  a continuous process ischemic necrosis. So thrombolysis (or more specifically fibrinolysis should be attempted immediately) .The other option is primary angioplasty,  which will not be discussed here.

The thrombus in STEMI  is RBC &  fibrin rich and often called a red clot. Number of fibrinolytic agents like streptokinase, Tissue palsminogen activator,(TPA) Reteplace, Tenekteplace etc have been tested and  form the cornerstone of STEMI management.The untoward effect of stroke  during  thrombolysis  is well recognised , but usully the risk benefit ratio favors thrombolyis in most situations except in very elderly and previous history of stroke or bleeding disorder.

Unstable angina is a  close companion of STEMI . Many times it precedes STEMI often called preinfarction angina. During this phase blood flow in the coronary artery  becomes sluggish gradually,and patients develop  angina at rest .But unlike STEMI there is never a total occlusion and myocardium  is viable but ischemic,  and emergency salvaging of myocardium is not a therapeutic aim but prevention of MI becomes an aim. It is a paradox of sorts ,  even though thrombus is present in  UA ,  It has been learnt by experience thrombolytic agents are not useful in preventing an MI .

 

Why  thrombolysis is not useful in UA ?

1.In unstable angina  mechanical obstruction in the form of plaque fissure/rupture is more common than completely occluding thrombus. So lysis becomes less important.

2. Even if the thrombus is present , it is often intra plaque  or intra lesional and the  luminal  projection of thrombus is reduced  and hence thromolytic agents have limited area to act.

3.Further in UA/NSTEMI since it is a slow and gradual occlusion (Unlike sudden & total occlusion in STEMI) the platelets  get marginalised and trapped within the plaque .Hence in UA  thrombus is predominantly  white  . Often, a central platelet core  is  seen over which fibrin clot may also be  formed.

4.All available  thrombolytic agents act basically as a fibrinolytic agents,  and   so it finds   difficult to lyse the platelet rich clot.There is also a small risk of these agents lysing the fibrin cap and exposing underlying platelet  core and trigger a fresh thrombus.This has been documented in many trials( TIMI 3b to be specific) So if we thrombolyse in UA , there could be a risk of recurrent ACS episodes in the post thrombolytic phase.

5. UA is a semi emergency where  there is no race against time to salvage myocardium .Administering a  stroke prone thrombolytic agent tilts the risk benefit ratio against it.

6. Among UA, there is a significant group of secondary /perioperative UA   due to increased demand situations. Here there is absolutely no role for any thromolytic agents,  the  simple reason is , there is  no thrombus to get lysed. 

7.Many of the UA patient have multivessel CAD and might require surgical revascualarisation directly .

 

So fibrinolytic  agents are contraindicated in UA so what is the next step ?

The emergence of  intensive and aggressive platelet-lytic agents.

A combination of aspirin, clopidogrel, heparin, glycoprotien 2b 3a antagonist formed the major therapeutic protocol in these patients.Even though these are called antiplalet agents some of them  like 2b/3a antagonist eptifibatide, tirofiban, and many times even heparin has a potential to dissolve a thrombus. So technically one can call these agents  as thrombolytic agents.

What are the unresolved issues

                                       Even though clinical trials have convincingly shown thrombolytic agents  have no use in UA .There is a nagging belief  THAT  there could  be group of patients  with UA , still might benefit from thrombolysis as total occlusions have been documented  in some cases with UA.This is  especially true in peri-infarction unstable angina (Pre & post) as there is a fluctuation  between total and subtotal occlusions ) .But bed side recognition of this population is very difficult.

Many would consider this issue as redundant now,  since  most of  these patients  are taken up for emergency revascularisations

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In a patient with renal failure and critical coronary artery disese , who is being planned for CABG and renal transplantation which should precede what ?

Posted in Cardiology - Clinical, cardiology -Therapeutics, cardiology- coronary care, Uncategorized, tagged , , , , , , , , , , on September 7, 2008| Leave a Comment »

                           

 

 

Chronic renal failure and CAD are common companions.Severe CAD  in patients with renal failure  pose an imposing task on the treating physicians.CABG  and kidney transplantation  both are major interventions.When a patient  requires both the decision making becomes much more difficult.

The possible  choices are

A. Do CABG first follow it with renal transplant .

B. Do  renal transplant first follow it with CABG.

C. Do CABG first  and  defer transplant &  advice life long dilaysis

D.Do  renal transplant and offer medical management / PCI for CAD if feasible.

E.Simultaneous CABG & renal transplant is a remote possibility .

F.In terminally ill , combined cardiac and renal transplantation is the ultimate option. (Possible in very few centres in the world)   

G.In severe co-morbid condtions avoid both and support life. Success is not in completing   the procdeures but in providing useful life !

Among the options the most prefered worldwide is option no 1. This has a caveat. If angina is dominant  CABG should precede transplant. If cardiac failure is dominant the issue need further scrutiny.

Given a situation ( DCM & End stage renal disese) , your patient could  undergo only one procedure,  which will you prefer ?

              This again is highly emprical but logic could still be applied. Never do  CABG with a sole  aim of improving severe LV dysfunction in ischemic DCM .It happens only in  journal articles & major clincal trials!.Of course mitral valve correction and LV reduction surgery might help.But in a patient with  renal failure prolonging the CABG on table time , with add on surgery is highly risky. So it would be logical to think intensively  for  postponement of  the CABG in a patient with class 4 cardiac failure and renal failure. Do only the transplant .

 What is the impact of end stage renal failure  on LV dysfunction ?

 End stage renal failure has a great adverse impact on LV function. Many times it is reversible.We will never ever know, if you do a CABG first on them. So always think twice or even thrice before voting  on this vital issue . Correction of renal impairment can improve the cardiac status dramatically in some.

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Don’t panic when you diagnose a left main disease in routine coronary angiogram : It may cost you a life !

Posted in Cardiology -Interventional -PCI, cardiology- coronary care, Uncategorized, tagged , , , , , , , , , , , , , on August 25, 2008| Leave a Comment »

                                                          Left main coronary  lesions are  fairly common  during routine coronary angiogram.These may be a critical or a innocuous lesion.The  word “left main” triggers a sort of alarm reaction to many cath lab staff as well as the cardiologists and surgeon.Many times, these left main lesions are detected in patients   with chronic stable angina who have stable symptoms. Left main disese has not been graded  clearly in literature . Often it is perceived , any lesion in LM is serious.

There is an unwritten rule,  rather a medical compulsion  to take a patient  with left main disease  for emergency CABG ( Now some centres ,emergency PCI) .Some institutions make it  a rule these patients  are posted  in the  next available slot in the theatre.

 The basic question we raise here is   “Should we consider all  left main  disease  as  an  emergency”?

Not really , especially when it occurs in a stable angina .One can wait , buy some time to fully evaluate and prepare  the patient  and may be the patient can be posted  as an elective case. It is a well recognised fact that, CABG carries adverse outcome when done as an emergency procedure. This is primarily due to inadequate pre op work up and resultant complications. It is also well known ,  surgical  back up team may not be available in full strength in odd hours .

This post is  to convey the message , that left main is  a serious disease but that doesn’t  mean it should elicit  a panic reaction and be taken as an ultra emergency . There has been many morbid and fatal outcomes in many hospitals due to this apparent  pseudo emergency !

 

Note* 1.Left main  disease during acute coronary syndrome is to be seen in different perspective.2.Some of the proximal LAD lesions are so tight and  could be more significant than left main lesions.

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