Feeds:
Posts
Comments

Posts Tagged ‘left main’

Human coronary artery branching pattern is unique in every  individual . Left circumflex shows many variations.

The important ones are  a separate origin , variation in the angle of bifurcation, the number of OMs  .Further, the length of  mainstem  LCX  and its course in the AV groove are quiet unpredictable.The diameter of LCX vs are generally equal  (or LAD >LCX).

The division of  left main is such that circumflex  generally gets a lesser share  of blood flow . If  LCX is dominant this  ratio  may be little balanced. But if the LCX  is huge LAD definitely suffers !When left circumflex equals the size of left main  the pattern is distinctly  unusual.

This patient   we encountered recently had 4mm sized LCX   and  presented with a tight LAD lesion .

This man's LCX probably will never sufffer from atherosclerosis !

Other observations about large bored LCX

  • Narrow ostiums are prone for  atherosclerosis .A large mouthed  LCX rarely involves  in left main  bifurcation lesions.
  • Disproportionate size of LCX when compared to LAD  can  have hemodynamic implication of provoking LAD disease  .

The implication of  differential  sharing of left main blood flow is not fully understood .It needs further insights.

Read Full Post »

Left main divides into two. Some times into three . Very rarely into 4

Look  at this angiogram ,  This looks  like  a quadrification, if not quadrification equivalent

Clinical implication

A 4 way division invariably means the OM and diagonal or going to be diminutive.These people are expected to have favorable coronary hemodynamics during ACS , and  left main lesions are  less likely  to  occur

Reference

This article is from Singapore medical Journal

Read Full Post »

NSTEMI constitutes a very heterogeneous population .The cardiac risk can vary between very low to very high . In contrast , STEMI patients carry a high risk for electro mechanical complication including sudden death .They all need immediate treatment either with thrombolysis or PCI to open up the blood vessel and salvage the myocardium.

The above concept , may be true in many situations , but what we fail to recognize is that , STEMI also is a heterogeneous clinico pathological with varying risks and outcome !
Let us see briefly , why this is very important in the management of STEMI

Management of STEMI has undergone great change over the past 50 years and it is the standing example of evidence based coronary care in the modern era ! The mortality , in the early era was around 30-40% . The advent of coronary care units, defibrillators, reduced the mortality to around 10-15% in 1960 /70s . Early use of heparin , aspirin further improved the outcome .The inhospital mortality was greatly reduced to a level of 7-8% in the thrombolytic era. And , then came the interventional approach, namely primary PCI , which is now considered the best form of reperfusion when done early by an experienced team.

Inspite of this wealth of evidence for the superiority of PCI , it is only a fraction of STEMI patients get primary PCI even in some of the well equipped centers ( Could be as low as 15 %)

Why ? this paradox

Primary PCI has struggled to establish itself as a global therapeutic concept for STEMI , even after 20 years of it’s introduction (PAMI trial) . If we attribute , lack of infrastructure , expertise are responsible for this low utility of primary PCI , we are mistaken ! There are so many institutions , at least in developing world , reluctant to do primary PCI for varied reasons.( Affordability , support system , odd hours ,and finally perceived fear of untoward complication !)

Primary PCI may be a great treatment modality , but it comes with a inherent risk related to the procedure.

In fact the early hazard could exceed the potential benefit in many of the low risk STEMI patients !

All STEMI’s are not same , so all does not require same treatment !

Common sense and logic would tell us any medical condition should be risk stratified before applying the management protocol. This will enable us to avoid applying “high risk – high benefit” treatments in low risk patients . It is a great surprise, the cardiology community has extensively researched to risk stratify NSTEMI/UA , it has rarely considered risk stratification of STEMI before starting the treatment.

In this context , it should be emphasized most of the clinical trails on primary PCI do not address the clinical relevance and the differential outcomes in various subsets of STEMI .

Consider the following two cases.

Two young men with STEMI , both present within 3 hours after onset of symptoms

  1. ST elevation in V1 -V6 , 1 , AVL , Low blood pressure , with severe chest pain.
  2. ST elevation in 2 ,3, AVF , hemodynamically stable , with minimal or no discomfort .

In the above example, a small inferior MI by a distal RCA occlusion , and a proximal LAD lesion jeopardising entire anterior wall , both are categorized as STEMI !
Do you want to advocate same treatment for both ? or Will you risk stratify the STEMI and treat individually ? (As we do in NSTEMI !)

Current guidelines , would suggest PCI for both situations. But , logistic , and real world experience would clearly favor thrombolysis for the second patient .
Does that mean, the second patient is getting an inferior modality of treatment ?

Not at all . In fact there is a strong case for PCI being inferior in these patients as the risk of the procedure may far outweigh the benefit especially if it is done on a random basis by not so well experienced cath lab team.
(Note : Streptokinase or TPA does not vary it’s action , whether given by an ambulance drive or a staff nurse or even a cardiologist ! .In contrast , the infrastructure and expertise have the greatest impact on the success and failure of PCI )
Final message

So , it is argued the world cardiology societies(ACC/ESC etc) need to risk stratify STEMI (Like we do in NSTEMI ) into low risk, intermediate risk and high risk categories and advice primary PCI only for high risk patients.

Reference

https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/226907

Read Full Post »


Coronary stents have revolutionised the management of CAD. Stents are metallic scaffolding devices that help keep the atherosclerotic plaque  plastered within the coronary arterial wall.Thus it gained the name angioplasty. Stents have aradial strength that  exerts a constant force on  the plaque . Since metals are unfriendly partners for coronary artery , we need to have minimum metal within the coronary artery.The stent struts weave around the lumen generally the stento/ artery area ratio should be as less as possible (15%).

But this has a trade off .The uncovered area of plaque tend to project into the lumen .This is many times not significant.But can be a problem if the plaque is very soft and bulk of the lipid core may reenter the lumen.this event is called plaque prolapse.

plaque-prolapse

What is the time taken for plaque to prolapse ?

Generally it is late event.But it can happen immediately after the procedure also.

Which type of lesions are more likely to have plaque prolapse ?

Eccentric and complex lesions especially with overhanging edges are prone for prolapse

What is the sequale ?

It can be benign.If there is a erosion due to stent struts can precipitate an ACS.It progresses into instent restnosis in many.

What is the angiographic appearnce ?

Angiographically it often appears as luminal  irregularity withi stented segment .

Many times , it may appear as a filling defect also.

Is there any specific issues in plaque prolapse in drug eluting stents ?

Coornary artery is not drugged uniformly by the drug eluting stents.In fact contact  lines of metalic struts  , through it’s micropore oozes the drug with polymer.Pathological studies have revelaed non homogenous drug penetration and resultant irregularity on the plaque surface.This could amplify the plaque penetration preferentially in few areas.

How to manage plaque prolapse ?

It should be managed as any other instent restenosis.Plaque resection with atherectomy devices has not solved the problem to the desired levels.A second stent is the most common approach advocated by the cardiologists.(Whic is not ideal though !)

Read Full Post »

                                                          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.

Read Full Post »