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Archive for June, 2009

The enigma of TIMI 3 flow !

Posted in Uncategorized, tagged on June 3, 2009| 2 Comments »

Coronary arterial obstruction  is  considered,  dangerous because it obstructs the coronary blood flow . Is it possible ,  for an  obstruction  to have  little  impact  on the blood flow  ? Fortunately ,”yes” , the physics of   fluid dynamics  is patient  friendly .It is  well known , coronary blood flow goes on smoothly, uninterrupted until very late stages of obstruction .*This  has created the concept of flow limiting lesions and non flow limiting lesion .

The most popular form of reporting coronary blood flow across a stenosis is TIMI grading. Originally used   following thrombolysis , now universally used for all angiogram (Is it appropriate ?)

TIMI Grading

Grade 0 (No perfusion): There is no antegrade flow beyond the point of occlusion.

Grade 1 (Penetration without perfusion): The contrast material passes beyond the area of obstruction but “hangs up” and fails to opacify the entire coronary bed distal to the obstruction.

Grade 2 (Partial perfusion): The contrast material passes across the obstruction and opacifies the coronary bed distal to the obstruction. However, the rate of entry of contrast material into the vessel distal to the obstruction or its rate of clearance from the distal bed (or both) is perceptibly slow.

Grade 3 (Complete perfusion): Antegrade flow and clearance  of the dye   distal to the obstruction occurs as promptly as antegrade flow .

When does a coronary blood  flow gets impeded  following obstruction ?

Contrary to the  popular belief , the distal blood flow in a coronary artery  is  less dependent on the degree obstruction than the status of the  distal microvasculature.Classical teaching tells us if a coronary artery narrows >70% diameter stenosis (90%area) the blood flow gets impeded on exertion . For resting blood flow to get blocked it needs still further narrowing .

These rules are written in the era  before we knew the concept of coronary vascular  reserve . We , have since understood  ( or confused !)  more about coronary microcirculation.The major misconception could be what we interpret as epicardial blood flow is actually reflect the status of coronary micro vascular integrity.

How else you explain a patient with a same degree of coronary obstruction has vastly different distal blood flow profile ! There are innumerable examples of patients with 50% obstruction having  TIMI one flow and a 99% obstruction with TIMI 3 flow  !

Have a look at this angiogram ,  / Click  here  to view the video

LCX TIMI 3 FLOW CORONARY ANGIOGRAM

What are the factors  other than the  degree obstruction that determine  the  distal  flow?

  • Acuteness of obstruction.
  • Status of   coronary microvascular bed
  • Interstitial  (Myocardial)  edema
  • Coronary microvascular  reactivity
  • Recruitment of collaterals
  • Coronary perfusion pressure (Aortic diastolic pressure – RVEDP/Coronary sinus pressure)

Final  message

The most important determinant of  blood flow distal to obstruction is the vascular reactivity , tone  and the integrity microvascular reserve .This rule  applies  both in  in acute  and chronic coronary syndrome  . In  CTOs  it may  not apply as distal flow is near zero.  Here  also  the  inherent  intraluminal resistance   of collapsed distal vessel  will determine the  distal flow.

Note :TIMI 3  flow  ,does not represent  a homogeneous class of coronary blood flow .They can have variable myocarial blush and frame counts.It may need further analysis.

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The wrong concepts in coronary spasm !

Posted in Uncategorized, tagged , , , , , , , , , , , , , , , , on June 1, 2009| 1 Comment »

Coronary arterial spasm is a commonly discussed entity  in clinical cardiology. Originally described by prinzmetal decades ago .It was reported to occur only in coronary care units as variant angina .There is nothing called stable spasm every episode of spasm is considered as unstable angina.

How common is coronary artery spasm ?

This condition thought to be very  common during ACS , but  notoriously difficult to confirm.In fact many of episodes are clinically suspected and never confirmed. There has been lot of provocative tests for confirming coronary spasm like ergonavine etc.None of these tests were  neither useful nor practical.

What are the clinical situations where coronary spasm occur ?

Old concepts die hard.Most of us believe , the most common cause for coronary spasm is prinzmetal’s  angina ie , angina   in normal coronary arteries or  with minimal lesions .Clinical experience ,  has taught us coronary spasm can occur in all spectrum of acute coronary syndrome or even chronic coronary syndromes.

Some believe every episode of STEMI will have a component of coronary spasm.

In NSTEMI/Unstable angina spontaneous coronary spasm is an important pathogenetic mechanism

Now,  we witness transient coronary artery spasm in the cath lab due to catheter and other hard ware.The spasm  here  , is secondary to mechanical stress and this in no way related to the coronary spasm described by prinzmetal in the pre cath era.

What is the link between coronary spasm and electrocardiogram ?

The most common  fallacy among  coronary care physician is , if it is spasm  there must be ST elevation

The classical cardiology teaching all over the world , has been so powerful  this myth continues to prevail over . The fact  of the matter is ,  the  coronary arterial spasm  , can never have any direct impact on the ECG. (Unless , coronary smooth muscle generate ST currents !)  . So , whatever  be  the effect of spasm it  is through it’s effect on the myocardial  blood flow.

Hence ,  it is not the coronary artery spasm that will dictate  the movement of ST segment . It is the impact of myocardial blood flow  to the layers of the myocadium  namely , endocardium, epicardium  , epicardium (  or a combination of  the above )  that will dictate ST segment dynamics.

What are the  the ECG features of coronary artery spasm ?

It can be

  1. ST depression
  2. ST elevation
  3. Only with T wave changes (Tall or Deep T invrsions)
  4. Flattish ST segment  or  rarely , entirely normal ECG indicating balanced ST forces

Among this , the most common manifestation of coronary spasm is thought to be ,  subendocardial ischemia and resultant ST depression .This classically occur in many cases of NSTEMI/UA .

This makes  ST depression  the dominant manifestation of spasm  ,

How coronary spasm can elevate the ST segment ?

If it  can   induce a transmural ischemia  it  can elevate a ST segment . Does  all episodes coronary spasm result in transmural ischemia ? No,not at all .in fact it happens very rare  as we have already seen .

To result in transmural ischemia , the spasm should be total &  sustained ,   at least for few minutes   to   completely   occlude  the blood flow .

Milder forms of spasm can elicit only  a  sub endocardial ischemia  that  depress the ST segment.

*There is a rare variety of spasm where subepicardium is more affected than endocardium and hence ST elevation may occur.

What is the effect of Nitroglycerine on coronary spasm ?

This is a very powerful coronary spasmolytic agent.We can witness it’s action more vividly in cath lab .

It brings back the ST segment to neutral position , from either a elevated or depressed state  .Many believe , ( may it’s a fact ) much of the early  benefit of angina relief in UA/NSTEMI is  amelioration of coronary spasm

Is coronary spasm a neural event or a biochemical event ?

The exact  answer is not known .It should be chemicals as  neural  signals are also mediated by chemicals.

What are the biochemical mediators of coronary spasm ?

  • Smooth muscle calcium : Calcium flux is the immediate cause for spasm
  • Mediators .Neural :Catecholamine ,
  • Thrombus  secretes  Thromoxane A2  which is a powerful vasoconstrictor

Smooth muscle calcium

Is  coronary vasoconstriction  and  coronary spasm  are synonymous ?

Both terms are synonymous . Vasoconstriction is often used to refer  constriction of  microvasculature

while  spasm  often describes  the event in large  epicardial vessel. Some times the term coronary vasomotion is used to describe  fluctuating coronary arterial tone.

What are the determinants of coronary artery spasm ?

  • Location (RCA>LCA)
  • Lesion characteristics -Eccentric overhanging lesion can trigger a spasm by  the plaque ‘s weight.
  • Thrombus content
  • Acuteness of the event
  • Adrenergic tone and nerve activity
  • Concomitant betablockade  .  Theoretical risk ?

What are the types  of coronary spasm ?

  • Discrete ring or band like  spasm
  • Segmental
  • Diffuse long segment  spasm
  • Multilevel spasm in same coronary artery
  • Pan coronary spasm entire vessel (rare)
  • Remote spasm away from catheter tip

Unanswered questions in coronary spasm

Can a totally normal  coronary artery go for spasm all of a sudden ?

It is thought to be rare. Even in prinxmetal series some amount of atherosclerosis was documented in most patients.

What is the relationship between spasm and adjacent lesion ?

Spasm following PCI :Can spasm crush a stent ?

Can a  coronary collaterals go for spasm ?

Logically  Spasm  can  occur  coronary collaterals .But it is difficult to document .coronary collaterals eventhough  has three layes as that of artery (Intima, media, adventia) th medial smooth muscles are less sparse. Advential lack vasa nervorum and hence neural input is less.So spasm is a rare event in coronary collaterals

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