Posts Tagged ‘unstable angina’

Now , some one wanted to know,  Can we diagnose unstable angina without Chest pain ?

Crazy question isn’t , Angina by definition  should have chest pain .There is nothing called silent angina , only silent Ischemia  .

  • We know Ischemia can occur silently .
  • We also know STEMI can occur silently (About 10 % of MI do occur without any symptoms )
  • If STEMI occurs  silently  why not UA/ NSTEMI combo ? (Collectively called as  NSTE-ACS)

The debate goes like this .If stable angina can present with equivalents ? what prevents  “Unstable angina”  to present with  Anginal  equivalents without chest pain ?

If  a diabetic patient who had a silent MI in the past  . . .  subsequently  experience  severe episodes of resting ischemia  , will he feel the pain , that is supposed to occur  with his  “unstable angina”  or not ?

Hmm , difficult to guess right,   So it seems highly plausible  UA/NSTEMI  do  occur silently ! Literature hasn’t looked into this specifically. Chest pain is built integral  into definition of UA , infact it is a symptom  complex rather than an disease entity by itself, while NSTEMI is ECG and enzyme combo ! Making the term  NSTE-ACS  look  perfect.

Any other technical explanation ?

The concept of Ischemic cascade says angina occurs last, well after biochemistry , wall motion defect and ECG , hence its distinctly possible for UA/NSTEMI present to be painless !

Final message

Anginal pain perception is related to intactness of neurogenic circuits and also probably the severity of Ischemia.If full thickness myocardial necrosis can be painless in few, nothing prevents from an episode of UA/NSTEMI  be truely painless .

Clinical implication of this conundrum

Can we admit a patient as UA/NSTEMI with out chest pain ?

Yes, it would seem so .

No, we can’t .

Indeed we can , if ECG changes are there .

No, we can admit even with normal ECG if its real unstable angina.

This is the crux of the problem in ERs all over the globe. Our knowledge base is simply not good enough. Every one of us has seen Troponin positive silent NSTEMIs ! but . . . to me still something is missing in the link .

Modern day approach 

Pain or no pain,any  fresh ECG changes ( Both T and ST shifts*) should be rushed to cath lab.Whenever you are not sure .Always better to err on the side of over investigation.That’s the mantra ! So ,you do an Angiogram , find an Incidental intermediatroy lesion which may not be responsible for the ECG changes but you are compelled to go after it FFR//iFR , OCT, IVUS and so on !

*There is huge list of non Ischemic ST/T shifts in ECG that can be read elsewhere .


Can’t agree with this article. Foolish to diagnose UA without chest pain. Never  treat ECG  in isolation unless its a convincing  ST elevation or depression with clinical input and thorough scrutiny of  past record . Realise , how important is  the basics principles of medicine taught  by Oslers and Cushings a  century ago.



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When a culprit thrombus keep the  myocardium as hostage . . . don’t storm the coronary artery  indiscriminately   !

When a single gun men  keeps 100 innocent people as hostages , threatening their  lives, rescue mission should start .No can can afford to wait. But, without knowing  the  culprit’s true nature the process of rescue mission is always going to be tricky .There are so many instances Newton’s third law  was reversed , when reactions  evoke more chaos  than the index action.

In the recent world terrorist events ,  the  rescue missions  were so delicate and  it was very  unfortunate we  lost  many   innocent hostages !  The reasoning is ,there  is no way we can avoid these. I wonder is it really true ? !

rescue missionNot all culprit lesions  are true ones.They simply threaten  our myocardium with  thrombus and plaques  in various forms .Don’t show aggression to pseudo threats  you may  ultimately end up with more damage.(What I call as crazy culprits!)

(  Read here , why unstable angina even though thrombus is sitting right inside the coronary artery attempting to lyse it causes more  damage !)

After thought

Iam sure ,bulk of  the Interventionists wouldn’t agree with this thought . They would decry , watching a person  silently when the myocardium  is on  fire is a serious crime !

But . . . we  need to  remember the process of extinguishing  the fire  with some more fire arms is a delicate game played in undefined  philosophical turf.

The only way to introspect  such events in life is , to accept any eventuality    arising out of “not pursuing”  a  presumed rescue mission with vigor. No need to be guilty about that,after all , it can be a myth !

Modern human cognition , growing with a staple  scientific  feed  on a 24/7  basis  is  unlikely to realise , restraint can be an effective tool  even in critical moments !

Oh,is all that I have  scribbled so far  is just a repetition  of 1000 year concept of  “Primum non nocere”

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This question always creeps in any coronary care unit.

Often times , there is a significant  histo-pathological overlap between severe degrees of  Ischemia* and  myocyte necrosis . (What is called micro infarcts, lacunar infarcts,  make us over diagnose MI). It is not yet clear , whether leaky myocyte cell membrane can release free cytoplasmic enzymes without actual cell necrosis.
Clinical Implication
Fortunately , there is not much .These bio markers are primarily used as prognostication tools .Many of these patients  need to  undergo early revascularisation. However , It is unwise ,to get alarmed by  just  Troponin positivity  in an other wise comfortable ACS patient.
* Some call severe degrees of Ischemia as Injury ! It is an old thought based entirely on ECG  .There is no specific cellular equivalent of electrical injury current !

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When the concept of acute  coronary syndrome was at infancy, when there was no echocardiography , when there was no coronary angiogram   when there was no coronary care units either , this man was able to identify a group of patients who are high risk to develop acute MI

These pateints are now refered to as  famous entity  unstable angina !

Serving in  Goverment institution of KEM hospital Bomay , he was instrumental in isolating reserpine which was a powerful anti hypertensive drug those days.

Realise , He is not a official cardiologist as the much hyped DM degree was not there  those days.His life is an strong evidence that , meticulous observation and documentation of simple facts from the bedside  is the many times greater than research done in  sophisticated laborataries !

Life history of Dr.Vakil (1911 -1974)


His famous article on Intermediate coronary syndrome


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It is a well known fact  ,   CABG and PCI  provides immediate relief  for patients with angina ,  which is refractory to medical therapy. Of course , this happens only if a critical occlusion of  at least one epicardial coronary artery is  opened . It need to be realised ,  angina  due to  microvascular  disease can not be cured by maintaining  epicardial  patency .

While angina  relief is prompt ,  dyspnea is not ! . If we  believe,  opening  up a  coronary artery  in a patient with LV dysfunction will  restore the LV function  ,  it  is grossly mistaken !

Why is it so ?

Angina  relief requires  simple  restoration  of  oxygen supply and correction of local ischemia .  This happens without any issue as the blood  seeps in to the ischemic cells and soothes the ischemic nerve fibres that trigger the pain signals   . While  ,  for LV function to improve , the blood flow has to be converted to mechanical activity in the form of myocyte actin/myosin interaction. For this,   there need to be an intact  cellular contractile mechanism . The myocyte architecture should be appropriate .In post MI ventricles we know there is  zig zag  orientation of myofibrils due to myocyte slippage that interfere with mechanical recruitment . Further , integrity of  extracellular matrix  namely the collagen frame work is also vital . Note ,  angina relief  is not concerned with any of the above .

And now ,  we also realise  dyspnea  in failing ventricles  is vitally  dependent on diastolic function ,  which is also very much  impaired in ischemic DCM .There is little proof for  PCI/CABG  to correct the  molecular   mysteries in  diastolic dysfunction !

Dysfunctional LV means what ? (read the link )

It is a collection of  variety of myocardial tissues . Viz : Fully  necrosed , partially necrosed ,  ischemic viable, non ischemic viable, ischemic non viable, non ischemic non viable , Apart from this patchy necrosis, patchy ischemic, areas are common. Finally , necrosed segments   may  also be perfused normally by  spontaneous reopening of an IRA.

One can imagine the complexity  of events in these segments  once we do the  PCI /CABG . The response  is highly variable and unpredictable. The major concept we  , the physicians  believe or ( to be precise made to believe !) is  the  sanctity  devoted to  the viable myocardium .For  many us ,  it is considered a  holy  exercise  to identify viable myocardium in patients following MI and then revascularise them if  found to have significant viable myocardium (Atleast 20% of infarcted area )

A full 2 decades were lost or (shall  we   say wasted on this futile exercise !) as   we have since  realised most of the cardiologists do not follow this rule .

Now , even a scarred myocardium is revascularised in the hope of recovery .As such , we have reached a stage where  there is no contradiction for not doing a PCI /CABG   with reference to LV dysfunction.

Now every  patient  with post MI  LV dysfunction  is considered to  have  some amount of viable myocardium that is  fit   enough  for revascularization

Are we justified in doing  this ?

Many clinical  trials  have revealed  , the  recovery of LV function  in these segments  has not been consistent at all .

The most surprising discovery is  a viable myocardium need not  be ischemic   .It might get adequate blood supply either  from invisible collaterals or trickle of antegrade flow .  Hence an adequately  perfused myocardial segment can  still be   non contractile . This shatters the myth  that  revascularisation must have a dramatic effect on the recovery of contractility in all viable segments.

The other major finding is  ,  even ischemic   viable   myocardium ( documented by metabolic activities PET etc)  need not regain it’s original contractility  after the ischemia is fully corrected .

*reference for  both the above statements are available from variety of sources including real life experiences .(Type C evidence )

Final message

  • Do a PCI/CABG promptly for patients with refractory angina.
  • Never  advocate PCI/CABG  for  a primary relief of dyspnea .  (Never is a harsh word,  let it be  “use it  with caution ” ! and  the  patient  should be  revealed  the whole facts  about  what we know and what we do not know regarding the complex  hemodyanmic events  in  revascularisation   )

Counter point

If  the above statements are really true ,   How does PCI/CABG   help  relieving  dyspnea  and functional class  what is your answer for thousands of patients  with CAD and ischemic DCM who have greatly benefited from CABG ?

The answer could  be  simple , The revascularization  piggybacks  over the   medical management (which , these patients pursue vigorously)     like  ACEI,  statins, salt restriction, betablockers  , optimal diuretics and tend to hijack the credits from the poor  drugs !

Read a related blog

Revascularisation for ischemic DCM

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We know human heart contracts and relaxes in an active manner .Systole happens when calcium is pumped from the cytoplasm into the actin myosin complex and diastole occur when the calcium is  returnded back into the sarcoplasmic reticulam .The rate of calcium reuptake  is detemined by the  molecules calmodulin ,  phospholamban and it’s functional status .

When the heart fails acutely , as in asystolic cardiac arrest , does it fail in systole or diastole ?

The seemingly simple question can never be answered dogmatically.

Pathological studies of post moretm specimens suggest contraction band necrosis is a feature of systolic cardiac arrest .We are not yet sure  yet . . . How a heart will appear when it stops in diastole .In fact , if a heart gets struck in systole it means systole has actually  occured  and  because it fails to relax  it  assumes a  stone like contracture  state .

While  the  molecular basis  are pretty much confusing  , what is clear is we do get number of clinical situations where a acute diastolic dysfunction may occur.

Flash pulmonary edema

The mechanism in the former could be sudden afterload mediated mechanical stunning while in the later ischemia mediated acute contractile and diastolic dysfunction.

In both situations there is severe pulmonary venous HT and class 4 pulmonary edema. The credance to concept  of acute diastolic dysfunction came to light , when  we noticed many of  these patient with acute LVF had preserved EF %   and absence of MR to explain acute pulmonary edema .

*Coronary vasospasm–induced acute diastolic dysfunction in a patient with Raynaud’s phenomenon http://www.springerlink.com/content/g1774g34544q2482/

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NSTEMI constitutes an important sub group of ACS. In fact it  forms the major  group. Real world data would indicate it   UA/NSTEMI could form up to 75% of all admissions for ACS in any cardiac emergency units. Risk stratification of NSTEMI is important and  is available. It is  one primarily with clinical features , ECG and troponin positivity. Classifying NSTEMI   with reference to underlying patho anatomy is not available.

Classifying  NSTEMI based on the following is  is suggested .

A.Based on the  extent  of infarct.( For example there is no entity called extensive NSTEMI  unlike STEMI)

B.Based on the Location of NSTEMI .

Currently , NSTEMI simply means there is an infarct some where in the heart ? Should we not localise it ? Is it not surprising , we have not attempted to localise  NSTEMI  so far ?

C.Based on the coronary anatomy : RCA NSTEMI vs LAD vs LCX NSTEMI.

The reason is two fold.

1.NSTEMI is often patchy , subendocardial . Some times  only islands of infarct can occur.But , .How common is segmental NSTEMI ? May not be common, still if wall motion defect occur it must be an segmental MI.Some estimate wall motion defect in NSTEMI is around 25%.

2.Is  there any clinical purpose for localising NSTEMI ?

Some would  think there is no real  purpose. That does not  mean ,  we should not attempt to do it. In fact there is an  important reason ,  we  need to  localise  NSTEMI. Triple vessel disease ,  is the common pathology underlying NSTEMI. They often have  multiple critical lesions as well. Identifying the  the  culprit lesion is not an easy task. If we know the site of infarct ,  however small it may be , it  helps us fix  the coronary artery.

A real dilemma could occur in patients  with NSTEMI , who has a  90 % lesion  in  RCA and  50 % proximal LAD lesion  . We ( tend to !)  take it as granted  ,  RCA  lesion is likely to be responsible for the NSTEMI. But  the real culprit  could be  the  recannalised LAD .  If it is so ,   the 50%  LAD lesion  could   be  more important and if you leave it free there is a strong  likely hood of recurrent UA. If we could some how located  the NSTEMI in the LAD region in this patient  , he could  get a PCI for LAD as well.

Of course , there is  an   universal approach available “Doing PCI for all suspected culprit lesion however mild it may be ”  . Unfortunately , it  increases the metal load for the  patient, which is an independent risk factor for a future ACS.

How to locate NSTEMI ?

So , it is often helpful to locate NSTEMI  . Of course ,  it needs little more efforts. A very meticulous echoc cardiography can aid in locating  the subtle  wall motion defects in NSTEMI . Perfusion studies/PET studies may be indicated in occasional patients.Myocardial contrast echo can be useful.

Coming soon

Difference between Anterior NSTEMI and inferior NSTEMEI

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