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Posts Tagged ‘acs’

Primary PCI  has proven to be the   best  option for management of STEMI . But it need to be  done very early by a an experienced team in a good facility . (Note ,  it is not the individual expertise that matters !  Ronalodo alone can never guarantee a   match win  !  )

Any treatment ,  which has a great therapeutic potential also  carries a hazard .

So , these treatment must be used with caution.  Not every STEMI patient , has a high risk of death.  In fact the mortality  in some of the subsets of STEMI ,  can be less than 1%. If , a  STEMI patient with a likely 1% mortality   is going to get a procedure with  3-4% ,  risk it is bound to raise a  validity  question ?

primary PCI PTCA STEMI CORONARY ANGIOGRAMS

What are the situations in  STEMI , where primary  PCI could be dangerous*?

* The  term dangerous here  means ,  Risk > Benefit .

Side vessel STEMI : STEMI in  branch coronary arteries. Main vessel STEMI(LAD,RCA,LCX ) has higher risk than side vessel STEMI( Diagonals, OMs, Septal) .

Side vessel  STEMI is not easy to diagnose in ECG ,  but an MI with ST elvation restricted to  only  2 leads  could be a side vessel STEMI.

The following could be some examples.

  • 1 /AVL , High lateral
  • V2 V3 ,   Septal
  • 3 AVF ,  PDA/RV/ Acute  marginal
  • V5 V6     OMs/Ramus

A spontaneously evolving  STEMI , with  ST segment   returning   towards  baseline  and T wave  getting inverted .This indicates IRA is either partially patent and  the coronary blood flow is in the salvage mode. Here , thrombolysis is going to be very effective .

Final message

In the management of  STEMI  , primary PCI could be  consciously avoided in some of the patients   to improve the overall outcome .

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04_16

How good is Troponin T or I  to rule out acute coronary syndrome in the emergency room  when a  patient presents  within two to three hours after the onset of symptoms ?

  1. Very useful
  2. Useful
  3. Rarely useful
  4. Not useful
  5. Not at all useful

The answer is  5 , can be 3 or  4 , never 1 or 2 !

If you are surprised with the answer

Findout why , read further

troponin-i-troponin-t1

19_trop-t-sen1

troponin-i-troponin-t-2Final message

Troponin has a definite diagnostic  and prognostic value in  STEMI or NSTEMI  but relying on a single normal troponin level very early after an ACS can be . . . futile.

Realis,   diagnosis of ACS , especially  STEMI , is primarily by ECG and clinical features . Even in NSTEMI biomarkers help primarily to risk stratify the event. Bio markers come into picture only in borderline  ECGs and in baseline ECG defect like LBBB/Pacing rhythm .

It should be recognised , the major draw back of cardiac markers is , it  does not represent real time cardiac myocyte  events. (But the good old ECG has this unique property !) .The myocyte secretion & release  kinetics , the effect of  native (and pharmocological ) reperfusion make it a unreliable  marker.Apart from the time lag  , the  laboratory methods to detect these  molecule needs further refinement.

For the current day cardiologists ,  it is  required to finish off the entire treatment  of MI  within 6  hours by doing a primary PCI . It is an irony , troponin begins to appear only by  then to be detected in the blood !

Further reading

A .All about troponin

http://www.annals.org/cgi/content/full/142/9/786

B.Troponin In aortic dissection

http://www.ncbi.nlm.nih.gov/pubmed/15887472

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pci-ptca-ebm-stent

Scientifically ,  the  indication for coronary revascularisation   should be  based on following

  1. Patient’s  symptom ( more specifically angina , dyspnea is less important !)
  2. Prov0kable  ischemia  ( A significantly positive stress test )
  3. Signifcant LV dysfunction with  documented  viable myocardium &  residual ischemia
  4. A revascularisation eligible coronary anatomy * TVD/Left main/Proximal LAD etc ( *Either 1, 2 or 3 should be  present  in addition )
  5. All emergency PCI during STEMI /High risk NSTEMI

Practically ,

A CAD  patient  may fulfill  “Any of the above 5 or  “None of the above 5” ,  but ,  if   a coronary obstruction  was  revealed  by coronary angiogram  and if he  fulfils The 6th criteria , he becomes  eligible for  revascualrisation

6th criteria

If the patient has  enough monetary   resources (by self  ) or by  an  insurance company  to take care of PCI /CABG *

*The sixth  criteria overrides all other criteria in many of the cath labs .Of course , there are few genuine ones still  fighting hard , to keep the commerce out ,  from contaminating cardiology !

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First and foremost is

Avoid the procedure if  not really indicated.A lesion which  has more thrombus load  than a plaque and it is ,  subcritical and not limiting the flow  , PCI may be inappropriate  especially if the ACS is stabilised.

  • Adequate anticoagulation  along with  2b 3a blockers should be used
  • Predilatation should be minimally used or to avoided.Direct stenting preferred.
  • In primary PCI suction devices (Export etc may be useful)
  • Distal protective devices  are  “hyped up devices” rarely useful in an occasional patient with good distal vessel diameter.
  • Pseudo stent approximati(fig 1) may occur. A Layer of thrombus may get plastered between stent and the vessel wall.In the post PCI  phase , with intense anticoagulation and antiplatelet regimen this layer may get dissolved and stent  may lose it’s grip and may dislodge or migrate.Another possibility is the dead space  beneath the stent  becomes a potential site for future  thrombus and ACS.

thrombus-and-pci

Fig 1

  • To prevent this complication , high pressure inflations and Post procedure IVUS (Intra vascualr ultraound may be done to ascertain lack of thromus between stent/vessel wal  interface)
  • Drug eluting stent evoked a special concern , when used in thrombotic milleu.This , has now been  proven to be  safe

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plaque-fissure-and-coronary-dissection

  • Plaque fissure is  the most common intra-plaque event that   precipitates  an acute coronary syndrome.
  • It is the  site of   attachment  for coronary thrombus
  • It can  either be spontaneous or PCI induced.
  • Plaque fissure can  either be  partial or complete and  may  reenter the lumen.
  • Eccentric plaques are likely  to fissure often  , as the  wall stress on the plaque shoulder region is  high  (Laplace law)
  • Angiographically  it is often difficult to differentiate  fissure from true coronary dissection.Both manifest as intraluminal filling defect.Coronary dissection  often extend beyond the length of plaque.
  • Many of the reported cases of spontaneous coronary dissection are thought to be  nothing  , but plaque fissures and their extensions.

Is plaque fissure a painful event ?

Plaques do not have neural innervation.So the plaque fissure is generally not painful.But when it extends into the media of vessel wall it can be severely painful.

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Left main coronary artery disease (LMCAD) often evokes  a panic reaction  among cardiologists .Not every LMD deserve that re. To  label  it as  significant, we have a criteria ,  that is 50% diameter stenosis.  So what you do , for a tapering  or narrowed left main with 40% stenosis. Isolated insignificant left main is rare *, but real incidence is not known.  LMCAD  is  most often due to  , atherosclerosis of left main coronary artery without limiting the flow.

What are the options ?

  • Leave it alone, with intensive medical management assisted by high dose statin(80mg)
  • Elective PCI with stenting , even though the lesion is not significant.

*If associated LAD  or LCX is there decision making is easier .

How  significant is a coronary stenosis ?

The significance of a coronary lesion with reference to “lumen diameter obstruction” is basically flawed. The significance of a coronary stenosis, by tradition is  based on it’s hemodynamic impact ,right from the  CASS days in early seventies.Unfortunately our mind set has not changed even after realising    non obstructive – sub critical lesion is more prone for acute coronary syndrome.  Is it not ironical to call a  40% lesion a non significant one !

So, the  significance of coronary stenosis is two fold.

  1. Hemodynamic  significance
  2. Clinical and  pathologic significance

The former predisposes to often chronic stable angina, later likely to result in ACS.

How will you approach a apparently insignificant left main disease ?

A 40 % lesion in left main is hemodynamically not significant , but pathologically very significant.It needs intensive treatment. Plaque passification with medical approach is first choice.If the lesion morphology is eccentric,  has irregular margins or involves  LAD  or LCX ostium doing a PCI or even a CABG is to be considered in spite of the lesion is  hemodynamically insignificant .

Why , PCI is   considered  “not appropriate”  for   less tighter lesions , even though these lesions  have great clinical significance ?

The answer is simple, The risks  and the  potential cost are more than the benefit !

And further ,  stents are  not innocuous devices  either  , they  always carry a risk of sudden occlusion as like  a sub critical lesion  !

Answer to the title question

True incidence is not known . Our experince (Class 1 c evidence) would suggest Left main disease constitutes up to 10 % of CAD.Among this one third would be hemodynamically insignificant

Suggested reading

Handbook of Left Main Stem Disease


edited by Seung-Jung Park

hbleftmn

//

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                                                    Drugs are poisons , whenever it is administered without valid purpose. it can enter human body  in many ways (Oral, intravenous, percutaneous etc ) And now we have another route namely intracoronary !

                                                   In quest for prevention of restenosis, many of the anti cancer drugs are now delivered directly inside the coronary arteries .These drugs are secreted  like a sustained release  tablet from the drug coated stents.These drugs are expected to prevent restenosis within the stented segment.But, after years of  intense debate and research  , we realised that ,  drugs  eluted from the stent  could damage the distal coronary vascular bed and coronary microcirculation.( And thus came the epidemic of acute stent thrombosis ! )

                                                The tender and sensitive coronary microvasculature  is constantly exposed to  these  powerful anticancer and immmunosuppresive  drugs .It is a great surprise , no body thought of  this dangerous drug -coronary artery interaction ! It required the genius of Renu virmani and others to point out this.

But still , the cardiology community by and large , fails to consider  this an important issue.This is proven by the fact, usage of DES is  still increasing  and used mainly as an off label indication.

Read this land mark article from circulation

picture1

http://circ.ahajournals.org/cgi/content/full/115/8/1051?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=1&author1=renu+virmani&andorexacttitle=and&andorexacttitleabs=and&andorexactfulltext=and&searchid=1&FIRSTINDEX=0&sortspec=relevance&fdate=1/1/2007&tdate=12/31/2007&resourcetype=HWCIT

 

Questions that need to be answered

  • What is the long term effects of drugging a coronary artery ?
  • Is no reflow or slow flow  more common after DES , because of the adverse drug reaction in the distal vascular bed ?
  • If a patient  with  DES  undergoes a CABG later what  would be  the impact of the  drug on the graft ? Will the functional vasodilatation   affected ?

Final message

                                  A drug , to get a legal clearance it has to undergo  hundreds of rigorous tests . Finally it is cleared for that  specific indication for which it is tested  .Just because a drug is cleared for one purpose ( Paclitaxel for malignancy ) it does not mean it is safe to use for any other  purpose for which it is deemed to be useful . Exactly the  opposite is happening   in the  the field of interventional cardiology . No body wondered to think what would be the effect of these drugs on the normal coronary endothelial cells and vasculature.Is it not a crime ,  without analysing this particular issue  , dozens of drug eluting stents have been released in the market . And now,  sounds of crying  foul is heard world wide !

Let us thank  , the so called negative forces in cardiology  for making this an  issue . In science ,  the watch dogs should bark  at  times of danger not wag the tail !

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This paper was presented in the just concluded 60th Annual scientific sessions of cardiological society of India , Chennai.India

POSITIVE  ALLEN’S  TEST  FOLLOWING RADIAL CORONARY ANGIOGRAM

Venkatesan  sangareddi , G.Gnanavelu, R.Alagesan,V.Jaganathan.

Department of cardiology, Madras Medical College, Chennai.

 

                          Radial  artery  has become the  major access  site for the interventional cardiologist in recent years. Radial approach has provided increased patient comfort and  less access site complication. Many  of  the   complications  are  unique to radial approach mostly due to  anomalies of origin, and course while others are  hardware related .Unlike femoral arterial access ,  compromise of blood supply to hand is never considered a  threat because of dual blood supply to hand  .But the fact  is that,  it  could be sub-clinical  and the hand is rarely assessed for vascular insufficiency after a radial procedure.

             The aim of the study is to assess the  impact of   radial  procedures  on the  blood flow  to  hand . 20 patients who had undergone routine  radial coronary  angiogram  formed the study population. All patients had negative Allen’s test prior to the procedure. The mean procedure time was   25mts (18-45) .Standard  hardwares were used. Difficulty in crossing at forearm and   subclavian   was observed in  4  patients. Extravasation of dye  in forearm was observed in two. Allen test  was  done 24 hours  after sheath removal and  repeated 48 hours after the procedure .  4 patients   showed positive Allen test  at 24hrs. One  patient   regained  Allen negativity at  48hours. The incidence of positive Allen test at  24 hours is 20%. The compromised blood flow was correlated with the  procedure time, and a difficult catheter course .

                 We propose,  radial procedures especially , when prolonged has a potential to compromise palmar arch flow .This phenomenon  is  either  permanent  or transient  and  may be attributable to enhanced  endothelial tone and sheath related injury. Irreversible  compromise  of blood flow to  palmar arch  may  also occur  in radial dominant hands. Further enhanced  sympathetic tone can  spill over to ulnar artery as well . 

             It is concluded, interventions through radial route has hitherto unreported adverse effect  of  “Post procedural  positive  Allen test”  . It  implies , radial  procedures  could  convert  a dual blood supply  pattern of the  hand to ulnar dependent  uni-modal  blood flow  in a significant  subset of patients. This is important   to recognise, as it   precludes further radial procedures in the same patient.

 

Final message

Hand function could be as vital as our heart’s ,   please handle with care to avoid this complication

 

Click on the slide to download PPT presentation

radial2

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                                     Hypertension is considered a major cardiovascular risk factor.Hypertension  can have multiple physiological and pathological effects on heart . The common response to  raised arterial pressure is the hypertrophy of the left ventricle ( LVH). This can increase the risk of heart failure in few ( Mainly diastolic failure)  It is a leading cause for stroke  and   less often a  coronary event.

What links Hypertension and  coronary artery disease

                                           Coronary artery disease is almost synonymous with atherosclerosis. There is no separate entity called hypertensive coronary artery disease. But HT can accelerate the process of atherosclerosis. It is widely understood, hypertension can cause  physical endothelial damage and functional impairment of endothelial function.The physical damage ie enothelial disruption , or erosion is a very uncommon phenomenon . So currently  there is sufficient clinical experience  HT is considered dangerous for coronary artery only if it is with the  company of diabetes and hyperlipidemia. (This will seem controversial as it is against the findings of iconic Framingham trial!)

What the medical community refers to hypertension , may not be really so inside  for the coronary arteries.

                                             The relationship between brachial cuff blood pressure and the intra coronary pressure has very little linear relationship. So one should recognise it is the intra coronary hypertension that has a immediate impact on the coronary events. Now only , we are beginning to understand the complexities  of the relationship between HT and CAD. If we analyse a series of individuals HT per se is not a very serious risk factor for CAD* , but it is a number one risk factor for stroke. 

Why HT in isolation  often result in stroke , rather than a MI ?

While HT  is notoriously common to result  intracerebral hemorrhage, the same HT  would not cause  intramyocardial bleeds . Why ?

What is protecting the myocardium against this complication ?

                                      The exact mechanism  is not clear.Acute surges of blood pressure can increase the risk of stroke many times  but  rarely precipitate  a coronary event(  But may cause a LVF) . The reasons could be the coronary endothelial shearing stress is less than the cerebral blood vessels.Both cerebral and coronary circulation has  auto regulatory mechanism . The coronary auto regulation is more robust in that it does not allow  intra coronary pressures to reach critical levels .There is no clinically relevant intra myocardial hemorrhage reported  even during malignant hypertension.

*But a  high intra coronary pressure can sometimes  result in spontaneous coronary dissection and plaque fissure .Lipid mediated injury is vey much facilitated in a high pressure environment.

Has Controlling blood pressure  to optimal levels  , reduced the overall CAD morbidity and mortality ?

                    The answer is yes, ( But not an emphatic yes ! ) Some studies had been equivocal. It is very difficult to say , how much benefit is attributable to BP reduction  per se  and   how much is attributable to indirect effect on atherosclerosis prevention.

Hypertension during ACS

                            High blood pressure during an episode of unstable angina or STEMI can increase the myocardial oxygen demand and worsen the ischemia. It requires optimal control with nitroglycerine ( Preferably ) or beta blocker and ACE inhibitors.Even though HT is commonly associated  with ACS,  one can not be sure the ACS is preciptated by HT. Many times the sympathetic surge during an ACS keeps the blood pressure high.It is a common experience the blood pressure suddenly dropping to normal or hypotensive levels once the pain and anxiety is controlled.

Hypertension during thrombolysis

                           High blood pressure is a relative contraindication for thrombolysis.It need to be emphasised here, It is the  the fear of stroke that make  it contraindicated .The heart can tolerate  thrombolytic agents delivered at high BP .In fact logically ,  hemodynamically and also  practically it is obseved , thrombolytic agents administered at relatively high blood pressure (140-160 systolic) has better thrombolysis than a patient who is lysed at 100mmhg.

                       The coronary pressure head which contain the thrombolytic agent (streptokinase and others ) need to have pressure jet effect on the thrombus.So the  mean coronary perfusion pressure becomes  a critical determinant of success of thrombolysis.

                            It is a paradox of sorts , very high blood pressures are a relative contraindication for thrombolysis and at the same time normal pressure patients fare less well to thrombolysis.

 Final  message

                        Hypertension continues to be a major cardiovascular risk factor.It has direct and indirect effects on the heart.Generally HT is more of a risk factor for stroke than CAD.A slightly high BP ( Just around the  upper limits of normal or just above it ) has a hemodynamic advantage during thrombolysis.(Class C evidence )

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Non ST elevation Myocardial infarction  (NSTEMI) is a major mode of presentation of acute coronary syndrome.

Patients present with clinical unstable angina and  elevated cardiac enzymes or troponin.

ECG features can be any of the following.

1.ST depression (70-80%)

2.T wave inversion(10-20%)

3.Both ST depression and T wave inversion

4Post MI NSTEMI  -ECG changes variable ( Ironically ,even a residual  ST elevation may be present)

5.Normal ECG.

                                     Bulk of the NSTEMI belong to ST depression group.NSTEMI with purely T wave inversion is less common but occurs mainly in perioperative settings, pre existing CAD.NSTEMI with normal ECG is very rare  but can occur.

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