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What is dfference between successful thrombolysis and successful reperfusion in STEMI ?

Posted in Cardiology - Clinical, cardiology -ECG, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, tagged , , , , , , , , , , , , , , on May 27, 2009| Leave a Comment »

Thrombolytic therapy ,  has been  the specific treatment  for STEMI for  many decades. Primary PCI*  is  shown to be  superior  than  thrombolysis  if   performed   early  by an experienced  team in a dedicated facility. (*Conditions apply). It is estimated ,   currently only a  a fraction  STEMI  population get primary PCI (<5%) in ideal conditions . Another fraction , get  primary PCI by inexperienced cardiologists  in low volume centres.

So , thrombolysis   remains, and  would continue to remain ,   the    primary  mode of therapy for STEMI  in the  present and near  future !

How do you assess the successful  thrombolysis ?

It should be recognised ,  there is a fundametal flaw in this  question !

The aim of thrombolytic therapy is  not  to   lyse  the thrombus  , but also  to restore the coronary blood flow to the  myocardium – also called reperfusion . One may wonder , why the term ,  thrombolysis  should ‘t be  used interchangeably with reperfusion. 

A successful thrombolysis  never guarantees  a good reperfusion , for the simple reason ,  distal blood flow in an  obstructed coronary artery  is dependent on ,  many factors  other than relief of obstruction.

Apart from the potency of drug,     other   important factors  that determine  successful  lysis &  reperfusion are  . . .

  • Timing of opening of artery , if the thrombolysis is delayed  ,  the distal myocardium is dead , and   it won’t allow blood flow to enter the mycardium.
  • Microvascular integrity is as vital as epicardial vessels.
  • Distal microvascualture  plugging by the thrombotic debri . This is called”no reflow “

So , we should  primarily assess myocardial reperfusion rather than epicardial thrombolyis ! following thrombolysis .

What are the parameters available to assess successful reperfusion /thrombolyis?

  1. Clinical : Relief from chest  pain. Angina relief  , though subjective is an indication for adequate reperfusion of ischemic myocardium.
  2. ECG-ST segment regression > 50%
  3. Cardiac enzymes: Early flushing of  intra myocytic CPK into systemic circulation and hence early peaking of CPK MB (<1ohours instead of 24h)
  4. Reperfusion arrhythmias(AIVR-Less specific) .Primary VF is now thought to be reperfusion related.
  5. Infract related artery(IRA) patency by coronary angiogram
  6. Distal TIMI flow/ myocardial blush score/ TIMI frame count

ECG ST regression ,  is a direct indicator  myocardial reperfusion   as the ST segment shifts  towards baseline ,  implies  of infarct current of injury . ST regression almost always correlate with good  recovery of LV function  in STEMI .

IRA patency , is an epicardial index , it  does not give information about myocardial blood flow . But ,  a good  distal TIMI flow generally indicates good reperfusion.This  again ,  is  not a fool proof  index,  as even many of the TIMI 3 flow patients  have severely damaged myocardium by echocardiography .

Final message

For the above reasons, one should always  make a distinction between successful lysis and successful reperfusion . Surprisingly ,  ECG  is  the gold standard for assessing successful reperfusion of myocardium ,  while CAG tell us  about epicardial patency and possibly reperfusion also.

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What is ischemic left ventricular failure ?

Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, tagged , , , , , , , , , , , , , , , on May 26, 2009| 2 Comments »

Apart from  acute  coronary syndrome,    cardiac  failure is   the most common clinical  presentation of  CAD. Cardiac failure ,  classically present with dyspnea on rest or on exertion , while angina is the dominant presentation in ACS.  

What if  ,  both these  occur together in an acute fashion ?

Yes ,  if it occurs  together it is called ischemic cardiac failure . Fortunately , this is quiet uncommon . It has   an adverse outcome,  especially if it occurs  as a companion of NSTEMI . Let us see how . . .(  Most of the episodes of cardiac failure  in CAD  means only  LV failure )

For cardiac failure to occur , there need to be a mechanical contractile dysfunction or defect . In CAD population , this can  occur in  one of the following way.

  • Loss of LV muscle (Acute  Myocardial infarction as in STEMI)
  • Mechanical defects (Mitral regurgitation/VSR etc)
  • An arrhythmia (Commonly VT or AF / CHB )  can precipitate  cardiac failure

Apart from these three , there is  an important mechanism of acute LVF, namely ischemic stunning of major part of LV resulting in severe mechanical dysfucntion.This is a dangerous form of cardiac failure (Pathologivcclaly it is thought to represent  contraction  band necrosis !) this occurs in global ischemic situations manifested as gross global ST depression.

So,  there are two types of  ischemic LVF  .  STEMI   occuring due to infarct( ± ischemia ) Other  one (NSTEMI)entirely due to ischemia.

Logically ,  one  may n’t   refer  STEMI related LVF as  ischemic LVF at all  , as infarct has already occured. While , NSTEMI related LV could be the ” True ischemic LVF “


What are the differences between cardiac failure that occur in  STEMI and NSTEMI ?


lvf in nstemi stemi

Is post infarct failure  ( The commonly used terminology  , now out of vogue ! )  a type of ischemic LVF ?

In the strict sense , it is not . Here the dead myocardium , is responsible  for the   failure .To label a  LVF , as  ischemic , ongoing ischemia must  be  documented and further it  should  be shown to  contribute   for the  mechanical dysfunction .

This is of vital importance ,   if you wrongly attribute ischemia  as a cause for  the LVF , the patient may be taken up for emergency  revascularisation .It is not going to help much (Infact , it may  worsen !) as  this cardiac failure is not going to be corrected  .What we require ,  here is an  aggressive medical management  protocol .


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Is there a time window for rescue PCI ? Why we are not insisting on it ?

Posted in cardiology -ECG, Cardiology -Interventional -PCI, cardiology -Therapeutics, tagged , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , on May 25, 2009| 1 Comment »

Failed thrombolysis is an important clinical  issue  in STEMI   as  successful thrombolysis  occurs  only in  about 50-60%  of pateints . The typical criteria to define failed thrombolysis is  the  regression  of less than 50% of sum total( or maximum)  ST elevation in infarct leads.

So what do you do for these patients with failed thrombolysis ?

It depends upon the patient’s symptom, hemodynamic stability, LV dysfunction .

They  should  get one of the following .

  1. Conservative medical management  with /without CAG
  2. Repeat thrombolysis
  3. Rescue PCI
  4. CABG

Medical management is  thought to be  too inferior a  management,  many of the interventional cardiologists  do  not want to talk about . But  , there is  an important  group of patients (Not often addressed in cardiology literature)  who  technically fulfill the criteria  of failed thrombolysis  , but   still  very  comfortable , asymtomatic  and in  class 1. These patients ,  have  a strong option for continuing the conservative management .

Repeat thrombolysis does not have a consistent effect but can  be  tried in some  stable patients. CABG  can be a genuine option in few

Rescue PCI

This terminology  has become  the  glamorous one since the  catchy word  rescue is tagged in the title  itself. For most of the cardiac physicians ,  this has become the default treatment modality.This is an unfortunate perception . What  one should realise   here is  , we are  tying to rescue  the myocardium and  the patient ,   not the patient’s coronary artery !

Opening up a coronary obstruction is not synonymous with rescue .

For rescue PCI ,  to be effective it should be done within the same time window as that for thrombolysis (ie within 6 or at the most  12 hours) .This timing  is  of vital importance  for the simple reason , there will be nothing to rescue after 12 hours as most of the muscle  would be  dead. Reperfusing a dead myocardium has been shown to be hazardous in some ,  as it converts a simple  infarct into a hemorrhagic  infarct.This softens the core of the infarct and  carry a risk of rupture. Further,   doing a complex emergency  PCI  ,  in  a thrombotic milieu with   presumed  long term  benefit ,  is  a  perfect recipe for a potential  disaster.

While the above statement may be seen as pessimistic view , the optimistic cardiologist would vouch for the“Curious  open artery hypothesis” .This theory simply states , whatever be the status  of the distal myocardium ( dead or alive !)   opening an obstruction in the concerened coronary artery  will benefit the patient !

It is  huge surprise , this concept   continues to  be alive even after  repeatedly shot dead by number of very good clinical trials (TOAT, CTO limb of COURAGE etc ).

The REACT study (2004) concluded undisputed benefit of rescue PCI for failed thrombolysis  , only if the rescue was done  within  5-10 hours after the onset of symptoms.The mean time for  pain-to-rescue PCI was 414 minutes (6.5hours)

Final  message

It is fashionable to talk about time window for thrombolyis but not for PCI  .The time window for rescue PCI is an redundant issue  for many  cardiologists ! . But ,  the fact of the matter is ,  it is not . . .

The concept of time window in rescue PCI  , is as important as ,   that of  thrombolysis. Please , think twice or thrice !  if some body suggest you to do a rescue PCI in a stable patient  ,  12hours after the index event .

Important note : This rule   does not (  or need  not  ) apply for patients in cardiogenic shock  or patient ‘s with ongoing iscemia and angina.

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If ischemia is a powerful trigger for ventricular arrhythmias ,Why cardiac arrhytmias are less common in NSTEMI ?

Posted in Cardiology - Clinical, tagged , , , , , , , , , , , , , , , , on May 10, 2009| Leave a Comment »

Acute coronary syndrome is the commonest cardiac emergency. STEMI and NSTEMI are the two clinical limbs of ACS. Generally they have distinct clinical, ECG, angiographic features.(Ofcourse, with some degree of overlap) . It is  a  mystery , both clinical presentations differ so much inspite of the common denominator  , namely ,  an injured plaque with add on thrombus  within the coronary artery. The primary difference between these two entities is, in  STEMI the occlusion occurs sudden and complete and in NSTEMI it occurs slow and incomplete

Cardiac arrhythmias in ACS

It is a  much published factoid  for  many decades, that  only one third of STEMI patients  reach the hospital alive ! The reason being , STEMI  is very much prone for primary VF.  Contrary  to this ,  most pateints with NSTEMI reach the hospital alive ! How ?

Both are ACS, if ischemia is a powerful trigger for dangerous ventricular  arrhythmia’s , NSTEMI should also behave  similarly .So what protects against arrhythmias in NSTEMI ?

  • We realise ,  by observational experience (Not EBM !)  It is the suddenness and totality of ischemia that trigger dangerous form of arrhythmia  .
  • Further, a balanced  ischemia in two contralateral segments (or global  ischemia) some how protects against development of ventricular  fibrillation .This may be due to preservation  of  electrical homogeneity  , and the spherical VT spiral waves are not sustainable.
  • In contrast , STEMI has a sudden  focal , ischemic  zone that initiates the VT and    ischemia free  contralateral segment  welcoming  and sustaining the  reentrant wavelet.
  • The observation of primarily single vessel disese in STEMI and multivessel disease in NSTEMI also give credence to this concept.
  • Further , ischemic preconditioning can exert an important anti arrhythmic  effect in NSTEMI as  patients with unstable angina have   slow, repetitive episodes of ischemia prior to the index event .
  • Post MI scar mediated VT/VF is independent of degree of overall ischemia
  • It is also established ,  a sub group of  STEMI pateints  who  had  preinfarction angina(  ie . a brief  period of UA/NSTEMI) have very low risk of SCD  supporting the concept of sensitising the myocardium against ventricular arrhythmias.

Final message

Even though , there is a convincing concept  of  Ischemia induced  cardiac arrhythmia in literature ,in real patients it is very difficult to link the two in many situations..UA/NSTEMI is the most common  acute ischemic event but the incidence of VT/VF here,  is far less than one would expect.In ACS , focal , total  ischemia is more likely to precipitate a VT/VF than multifocal and global ischemia.

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How good is Troponin T to rule out acute coronary syndrome in the emergency room ?

Posted in Uncategorized, tagged , , , , , , , on May 7, 2009| Leave a Comment »

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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Can stable angina occur at rest ?

Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, cardiology- coronary care, Infrequently asked questions in cardiology (iFAQs), tagged , , , , , , , , , , , , , , , , , , , , , , , on November 11, 2008| 1 Comment »

                                        Angina pectoris , classically occur on exertion and gets relieved on rest .This is called typical chronic stable angina as described by Heberden (CSA ) .  Unstable angina(UA), the term originally described by Noble O Fowler in early 1970s. ( Also being referred as  intermediate coronary syndrome , preinfarction angina etc).The definition for unstable angina has evolved  over the years  and currently  refers to .

 1.All new onset angina of any degree* Some include severe angina only ! New onset angina of very mild degree on exertion could be the onset of the first episode of  stable  angina. 

 2.Rest angina of more than >30 mts not relieved by taking sublingual nitroglycerine.

 3.All Post MI angina

 4.Any angina in patients who have been stented by PCI.

How to recognise a patient  who is shifting from  stable angina to  UA ? 
UA is  to be suspected when  a patient develops. 
5.More frequent episodes than usual
6.Angina occurring at lesser level of exertion than before 
7.Angina radiating to new site ( Example : Chest pain radiating  to jaw rather than to the usual left arm or vice versa)

Why the first episode of angina is given a special status and often considered critica ?

Angina is the  clinical expression of   myocardial ischemia.The course of  the  first  episode of angina , can not be predicted.It could be a the beginning of a chronic disease process, or it could be a progressive coronary occlusion as in unstable angina /NSTMEI , or the onset of even a STEMI.
In contrast a patient with chronic stable angina  has a predictable chest pain , at a particular level of exertion, radiation to same site, same character, and the patient knows for sure the pain  would promptly dissappear  when he takes rest or nitroglycerine  tablets.

What is the underlying pathology in UA ?  

Generally it is very rare for  a stable plaque to produce a  serious episode of unstable angina .It  requires  an unstable plaque* to  precipitate an unstable angina !
Unstable plaque refers to any plaque which is eroded, fissured, ruptured or  hanging  eccentrically ,  with
an active thrombus.

What is the significance of post PCI angina?

It is an irony, any angina following PCI is to be considered unstable as sudden occlusion of stent is quiet common.This is a paradox of sorts as one would wonder in a patient  with CSA who undergoes PCI with stenting  of left anterior descending coronary artery  (LAD)  all his subsequent episodes of angina  will be labelled as UA  even if a stable angina occur in his other coronary artery.And these patients would go for early invasive approach and potentially inappropriate interventions even if they are at low risk !

Is all angina at rest can be termed as unstable angina ?

No, but many times ,  rather most of the times  cardiologist believe all rest angina to be unstable.

What are the situations where stable angina can occur at rest?

An episode of angina during mental stress, or post prandial* state are very common in patients with CSA. This gets relieved after the stress. Some times  patients with CSA during episodes of fever may get angina at rest .These are considered variants of stable angina.
Post prandial angina , may be considered by some as unstable

How often a diagnostic confusion occur between CSA and UA ?

Generally, this issue is rarely addressed in cardiology literature , for the  simple reason it is never considered an  issue at all !
According to Canadian cardiovascular society grade 4 stable angina  is almost similar to unstable angina , as it denotes angina occurs with minimal effort or even at rest. In fact CCSC grade 4 should be termed as UA.

Can ECG be useful to identify stable angina from unstable angina ?

                                    ECG will some times  come to our rescue when one is confused between stable and unstable angina even though resting ST depression can occur in both stable and unstable angina . Statistically , if ST depression is noted during an episode of angina it is more likely to be UA rather than CSA. . Apart  from ECG , Troponin T or I levels may be elevated in some of the patients with unstable angina. Rarely stable angina can also show elevated troponin.

In patients with systemic hypertension and LVH or cardiomyopathy resting ST depression may not indicate UA 

So differentiation between, stable and unstable angina even though appear simple and  straight forward, it requires a diligent appraisal of history , physical examination (Aortic stenosis /HCM  may cause stable angina)  and ECG, enzyme evaluation.

Final message

In any coronary care unit ,  admissions with initial diagnosis of  ACS/UA/NSTEMI , subsequently turn out to be simple stable coronary artery disese . This error happens because the chest pain  or ECG changes  are aggravated by non cardiac factors like a mental stress or a post operative stress  or fever etc.
There could  be another school of thought, that is to err on the side of  safety, and manage all  rest angina as UA  .But the hazards of unwarranted therapy might exceed the risks of leaving these patients alone.
In this context ,there is a need for a new definition for unstable angina .
One ideal version could be . . .
  • Any angina , of any degree  which is caused  mainly by the supply side defect (By a acute thrombotic /disruptive plaque   occluding the  coronary lumen  with a imminent danger of myocardial infarction is to termed as real UA.
  •  All post MI and post PCI angina are unstable angina
  •  Rest angina which occurs due to increased demand situations need not be  labelled  as unstable angina for the simple reason  there is neither an active plaque nor a  fresh thrombus likely  in these patients. They rarely develop  recurrent angina or MI . The mechanism of angina at rest here is most often due to a tachycardia and resultant increase in MVO2 .(myocardial oxygen consumption) .Currently they are called as secondary unstable angina.In fact , anti thrombotic drugs are misused in these situations as they satisfy the criteria of UA/NSTEMI.

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What are the most common indications for coronary arery by pass surgery?

Posted in cardiac surgery, cardiology -Therapeutics, tagged , , , , , , , , , , , , , , , , , , , , on November 5, 2008| Leave a Comment »

                                Coronary artery  by pass graft surgery has become the most common cardiac surgery done world over ever since it was first introduced by Favalaro in 1969.The common indications  are, triple vessel disease and left main disease in any of the following situationsE.

Elective CABG(Non emergent)

1.Chronic stable angina

Either emergent or elective

1.Unstable angina

Emergency CABG*

1.Acute myocardial infarction.-Cardiogenic shock

2.Failed thrombolysis

3.Failed primary PCI

4.Complications during routine PCI(Cath lab crashes !  etc)

5.As an associate procedure after a  mechanical complication during MI (Septal rupture, Acute MR etc)

*In emergency situations even a single vessel disease would require a  CABG

Hybrid CABG

Combining CABG and PCI in the same patient is followed in very few centres .(Example LAD graft and RCA angioplasty)This is done in patients who have co morbid conditions who can not tolerate prolonged surgical times.Further there can be situations  one lesion is very ideal for PCI  while for other grafting is the only solution.

Controversial CABG

1.CABG as a primary revascularisation  in STEMI*

(Rarely done now , almost obsolete , primary PCI has almost replaced it  . . . but it is still  useful if performed within 6 hours of MI )

2.Incidentally detected CAD*  following routine coronary angiogram.

( *CABG for incidentally detected asymptomatic CAD is  increasing in many parts of world )

Inappropriate CABG

         If it’s triple vessel disese it must be CABG -CASS study (1980s)

                       Coronary artery surgery study (CASS) still has considerable influence among the  cardiology  community in the decision making process  for CABG , even though it is many decades old .There has been a phenomenal development in both medical as well as interventional techniques since  CASS . (Thrombolysis, Statins, ACEI, PCI  DES to name a few) .

                     When CASS study was done many decades ago,it was believed triple vessel disese constitute a  homogeneous population and  carry  the same clinical significance . For example a 90% proximal LAD , 50% RCA and 50% OM technically qualify for a CABG and unfortunately , some of them are  subjected to it even in  2008 !  Now we clearly know, it is not the number of diseased vessels  that is important, but it’s location, severity , LV function, presence or absence of diabetes . Finally , the presence of revascularisation eligible myocardium must be documented in all post MI patients . (Technically referred to viable & ischemic myocardium ).              

              Currently , with the  PCI  & medical management has grown so much, CABG should be reserved only for, critical triple vessel disese , with at least one proximally located lesion (Mostly  LAD  or Left main ), especially in diabetic individuals.

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Which is the most important factor that determines “Failed thrombolysis” in STEMI ?

Posted in Cardiology -Interventional -PCI, cardiology- coronary care, Infrequently asked questions in cardiology (iFAQs), tagged , , , , , , , , , , , , , on November 2, 2008| Leave a Comment »

Which is  the most important factor that determines thrombolysis failure in STEMI  ?

  1. Thrombus load .
  2. Drug efficiency
  3. Time delay
  4. Presence of a mechanical lesion
  5. Hemodynamic instability

Answer : 3 .(Though all 5 factors operate )

Failed thrmbolysis occur in about 40-50% after streptokinase and slightly less with TPA   and TNK-TPA . Delayed arrival and late thrombolysis are  most common cause of failed thrombolysis. As the time flies , the  myocardium gets damaged and the intra coronary  thrombus gets organised .Both these processes make delayed thrombolysis a futile exercise.

               Not all STEMI patients have large thrombus burden. There need to be a critical load of thrombus for thrombolytic to be effective

Some may have a major mechanical lesion in the form of plaque fissure, prolapse and it simply blocks the coronary artery mechanically like a boulder on the road  . The poor  streptokinse  or the rich Tenekteplace !  nothing can move this boulder .The only option here is emergency PCI .

How will you know when the patient  arrives in ER with STEMI whether his/ her coronary artery is blocked with soft thrombus or hard mechanical boulder ?

It is impossible to know.That’s why primary PCI has a huge advantage.  But still thrombolysis is useful as some amount of thrombus will be there in all patients with STEMI.Lysing this will provide at least a  trickle of  blood flow that will jeep the myocardium viable and enable us to take for early PCI.

Final message

The commonest cause for thrombolytic failure is the time of administration and the degree of underlying mechanical lesion  . So  it does not make sense  to blame  streptokinase always !

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What is the link between hypertension and coronary artery disease ?

Posted in Cardiology -Interventional -PCI, cardiology -Therapeutics, cardiology- coronary care, Infrequently asked questions in cardiology (iFAQs), tagged , , , , , , , , , , , , , , , , , , , , on November 2, 2008| Leave a Comment »

                                     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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Is the terminology of “Non q MI” obsolete or still relevant ?

Posted in Cardiology -Interventional -PCI, cardiology- coronary care, Infrequently asked questions in cardiology (iFAQs), tagged , , , , , , , , , , , , , , on October 19, 2008| 4 Comments »

                                Acute coronary syndrome (ACS) is currently classified as STEMI and NSTEMI.This classification came into vogue  primarily to  triage patients for thrombolysis eligibility , as ST elevation is the  only criteria for thrombolysis.The  earlier term  non q MI  is largely used  to denote the  present day NSTEMI. In the past q  MI was referring to transmural MI non q MI  to non transmural  pathologically.(Of course , now we know  the relationship between q waves and transmurality is not good )

So when can we still use term non q MI ?

These terminologies of STEMI and NSTEMI are made on admission  at the emergency room.  ACS being a dynamic entity these  patients can  have rapidly changing  ST shifts , from depression to elevation and vice versa. Fresh T wave changes can also occur .Q waves  may or may not develop ,  depending upon the damage sustained to the myocardium and the efficacy of thrombolysis / PCI. So it should be emphasised here STEMI,  NSTEMI ,  q  MI ,  non q MI are the  descriptions of the  same group of patients in different time frames. The common mode of  evolution  of  STEMI  is  to q MI and NSTEMI  into non q MI. Cross overs can occur.

 

 

 The problem here is NSTEMI getting converted into STEMI  is quiet common and has no nomenclature issues . But  when   STEMI down grades  into NSTEMI  there is apparent  nomenclature incompatibility .This category of  patients have  no other labelling option other than “A STEMI evolving into non q MI”. Because one can’t label  STEMI  evolving into NSTEMI as  many of  them  will  have a residual ST elevation as well.

What is the final message ?

The term non q MI is still relevant and is used at discharge , in a patient with STEMI when he or she evolves without a q wave .In the setting of unstable angina , NSTEMI has largely replaced  the term  non q MI either on admission or at discharge.

Before I close

                 The important point to remember here  is NSTEMI getting converted into STEMI  is an adverse outcome and  in fact, it is  a complication and the patient should get an immediate  thrombolysis or PCI , while a STEMI getting converted into non Q MI is generally a  major therapeutic success.( Effective salvaging and preventing q waves )

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