Archive for October, 2009

Pulmonary embolism is  one of the  important  causes of acute chest pain . It can mimic  acute coronary syndrome . In fact along with aortic dissection  , it forms  a  differential diagnosis for STEMI especailly if the ECG is not typical.

pulmonary embolism chest pain dvt d dimer ventilation perfusion

The Chest pain of acute pulmonary embolism can originate in one of the following structures  with different mechanism

  • Lung parenchyma ( Necrotic pain ?)
  • Pluritic pain in adjacent necrotic segment
  • Main Pulmonary artery and it’s branches
  • Right ventricular mechanical stretch
  • Right ventricular ischemia
  • Hypoxia induced LV ischemia with coexisting CAD.
  • Multiple contribution from any of  the above *

It should also be remembered , medicine never respects logic, as some times  an episode of pulmonary embolism can occur without any chest pain

Localisation of chest pain

One can imagine ,  how difficult for the  nervous system to zero in on the origin of this  pain as  the structures involved in acute pulmonary embolism are in different planes  and in different depths  within the chest cavity . Patients  often complain vaguely  the site of pain but  what is universal is severe resting pain deep within the chest . If the ischemic lung segment  transmit pain signals , the location and radiation depend on the  bronchpulmonary segment involved.This again adds on to the complexity in the  genesis of pain  .It can be virtually any where in the back or front of chest.

But , the central and retrosternal chest  pain are equally common as invariably the central pulmonary arteries go for a acute stretch which can be severely painful .In fact , current thinking is it could contribute maximum  for the intensity of chest pain. Similarly,  acute dilatation of RV result in mechanical pain. RV sub endocardial ischemia may   also contribute .An intact bronchial  circulation( From aorta)  can limit the  ischemic lung pain .

Final message

Analysing  the chest pain of acute pulmonary embolism can be an  interesting academic exercise . It could arise from multiple structures with different mechanisms. It may not be much significant with  reference to management . But it has a diagnostic role.  A pain which is severe , and  atypically located should raise the suspicion of acute PE especially  if the patient has associated dyspnea.

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Rescue angioplasty as a concept in PCI is advocated for the past  two decades. Rescue angioplasty  continues to enjoy the  controversy over the years. A procedure which fails to shrug off the controversy for so long   inspite of multiple studies ,  would indicate there is something seriously wrong in the  procedure  or in the conceptualization.

The fundamental question   that  is often  and not answered properly is :

What is being rescued in R angioplasty ?

Is it the

  • Patient’s life ?
  • Myocardium  ?
  • Rescues ischemic myocytes
  • Infarct related  artery ?

*Or it simply rescues physician  from the legal issue arising out of  labeling his patient as  failed thrombolysis

The term rescue generally implies  tackling an  impending crisis .The threat is either  to the patient’s life or to the myocardium or both.

In STEMI when the initial reperfusion strategy fails (Usually thrombolysis)  R -angioplasty is considered. Here the aim is  to  rapidly  rescue  and salvage  myocardium . The problem  here is   , contrary to our expectation   the population of failed thrombolysis is not a homogenous one .In one end of the spectrum ,  is a patient with  persistent ST elevation ,   totally comfortable and pain free and  hemodynamically stable.The other end is , deteriorating blood pressure , tachycardia , progressive angina and impending cardiogenic shock. Considering the above situations it is very simple to guess who will  require the rescue  and  who will benefit more. In fact,  R -angioplasty  in   patients with  asymptomatic  failed thrombolysis  without ongoing  ischemia defies logic and conveys no meaning !  .This is especially true if the patient has crossed 12 hours of time since the first symptom.

In deteriorating patients R- PCI has a role where one can potentially  arrest the progression of cardiogenic shock  or even reverse it.

A third  group  among failed thrombolysis have  predominate  angina  with  hemodynamic stabilty. This group will benefit from R angioplasty  irrespective of time window , as the pain is often due to a critical non IRA lesion .Technically again we can’t call this PCI as rescue as nothing is done to salvage the myocardium . (Of course one wish to call it so ,  as the  patient is rescued from angina !)

A tricky issue is to know where does the pain come from in a post MI patient ?

It should be realised a post MI patient can have variety of source of chest pain. There has been instances where a persistent  pericardial pain has resulted in emergency  R-PCI !

The critical question that  has not  been  answered by cardiologists is

How long a STEMI pain last and when does post infarct angina begin in a  susceptible patient .


In other words how do differentiate present(Index event)  infarct angina from post infarct angina ?

Studies on pain signal transmission (medullated type c)  would suggest a dull aching retrosternal pain may occur in a substantial number of  patients  following STEMI .These pain signals come from  necrosed cells and not from  ischemic cells. This pain ceases after complete  ischemic destruction of nerve endings . The threshold , duration and central perception of this pain is highly variable.

One can imagine the importance of the above issue ,  as   there is a potential  to  misdiagnose recurrent post MI angina   for the relatively benign infarct related pain. Though experience have suggested a 12 hour cut off to define post MI angina ,  it is too empirical .

Final message

  • Rescue angioplasty remain as  disputed entity in vast majority of  post MI population .
  • It is most useful when  it is done in  impending cardiogenic shock .Note the word. Impending  . . . not established cardiogenic shock. (After prompt recognition of failed thrombolyis ,  within  overall time window < 6h*  ideally ,  but may be done  to up to 12h) There is no role for routine rescue in all failed thrombolysis patients , for the simple reason there may not be any clinical or  live myocardial  targets for rescue.

Need for seperate time window for rescue angioplasty

* Even this 6 hours is emprical . We need  seperate evidence based time window exclusive for rescue angiopalsty .I would personally believe this could  be as short as 1-2 hours .

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Exercise stress test is the most commonly used non invasive  diagnostic test for CAD.

It is also useful in the functional capacity evaluation.Even though medical management of CAD is a proven and accepted  method of therapy in CAD . There  is always a   perception  even   among the  cardiologists  medical management  is an inferior form of treatment.  This is primarily due to peer group  pressure rather than based on solid scientific concepts.

What is the effect of medical  management on  the common CAD parameters ?

Relief of angina  . It is a simple , and easy parameter to assess.

Functional capacity . Increased exercise capacity  is a good marker of successful medical therapy

The effect  on stress ischemia could be most objective way to assess the success of medical therapy.

But , unfortunately this does not come in the regular scheme of things  for many  cardiologists following medical  management. If we are able to document reversal of stress  test positivity it could be the ultimate marker of success in medical revascularisation. EST is an approved method of assessment of efficacy of optimal medical  management .Still ,  in day to day cardiology practice this is rarely done for the simple reason the patient often stumbles upon an  interventionist and lands up in a PCI or CABG !

Following  things can happen over EST following medical management

  • Complete correction of inducible   ischemia
  • Delayed appearance of ST depression with increased exercise capacity
  • Duration of ST depression can be reduced
  • Convert painful  ischemia into silent ischemia*
  • No response **

* Conversion of painful episodes into silent episodes may not be a real success  in physiological terms.But in patient point of view it is .It should be  recalled  even in  CABG  pain relief  is a major clinical  outcome .

** Could be termed as failure of medical management , but there  is a  group of patients who have increased exercise  capacity but still EST is positive

Real world experience of large case studies (Individual communication : Large community based stress test in over 9000 patients ( Gnanavel et all Ganesh clinic Thiruvannamalai ,India ) strongly suggest optimal medical management would indeed reverse exercise induced ST depression.

Why can’t we call medical therapy as a revascularisation procedure ?

Human mind does not accept certain things. Simply swallowing few drugs can never make us believe ( Especially the current generation cardiologists !  )  it can be  equivalent to a PCI/CABG

While , restoration of  TIMI flow ,  %  stenosis , Net luminal gain,  are the popular   scientific parameters fro effective revascularisation , the following are  the  desired outcomes  clinical well being , relief from pain, reduction of plaque volume, plaque stabilisation, maintenance of  collaterals , microvascular patency ,  reduction of recurrent events .The irony in CAD management  is  in many points clinical endpoints can be achieved without mechanical  the above  mechanical end points !( As we learn from the OAT, COURAGE trials where we learn t arterial patency is nothing to do with major  clinical end points )

While PCI and CABG inherently convey they are revascularsation procedures , realistically looking medical  therapy also does improve the vascularisation espcially where it is needed (Micro)

In the overall interest of  CAD community , and with good scientific basis ,  it is vital  to  emphazise medical management of CAD  is  also a  form revascualrisation .It is better to call OMT(Optimal medical therapy )  as medical revascularisation .This will help us  to neutralise the unfair” semantic  advantage” the PCI and CABG enjoys as   revascularisation modalities !


Refer: 1.AVERT study :Atorvastatin equals PCI .2.Regular excercise equivalent to PCI (esc2009)

Final message

Medical management , do reverse  the positive EST in most of the patients provided the drugs are optimally used

Stability provided by  medical management   in coronary micro and macrocircualtion is  often  significant and it can either directly  or indirectly improve coronary perfusion .  attenuate ischemia ,  improve exercise capacity and relieve symptoms. To confirm this , every patient  with medical management should periodically undergo exercise stress testing.

* One may argue , without knowing coronary anatomy  it is dangerous to  assume things and every patient with positive EST should udergo CAG. Yes ,  It may be true, ischemia due to  critical lesions in proximal locations can never be corrected with drugs

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