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Posts Tagged ‘d dimer’

The delicate relationship between D-dimer and aortic dissection !

Posted in Cardiology - Clinical, tagged , , , , , , , , , , on November 15, 2009| Leave a Comment »

Role of d dimer in acute aortic syndromes

D -Dimer is a marker of  intravascular fibrinolysis .It is a degradation product of fibrinogen. A level more than 500ng/ml is significant.In acute aortic dissection this level is reported to be more than 2000ng/ml.

The beauty of this molecule is it is elevated in three important chest pain emergencies.

  • Acute myocardial infarction
  • Pulmonary embolism
  • And now aortic dissection.

The issue is not simple , as we know any intravascular coagulation and lysis can elevate this molecule.In patients with chronic CAD as like a chronic thrombotic lesions within the coronary arteries can also elevate d dimer.

Similarly , in portal, cortical, deep venous thrombosis all result in elevated D dimer.

So , such a non specific test  , how can be  useful in the diagnosis of aortic dissection ?

Yes, you are right ,

D Dimer helps us  not in diagnosing aortic dissection but  helps us in ruling out a possible dissection

D-Dimer levels <500 has a negative predictive value of 98% .

What is the bio- chemical  dynamics of  D dimer in dissection ?

D dimer in aortic dissection is mainly secreted within the false lumen. For d dimer to secrete into  systemic circulation  the clotted area should be exposed to a adequately flushed systemic blood at a good perfusion pressure.The contact area between the clot and fresh blood  is of critical importance.

d dimer aortic dissection false lumen

So ,  even though it has been reported d dimer has near 100% negative predictive value . . . is there a chance a dissections might occur with normal  d dimer levels ?

Yes, very well possible with due credits to published data

  • A dissection without thrombus(Rare . . . but still possible !)
  • A clot confined to false lumen with entry or exit points sealed.
  • A dissection without a exit point.
  • Intramural hematoma with no communication with aorta

Infrequently asked questions

  1. Time window ? Dimers are mainly useful in  patients who report before 24h after the onset of chestpain.
  2. How long it takes for the dimers to  get excreted ?
  3. Can coronary dissections in STEMI elevate dimer ?

Final message

D dimer is  mainly useful in  “not making a diagnosing” aortic dissection.

If  dimer levels are strongly  positive and  clinically the patient  has  has no evidence for acute MI or acute pulmonary embolism  and continues to have chest/back/atypically located pain  suspect aortic dissection , and order for further imaging like TEE,MRI, MDCT etc.

* Do not forget the role of routine , simple bedside transthoracic and suprasternal echocardiogram.It can diagnose dissection correctly in good number of patients.

** Never oder for costly thoracic imaging whenever d dimer is elevated.

*** When you send the sample for dimer make sure to mention  the clinical likelyhood of dissection .If it is very high the lab has every reason to reject the sample and suggest you to go ahead with thoracic images.

This is because ,  it could be costly miss . . . if you depend on dimer to diagnose a dissection

Imagine this scenerio , while your patient has a absent left radial pulse due to dissection and you are waiting for the lab report to arrive !

Never use it for diagnosing aortic dissection.

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Origin and location of chest pain in acute pulmonary embolism

Posted in Cardiology - Clinical, Infrequently asked questions in cardiology (iFAQs), tagged , , , , , , , , , , , on October 21, 2009| Leave a Comment »

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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Land mark concepts in cardiology : Biochemical diagnosis of aortic dissection

Posted in cardiac surgery, Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, Uncategorized, tagged , , , , , , , on January 19, 2009| Leave a Comment »

                                       Aortic dissection is a complex cardiac problem and a  killer disease .Even though it is a fancier to make a  diagnosis  of aortic dissection in any intractable chest (or back )pain   the  most common error  committed by physicians is failure to recognise it  .

Is it possible to diagnose or atleast suspect aortic dissection  by a rapid screening biochemical test ?

Yes,  it seems so, 

  1. D Dimer , a product released consequent to  intravascular thrombosis is elevated  by >500ng in most of the patients with dissection.
  2. Aortic smooth muscle heavy chain estimation is the other option.

aortic-dissection-d-dimer

Read this original article by Patrick Ohlmaan

Click on the link

http://www.medscape.com/viewarticle/530783_print   Courtesy Medscape

 What happens once a diagnosis of aortic dissection is made ?

It is not a great achievement to make a diagnosis of aortic dissection.It is only, a  beginning of a long  and often   tedious decision making process . A real tough task , on hand for the cardiothoracic  surgeons. It is a team work , needs the interaction of cardiologists, radiologists and cardiac surgeons to bring an optimal outcome.

The major issues are

  1. Never try to  manage this problem in a small hospital or facility. Always send the patient to a teaching hospital ( of course , not all teaching hospital can  tackle  this   either , so enquire about their expertise ! )
  2. No credits for making a simple diagnosis of dissection.One has to exactly locate the entry point and exit points if any.
  3. Aortic root and arch  involvement  is of major importance in determining the modality of therapy.
  4. Debaky classification is not  of academic interest ! it has a purpose . Generally type A dissection(Proximal ) require emergency surgery
  5. Differentiating true lumen from false lumen is of critical importance , it needs a meticulous transesophageal echocardiogram.( Some times one may , never  be  sure which is true and which is false lumen  , funnily .in descending aortic  dissection it may never matter for the patient !) Self healing of many dissections with thrombus is possible. 
  6. Controlling hypertension with powerful parentral antihypertenive drugs (Labetalol . . . ideally )  is vital.
  7. Side branch  involvement (spiral dissections) especially arch vessels and renal arteries  make this entity much more complex
  8. Isolated distal dissections and some low risk proximal dissections  can indeed  be managed conservatively(Also called non surgical ! ) Some cardiologists or even institutions  hesitate to  put a aortic dissection with medical management .They feel it is inferior form of treatment . . . but realise , it is not  necessarily so !)

 

What is the other bichemical marker for disscetion ?

The aortic smooth Muscle Myosin Heavy Chain was proposed as a useful marker for diagnoisng dissection.

Diagnostic Implications of Elevated Levels of Smooth-Muscle Myosin Heavy-Chain Protein in Acute Aortic Dissection: The Smooth Muscle Myosin Heavy Chain Study  Toru Suzuki, MD; Hirohisa Katoh, PhD; Yasuhiro Tsuchio, MD;  Annals of internal medicine 3 October 2000 | Volume 133 Issue 7 | Pages 537-541

 The abstract from annlas of internal medicine follows Readers from India can get the full text article free

  1. http://www.annals.org/cgi/content/abstract/133/7/537 
  2. http://www.annals.org/cgi/content/full/133/7/537
  

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