What is a normal coronary angiogram & What is a normal coronary artery ? Do they mean the same ?

Coronary angiogram is a video graphic  snap shot of coronary arterial lumen which is filled with radio opaque dye. This is some times called as coronary luminogram . It is a paradox , when we say normal coronary angiogram we can only mean  normal coronary lumen. But  generally, this can provide sufficient  information regarding the status of  coronary blood flow.There are three structured layers in coronary artery wall . Coronary angiogram  can not give any information about the status of the intima, media or adventia .

Lesions A to F may be totally missed by conventional coronary angiogram

A patient with normal coronay angiogram can have diffuse  atheroscelrosis or  localised atherosclerosis within the media of coronary artery .Many times these atherosclerotic plaques grow outward into the adventia and fail to encroach upon the lumen to be detected by coronary angiogram. These plaques , even though has an hemodynamic advantage, in that it doesn’t block blood flow , has a serious risk for sudden rupture and result in an acute coronary syndrome.

So what is the message?

A normal coronary angiogram can never convey a meaning of normal coronary arteries.

A person who has a normal coronary angiogram has no guarantee that he won’t develop a coronary event in the near future.(But the the chances are very low)

If coronary angiogram has serious limitations  what is the next alternative ?

Intra vascular ultra sound imaging(IVUS) can give us an idea of the coronary arterial wall anatomy. This investigation , though available for clinical application is too complex for regular use.So , you  can’t subject every patient with normal CAG  to an IVUS  (Intra vascualar ultra sound) to confirm the normality. The best option is what we follow every day in our practice  .Tell your patients   with normal coronary angiogram , that they are likely to  have  normal coronary arteries  ! don’t add up to their anxiety by saying,  in spite of normal CAG  still they  can carry  gross atherosclerosis in their  arteries. Anxiety can precipitate an coronary event. Too much technical information to the patients  can be counter productive. Instead  advice regular life style modification,  blood pressure ,diabetes, lipid  control  etc .

Why thrombolysis rarely fails in right coronary artery ?

Differential response of thrombolysis between left and right coronary system

• Thrombolysis is the specific treatment for acute myocardial infarction. ( Privileged few , get primary PCI))
• Failed thrombolysis occurs in significant number of patients ( 30-40%).
• Persistent ST elevation  120 minutes after thrombolysis is best indicator of failed thrombolysis.
• It has been a consistent observation  failed  thromolysis almost always occur in anterior or LAD myocardial infarction. 

In a simple study we have documented  patients  with inferior MI  rarely had persistent ST elevation and thrombolysis  has been  almost always successful ( Except in few patients associated lateral MI)

 

The mechanism of better thrombolysis in right coronary artery  is simple.The success of thrombolysis , apart from early time window , is directly correlated with pressure head  and the duration of contact between the thrombolytic agent and the thrombus. In right coronary circulation the  blood flow is continuous ,  occurs  both in systole and diastole that facilitates the maximum delivery of the thrombolytic agent . Further there is a favorable  pressure gradient  across RV myocardium  as the transmural occluding pressure across RV is considerably less then LV myocardium. 

 

 

This paper was presented in the  “Annual cardiological society of India scientific sessions”

at Chennai, Tamil Nadu.India December 2000

Click to down load PPT full presentation

What is no reflow ? What is the mechanism of no reflow ?

No reflow is the terminology used primarily in cath labs where, even  after a successful opening and stenting  of a coronary artery the coronary blood flow is not  restored to myocardium . The point to be emphazised here is blood do cross  successfully the site of  the obstruction but fails to enter the muscle segment  to which the coronary artery is supplying. So the paradoxical situation of artery  being open but the  myocardium is closed to receive  blood flow  happens . This is termed as no -reflow.  Actually it is a  misnomer , and  ideally it should be called “no flow” because  normal distal flow  does not  occur (After PCI)  in the first instance  to get interuppted  later on  and be labeled as  no re-flow.  .The only positive effect of PCI in these situation is blood flow would have improved by few centimeters ie till it reaches  but falls short of myocardium . In fact no reflow , can be termed as  glorified and concealed  terminology  for  PCI failure . It needs urgent action . No reflow is also called as myocardial epicardial dissociation.

Mechanism of no reflow.

Curious case of open coronary artery and closed myocardium !

Coronary  microvascualr plugging  is mainl  due to thrombus and atheromatous debri , myocardial  edema , microvascualr spasm may also contribute.

Where can it occur ?

• First described in cath lab, especially following primary angioplasty.
• It can very  well happen following thrombolysis in STEMI.

• Can occur in venous grafts.

How do you recognise no reflow?

In cath lab it will be self evident from the check angiogram. Some times it is less obvious and may  require, myocardail blush score, TIMI frame  count, contrast echocardiography, PET scan etc. In post MI a very simple method to recognise this entity could be the observation of persistent ST elevation in ECG .

Treatment.

Extremely difficult. Almost every coronary vasodilator has been tried.(Nitrates, nicorandil, calcium blockers, etc).Success is less than 30%.  High pressure flushing with saline inside the coronary artery is advocated by some.Others believe it’s dangerous to do it. So prevention is the key. Avoid doing PCI in complex, thrombotic lesions. Use thrombus suction device like export catheter(Medtronic). Distal protective devices are double edged devices , useful only in experienced hands.

Unanswered question

What is the size of the particle (thrombotic and atheromatous  debri)  the   coronary microcirculation safely handle and push it into the coronary venous circulation and the coronary sinus for disposal ?

If we can lyse the thrombus into micro particles by some mechanism and make it traverse the coronary circulation this complication of microvascuar plugging can be treated and prevented .

What is the final message ?

• No reflow is relatively common condition during emergency PCI done for ACS patients
• More common in complex thrombotic lesions.
• Can also  occur in STEMI
• Treatment is often vexing . In fact the treatment of this condition is so difficult , it can be termed  almost synonymously with “Failed PCI” if flow is not restored.
• Suceesful treatment of no reflow  means not momentry restoration of  myocardial flow  by mechanical and pharmacological modalities ,but to maintain sustained myocardail  perfusion. This  we realise, as patients who have had a no reflow during  a PCI, do not perform as well in the follow up  .
• So prevention is the key.

Some possible truths about human heart

Heart rate and human survival has an inverse relationship. This is in fact true for  all mammals.The tortoise which has a heart rate of  6/mt lives for over 200 years. The rat which has heart rate of 500 dies does not even  celebrate it’s first birth day ! Human beings with an average heart rate of 70 lives for 70 years. 

There is a belief  human heart is programmed to beat for certain trilion beats in it’s life time .It is possible ,  with evidence mounting this belief  could  indeed be true .

People with low heart rate simply outlive the ones with  fast heart rate ! Is this due to simple fact they conserve their heart rate .Each human has a reserve of few trillion heart beats for usage in his or her life time .So if this is true what does regular vigorous  exercise do to our longevity ! These are pure fantasy questions that need to be answered !

The truth may be regular excercise even though raises the heart rate to high levels it keeps our vagal tone high and maintain the basl heart rate low and there by conserving both heart rate and myocardial oxygen consumption.The other evidence for heart rate being vital in prolonging life is the proven benefits of beta blockers in patients with decompensated  heart.

Read the excellent issue dedicated to the  importance of heart rate for human survival especially in relation to cardiovascular disease .

From the  publishers of dialogues in cardiology .This knowledge sharing comes free of cost

Courtesy of  Servier

http://www.dialogues-cvm.org/pdf/19/DCVM19_05.pdf

Conquering atherosclerosis : Why we are not getting the desired outcome ?

Atherosclerosis   remains the number one cause for all vascular disease of human beings. It probably  kills more  patients than all other causes put together .

Modern medicine has never conquered the disease. How  the vascular system ages and why some develop premature atherosclerosis remains largely speculative. While it is true , we have identified some major risk factor for development and progression of the atherosclerosis  , patients with out any of those risk factors do develop severe atherosclerosis !So researchers sought to look for some other risk factors . There lies the difficulty  and irony .

We always tend to the research with the affected population .When we know millions of people with the so called risk factors live comfortably , there lies an opportunity  to  analyse why they are protected against the onslaught of atherosclerosis .It is always convenient to blame it or bless it on the genetic predisposition .But we need to look beyond that .Of course  . every genetic expression has to  manifest phenotypically .

While the search for all those hidden secrets has to continue , we should also realize in pursuit of breakthrough we some times waste our energy in false targets  for too many decades !

The reality as on today is ,  there is no reliable  &  undisputed drug available to arrest atherosclerosis  (Some would love to call statin so . . . )

While  our basic science colleagues struggle  in molecular  factories and biological models in pursuit of answer against  atherosclerosis , our elite  cardiac physicians   carry on with the cosmetic touches over this   progressive disease  in  sophisticated cath labs.

Let us hope  man prevails over nature . . .

A cartoon , Just for laughs . . .

Why we struggle to prove the benefitial effect of strict diabetic control on cardiovascular events ?

Diabetes is the scourge of mankind .( Womankind too ! In fact it affect women more than men !) When we say DM  & Cardiovascular disease we mean the type 2 maturity onset DM  .Even a lay person  can  recognise  the strong  link between DM and increased cardiovascular mortality .

While logic would make the same lay person believe , that  proper  control of diabetes will eliminate  CVD risk that was acquired . Alas . . . how foolish science can be

The problem in medicine is 1 + 2 is  3  only if it’s counted antegradely   , 2 + 1 is rarely three !

Unfortunately even many of the medical professionals  do not realise this fact and keep the  logic  above reality and continue to believe in what they believe .

When we find,   a  disease process that tend to  continue even after the  offender ( Here incresed blood sugar ) is removed  then there is questionable relationship between the offender and the victim .

This is what we have learnt in over 50 years of diabetic research . Now we have so much controversy and confusion.The savior of diabetes insulin itself may be the offender (ACCORD Trial ) Or is it insulin like growth factor , or circulating peptides ( named and unnamed )

So the debate and research  goes in an unknown  and uncharted direction  . . . The drug companies periodically need some studies to bond the link between DM and CVD to keep the per capita consumption of antidiabetic drugs .

And the only fact remains  true is a good life style with physical activity  with peaceful pursuit of life  will keep the diabetes at bay . . .

So till that time we reach the reality ,  there is no other option  but to experience articles which add on to the  confusion rather than clarity .Read the latest metanalysis  about the link between DM & CVD  . . . and  I can assure you the confusion is  guaranteed

http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(09)60697-8/abstract#

Expect soon another trial , that contradicts the above trials conclusion  .

Title talk

So now  you can answer  the title question : Why we struggle to prove the beneficial effect of strict diabetic control on cardiovascular events ?

We struggle because  , the beneficial effect is so little or  even may be non existent !

Beware of non infarct q waves : A women with an unusual pathological q waves

Looks very much a infarct of  infero posterior territory is it not ?

Have a look at her 2D echo still picture . . .

Are you convinced ?

This women had normal LV systolic and diastolic function with no evidence of constriction.

The explanation for the asymptomatic pericardial thickening is due to a healed  chronic pericarditis .This sort of localised thickening in the posterior aspect is all the more likely following a loculated pericardial effusion.Tuberculosis is a very likely etiology.But this women do not have any markers for tuberculosis.Since she is symptomatic no treatment was offered.She is being followed up.

Discussion .

Q waves are not ” sacred waves” to diagnose myocardial infarction.It simply indicates the  direction of current flow is away from the  recording lead of the ECG .Any thing  electrically inert , that come in the interface between the heart and the recording electrode   can record a q waveWhat are the pathological entities that can produce q waves other than infarct ?

• Fibrotic myocardium(DCM-Cardiomyopathy)
• Myocardial Scars
• Myocyte dis array(LVH, HCM)
• Air,fluid in pericardium /pleural space
• Pericardial thickening (As in this patient)
• Electrical shortcircuits (WPW syndrome)
• Rarely pure ischemia without necrosis can produce q waves (Electrically stuned myocardium)

Final message

Localised pericardial thickening is  a rare  (?unrecognised) cause for pathological q waves , that may mimic a MI.

Let us clear the confusion about ventricular tachycardia :Is it a regular or irreguar tachycardia?

Ventricular tachycardia is the most common wide qrs tachycardia.It is generally taught VT is a  regular wide qrs tachycardia.It indeed appears regular most of the time but in reality it is not.

There are few  situations it shows irregularity . Of course , this irregularity may be due to the associated phenomenon ,  even as the VT focus  fire regularly. But for a physician what is manifested in the given ECG matters.

Frequent capture beats and fusion beats.

We know   AV dissociation is sine qua non of VT. Not withstanding this fact , the sinus impulses always try to enter into the ventricle and looking for the door at AV node to open.Even a fraction of a second is enough for the sinus impulse to sneak through it , the only question is the timing .It should be noted that an  intact VA conduction precludes antegrade AV conduction and fusion and capture beats are rare. So whenever the VA conduction lags behind or sluggish , more capture  beats occur.This obviously make  a VT irregular. This sort of irregular VT can occur in up to 20% .So it is indeed wrong to assume that the  presence of  irregularity one should make a diagnosis of VT.

VT induction phase cycle length fluctuations.

The other reason for VT may be irregular  during the early minutes after the onset of VT. Here the electrical circuit fluctuates till it attains a steady state.

The  VT often takes off  with a turbulent course (Bumpy myocardial boulders due to electrical reactionaries and mechanical scars ) Then the circuit optimises .This happens more so in post MI scar induced VT where the tract can be long and circuitous with considerable delay in conduction. But, once the VT reaches the cruising speed it becomes fairly regular. In ischemia mediated micro reentry or automatic focal VT cycle length variations are less common and they maintain the classic property of the VT namely the regularity.

Drugged VT: The Amiodarone effect.

The effect of class 1 a or 3 drugs on VT is a complex one.Either they revert to SR or it may reduce the VT rate, widen the qrs complex, and make it little irregular.This is especailly common after the cumulative amiodarone effect.

Polymorphic VT

The VT that has polymorphism obviously will be irregular.Torsades is the typical example.

Multifocal ventricular tachycardia(MVT)

Every one is aware of multi focal atrial tachycardia.It is surprising the MVT as an entity is rarely described in literature.Are the ventricles protected against such arrhythmia ? When multifocal VPDs occur very often why it is not transforming into MVT ? It is  possible , once a VT is  initiated it suppresses the other focus like a overdrive pacer  and extinguishes all surrounding electrical activity. But as in parasytolic tachycardia MVT can occur occasionally when  each focus is protected against the other by an entry block.

A VT may switch over from one focus to other.During the time of transition or competition between the two focus if you happen to record a ECG it can be really irregular  and chaotic !

Final message

VT is a regular wide qrs tachycardia  in majority.But this rule is applied only in monomorphic unifocal VTs. Even in monomorphic VTs there are  occasions it may show irregularity due the associated phenomenon.A grossly irregular wide qrs tachycardia always indicate a antidromic AF with accessory pathway.

* Title talks : With due respect to the  experts  ,there is no reason for getting confused .For the  practical working formula VT can be considered as regular tachycardia.

Cardiologists awake , lets us learn echocardiography right from the fetus : The link to excellent resources for learning fetal echocardiogrphy .

Fetal echocardiography is an important imaging modality for screening fetuses with congenital heart disease.Not all cardiologists are familiar with this imaging . Obstetricians are also not well versed in these techniques.So, finally,  it is left to few specialised radiologists to do this job. The issue here is  they are less  in number and the need for the experise is huge.  Further , the fetal cardiac hemodynamics and anatomy  are too complex to comprehend for a non cardiologist . So it is argued every clinical cardiologist to get trained in the basics of fetal echocardiography.

There are dedicated institutes and people who do this mode of imaging.

One such place is www.fetal.com

See for yourself the excellent information and knowledge resource in this site.

http://www.fetal.com/FetalEcho/04%20Standard.html

Other .popular books on fetal echocardiography

Julia A Drose

Simcha yagal

Juri W. Wladimiroff, G. Pilu

Lindsey Allan

When God performs a bypass surgery what is the chances of failure ?

Coronary artery disease is the major determinant of human  health and longevity  in this  modern era! Obstruction of a coronary artery either sudden or gradual  forms the basis of  CAD .

When a free flowing  river stumbles upon an  obstruction , it does not die , it finds it’s way to the sea. Similarly , God is kind enough to provide  alternate channels for blood flow to heart at times of crisis .Contrary to the perception , collaterals develop not only in chronic occlusions but also in acute occlusions.

A person who dies due to a primary VF few minutes after an acute occlusion is in all probability experiences his fate  ! While those who survive are protected by the immediate recruitment of collaterals and this prevents the   remote myocardium  from triggering a VF.

In chronic CAD, the collaterals are much more effective. Now we have evidence with OAT and COURAGE *trials for this. Some times , the LAD is fully supported by the RCA the flow is better than a graft.

*These trials showed us opening occluded coronary arteries routinely do not confer additional benefits.

Coronary collateral circulation is most poorly understood phenomenon in cardiology. But it comes as helping hand whenever required  only for those humans who deserve it !  God has kept the secrets of coronary  collateral circulation with himself !

A excellent article on natural by pass from circulation patient pages.

http://circ.ahajournals.org/cgi/content/full/116/11/e340

Link to related you tube video

http://www.youtube.com/watch?v=qQfUttiDgE8

What does the term junctional tachycardia mean in current era ?

Cardiac rhythm disorder remains  as a  fascinating  clinical cardiac  problem  to  the physicians for many decades. The joy of decoding cardiac arrhythmias and categorizing into supra ventricular , junctional, ventricular tachycardias is unique ,  even as  many of these patients are struggling for life !

Initially the tachycardias were labeled with reference to their origin .Later as we recognised the locating the  origin is not an easy exercise , we introduced a practical classification  : Narrow and wide qrs tachycardia  emphasizing the fact that , both SVT & VT  can be either narrow or wide !

Traditionally there is much more  confusion in labeling the  narrow qrs tachycardias than the wide  qrs tachycardia.

Is the term junctional tachycardia still relevant ?

To answer this question we need to know what exactly we mean by the term Junction.

• Is it a particular anatomical spot  called AV node ?
• Is it a diffuse area in the vicinity of AV node ?
• Is the early part of the his bundle included in the junction ?
• Or  Is it formed by  the entire rim  of both  AV groove formed by the fibroskeleton  that form a electrical  barrier between atrium and ventricle ?

Answer:

The answer to the above question is very simple “we don’t know yet !”

The nearest fact is , for the electrophysiologist,  AV junction refers to the electrical  junction box of  that connects the specialised wires coming down from the atria and from there it connects  to the specialised his purkinje fibres of the ventricle .

Is AV node  anatomically distinct structure?

No .It is not. It is a collection of different conducting cells with varying properties.The term AV node need to be abandoned by the cardiology community for the simple reason there is no such entity.

In fact the AV junctional cells are are now called as pure atrial,atrial approach CELS ,  junctional approach cells, junctional cells,transitional cells,  ventricular approach cells.These cells interdigitate with each other , and has unique cell to cell communication.The cells that are above the AV junction share atrial electrical properties while the cells that touch the his purkinje  acquire some of the properties of specialized ventricular conducting properties.

What is the function of AV junction ?

One should realize  it is the AV junction does a  a very unique job of great importance  for human   survival ! Even though SA node is the pacemaker of the heart , the AV junction does the extraordinary it receives the impulse and delays it for about 200 millisecond and then hand over it to the ventricle.

The rules that govern the  nature is so fascinating  , this delay is vital for the venous return to enter the ventricle from atrium other wise , the ventricle is under filled and cardiac output falls.The bulk of the PR interval is contributed by the AVconduction delay (also called as AH interval )

What is the clinical relevance of this new found physiology of AV junction ?

It is to be understood the electrical properties of the AV junction is determined by neural innervation the ionic currents.Much of AV junction is under the dominant control of vagal fibres, while the ventricles get more innervation from sympathetic neurones. There is considerable overlap in the AV junction area.

The classical dual nodal physiology of AVNRT is nothing but longitudinal physiological splitting of AV junction  .Strands of slow conducting cells and fast conducting cells are arranged in such a way to create a reentrant circuit.The atrial approaches in the posterior aspect contain mainly slow pathway. and anterior aspect near his contain the fast pathway.

Some times  clusters of AV junctional cells are scattered around the upper septal area giving a slow conducting properties to ventricle.These cells can be site for reentrant septal or fascicular VT.

The overlap of  these AV junctional cells explains the verapamil sensitivity of some of the VTs  arising in the vicinity.

What are the tachycardias that can be termed  as junctional tachycardias ?(JT)

By logic and realism  any tachycardia that originates in the AV junction either by reentry or ectopic activity shall be called as JT

By tradition , we have been illogical.

AVNRT is never referred to as JT  in spite of the fact that,   it is initiated by a pathological reentry right  in the middle of AV junctional tissue.

So currently we are authorised to call only few arrhythmias as true junctional tachycardia  .

• Non paroxysmal junctional tachycardia( NPJT)
• Incessant junctional tachycardia
• Permanent  junctional reciprocating  tachycardia(PJRT)
• Accelerated junctional  rhythm

NPJT

This occurs in following situations

• Digoxin toxicity(Classical description)
• Post operative hearts
• Occasionally during acute MIR
• It may be observed during AV nodal ablation in EP LAB

NPJT is an automatic tachycardia .arising focally from AV junctional tissue . Ideal terminology should be focal junctional tachycardia(FJT) .The rate is between 70 -140. Accelerated junctional rhythm can be termed as a benign form of JT.DC shock has no role.

Incessant junctional  tachycardia

This was first described in infants .Thought to be congenital in origin.Now adult forms also recognised.Very malignant arrhythmiaRate is between 150-300. AV dissociation is the norm.May mimic atypical atrial flutter or ectopic atrial tachycardia .High risk for tachycardic cardiomyopathy. Amiodarone may be effective.Surprisingly ,verapamil may worsen it .There is a overlap between adult postoperative NPJT and Incessant JT.DC shock is not effective may worsen . RF ablation rarely effective.

Permanent form of junctional tachycardia

It is not clear what the  term permanent denotes ! May be because   these tachycardias occur with fixed anatomical substrates.In fact this can be called as a type of AVRT. But the difference is the retrograde ventricular circuit does not travel in any free wall but within the septal his bundle   . PJRT,  infact  may be labeled as AHRT -Atrio hisian  recipocrating tacycardia

It is a reciprocating tachycardia with antegrade condction through AV node and retrograde through a slow conducting accessory pathway in posteroseptal location.

The rate is between 90-150. Mimics long RP tachycardia like AT or fast slow AVNRT.Some believe , In fact a fast slow AVNRT can be  nothing but a variant of PJRT.

DC shock may be effective only to recur again.RF ablation is very effective .

Final  message

Junctional tachycardias are a unique group of narrow qrs  tachycardias  with differet mechanisms.It is diagnosed in specific clinical settings. They are generally difficult to treat,as the mechanism is often ectopic in nature (Except PJRT).Accelerated junctional rhythm can be termed as a benign form of JT. AVNRT need not be confused with JT , even though it may considered as a junctional reentrant tachycardia.

 

Reference

Rosen Circulation 1973

The delicate relationship between D-dimer and aortic dissection !

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.

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.

What are the determinants of qrs width in ventricular tacycardia ?

Every one knows VT  presents as a wide qrs tachycardia  .Few of us ,   know VT can be narrow or even a normal qrs complex . But .none of us know what is the exact reason , why the width of  qrs complex  in VT swings from narrow  to wide.

Factors determining qrs width in VT.

• Origin of VT :Septal, freewall , apex etc
• Epicardial exit points make it wider
• Rate dependent Intraventricular conduction (VT with aberrancy a possibility ?)
• Drugged VT(Cumulative dose of amiodarone widens the  VT  )
• Associated LV dysfunction/Myopathy
• Electrolytic milieu (K + etc )
• Preexisting bundle branch blocks (Surprisingly common and still more a surprise some BBB  may convert  a VT from wide qrs to narrow qrs ) 

* Another unique , but common observation is  variation in qrs width between different leads.This again points to different exit points and tachycardia circuits traversing and looping around the epicardium to endocardium at different depths  from the chest wall leads.

The commonest explanation of VT being narrow is it’s origin near the septum and travel down the fairly physiological his purkinje tracts and resultant uniform depolarisation.While myocardial,free wall apical VT are bizarre and wide. We now know , many factors come into play in determining the  qrs width.In fact , we are only beginning to understand the complex conduction pattern of VT.