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Archive for January, 2009

Lignocaine , probably has saved more lifes  world over  than any other cardiac drug .

It was the only choice for ventricular tachycardia  till 1990s, both in pre and post  thrombolytic era.Every coornary care unit has reverted tens of thousands of  unstable VTs with this simple and cheap intravenous drug.the utility value of lignocaine is not limited to ischemic VT alone it is effective in in almost all forms of VT.It was classically administered in two or more boluses followed by an infusion.

What happened to this wonder drug  with great performance record ?

The  power of   statistics , and inappropriate interpretation by the scientific community  has left a serious blow to this wonder drug .Now the drug has been made redundant, and mainstream cardiac literature has made everyone feel  guilty , if  anybody  uses this drug for VT .

Why did lignocaine lose the battle ?  The reason is three fold

  1. The advent of  much fancied Amiodarone
  2. One negative study  for antiarrhythmic drugs in post MI period (CAST) 
  3. And two so called  positive studies  for Amiodarone (ALIVE & ARREST) has sounded the death bell for this drug  which has resuscitated millions of life !

CAST study http://content.nejm.org/cgi/content/abstract/321/6/406 

All , CAST  said was routine suppression of  asymptomatic ventricular arrhythmias  in the post MI period is unwarranted. But you know , how this  world interpreted it  “Lignocaine  has no role in ventricular arrhythmias in post MI setting ”  The most funny thing  was  lignocine was never used in CAST study .

The  studies involving one to one comparison  of Lignocaine and Amiodarone (ALIVE and ARREST study) was also not interpreted  properly.These studied only shock resistant VTs. What about the role of lignocaine where defibrillator was not available ?

Link to ALIVE and ARREST  read and make your own conclusion.

http://content.nejm.org/cgi/content/abstract/346/12/884

http://content.nejm.org/cgi/content/full/341/12/871?ijkey=8fa241f3cebb86a177632ec6ccadfb5a3ded7bc2

 Final message

  • Lignocaine is not  only a topical anesthetic  , it is powerful and gentle myocardial anesthetic when administered in post MI period.
  • With this property it  successfully cardioverts and prevents dangerous ventricular arrhythmias.
  • Time tested and worthiness proven.
  • While , we are made to believe  the success rate of  Amiodarone in VT is far superior than ligncaine .It is a falsehood.
  • Any experienced cardiologists will recognise ,  many times even  Amiodarone resistant VTs often respond to Lignocaine .
  • The fact of the matter is , without a good quality  one to one study  , lignocaine was ditched. One reason for this could be  Lignocaine ,  is a generic drug and has no market value.

Let us take home , the message (scientific or unscientific ! ) Lignocaine still has a great role to play in the management of dangerous ventricular arrhythmias .The only caution is ,  it should not be used routinely and indiscriminately in all asymptomatic patients with  VPDs or nonsustained VT . (Acknowledging CAST conclusion.)

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Cannon waves occur classically, during  ventricular ectopic beats .(Commonly irregular) regular cannon waves occur during Junctional tachycardias with 1:1 VA conduction

Cannon like wave may appear  in the jugular vein if the VPDs is timed in a such a fashion ,the atrial systole occurs with a closed AV ( Tricuspid and mitral valve ) so the atrial  contractile wave is reflected back into the veins.This not only happen in right atrium but also  in the left atrium , but the cannon waves are sent into the pulmonary veins , which is not visible. As by  tradition  cannon waves are  meant to be seen only in neck veins , we rarely realise   the importance of such waves in the pulmonary veins.

There must be some significance for this  abnormal pulmonary venous waves  which  travel  in a retrograde fashion.In fact , with  the advent of echocardiography, we realise  pulmonary flow reversal is an important contribution for raised PCWP.

The dyspnea during multiple  VPDs can be due to

1.Transient Mitral regurgitation and resultant elevation of PCWP.

2.Pulmonary venous cannon waves and  it’s effect on  J receptors.

3.Many of the intermittent  episodes of  dyspnea  (Especially paroxysmal nocturnal dyspnea ) , other wise unexplained could be due to this pulmonary venous cannon waves.

4.It also need to be studied how this pulmonary venous cannon waves distribute themself into the 4 pulmonary veins.

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Angina is classified in many ways .The most useful , clinical classification is stable and unstable angina . While  ,the former generally is considered   innocuous  the  later conveys a sinister  signal to the patient as well as  the physician. 

Why stable angina is  stable ?

In stable angina

  • The patient knows how the pain is going to behave by his past experience.
  • Very predictable .The patient knows at what distance it’s going to come
  • He also knows when  it will disappear.(For some , with rest for others with nitrates)
  • He also knows where the chest pain will radiate.
  • If some thing is unusual it is unlikely to be  stable angina , also any  first episode of angina is considered unstable as one wouldn’t  know how the angina is going to behave !

How is that stable angina has such a learned behaviour ?

The main reason for  the beningn nature of  stable angina is the coronary artery has “stable plaques”

Stable plaques produce stable angina  ,Unstable plaques cause unstable angina

Stable plaque s restrict blood flow only at times of  increased demand( ie supply side ischemia.) There is no thrombus in these plaques.As soon as the exertion ends the angina is relieved.So in chronic stable angina, the patient is stable, the angina is stable , the palque is stable , the coronary blood flow is stable.

Unstable palques have erosion and thrombus , and it interferes with blood flow even at rest .So in  unstable angina, not only the angina is unstable , the plaque is unstable  ,coronary blood flow is unstable. So it is obvious unstable angina , may not be relieved by bed rest.It needs intensive treatment.

Is there a overlap between stable and unstable angina?

Yes. In fact it is more common than we realise.

Read this post http://drsvenkatesan.wordpress.com/wp-admin/post.php?action=edit&post=2177

Related topics

How is a stable palque converts into a unstable plaque ?

How do you identify these vulnerable plaques ?

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                                    Competence of mitral valve is vital  for proper hemodynamics of  heart .A trivial mitral regurgitation ,is observed in nearly 10-20% of normal population detected by doppler echocardiograpgy .This is other wise clinically insignificant. In fact , it is expected  , the sonographers do not report this,  as it might increase the patient anxiety.

Can a mildly incompetent mitral valve be a hemodynamic advantage ?

Left ventricle , physiologically can have only one exit, namely LVOT and aortic valve.If there is normal  impedance , at this level (LV after load )  it  is refered to as  physiological .In disease states , as in cardiac failure there is raised after load or LV wall stress.this makes the LV struggle to pump blood into aorta.The more the dilatation the more the wall stress (Laplace law). more the wall stress more the after load.

 The  main principle of management of cardiac failure  for decades  has been promoting  LV inotropism .Now we have realised this is fundamentally a wrong concept, (Except in acute heart failure). Hence the main option available now is to reduce the after load , ACEI do that most effectively and proven to improve survival.

What is the effect of  trivial or mild MR on LV after load  ?

It is a hemodynamic fact for MR  to increase LV contractility  and Dp/Dt  due to a relative reduction of after load.

In patients with cardiac failure , even a mild improvement in LV contractility can give a  symptomatic improvement .

 

09tmr1

Can mitral valve act as controlled safety valve allowing only a trivial or mild MR ?

This may be difficult . But it happens naturally in many of our patents in cardiac failure .

Probably , these are same  patients who come under the 20% incidence of physiological  doppler  MR .Other group could  form the  functional MR*

We have found, patients with  DCM  with mild mitral regurgitation tolerate excercise better than patients who have very competent and rigid mitral valve.It is presumed a mitral valve which gives in a little bit , decompresses the LV with a symptomatic benefit.But if the MR , is occurs in an eccentric path or it results in significant volume burden the potential advantage becomes a liability.

Related issues

*Functional mitral regurgitation. Functional MR is said to occur , when patients with cardiac failure, and resultant dilatation of mitral annular ring, and lack of opposition of leaflets

While milder forms of MR are well tolerarted  , when it occurs  acutely ( even if it is mild) ,  it can be dangerous and result in sudden pulmonary edema  .This usually happens in acute MI or infective endocarditis etc.

 Final message

  • Minimal or mild  mitral regurgitation without any significant volume overloding  in some of the patients with dilated cardiomyopathy  could bring  a hemodynamic advantage .
  • So one may not unduly worry about , a mild MR (central jet) in patients with DCM.It could be after all a safety exit for overstrained LV

We will report the results of the ongoing study about the impact of presence /absence    of  mild MR on the 6 minute walk test in patients with dilated cardiomyopathy.

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  • Gastric pain is a great mimicker of cardiac pain.
  • It may have , almost all the typical characters of angina . . . in some cases ECG changes too.
  • The confusion is complete ,  as esophageal pain can also  be relieved by sublingual nitrates !
  • The issue is further complicated, when  esophagus and coronary artery share  the same neural codecs, and each may induce spasm among themselves !
  • It is thought , of course with  some  evidence !  many of the syndrome X  patients ( positive stress test with normal coronary arteries )  have esophageal motility disorders.
  • The ST segment depression during EST  in these patients  is apparently attributed to  stress induced esophageal spasm !
  • And many of the patients with variant angina  ,  have associated esophageal sapsm .

Read this land mark concept paper  documenting the neural link between esophagus and the coronary artery

Click on the article

esophagus

 

Final message

  1. Don’t ever forget the esophagus in your scheme of things when evaluating  CAD.
  2. Realise  that esophageal disorders  not only cause non cardiac pain but also cause    ischemic chest pain (Also called linked angina)
  3. EsophagEal  smooth muscle cell  can  exert electrical influence on the ST segment of  cardiac ECG !(After all every cell

has an action potential )

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                                         Coronary arteries are the major site for human atherosclerosis .CAD is considered the ultimate determinant of  cardio vascualr health of our global population.Coronary atherosclerosis has a predilection for proximal sites and branching points.Typically it occurs in leftmain, LAD ostium, LCX ostium, proximal LAD, diagonal origins, OMs RCA  and its branches .

4010940_766_gr1

Septal branches , even though divide very early  from the LAD , it  is  uncommon  to get affected by coronary atherosclerosis.  Even for an experienced   interventional cardiologist  , it  would be very rare to have  performed a  PCI for septal disease.

Why septal branches of LAD is rare to suffer from atherosclerosis ?

We don’t know the answer yet.

But , it is thought,septal branches are near perpendicular branches .The branching angle and incidence of atherosclerosis has a peculiar relationship.IAt any bifurcation  point , the atherosclerosis tend to occur ,  if the angle is more acute , and is  less common in abtuse angles .It is  almost rare  ,  if branching happens at   exact  90 degree angle or so !

The other reason for septal branches being immune to atherosclerosis is  , it runs within the muscle in its major course. The constant squeezing action(. . . and possibly bridging also)  makes it difficult for the  process of atherosclerosis to sustain and grow .

Can you still get a  septal CAD ?

Yes,  usually as  a component of bifurcation or trifurcation lesion. Some times a diagonal and septal are very close together and  atherosclerosis involves  both ostia.

What is  the implication for the  cardiologist to perform  a PCI with stenting in a septal branch of LAD  ?

PCI and stenting in the septal branches are more prone for crushing and fracture   as it is constantly exposed to the mechanical effects of muscle contraction.

Any other significance for septal branches of LAD ?

  • Isolated septal myocardial infarction can occur.This could be even a embolic manifestation.
  • Septal branches of LAD are potential target for therapeutic embolisation (By injecting alcohol)  in patients  with hypertrophic obstructive cardiomyopathy(HOCM) .This manover aims to produce a controlled septal myocardial infarction and thus paralysing the left ventricular outflow tract and reduce the dynamic LVOT gradient. This form of treatment, was glorified till recently now considered experimental !

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                                       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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