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Archive for the ‘Cardiology -Therapeutic dilemma’ Category

The ECG changes in ACS can be  “as dynamic as”  an occluding thrombus. The initial events include sudden total occlusion, early lysis, a trickle of flow, partial re-occlusion, reflow, no-flow, etc. The extent of transmural vs sub-endocardial ischemia, the competing force of re-perfusing vs necrotic wavefront, would define  ECG findings. This makes the ST segment labile in the early hours of ACS. This is also the basis of some cases of  STEMI evolving into NSTEMI and vice versa.

A 65-year-old man  presented to with this ECG,

 

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Does this ECG allow you to go ahead for thrombolysis? It actually looks like NSEACS with ST elevation in AVR suggesting left main lesion

The initial diagnosis of  NSTEMI was made, and hence thrombolysis was not considered. Even as the fellows were mulling over the diagnosis, one of them could find one more ECG available taken a few hours ago in another hospital.

It had something on it ,

img-20160423-wa0009_1_1.jpg

This ECG taken a few hours ago, shows ST elevation in 1 and AVL, and few VPDS in the chest leads unmasks the anterior ST elevation.

The moment we saw this ECG it was decided to go ahead with thrombolysis.The final ECG after thrombolysis with (Streptokinase) showed further stabilization. The question of thrombolysis in NSTEMI though not indicated in general, in selected situations we need to Introspect!

img-20160423-wa0011_1.jpg

How to manage a patient who presents as NSTEMI but had STEMI a few hours ago?

Four ways to ponder!

  • This patient should not be lysed as we have to treat the current event, not the past.  ,(Its NSTEMI and no need for lysis) Just heparin, dual antiplatelets. That will do.
  • One can go ahead with lysis as there is evidence for STEMI in prior ECG.
  • There is ST elevation in AVR even in the second ECG and so you have to thrombolyse !
  • “Come on guys, . . . don’t live in the primitive era of managing ACS in CCU . Forget the ECG take him to the cath lab , suck out all thrombus and deploy a stent and come out”.

* The last one , though appear practical (and most of us would love that ) is an unprofessional way of practicing cardiology. Management of ACS requires sound principles of ECG and its correlation with the Intra-coronary and myocardial pathology.

What happened to this patient?

He did well, free of angina with minimal LV dysfunction. He was discharged. Will be reviewed later, for further evaluation. This is a typical example of a patient with ACS managed successfully without entering the cath lab.(A forbidden practice and a potential coronary blasphemy )

Final message

ECG changes are as dynamic as the Intra-coronary blood flow in ACS. Multiple factors determine ST elevation or depression. While thrombolysis is reserved for STEMI,  NSTEMI has little or no benefit to accrue with thrombolysis. However, this is applicable only for de-novo NSTEMI  and may not apply for  STEMI in transition into NSTEMI as in the above patient.

 

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Answer  : I guess all mechanisms  contribute.Though E appears unlikely,  its backed by evidence (Ref 5)

Balloon pericardiotomy is done as a drainage procedure in recurrent pericardial effusion. It is actually a replication of surgical pericardial window by Interventional cardiologist.The window not only drains the effusion , it also act as a continuous drain. Though the  benefits are real (Pericardial fluid is shunted away from the pericardial space)  the exact mechanism of its benefit is not clear .

By concept , the catheter and  balloon should not cross the pleural space , (As pneumothorax may ensue) but still pleural effusion is a common consequence of this procedure .How is this possible ? One probable explanation is, the pleural space has some hidden communication with pericardial space .The other possibility is that, balloon creates virtual tissue channels  in the para-cardiac spaces of mediastinum .The extra-cardiac lymphatics does the drainage job without true shunting  pericardial space into the pleural space..

There is an article  from Annals of thoracic surgery which specifically   looked  into the  mechanism of benefit of  surgical pericardial window and came to a surprise conclusion, ie, it is not the continuous  drainage that keeps the space dry , rather it is likely the window  somehow obliterates the pericardial space permanently.(Sugimoto 1990,Annals of thoracic surgery )

Future  Innovation  : A technical add-on to  balloon pericarditomy  could be , delivering a covered stent across the pericardial space  into  peritoneal space like a VP shunt done by  Neurosurgeons.(If no body has done this , Can I claim the patency  for this  !)

The procedure

 

percutaneous balloon pericarditomy

Image used from Daniel A. Jones & Ajay K. Jain, Journal of thoracic Oncology , 2011

Risk of procedure

The procedure carries a definite risk especially  if done in an  emergency fashion. The aim of  procedure is two fold one to drain pericardial effusion second to prevent recurrence of effusion  .Since procedure carries  considerable risk  its to be performed  only in malignant effusion that are documented to be recurrent.

Surgical vs Balloon window  and other alternatives

Surgical window  creation is well known procedure , ever since Palacios (Ref 1) in 1991 described this per cutaneous approach as an alternative to surgery has become less popular. The risk of anesthesia and co-morbidity makes balloon pericardiotomy attractive. But surgical window creation still may have a role. A video  assisted pericardiotomy by thoracoscopy is also possible .Another option is injecting sclerosing agents into pericardial space .This time tested simple modality probably requires  more attention.

Need for subsequent pleural tapping

It should be realised this procedure may just  shift the  fluid from pericardium to pleural space. Some of them become significant effusion that requires pleural space drainage.

Concern of risk of dissemination of malignancy

Its a real issue , there has been instances of accelerated death after the procedure. Hence this procedure is a trade-of  between patient comfort and quality of life with a  potential risk of dissemination impacting  the longevity of life .

1.Palacios IF, Tuzcu EM, Ziskind AA, Younger J, Block PC. Percoutaneous balloon pericardial window for patients with malignant pericardial effusion and tamponade. Cathet Cardiovasc Diagn 1991: 22;244-249.

5.

 

 

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Dengue is a global infectious disease caused by Flavivirus  (RNA) transmitted by day biting mosquitoes Ades aegypti .It is primarily a tropical or sub tropical disease , India is marked  among the epicentre . 75% of dengue infections  are asymptomatic. Among  the remaining 25 % only 5 % develop severe dengue and a fraction of them go for a dreaded  circulatory and bleeding complication leading to a likely fatality.Severe hypotension is the hall-mark in dengue shock .

The mechanism of shock

The sine-qua non of dengue shock is the  capillary leak syndrome .This is due to some unknown vascular toxins acting in micro circulatory network making it exude fluid .This is something similar to septic shock where mal-distriubution of fluids in the extravascular  or third  spaces occur . This is also referred to as  re-distributive or vasodilatory shock due to lack of effective circulatory volume. Significant serous cavity effusions  (Both pleural effusion and ascites )  contribute to the shock syndrome .  Meanwhile there can be accompanying  fluid loss due to vomiting as well  .Adding further complexity ,direct cardiac involvement in few in the form of myocarditis can cause lung congestion and confusing the true mechanism of shock .This has important  hemodynamic implication as overzealous fluid therapy without recognising a possible myocarditis can be counter productive.Few sick patients will drag the lung into the vicious cycle ending up with ARDS , refractory hypoxia and worsening shock.

*To reemphasize , even though there are  multiple components  for dengue shock , the capillary leak  is the dominant theme .

Timing of shock

The onset of shock peaks after 24-48 hours of fever .It may  even be delayed well after subsidence of fever (Deffervescence phase )

Differential effect on diastolic and systole pressure

Dengue primarily drops the systolic  pressure  due to hypovolemia .The diastolic BP may be kept artificially high due the heightened adrenergic tone .This is ironical , as even the fluid  is sequestrated into dead  space patient may appear stable but it can fall dramatically without any warning once the sympathetic reserve is exhausted .This is the hallmark of dengue circulatory  shock .

*Note : Dengue shock typically  narrows the pulse pressure, that’s responsible for the feeble thready pulse.This is in contrast to septic shock* where the PVR is low, pulse pressure is either normal or even apparently high.(* Not all situations)

Clue from hematocit regarding the status of shock

Initially the heamtocrit  tends to increase  (hemo-concentration )  as fluid extravasates . Later it strikes a balance as we attempt to replenish with fluids. During recovery as fluids reenter vascular compartment or due to sustained fluid therapy the hemo-dilution can occur and heamtocrit  may fall.

How  common is  myocarditis  in  dengue fever ?

Fortunately ,dengue fever rarely affects the heart directly  .(Of course, shock can be a killer even without involving the heart) Myocardits due to dengue virus  is randomly reported in literature (Ref 3,4). My guess is , the true incidence should be far  higher as most of the dengue cases are from countries where publications are rare ! Bed side echo will reveal a minimally dilated Left ventricle with global hypokinesia  and moderate to severe LV dysfunction. No need to prove myocarditis  by virology ,biopsy etc. ( (New onset LV dysfunction with S3 , tachycardia is suffice) .Treatment is only supportive and Inotropic  agents may be helpful. Recovery in LV function is usually complete in those who survive.

Acute pulmonary edema though expected with LV dysfunction , overzealous fluid therapy can be a trigger for this complication . Involvement  of  conduction system is  another evidence for myocardial pathology. AV block  (J Clin Diagn Res. 2015 May; 9(5)  and Atrial fibrillation have been described in association with dengue.

Treatment

  • Anticipation and prevention of onset of  shock syndrome is  the key .
  • Careful monitoring of child is required.
  • Altered mentation is vital clue
  • Continuous fluid resuscitation is the only proven treatment .
  • Platelet infusion is required in clinical bleeding generally <10000)

Steroids, Immuno-suppression ,globulin have limited or no value  even in fulminant dengue fever .

Post-ample : Role of cardiologist in dengue shock .

Once , recently  I was called to see a child  with  refractory dengue shock .It turned out to be a helpless consult for the parents who had great faith in me .They believed  as a  modern day cardiologist ( circulatory specialist ?) with sophisticated devices I will be able revive the vascular system .I regretted ,there is nothing specific can be done ,the entire circulatory system is leaking and had lost its tone ,we have to wait ,watch and pray .

I realised on that day , how these tiny mosquitoes can expose us  . . . the  much hyped cardio vascular specialist’s  skills who live a celebrity life,hopping between cath labs , still unable to deliver at a critical time of need !

Reference :

1.Capillary leak syndrome in dengue fever.New Delhi: WHO Regional Office for South-East Asia and Manila: WHO Regional Office for the Western Pacific.Dec-2011

2.

dengue myocarditis

3.Kabra SK, Juneja R, Madhulika, Myocardiald ysfunction in children with dengue haemorrhagic fever.Natl Med J India.1998Mar-Apr; 11(2): 59-61
4.Wali JP, Biswas A, Chandra S,  Cardiac involvement in Dengue Haemorrhagic Fever.Int J Cardiol.1998 Mar 13; 64(1): 31-6.

5.Horta Veloso H, Ferreira Júnior JA, . Acute atrial fibrillation during dengue hemorrhagic fever.Braz J Infect Dis.2003 Dec; 7(6): 418-22

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A cardiologist  is  a physician who has  trained himself  in a special  way  to deal with any problem of heart.Ironically , it exists only on paper.The field has developed so vast  no one can master everything .There is no such  “Pan or global cardiology expert” .In fact it would be shortly become unethical to try to become one !

Pediatric cardiology  has developed into such a big field , doing a echo in newborn or  infant has become a comprehensive job and  requires  special talent .This unique  and excellent study from Narayana Institute , Bangalore published in the  prestigious Annals of pediatric cardiology   throws up interesting realities about the quality of echo report done by adult cardiologists in children .The error rate  appears  huge and stands at  prohibitive 38%. While many errors were minor , major  were also not insignificant (23%)

pediatric echocardiography by adults cardiologist

With bulk of the pediatric echo  involves  in the critical decision making  process of device closures and interventions the  data required  becomes vital .The commonest cause for  error is probably not due lack of  knowledge and but to due to lack of commitment and  continuous  exposure in doing echocardiograms in  those age group.

While this paper  decently skirts the issue of quality of pediatric echo done in medium sized hospitals without pediatric cardiology service ,I can say the error rates or inadequate reportage could be significant  in such hospitals  with apparently good ranking .

Final.message

Of course ,we have many  adult cardiologist who do  excellent  pediatric work , It looks like , as a general rule  performing pediatric echocardiograms  by non -institutionalized  adult cardiologist  may not be appropriate ! It may be wise for them to avoid doing echocardiogram in small infants with  truly complex disorders (even perceived  complex) till they gain the required expertise and confidence.

I recall an  adverse  issue happened years ago ,  when I had  missed an associated    PAPVC  in ASD that made my surgeon anxious on table .In a country like ours there is no one to audit our work , “our conscience remains the only option” to deliver the best for our patients  especially so, when they are tiny lives in distress.

After thought

Who am I to suggest  who should do echocardiogram ? , after all every cardiologist is licensed  to do that . One simple  suggestion  would be , if  not confident  they can at least mention in their report it is only  preliminary evaluation and need to be followed up with  an expert . I do that whenever its required  and gives me peace of mind as well !

More controversies* to come

Can adult cardiologist do pediatric intervention ?

* Controversy : One of the meaning for this word  is  “It is a thought  process  set into motion , that aids digging up hidden truths ”

Reference

 

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Brugada syndrome is due to a genetically  impaired  sodium channel activity  ( SCN5A)  in phase o, of action potential .This results in phase 1 (Ito channel) failing to inscribe the transition between phase 0 and  1 that result in loss of  dome .This loss of dome is dominant in epicardial cells compared to endocardial cells.This result in  electrical heterogeneity and a hence a voltage gradient in repolarisation phase  that can trigger a Phase 2  reentry mediated  VT /VF.The above said defects are either dormant, manifest, self extinguishing , dynamic  subjected to autonomic tone , ambient myocardial temperature (Febrile VTs) making this a complex entity.

There are three distinct types according to surface ECG.It can be either spontaneous or induced. The arrhythmic events and prognosis and hence management differs according to the types.

mechanism of brugada syndrome three types of ecg 2All types carry  a minimal risk of SCD , variable though . Of course  syncope  has to be  much more  common. Curiously every episode of syncope is seen as naturally aborted SCD by physicians ! (No one  to be blamed for this .The definition of syncope is like that !If the patient doesn’t wake from syncope it becomes death !).

When a patient with Brugada  has a  syncope , it  doesn’t  imply  he  experienced a dreaded VT or VF.While SCD is invariably due to ventricular fibrillation , a spontaneously terminating VF  as a cause for syncope is rare in Brugada . (Ref 2 : ILRs have documented though in few)

So what exactly is the cause for syncope in Brugada ? The issue is  real  and critical in clinical decision-making. We are beginning to document variety of mechanisms. Following are the possible causes

  1. Sustained  VT or NSVT with
  2. Non sustained self terminating  VF
  3. Extreme bradycardias (Vaso vagal )
  4. AV blocks
  5. Unrelated neurogenic

Final message

It is to be strongly emphasised a significant subset of Brugada patients especially in Type 1   Brugada (spontaneous or drug induced )  the mechanism of syncope is often not related to the dreaded VT/VF. It can simply represent high vagal tone and unexplained dynamism of autonomic activity .ICD is not a default indication for all those with syncope in Brugada syndrome.Think , pause and decide when you deal with such patients. ICDs are true revolutionary devices  . . . no two thoughts about it,but it can make a hell out of heaven if used in an inappropriate situation !

Reference

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Aorto ostial  stenting requires extra caution and special technique. It always  worry us  what if  few mm of  metal might project into Aorta when we stent a RCA or left main ostium.

To  prevent this ,Merit- medical  has innovated a catheter that help us position the stent exactly at the ostial level .It is  done  with a help of an octopus like buttressing arm that support the aortic wall when the stent is deployed .

Watch the video.

 

Reference

Merit-medical 

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Your clock starts  now !

 

clock gif  dr s venkatesan002

Chronic stable angina : Most can be effectively managed  by  optimal /intensive medicines and life style Interventions .About 10% will require PCI/CABG.

ACS – STEMI:  Primarily  managed  with  rapid and competent  pre-hospital care with prompt thrombolysis in or out of hospital .Patients  with  large STEMI who develop complications (Again about 10 %)   require PCI and few additional  lives can be saved.

ACS-NSTEMI : This is  the group that demand  an  important role for PCI . All true high risk UA/NSTEMI patients  should receive urgent coronary  angiogram and critical lesions  should either be stented or  sent for CABG  (If the lesions are multiple and complex ) The field of interventional  cardiology  is  expected  to play a major  role in  this category of  patients for the simple reason , we  not only give dramatic  relief from angina and also prevent a  potentially a huge MI that is waiting to happen !

* It is vital to emphasise  the “Aim and  objective” in  NSTEMI  management  is critically different from other two. We know ,  in CSA   the aim is to give relief  symptoms  and improve excercise capacity . Both PCI/CABG  are  unlikely  to prevent a future MI in CSA..In STEMI it has already occurred .The aim is to salvage myocardium  and prevent  future events. While PCI can do the former , it can’t do the later . In STEMI scenerio ,we have very good  alternate  modality called thrombolysis which can easily beat the  pPCI  in , cost , availability and time  (and  hence efficiency as well  in  most  countries !)

Counter thought

The above suggestion  is too simplified ,generalized , misleading , and  unscientific, should   strongly be disagreed. For those people who disagree , I provide an alternate scheme  .It is ultra short ,comes in  5 lines .Very practical  and  scientific too  !

In any  patient , who is  suspected to have either  acute or chronic  coronary syndromes ,take them to the cath lab in an  urgent or semi urgent fashion .Do an angiogram and stent all lesions  that you feel important . If  stenting is not possible  manage  with optimal medicines and /or send them to the surgeons.

Final message

The essence of catheter based coronary care is simple.We complicate it. To understand this concept  100’s of cardiology  journals  and as many conferences and infinite  number of books are churned out every year !

 

 

 

 

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Current guidelines advice us to wait for 40 days following STEMI to implant ICD in most high risk patients.

Why this  cool off period.? *

  • Essentially  we are waiting for the Infarct healing process to be completed.
  • By this time electrical stability may be restored. The  risk of VT/VF  declines per naturalis.
  • LV function recovery  is possible. As stunned and hibernating myocardium resumes its mechanical function and patient might  jump out of the MADIT-2  cutoff point. (EF< 30%)
  • Introducing  ICD very early  after STEMI may be a myocardial irritant and that it self can generate  arrhythmias.
  • There is a possible interference by the leads in the physiological remodeling  process.

Final message

So the cool off period is  not only to reduce  the unnecessary  ICD implantation  but also to  avoid lead related issues .

*  This 40 day rule is based on one  large study from Germany. (DINAMIT, 2004  ) . However  few believe  the rule is not absolute. There can be individual   exceptions in high risk patients with critical LV dysfunction .

Other  wise   . . . How do you digest  a death occurring on  35th day  in a patient  who is waiting for an ICD scheduled one week later ?

Reference

DINAMIT trial ICD nejm

Link to  ACC/AHA  Guidelines for ICD Implantation 2013

New development

How to bridge the 40 day gap in really high risk post MI patient ?

We can’t keep him in CCU. Here comes the role of WCD (Wearable cardiovertor defibrillator.) Life vest is  from Zoll . WCD can act like a bridge till the 40 days when the patient becomes eligible for ICD.

http://lifevest.zoll.com/

 

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As the medical care advances  human care  has taken the back seat. It is said super specialists  read more and more about less and less ! In the  process they  fail to see the  patients  as a single biological unit  instead as collection of organs .

While  organs in turn are looked as  pile of data.Hence the  treatment they provide lack the soul !

In the prevailing circumstances , how do we ensure  modern medicine  does not interfere with  these vulnerable souls,either to live in peace or leave in peace ?

Medical Ethics

Image : Source and Courtesy of http://illuminationstudios.com

It appears doctors are not at fault . The system is  biased towards raw science .Highly trained  doctors are tied down by  both  true and pseudo  scientific Intellect .Often  times they are compelled to do some procedure or interventions  just to  justify  the  premier status of the hospital  .While few do it  to show off  their expertise or  to impress  their peers   others are simply bound by rigid and obsessive  protocols and guidelines . Few others do it  for the burning  desire  of  scientific accomplishment .

One can offer hundred reasons for doing a procedure . . . but we always struggle to justify  with a valid reason for not doing a investigation or  procedure !

In fact , the  concept of appropriateness  criteria came out with good intention .But , it had failed miserably.

The irony is  . . . we need to indulge in something to avoid something.

Example 1 If homocystiene and  hsCRP vanish from the CAD screening industry   Adiponectin and Vitamin D3 comes in with a thunderous applause like a new Hollywood movie  !

Example 2: In cath lab  for leaving alone an insignificant  coronary stenosis , we have to do  another procedure  called FFR to satisfy  scientific ego ! (I know one senior doctor , who left a 80% LAD  lesion for medical management without FFR ( with all his clinical acumen )  was ridiculed for being unscientific !)

Here is a recent perspective article NEJM has discussed  this  important issue that plague us

Why should big  Tertiary  teaching hospital  are  flooded  with super specialists  which by default shun basic human care ?

Read this article*

Super specialist tertiary care hospital NEJM

*The article I have quoted  may  not  be completely relevant here  . . . It  answers  few of the queries raised!

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A STEMI patient arrives late after 48 hours with chest pain .There is  persistent ST elevation.

What is the likely mechanism of this chest pain ?

  • Index infarct pain continuing . . .
  • Post infarct Angina-IRA territory
  • Re-infarction following intermittent re-perfusion  and re-occlusion
  • Remote  ischemia from a branch of IRA
  • Ischemia from a possible  non IRA lesion in a multivessel CAD

If this patient  comes to a non PCI eligible centre. Will you lyse him  ?

If post infarct angina is  unstable angina  . Isn’t  thrombolysis  contraindicated in UA  ?

How to differentiate Post Infarct Angina from Re-Infarction ?

A very tricky issue indeed.

Unless fresh ST elevation with fresh enzyme peak is documented these entities  cannot be differentiated.

(Even  fresh ST elevation can be related to infarct expansion ,stretch or early acute remodeling.Fresh enzyme  release or new peak  may not represent new infarct always .It can be due to intermittent re-perfusion of IRA .It may  simply represent a  enzyme  flush from the index infarct zone)

What is the practical , realistic , (Unscientific !)  solution  ?

Why break our head ? Never bother to differentiate PIA   from Reinfarction  etc . Let  it  be any thing . Do a emergency CAG .Stent  whichever  lesion looks good  for the same . Of course , make sure he has enough insurance coverage .

 

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