Archive for the ‘cardiology -Therapeutics’ Category

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.


  • 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


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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When a culprit thrombus keep the  myocardium as hostage . . . don’t storm the coronary artery  indiscriminately   !

When a single gun men  keeps 100 innocent people as hostages , threatening their  lives, rescue mission should start .No can can afford to wait. But, without knowing  the  culprit’s true nature the process of rescue mission is always going to be tricky .There are so many instances Newton’s third law  was reversed , when reactions  evoke more chaos  than the index action.

In the recent world terrorist events ,  the  rescue missions  were so delicate and  it was very  unfortunate we  lost  many   innocent hostages !  The reasoning is ,there  is no way we can avoid these. I wonder is it really true ? !

rescue missionNot all culprit lesions  are true ones.They simply threaten  our myocardium with  thrombus and plaques  in various forms .Don’t show aggression to pseudo threats  you may  ultimately end up with more damage.(What I call as crazy culprits!)

(  Read here , why unstable angina even though thrombus is sitting right inside the coronary artery attempting to lyse it causes more  damage !)

After thought

Iam sure ,bulk of  the Interventionists wouldn’t agree with this thought . They would decry , watching a person  silently when the myocardium  is on  fire is a serious crime !

But . . . we  need to  remember the process of extinguishing  the fire  with some more fire arms is a delicate game played in undefined  philosophical turf.

The only way to introspect  such events in life is , to accept any eventuality    arising out of “not pursuing”  a  presumed rescue mission with vigor. No need to be guilty about that,after all , it can be a myth !

Modern human cognition , growing with a staple  scientific  feed  on a 24/7  basis  is  unlikely to realise , restraint can be an effective tool  even in critical moments !

Oh,is all that I have  scribbled so far  is just a repetition  of 1000 year concept of  “Primum non nocere”

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Every one talks about  coronary excesses ! It happens  both  in acute and chronic  fashion , not withstanding the inappropriately  understood  . . .   appropriately  released  guidelines  on inappropriateness ! The  burden  of coronary syndromes of the humanity, I am afraid would  include these man made excess as well !

I stumbled upon two  small  “gems ” in this other wise wild dark  cardiology literature  .One from Kamaer , Netherlands and other from  Escaned from Spain.

Both  talk about a  simple and logical modality in the management of STEMI . If bulk of the STEMI events are due to coronary thrombosis just tackle it  . No more  . . . no less” Stent only , if there is tight residual lesion.

1. From Amsterdam , Holland.

krammer thrombus aspiration alone priamry poba for stemi no stent

2.This one is from Spain.These studies I am sure , only a fraction of the interventional community would have read .Reason ? We are always hijacked by the moments of glamor ! I am just sharing them .hope few are benefited

primary POBA thrombus aspiration alone for stemi no stent stemithrombus aspiration alone for stemi no stent priamry pobaThese two studies with total number of 44 patients has a potential to redefine  the entire practice pattern of acute interventional coronary care.(Of course , if only , we are ready to make sense out of it !)

But , the concept will be heavily banished by strong visible and invisible forces   for the simple reason it suggests a true possibility  of knocking  out the role of  stent from acute STEMI arena.

When I discussed with my colleagues  for a large scale study  on isolated thrombus aspiration in STEMI , they told it  is not possible for ethical reasons !

I was amused , denying such a study is biggest ethical blow to the field interventional  cardiology !

Final message

Proof of concept does not require numbers .A study with less than 50 subjects  can be far superior than multi-centre ,multi-blinded , self steered ,peer reviewed largesse ! The truth of the study lies in the core consciousness  of people who do it , not in the numbers and exotic statistical methods !.

After all , one of the greatest medical study  was  done by James Lind  (Father of RCT) who discovered vitamin c as an antidote for scurvy,  with a hand full of sailors  while they crossed the Atlantic many centuries ago !

After thought

You say , thrombus aspiration is great , Why the hell , TAPAS , INFUSE AMI, and TASTE studies  confuse us regarding thrombus aspiration  ?

Don’t blame it on thrombus aspiration .We do it perfectly . It is because of what  we do after that ! We decorate the coronary lumen finally with a piece of metal cherry  undoing all the goodness of a great pudding !

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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 ?


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.



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Coronary artery disease (CAD)  is man-kind’s  greatest threat in modern times.CAD ,diabetes ,Hypertension, obesity, mental illness  has become an epidemic  even among the young !


Lifestyle diseases cad risk smoking alcohol

There is a simple solution for  lifestyle diseases !

Just  . . .  Remove style from your life !

lifestyle diseases coroanry cardiology medical ethics inappropriate stents over treatment excess medical care , bio ethics,

Instead . . . try to live like these  Tibetian villagers

life purpose of living

Final message

One study which researched all lives who crossed 100 Years  concluded something like this !

“To live a longer and healthy life* ,Get up early  , have a purposeful daily chore that must include a physical component , work with conscience ,love every one sync with the nature and  lastly and most importantly remove style from your life !

Choose  your life . . . It is simply there in your hand for grabs !


* Please note , Doctors  are never listed in the top with relevance to health of mankind  ! They simply cure some illness !

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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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