Advertisements
Feeds:
Posts
Comments

Archive for August, 2015

Coronary care units are the place, where acute myocardial infarction patients are housed. Thrombolysis is still the primary modality of treatment world over .Large infarcts, ,  impending or established cardiogenic shock are major source for mortality .

Acute  left ventricular failure (LVF ) in CCU has to be swiftly managed in whatever phase of MI .Standard regimen of sedation, diuretics, Nitro glycerine, and Dobutamine are administered are often not good enough  .( Its true  many of these patients are to be taken for emergency PCI ) Still, medical management of LVF has a huge impact on the outcome.

While cath lab  procedures are given top priority , I have seen many times, simple concepts in CCU not getting proper attention.Continuous positive airway pressure(CPAPA/Bilevel-NPPV) aided  oxygen administration has a critical role to play in this setting.

  • It reduces the work of breathing
  • Opens up wasted Vp/Vq zones in lungs
  • Interstitial gas diffusion is facilitated by keeping the respiratory units
  • Keeps a check on the LVEDP from going to very high levels in an indirect fashion (Lung helping heart !)

Why not Intubate these patients ?

It’s true Intubation and ventilation may be required ultimately in many of these patients. .It has its own issues of prolonging the stay and infection .

Final message

Even though the clinical trials do not show consistent  impact on long term survival , we have time and again found this modality useful .Timely administration of of CPAP definitely halts the progression of mild forms of LVF to full fledged cardiogenic shock and leads to recovery in many .

CPAP/Bilevel-NPPV is  important hemodynamic stabilising tool , that should be used liberally whenever possible .

Reference

There has been number of studies exploring the role of CPAP in acute LVF during STEMI.

Advertisements

Read Full Post »

A land mark concept , that changed our understanding about the mechansim of genesis of Atrial fibrillation happened  in the year 1998 .( Haïssaguerre ,Spontaneous Initiation of Atrial Fibrillation by Ectopic Beats Originating in the Pulmonary Veins N Engl J Med 1998; 339:659-666). He proved AF originates in specific focal points from the pulmonary vein ostia at its draining point in LA.Even though there only few selected focal points it was difficult identify those and hence empirical RF ablation of all 4 pulmonary vein became a standard practice. 100s of thousand of these invasive procedure were carried out in patients with chronic AF.

Now, in a span of 10 years , we realise many of these patients require second or third siting of ablation.The irony is , there are many non pulmonary connections  that require repeat ablation.

Common mechanism for recurrences are

  1. Inadequate first ablation
  2. Reconnections
  3. Inflammation and fresh scars
  4. Additional venous focal  sites (coronary sinus  ,SVC, Vien of marshall)
  5. Multiple mechanisms /*Non- focal , systemi AF mediated by neurohumoral triggers ?

A study from the prestigious JCE in May issue of 2015, reveals a starling fact , that about 50% of AF patients  have additional connections  other than pulmonary vein that require ablations at a future date.

If proven right ,  just wonder how much of knowledge and its dissemination  , efforts from  EP industry , technology transfer  over the years is threatening to become redundant .Let us hope,we will somehow conquer the AF either electrically or pharmacologically.

pulmonary vien ablatioan atrial fibrillation carto non pulmonary vien connection

A strong message comes out from this. In modern science, one need not be unduly excited about a new breakthrough.Proof of concept will have to overcome the ultimate test , ie time .

Read Full Post »

We essentially live in our blood vessels and age in our arteries.CAD is the principal  cardio vascular disease, which  God has created in Homo-sapiens to ensure they  do not stay more than “allotted life span” in this planet. Of course , the current generation cardiologists equipped with scientific weapons , have since decided to take the fight directly in the Almighty’s domain .Contrary to the popular medical doctrine, treating an established CAD seems to be easier task than preventing a new onset CAD.

While , arteriosclerosis is a normal aging process, atherosclerosis could be an  aging as well as a distinctive pathological process. However , athero-thrombosis  is a definite pathology of vessel wall .We know at any time atherosclerosis  can transform into  athero-thrombosis  and result in  clinical event depending upon the  triggers and other associated conditions, which we refer to as major or minor  risk factors.

In scientific terms ,

  • Primary prevention  of CAD is preventing first episode of  Coronary  event*(Typically , CSA, STEMI/UA,NSTEMI/SCD,)
  • Secondary prevention  is  prevention  of  second  or subsequent episodes following the first clinical event.(*What if , if  the first event is silent and never known ? )

For all practical  purposes CAD and  coronary atherosclerosis is synonymous. Can we  prevent atherosclerosis in human biological system ?  What are we  supposed to refer to  such a preventive measure , if any ?

We are biased towards obstructive CAD as we often  think it is the  the only form of CAD .Then , how do we diagnose , treat and prevent a minimal non flow limiting plaque , coronary endothelial dysfunction , or  acute coronary erosion that can occur in very early stages of atherosclerosis, in other wise healthy persons.(Routine IVUS ,OCT ? Futile isn’t )

  • Preventing  sub-clinical  CAD  from manifesting  as clinical CAD , is technically   primary prevention”  but still  patho-biologically  secondary prevention.
  • Preventing a CAD in a patient  with peripheral vascular  disease  or preventing CAD in a patient with TIA or stroke is secondary prevention for cerebrovascular disease but  falls within the definition  of primary prevention of  CAD.
  • Then  comes the new semantics :Primordial prevention .This could be same as primary (or another  version of primary prevention ).Primordial prevention is preventing development  the risk factor  itself (Like DM,HT, Dyslipidemia )

So ,whenever , we talk about primary prevention of CAD by Aspirin or Statins ,realize the complexities involved .Before i finish, let me make you  dizzy further with this quixotic one . In a multivessel CAD, as the  atherosclerotic  plaques are scattered across the coronary arteries in various stages of  maturity  , long term Aspirin  following  anterior STEMI has to secondary prevent an event  in LAD territory  . . . but   primary prevent a plaque disruption in RCA territory !

Reference

1.USPSTF Guidelines : Aspirin for the Prevention of Cardiovascular Disease: Preventive Medication

Read Full Post »

TAVR is the new state of the art Aortic valve replacement procedure done by cardiologists .Nearly 200 thousand implants have been done , and it is
backed up by major trials TAVI TAVR valve dislodgement embolism partent a b What keeps the Aortic prosthesis in situ in the aortic root/Annulus  ?

The valve is not actively fixed but passively positioned in aortic root by either self expanding or balloon expanded valve  system .It retains the position by two different forces acting on the valve in two difffernt directions , but work coherently to keep the valve static .The radial force of the hardware is centrifugal and the elastic force exerted by annulus is centripetal .It may appear mysterious how these oppose each other in a balanced way and arrest the valve in the desired site. Fortunately, there is little  supero- inferior force operating and hence the chances of dislodgement is low .It should also be mentioned we are not yet clear about the best site for TAVR. Annular , supra annular ,or is it at lower virtual annulus , all has some advantages and disadvantages.

Is progressive aortic annular dilatation possible in these degenerative aortic valve ?
Aortic stenosis is chronic degenerative disease. Generally we expect the annulus is narrow and fixed. However for some reason if the aortic annulus loses it constricting force or the root dilates or fresh calcium deposits, there is definite risk  (Not theoretical :See Reference ) of valve destabilisation  , dislodgement and embolisation . *It is vital to understand the para-valvular leak could be a  remote precursor of such potential dislodgement as it represents  micro gaps  in the prosthetic / tissue interface.

How many such  embolisation of valves  are reported following TAVR ?

While the incidence of para valvular leak is common ,(up to 20%) fortunately valve embolisation is reported between .3 to 7.5% (Ref 2). Stastically , subclinical   destabilisation, malpostion  and dislodgement should be more common. The timing of displacement is not clearly reported in literature .It can occur  at any time between few hours after implantation to a much delayed (months after ) complication .

Final message

TAVR is a major break through in Interventional cardiology .It gives us hope for possible TAMR (mitral) and other valve repair modalities .Though dislodgement of prosthesis appear a rare event it is tempting  to ask ,  whether we should work towards a actively fixing valve in aortic root ? That remains a open question !

Reference

1. A survivor of late prosthesis migration and rotation following percutaneous transcatheter aortic valve implantation. Pang PY, Chiam PT, Chua YL, et alEur J Cardiothorac Surg 2012;41:1195-6.

2.Thirty-day results of the SAPIEN aortic Bioprosthesis European Outcome (SOURCE) Registry: A European registry of transcatheter aortic valve implantation using the Edwards SAPIEN valve.Thomas M, Schymik G, Walther T, et al. Circulation 2010;122:62-9.

3.Migration of the transcatheter valve into the left ventricle Christopher Cao , Su C. Ang , Michael P. Vallely Mart Annals of Cardiothoracic Surgery Vol 1, No 2 (July 2012 4.Delayed Transcatheter Heart Valve Migration and Failure Vuyisile T. Nkomo, Rakesh M. Suri, ,J Am Coll Cardiol Img. 2014;7(9):960-962.

Read Full Post »

TGV is the most common cyanotic heart disease to present at birth.The outcome is dismal unless it is intervened at the earliest .It becomes a real  emergency if the dTGA is associated with intact IVS and IAS. (Though foramen ovale /ductus  may help for a while prolonging the survival . Often times , it is restrictive and demands immediate septostomy if primary arterial switch correction is not attempted )

Presence of VSD provides vital time interval to plan  surgery in a less emergent fashion. Otherwise , arterial switch if  contemplated one has to do it before 2-3 weeks (Rarely up to a month ) .The principle is to reverse the circulation before the  systemic left ventricle regress its myocyte function as it is exposed to low pressure pulmonary circuit .

Hemodynamics

We know , dTGA  has two parallel circuits in a bizzare hemodynamic disconnect .The right sided  pulmonary circuit sustains  the systemic blood flow with deoxygenated blood.The left sided systemic circuit recirculates oxygenated blood into pulmonary circulation again and again.

Survival depends upon , the anatomical communication between two circuits and the effective quantum (Deoxygenated)  of blood flow to the lungs .

Which communication is best for survival d TGA ?

The key is to understand   what we mean by “mixing  vs  shunting”  and the effective pulmonary blood flow (ie quantum of truly deoxygenated blood reaching lungs  vs oxygenated blood recirculating  the lungs in a hemodyamically wasted loop

It appears both atrial  ventricular level  mixing is good for maintaining adequate O2 saturation than PDA .

What does PDA do ?

Ductus is expected to persist in  dTGA  when  IVS and IAS are intact  . It is not clear  what determines the persistence of duct  in dTGA with intact IVS. Principles of natural  hemodynamic adoption would argue , all patients with dTGA should never close their ductus and foramen ovale. While , In reality it may be true for PFO to persist, ductus often gets closed on schedule* , aggravating  the hypoxia .(Both flow mediated myogenic resposne, O2 content of ductal blood and size are the determinants of ductal closure)

The ductal circulation in dTGA can be complex . It initially  acts as a channel to mix both arterial and venous blood flow .It can become a liablity  if its large , as the pulmonary vascular resistance falls,  blood is shunted from aorta to pulmonary circulation and potentially precipitate failure .Please note,  this shunting  also can  improve  the saturation as it diverts aortic blood into lungs ,still the ultimate usefulness will depend upon intermixing  at some other level  other than ducuts , ie either atria  or ventricle .One should  realise  ductus can never bring  good admixture as it happens outside the heart .It is obvious intra cardiac  mixing  with ASD and VSD  is always better and devoid of providing differentially saturated blood  to the extremities  , which is an inherent feature  PDA mediated  mixing .If ductus  is the only means of mixing and shunting  the lower half of the body has  an advantage as it is perfused continuously by oxygenated blood .This  may manifest as  reversed differential cyanosis in few combinations of TGA physiology. (Relatively pink  lower limbs and cyanosed upper extremity )

Summary

Ductus can be a double edged friend or single edged foe  in dTGV . It depends upon the size , quantum of shunt and associated  channels of mixing like ASD and VSD . If it occurs with  intact IAS and IVS it plays a role of  life sustainer.

Presence of ductus is definitely useful  initially.It can either help by mixing, intermittent bi-drectional shunting  or committed left to right shunting .This is why we attempt to  preserve its patency or even recannalise it by stenting  in such situations .The later can be used to buy time and train the regressing LV .However ,large ductus can be counter productive  if additional shunts are also present where one should even contemplate closing it .

Reference

1.

pda in dtga ductus ductal flow in tga2.Transposition of the great arteries with intact ventricular septum and patent ductus arteriosus. Waldman JD, Paul MH, Newfeld EA, Muster AJ, Idriss FS.Am J Cardiol. 1977 Feb;39(2):232-8.

Read Full Post »