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Ectopic beats or premature depolarisations are the commonest  cardiac arrhythmia encountered . Human heart , is a  non stop  electro mechanical organ ,  and it is not surprising   ectopic beats are so common  and can literally originate  from every cell of heart. But , generally it   emanates  primarily from  the special conducting cells . At times  ,  even  other cells (Myocytes, interstitial cells )  can generate abnormal electrical potential.These ectopic electrical potentials  can be compared  to  electrical load shedding when there is excess electrical strain .

Vast  majority of ectopic are benign  in human population. When this occurs ,  in the milieu of underlying heart disease or during ischemic  episodes they become clinically important and initiate a sustained arrhythmia.

Classically and traditionally ectopic beats are described in the

A.Ventricle :      Ventricular premature beats, (VPD)

B.Atrium:             Atrial premature beats(APD)

C.AV junction : Junctional premature beats.(JPD)

If you note , one important structure is missing from the list.

Yes , it is  SA node.  Can it result in premature depolarisation ?

When do you suspect a SPD(Sinus premature depolarisation)

  • It manifests a  an sudden unexpected , sinus beat exactly as the previous sinus beat. Followed by a pause.
  • The P wave morphology exactly is similar to prior p wave.
  • Many times we miss this entity as we tend to over  diagnose APD than SPD.
  • SPDs tend to occur in bigeminy rhythm.

Differential diagnosis

  • Sinus arrhythmia and pause
  • APD
  • SA node echo beats (Part of SA node reentry)
  • SA blocks

How do differentiate  a sinus arrhythmia from sinus premature depolarisation (SPD ) ?

Sinus arrhythmia occurs in a baseline bradycardia environment.

It does not not come as   “on -off ” pattern . It has a gradual onset offset dynamics.

Clinical significance

This is a clinically unimportant arrhythmia* .This  is probably the reason , it is not a popular concept .

*But it can confound in the diagnosis of  , other important rhythm  disorders.it could be a expression of  sinus node dysfunction and a precursor of  inappropriate  sinus tachycardia The significance could be substantial in atrial triggered  based  pace maker rhythm

Final message

When you confront an unexpected , early , sinus beat not accountable to sinus  arrhythmia  or APD

suspect SPD.It is  not rare , it is a  grossly under diagnosed entity.

Reference

Sinus premature systole  http://www.chestjournal.org/content/64/1/111.full.pdf?ck=nck

Pacemaker rhythms  result in classical ECG with  LBBB morphology.It is a universally understood  fact that  RV pacing would  produce LBBB and LV pacing a  RBBB pattern in surface ECG.As with any other rules in medicine , it is not 100%  perfect .(May be 70%)

In the process of oversimplification of rules  we have forgotten a simple fact , that is, interventricular  septum is  shared by both the ventricles . ( functionally and electrically )

In due course , cardiologists and electrophysiologists  have  recognised this fact. A pacemaker lead hitching on the IVS  can behave independently and disobey this  golden rule of pacing.(RV-LBBB,LV-RBBB). Depending upon the orientation of the lead and the pressure it exerts  on the tissue  and degree of penetration of the screwing lead into the septum, the resultant   ECG can  either have a complete RBBB pattern ,  partial RBBB or partial LBBBB or combination of both.

Can RBBB pacing be stable ?

Yes.,  provided the the fixity of the lead and other parameters like impedance and pacing threshold are good.

Before labelling RBBB pacing as safe one should rule out pathological RBBB pacing like septal perforation and

accidental entry into LV through foremen ovale.

Is coronary sinus pacing an acceptable alternative  for  long term permanent pacing ?

The answer is generally ” No ” ,  but it needs rethinking.

A coronary sinus pacing may happen accidentally.The leads get located  either in the main stem coronary sinus or it”s tributaries.the morphology of ECG depends upon the branch it enters.Leads when they reach LV aspect result in RBBB morphology.

Can  we do intentional coronary sinus  pacing for complete heart block ?

There are many accepted  references in literature  that terms   RV pacing as unphysiological and has high risk of precipitating or aggravating cardiac failure. So currently , alternate sites of pacing are explored.( Septum, his bundle , biventricualr etc)

It is an irony , in this era of cardiac resynchronisation therapy where we do coronary  vein pacing  , the same concept is not being tried for regular  permanent pacing in special and difficult situations.( Severe TR, Left sided SVC, AC canal defects etc)

Final message

  1. RBBB morphology following  permanent pacing  need not elicit a panic reaction provided all parameters are stable.
  2. In patients  with difficult RV anatomy* ,  who need permanent pacemaker implantation a modified  coronary sinus pacing can be a solution .But as of now no such speciifc leads are available.EP Industry should take a note on this .

*Epicardial pacing is an option in such situations .But it requires surgery.

Ref:

Safe right bundle branch block pattern during permanent right ventricular pacing Journal of ElectrocardiologyJanuary 1, 2003   Yang, Yung-Nien ; Yin, Wei-Hsian ; Young, Mason Shing

Yes , we can .         Abstract : Link to Indian heart journal

b1

Vegetation Negative Infective-Endocarditis

S Venkatesan, G Gnanavelu, G Karthikeyan, V Jaganathan,  R Alagesan,
M Annamalai, S Shanmugasundaram, S Geetha, A Balaguru, G Anuradha

Madras Medical College, Chennai


The definitive diagnosis of infective endocartitis (IE) remains a contentious clinical issue. Many diagnostic criteria have been advanced. However, none has withstood the test of time. Currently Duke’s criteria is considered as de facto standard. Documentation of vegetation within the cardiac chambers and positivity of blood culture is the sine qua non of IE and evidently they constitute the major criteria. Ironically, according to Duke’s criteria, IE could still be diagnosed in the absence of vegetation, provided it fulfils other major criteria of culture positivity. In this context, we report our analysis of patients with IE without vegetation. Out of 24 patients admitted between 2004-2005 in our hospital with the diagnosis of IE, 4 patients failed to show vegetations. All had rheumatic heart disease (RHD) and presented with prolonged fever. All had severe eccentric mitral regurigitation (MR). One had severe aortic regurgitation (AR) also. One had flail posterior mitral leaflet (PML). All had blood culture positive – 3 for staphylococcus auerus 1 for pseudomonas. None had vegetations on the first echocardiographic examination. Transesophageal echcardiography (TEE) also failed to detect a vegetation or abscess. The diagnosis of IE was made on the basis of Duke’s criteria (1 major and 3 minor features). Treatment was started based on culture positivity and sensitivity. All patients underwent serial echocardiography every week for 6 weeks. New mobile vegetation was detected in 1 patient in anterior mitral leaflet (AML) measuring 12 mm after 2 weeks. Three patients never showed any evidence of vegetation. One patient developed cerebral vasculitis and another renal insufficiency during the course of treatment. Two patients stabilized with medical management. One expired and other had refractory cardiac failure and was referred for emergency surgery. The mechanism of absence of vegetation in IE could be varied. Simple temporal dissociation between appearance of vegetation and the clinical syndrome should be the first possibility. Further, vigorous antimicrobial treatment might have prevented the formation of vegetation. But, as we have seen in few patients, it never appeared. This was possibly due to layered vegetation like that of a thrombus on the surface of the valve or adjacent myocardium. The process of vegetation formation need not be endoluminal, it can burrough into the tissue plane intramurally without projecting into the cavity. Spontaneous rupture of chordae secondary to inflammation without any vegetation is another possibility.

We conclude , even though vegetations are considered sine quo non of IE in many clinical situations, IE occurs without vegetation. The mechanisms could be varied.

Download full  PPT presentation

infective-endocarditis-csi-2005

infective-endocarditis-csi-2005

infective-endocarditis-vegetation-csi-2005

ebstein-anomaly

Down load high resolution PDF file

ebstein-anomaly

Ref:

An excellent article from H.Watson in british heart journal

HERNANDEZ FA  The intracavitary electrocardiogram in the diagnosis
of Ebstein’s anomaly. Amer J Cardiol 1: 181,  1958

A perfect illustration  to understand

What will happen if the aorta is obstructed at the level of isthumus ?

One of the great illustrations I have come across

co-arctation-collaterals

collaterals-in-coarctation-21

Courtesy

Dr.Jesse Edwards (Fowler’s Text book of cardiology )

To  Download a PDF version and Zoom into the Aorta  as deep as you would like !

collaterals in coarctation of aorta

Also watch

Collateral in co arctation   : A video

PDA is a common congenital heart disease.It results in progressive left to right shunting.

Development of pulmonary hypertension is the major complication.PDA need to be closed once the diagnosis is made.Until recently surgery was the only option.Now we have device, coil closure   available. Not all ducts are amenable to device closure.

For a duct to be closed by device we have to know the exact anatomy of the ductus.echocardiography has  limitation to  accurately image the ductus. Angiogram is the specific method.

What is  the normal length of patent ductus  arteriosus ?

The length of duct is very variable it can vary between 1 mm to 35  mm.

A 2 mm PDA is nothing but direct adherence of aorta and pulmonary artery (Ultra short form , similar to AP window )

pda-size-ductus

What is the branching angle of ductus from aorta and the entry angle at the pulmonary artery ?

This is an important determinant of technical success of device closure .Very abtuse or acute angled ductus can

face difficulty in deploying devices. The normal angle in lateral view is between 30-60 d

How do you classify PDA ? .

There is only one classification of PDA available  based on angiogram .Krichenko*

pda-4

pda-2

pda-31

Taken from  *Krichenko A,. Angiographic classification of the isolated, persistently patent ductus arteriosus and implications for percutaneous catheter occlusion. Am J Cardiol. 1989; 63: 877–879

Review article on PDA

http://www.circ.ahajournals.org/cgi/content/full/114/17/1873

British Bifurcation Coronary Study: Old, New, and Evolving Strategies (BBC ONE)  concludes complex crush ,   culotte technique are to be  avoided  . Single  stent  is better than two stents  in bifurcation lesions .

Unanswered question

If  single stent is better than two , is  it not logical ,  ” No stent” would be better than single  stent ?

This question may sound a straw man like ! But the truth is  the success of  medical management  in COURAGE and OAT study  may  be  due this concept !

BBC ONE: Fewer MACE with provisional T-stenting for bifurcations

CABG is the most common cardiovascular surgery  done world wide .

When the ventricle is dilated it is a common practice to do a ventricular  reduction surgery.

It was a logical to expect benefit when we correct the adverse remodelling of heart  that aoccur following an MI.

The STICH trial compared  plain CABG with ventricular  reconstruction and reduction .

Unfortunately , in medicine , the logics often fail  as this study  found no  mortality advantage .

Click here to read the land mark article from NEJM

Coronary collateral circulation is the most poorly understood, and often neglected concept among the cardiology community.There is a general perception , in obstructive CAD ,  coronary collaterals are an inferior modality of  back up blood supply than artificial collateral (Also called CABG ) ! One of the reasons,  it is   been ridiculed by many  mainstream cardiologists is   because  , it comes by nature , and also free of cost !

The often quoted statement* ,collateral blood flow can not sustain blood flow during exercise ,  is not based on solid scientific data. In the real world , there are thousands of patients actively pursuing life with chronic total occlusion and good collaterals.

It is surprising , there is no  physiologically valid ,  controlled study available to compare CABG with natural collaterals

*When repeatedly told , a  statement becomes a fact !

It can be assumed (Unscientifically ofcourse ! )   the  remarkable  success  of medical therapy  in COURAGE  and the OAT * study  can be attributable to the naturally occurring coronary collateral circulation.

* Summary of COURAGE & OAT : A   block  in the coronary artery  need not be opened  to prolong human survival !

You draw your own conclusions from the  following case study

A 40 year old women , with stable angina and good physical activity

Her angiogram shows.

coronary-collateral-2

RCA injection

coronary-collateral

Coronary artery  perforation is a dreaded complication of PCI. Perforations are the Interventional cardiologists ultimate worry   as they need to  manipulate their  hardware for  long periods in many complex lesions.  Especially  it is a  real threat in chronic total occlusions.

Still , an important fact is ,  many of the coronary perforations are not life threatening ?

How is this possible ?  (Type 1 Ellis has zero mortality Read below)

As the guide wire injures and perforates the cor0nary vessel,  it results in  small puffs of dye extravasating  into peri coronary space .

The coronary artery , which is located   within the  atrioventricular groove  (LAD), or AV groove (LCX, RCA) have  two distinct anatomical relationship with reference to epicardium and pericardial space.

50 % 0f circumference of the coronary artery is  hugged  by the myocardium  another 50% or so is related directly to the pericardial aspect.

Guide wires hitting on the myocardial aspects face a stiff resistance than the pericardial aspect. So , generally the risk of perforating pericardial aspect is more than myocardial aspect

Even if , the coronary artery is punctured on myocardial aspect , no great danger occur as there is no potential space for the blood to drain and further,  the  elastic nature of myocardial muscle plane effectively seals the leak. At the most , mild myocardial staining is noted .

coronary-perforation-2

While ,  perforations  into  the pericardial space  , often threaten with a tamponade. The fact that pericardial space has negative pressure and  the mean  coronary arterial pressure around 40mmhg ,  it is  , all the more likely blood is sucked into the pericardial  space. Of course , very minute  perforations  even into the pericardial space ,  could  be self limited and  benign.

coronary-perforation

What is unrecognised coronary perforation?

Many times , the guidewire goes in a false track in the tissue plane.This is  nothing,  but perforation without hemodynamic implication. Most often , these are the instances of guide wire entering the epicardium.They mimic , false lumen entry , dissections, etc. There are occasion , where false lumen of the  coronary artery were  stented.

What are the  factors which increase risk of perforation ?

perforation-6

 How do you classify coronary perforations ?

perforation-3

*Ellis SG, Ajluni S, Arnold AZ,  Increased coronary perforation in the new device era. Incidence, classification, management, and outcomeCirculation. 1994;90:2725–2730

 

How do you manage coronary perforation?

Simple guide wire induced perforations are less trouble some unless we have crossed it with balloon without realising the fact the wire has entered the pericardial space. So, caution is required and always watch for guide wire tip movement which is often funny looking wihtin false lumens or very freely moving within pericardial space. Anticipate the complication especially so when you do CTOs and venous graft PCI.  Keep one cath lab  tamponade crash  bin  in ready mode before embarking upon a complex PCI

  • Neutralise the heparin action with protamine is the first step
  • Most are self limited, no intervention is required  but requires close observation for next 24 hours.
  • Temporary balloon occlusion may be suffice in many cases
  • Tamponade requires immediate tapping. Small collection without fall in BP can be observed.
  • keep doing the echocardiogram liberally to assess the leak and watch for any new collection.
  • PTFE covered stents if prolonged leak.
  • Emergency surgery may required in few.

2018 update 

This is  nearly 10 years old article. Now, we have gained much experience and hardware utilisation have rapidly expanded. While expertise has minimised this complication , more PCIs in complex lesion subset tend to keep the incidence static , if not higher.(Its around .5% )

Tips to use balloon occlusion during perforation

Perforations which are active and flowing should be immediately occluded with a balloon either at the site of leak or just proximal to it. Doing a proximal occlusion is easier in emergency , as often times its technically difficult to reach the site of leak especially in CTOs where the leaky site is not defined clearly or forward looking (Local balloon inflation across the leaky site is not feasible )

 

How long to occlude , Intermittent /complete, proximal ? or at the site of perforation ? These queries are answered in Ref 4

Reference

1.Largest report (1762 cases) of perforation from British Cardiovascular Intervention  Society Database Circ Cardiovasc Interv. 2016;9:e003449.

2.Al-Lamee R, Ielasi A, Latib A,. Incidence, predictors, management, immediate and long-term outcomes following grade III coronary perforation. JACC Cardiovasc Interv. 2011;4:87–95.

3Xiangfei Wang and Junbo Ge Balloon Occlusion Types in the Treatment of Coronary Perforation during Percutaneous Coronary Intervention   Cardiology Research and Practice Volume 2014, Article ID 784018,

4.A very good review comes from Royal Hospital, Muscat, Sultanate of Oman

 

iFAQs in coronary perforations

1.Does the plane of the coronary artery (Sub epicardial within the fat layers)  determine the likely hood of tamponade ?

While myocardial tissue can resist flow we are not sure about sub-epicardial fat on the pericardial aspect.

2.How common is Intra-cavitory perforation ?

Perforations into chamber is invariably associated with septal branches (PCI to septal branch itself is less common )