Dr.S.Venkatesan MD

Archive for 2009

Why sinus node dysfunction rarely kills a patient ?

Posted in cardiology -ECG, Cardiology-Arrhythmias, Uncategorized, tagged chb, complete heart block, permanent pacemaker, sinus node dysfunction, sinus pause, siuns arrrest, snd, ventricualr pause on April 22, 2009| Leave a Comment »

Sick sinus syndrome or sinus node dysfunction (SSS, SND ) is one of the common cause of symptomatic bradycardia .The other cause for pathological bradycardia is complete heart block.Together , these two entities share 99% of indications for permanentpacemaker implantation.

The sinus node can get affected in various diseases . The commonest cause for SND is age related.This is manifested as inappropriate bradycardia .The other common presentation of SND is exaggerated bradycardia to betablockers and calcium blockers.In fact , some consider drug induced bradycardia is nothing but , unmasking of underlying SND.Pathological states that result in SND include hypothyrodism , infiltrative and inflammatory diseases . (Surprisingly , ischemic SND is a lesser clinical problem when considering the rampant CAD in our population )

What is is a fundamental difference between SND and complete heart block* ?

Sinus node is the proximal most pacemaker of the heart. When it fails the chances of a subsidiary pacemaker coming to the rescue is far greater than a complete AV block. Further the quality and stability of the escape pacemaker is better in SND. In fact , in pure SND ( With out AV nodal disease) a sinus arrest is rarely fatal as escape rhythm occur without fail.

* It should be emphasised , there can be associated AV nodal disease in significant (10%) number of patients with SND .This may be present either at the time of diagnosis or it can develop later in the course .This has important implication in the selection of pacemaker .The discussion here is confined to isolated SND .

How common is ventricular escape rhythm in SND ?

It is very rare. the ventricle never gets a chance to come to the rescue as invariably junctional pacemaker takes over at times of extreme sinus pause/arrest.For the same reason , pause dependent VT (Brady dependent ) is also less common in SND .

What is stokes Adam’s attack ? How common it is seen in SND ?

It is the cardiogenic syncope due to extreme bradycardia. This classically occurs in complete heart block , when

the the escape rhythm becomes either very slow or temporarily goes for sleep .This results in a huge pause (unlike sinus pause of , the pause here is ventricular pause , this is actually an asystole ) it can immediately trigger an VT or VF .

If SND is not life threatening why pace maker is indicated in them ?

The pacemaker is primarily indicated for prevention of dizziness , near syncope or syncope.So primary impact is on improving quality of life , not reduction in mortality. While in CHB pacemakers improve symptoms and survival.

Which form of SND can be dangerous ?

When SND is associated with rapid atrial fibrillation some times it can trigger a VT/VT if , these patients also have

a fast accessory pathway with short refractory period. (<250msec)

Final message

If you have only one pacemaker at your disposal , but there are two patients , one with SND and other with CHB please put the pacemaker to the patient with CHB , even if the later has insurance coverage and the former is not .You are justified in diverting the pacemaker !

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What do we mean by the term “LV dysfunction” ?

Posted in cardiac drugs, cardiac surgery, Cardiology - Clinical, Cardiology -unresolved questions, Uncategorized, tagged lv dysfcuntion on April 20, 2009| 12 Comments »

LV dysfunction , perhaps is the most common medical term used by physicians world over.But surprisingly , It is not easy to infer what they mean by it ! The term literally means left ventricle is not functioning all right .

LV dysfunction can be classified by many ways.

Symptomatic vs Asymptomatic
Global vs Regional
Reversible vs Permanent
Systolic vs Diastolic
Ischemic vs Nonischemic
Primary vs Secondary ( Muscle vs valve etc)

If you analyse the above classification LV dysfunction can mean different things to different people , at different times.Though systolic dysfunction , as reflected by low EF % ( Less than 50% ) is the major cause of LV dysfunction the issue is not simple.

Is coronary artery disease ( CAD ) a must for LV to become dysfunctional ?

No , not at all .CAD is the leading cause of LV dysfunction .Primary muscle disorders -cardiomyopathy is an equally common entity. Valve disorders especially aortic valve stenosis is another common cause for LV dysfunction. Further , systemic hypertension, diabetes mellites, renal failure, can result in serious impairment of LV function .Some drugs ( Adriamycin ) can either precipitate or aggravate LV dysfunction.

If physicians themselves are confronted with such complexity , how are , our other medical colleagues (Forget about the patients ! ) will understand the concept of LV dysfunction.

But , the crux of the matter is every doctor believes LV dysfunction is synonymous with low ejection fraction. A surgeon or an anesthetist is quiet happy to operate if the ejection fraction is above 60% .

Can a patient have significant LV dysfunction with normal Ejection fraction ? (EF )

Yes , this can occur in advanced degrees of diastolic dysfunction, where cardiac contractility is normal but

fails to relax adequately .

Is diastolic dysfunction less dangerous than systolic dysfunction?

May be , that is the dominant opinion , but there are sufficient evidence emerging that opinion is wrong.The main reason for diastolic dysfunction to send a ” not so sinister signal ” is over diagnosis of grade 1 diastolic dysfunction in the general population . The echocardiologists considered it fashionable for a quiet a longtime (Many have changed since then !) to report all patients with reversed E :A ratio in the mitral inflow doppler profile as diastolic dysfunction. This has resulted in thousands of asymptomatic , healthy people getting labelled as grade 1 diastolic dysfunction undermining the importance of this entity.

The fact of the matter is true diastolic dysfunction is indeed dangerous , if not more dangerous than systolic dysfunction for the simple reason , there is no specific treatment for this condition

To improve the specificity to diagnose genuine LV diastolic dysfunction it is suggested to remove grade 1 diastolic dysfunction from the literature .

Other causes of LV dysfunction with normal EF

Some times , there can be wall motion defects and mitral regurgitation but still the EF can be normal .
Mitral valve dysfunction can be a part of LV dysfunction .The EF is either not affected as ischemic damage might be confined to papillary muscle.
Vigorous compensation from non ischemic areas can normalise an EF

What is the difference between LV dysfunction and LV failure ?

Many times both these terms are perceived to convey the same meaning .But it can never be used synonymously .Cardiac failure is a clinical entity while LV dysfunction is a derived technical parameter by and large an echocardiographic enity. Cardiac failure is defined classically as a clinical syndrome .(elevated jvp, edema * S 3 rales etc) Neuroueohormonal activation can occur with both.

A patient with LV dysfunction when destabilsed develops LV failure and after stabilisation of LV failure he is brought back to the baseline LV dysfunction

*What is the link between LV dysfunction and RV dysfunction ?

RV can not be silent companion when the LV fails . There always have been link between the two.

LV dysfucntion begets RV dysfunction and LV failure can trigger a total heart failure

Apart from the classical concept of ventricular interdependence , where inter ventricular septum plays a pivotal role , now there is strong evidence to prove both LV and RV myocardial muscle bundles are interwoven . In fact failing LV drags the muscle bundles over RV also (Friendly pull , let us die together !) and this is classically seen in idiopathic dilated cardiomyopathy where all four chambers of the heart dilate. There is also biochemical evidence the RV myocytes deplete thier norepinephrine stores in LV failure.

Is there an entity called transient or temporary LV dysfunction ?

The classical chronic reversible LV dysfunction also called hibernating myocardium is a different topic shall be discussed later.

Can acute ischemia cause LV dysfunction ?

Yes .This can occur during ischemic stunning of myocardium during NSTEMI .This can result in acute pulmonary edema* at times.This can be termed as ischemic LV dysfunction as there is no myocardial necrosis .

* The pulmoanry edema mentioned here is the flash pulmonary edema carries very dis prognosis.

What is the cause of LV dysfunction in critical aortic stenosis ?

Is it fibrotic ?

Is it necrotic ?

Is it ischemic ? (Associated CAD )

Or is it simply a mechanical inability* to contract as the outflow is closed ?

There is no specific answer . All the above factors may contribute .*But the fact that most patients recover full normal LV function following aortic valve replacement would make the last explanation more likely.

What does the term LV dysfunction mean to a cardiac surgeon when he plans for a CABG ?

LV dysfunction becomes an important determinant of overall outcome in patients who are going to receive a CABG .The surgeon will have contingent strategies during peroperative and post operative phase while operating in hearts with severe LV dysfunction.

How much of LV function is going to recover after CABG ?

This can not be predicted accurately but CABG may not resucitate all dying myocytes and bring life in them .The buttressing effect of blood within the dysfunctional segement can improve contractility and reduce the wall motion defect(This is an indirect mechanism of improving EF )

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How does coronary revascularisation improve LV dysfunction in patients with ischemic cardiomyopathy ?

Posted in cardiac drugs, cardiac surgery, Cardiology - Clinical, cardiology- coronary care, Uncategorized, tagged akinetic myocardium, cabg, cabg vs medical management, is cabg useful in lv dysfunction, lv dysfunction, myocardium, pci, revascularisation on April 20, 2009| 2 Comments »

The answer to this question is not easy , as one would tend to believe . In fact this question , takes it for granted revascularisation will improve the LV dysfunction in patients with severe LV dysfunction.

The truth is , we are not sure about the mechanisms . How revasculariastion will have an effect on chronically dying or dead myocardium ? (Acutely dying myocardium is a different story, where revascualrisation has a profound effect , that is called salvaging the myocardium )

This issue is of great clinical significance in end stage ischemic heart disease .A typical myocardial segment in ischemic cardiomyopathy has millions of the dead cells interwoven with dying cells with occasional clusters if live cells scattered all over .Once the process of myocardial apotosis sets in , myocardial cell death does not result in segmental destruction instead an universal cell death.(Paracrine signals of cell death that spills over to adjacent segments ) The current standards of revascualrisation (PCI and CABG) aims to provide blood flow in a segmental fashion. Even if the blood flow is restored in an obstructive vessel it is not clear , how it is going to enter the chronically atrophied myocytes.

Meanwhile , many studies are available suggesting coronary revascularisation does indeed improve LV dysfunction. These evidence has never been conclusive .Real world experience would also confirm this simple fact , that angina relief is definite following revascularisation but not dyspnea relief in patients with LV dysfunction .

So , when seeking the guidelines for revascularisation ( PCI or CABG ) in patients with CAD one need to ask this specific question

Does the patient has

A.Angina alone

B.Angina and dyspnea

C.Only dyspnea

If the answer is C , assess the patient again , rule out systemic causes of dyspnea (Anemia, renal function etc) rethink or postpone revascularisation.If primary or secondary LV muscle dysfunction has set in revascularisation has little value.

What we don’t know about coronary collaterals ?

Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, cardiology- coronary care, Cardiology-Coronary artery disese, Uncategorized, tagged collaterals, coornary collaterl circulation on April 17, 2009| Leave a Comment »

Coronary collateral circulation is the God’s gift to mankind.It has potential benefits ( and of course real benefit !) both during acute and chronic coronary syndrome.

Collaterals in CCS

The classical role of coronary collateral is in patients with chronic stable angina.It is quiet common to see patients with totally occluded LAD or RCA with normal LV function maintained by extensive collaterals .

Collaterals during ACS.

An intact and functional collateral circulation can prevent an NSTEMI from converting into STEMI.In fact many of the patients with unstable angina patients carry on with viable myocardium just because thaey have good collaterals.It gives us a time window to intervene .Some times the col laterals are good enough and help us avoid a revascularisation in toto.

Collateral’s in STEMI.

This is not well understood. Some researchers reported opening up of collateral channels very early after a STEMI. Logic would suggest , anatomically patent functionally closed collateral channels are always available at time of crisis. But not every one is blessed with such rescue mechanism.

What determines the native collateral channel development in human cor0nary circulation ?

When the answer is unknown , it moves to the genetic domain also called – God’s domain .

Our ignorance in decoding coronary collaterals is vast.

The chief cause of this ignorance is we always tend , not believe things which we don’t see.

Coronary collaterals channels need to atleast 1mm to be visualised by CAG.There could be a vast network of micro collaterals out there within the myocardium invisible to current imaging methods. (In fact , this has a link with outcome of the COURAGE study )

Is coronary collaterals have all the three layers of an artery ?

Yes .But the media lacks muscle.

Is coronary collateral less prone for spasm ?

May be.

The drugs we give , Calcium blockers , betablockers, and nitrates have same hemodyanmic effects as in native coronary circulation ?

We don,t know as yet. Nitrates are supposed to improve collateralisation

How common is atherosclerosis to involve the coronary collaterals ?

How often is an ACS precipitated by an collateral occlusion ?

May be more common than we think.

Can we stent a 2mm wide collateral to maintain the patency in case of a CTO ?

A question need to be answered by current generation interventional cardiologists.

Is coronary collateral gives protection against primary VF ?

In one sense , the number one killer of mankind is in fact not STEMI but the VF that follows it .

Why only a few develop a VF following an MI ? What determines the arrhythmic response to ischemia ?

Some anecdotal observation of suggest a role for early coronary collateral opening in the prevention of VF .

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A new marker for transudate in pleural effusion

Posted in Cardiology - Clinical, cardiology -Therapeutics, Cardiology-Coronary artery disese, tagged atrial naturetic peptide, bio markers for cardiac failure, bnp, cardiac failure, nt prpbnp, pleural effusion, transudate vs exudate on April 17, 2009| Leave a Comment »

Diagnostic issues in cardiac failure : A febrile pleural effusion in a patient with LV dysfunction .

Is it a transudate or exudate ? How to confirm the pleural effusion is primarily cardiac failure related ?

When the classical protein criteria is inadequate or prone for errors

Try this more specific marker within the pleural fluid

N-Terminal Brain naruretic peptide

Pleural fluid NT-proBNP is very useful in establishing the diagnosis of HF-associated effusions, and it confirms this diagnosis . The measurement of NT-proBNP rather than serum to pleural protein gradient is recommended for identifying mislabeled cardiac transudates.

Reff :Biomarkers of Heart Failure in Pleural Fluid. Chest. 2009 Apr 10.

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Everything about radial artery spasm and friction

Posted in Cardiology -Interventional -PCI, Uncategorized, tagged femoral artery, radial artery, radial artery friction, radial artery spasm, radial coronary angiogram on April 16, 2009| Leave a Comment »

Radial access for both diagnostic coronary angiogram and PCI has been increasing steadily.Many centres have adopted an exclusive radial approach. Newer , radial specific hard ware is being produced.(Link) .It is surprising , radial approach has gained momentum primarily outside USA (Europe , Japan, India ).The advantages of radial access is primarily , patient comfort, less local site complication.

Prerequisite for radial approach.

The importance of pre procedural Allen test to document dual blood supply is well established but the less appreciated concept is preprocedure radial artery size assessment . It could be as important as Allen test .

The normal diameter of radial artery lumen is 2.4mm (Range 1.8-3.0) .Some population have still smaller radial lumen(India KA.Sambasivam et all mean 1.8mm). Compare femoral artery (8.5mm diameter, 4 times bigger )

Imagine this situation , a 1.65 mm (5 F) diameter catheter trying to enter a 1.7mm radial artery !

Is it not a futile excercise ? Many of the failed radial access is due to radial artery /catheter mismatch .

There has been occasions , when the radial sheath is larger than radial artery itself !

So the size of the radial artery becomes vital in planning radial CAG.

What are ways one can estimate the size of the radial artery ?

Volume of pulse (Still Useful , but can fool us some times!)
Thick radial walls (Monckeberg,s sclerosis)
Ultrasound imaging

Radial artery spasm

Radial artery has more medial smooth muscle and further the fibres criss cross the artery. Further , the radial artery is richly innervated by sympathetic nerve terminals.

The major factor that determines likely hood of spasm is

Pain intensity.
Amount of free space between sheath and vessel wall
The frictional force between sheath and artery wall is the powerful trigger for spasm and pain.

What is the biochemical mediators of radial artery spasm ?

It is logical to believe all vascular spasm are due to calcium .But it is not. Calcium blockers have no definite relief for spasm.Nor adrenaline mediated alpha receptor stimulation has a major contribution for RAS. Phentolamine is useful

Is there a objective and quantitative method to assess radial artery spasm ?

Removal of the radial requires some force. Kiemeneij ( Measurement of radial artery spasm using an automatic pullback device. Catheter Cardiovasc Interv 2001;54:437–441.) demonstrated if one require > 1kg force to remove a sheath it correlates with clinically significant spasm.

What are the serious sequel of radial artery spasm ?

Radial artery rupture and radial artery avulsion has been reported when attempting to remove the sheath from spastic arteries

Management of radial spasm

There are two aspects to this problem

Prevention of spasm
Treatment of established spasm

How to prevent or reduce radial artery spasm ?

Radial artery is a very sensitive artery .The incidence of spasm can be up to 20% The spasm can be due to

Hardware, technical ,anatomical factors.

Apart from above three factors, the most important is anxiety related .The key principle is , sedating the radial artery is as important as sedating the patient .

Sedating the patient

Explaining to the patient about the procedure can allay the anxiety. It is a fact , the tactile perception of catheter movement in radial route is more than the femoral .In very anxious patients (Some centres use it routinely ) IV sedation (Midazolam)

Sedating the radial artery.

Local anesthesia : Subcutaneous lignociane , though widely used has a drawback.It can aggravate pain, induce spasm , accidental entry into lumen may cause a hematoma .All can potentially make the pulse feeble. So care should be taken in giving minimal lignocaine ( At a specific point needle entry) with a short needle . One should watch , the grace with which experienced radial interventionist give the local anesthetics !

Arterial cocktail

The arterial cocktail consists of combination of Nitroglyceine (200 mcg) , Xylocaine (50 mg) Verapamil (5 mg) an. Heparin(5000 IU). Sodium bicarbonate (4%) is optional to neutralise the acidity of the solution

How to administer ?

Ideally spasmolytic cocktail should be given before the sheath is introduced immediately after puncture . As the drugs has to get in contact with the arterial wall .if cocktail is given after introduction of sheath one of the following may be done.

Give the drug as it enters the artery.
Pull back the sheath when injecting the drug.
Use a side holed sheath.

Technical issues to prevent radial artery spasm

Try to puncture in single prick . If the first puncture is not successful , don’t attempt to cross a spastic radial artery Remember (Unlike femoral ) successful puncturing of a spastic radial artery may be the beginning of a vexing and tiring procedure.So if we have lot of difficulty in getting in , please avoid the procedure and switch to femoral . (Spastic signals may spill over to left hand also !)

Remember unlike femoral cathetrisation , in radial access, getting out the catheter could be more tricky than getting in !

Avoid procedures that would require multiple catheter , guide wire exchange .Complex lesions and in emergencies.( Some experts do Primary PCI through radial !) .Now dedicated radial hardware are available.

Sheath selection (Visit : Arrow International )

Long sheaths have been used in the past. It makes the spastic segment lengthier.Now short sheaths are increasingly used. Long sheaths (20-25cm ) give better suppport during catheter manipulation. Side holed sheaths is a newer innovation. This maintains the blood flow on the sides of sheath and reduces friction with vessel wall .Further, it can deliver the arterial cocktail to vessel wall and effectively prevent or reduce spasm.

Catheters : Use 5 F/6F. Rarely 7f are used.

Guide wires :Hydrophilic guidewire are radial friendly.

How to manage established severe spasm ?

For severe spasm with sticky sheath / catheter

Increase the analgesia with morphine
Repeat NTG and Verapamil
Warm compresses over the forearm
Never pull with force
Wait for an hour and try pulling again (Often successful )

Last resorts

An axillary block

Vascular surgery

Reference and further reading

For excellent collection of radial access resources please visit www.radialforce.org

(Much of this blog’s content is based on this article )

http://www.invasivecardiology.com/article/5446

http://meeting.chestjournal.org/cgi/content/abstract/130/4/201S-a

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Can premature beats (Ectopic beats) occur in SA node ? Yes, it can . It’s called sinus premature systole.

Posted in Cardiology - Clinical, Cardiology - Electrophysiology -Pacemaker, cardiology -ECG, Uncategorized, tagged apd, atrial premature beats, atrial premature depolarisation, ectopic beats, jpd, sinus extrasystole, sinus node, sinus premature beats, sinus premature systole, ventricular premature depolarisation, VPD on April 14, 2009| Leave a Comment »

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

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Can right ventricular pacing produce an ECG with RBBB morphology ?

Posted in Cardiology - Electrophysiology -Pacemaker, cardiology -ECG, Cardiology-Arrhythmias, Uncategorized, tagged coronary sinus apcing, electro physiology, lbbb, lv pacing, pacemaker, pacemaker lead perforation, rbbb, rv pacing, rv pacing with rbbb morphology, septal pacing on April 13, 2009| 1 Comment »

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

RBBB morphology following permanent pacing need not elicit a panic reaction provided all parameters are stable.
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 Electrocardiology January 1, 2003 Yang, Yung-Nien ; Yin, Wei-Hsian ; Young, Mason Shing

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Can we diagnose Infective endocarditis without vegetation ?

Posted in Cardiology - Clinical, My presentations, tagged chordal ruptre, cultre negative infective endocarditis, duke criteria, flail mitral valve, ie, infective endocarditis, minor infective endocarditis, native valve endocarditis, vancomycin, vegeation, vegetation negative endocarditis on April 10, 2009| Leave a Comment »

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

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.

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