Dr.S.Venkatesan MD

Is there a time window for rescue PCI ? Why we are not insisting on it ?

May 25, 2009 by dr s venkatesan

Failed thrombolysis is an important clinical issue in STEMI as successful thrombolysis occurs only in about 50-60% of pateints . The typical criteria to define failed thrombolysis is the regression of less than 50% of sum total( or maximum) ST elevation in infarct leads.

So what do you do for these patients with failed thrombolysis ?

It depends upon the patient’s symptom, hemodynamic stability, LV dysfunction .

They should get one of the following .

Conservative medical management with /without CAG
Repeat thrombolysis
Rescue PCI
CABG

Medical management is thought to be too inferior a management, many of the interventional cardiologists do not want to talk about . But , there is an important group of patients (Not often addressed in cardiology literature) who technically fulfill the criteria of failed thrombolysis , but still very comfortable , asymtomatic and in class 1. These patients , have a strong option for continuing the conservative management .

Repeat thrombolysis does not have a consistent effect but can be tried in some stable patients. CABG can be a genuine option in few

Rescue PCI

This terminology has become the glamorous one since the catchy word rescue is tagged in the title itself. For most of the cardiac physicians , this has become the default treatment modality.This is an unfortunate perception . What one should realise here is , we are tying to rescue the myocardium and the patient , not the patient’s coronary artery !

Opening up a coronary obstruction is not synonymous with rescue .

For rescue PCI , to be effective it should be done within the same time window as that for thrombolysis (ie within 6 or at the most 12 hours) .This timing is of vital importance for the simple reason , there will be nothing to rescue after 12 hours as most of the muscle would be dead. Reperfusing a dead myocardium has been shown to be hazardous in some , as it converts a simple infarct into a hemorrhagic infarct.This softens the core of the infarct and carry a risk of rupture. Further, doing a complex emergency PCI , in a thrombotic milieu with presumed long term benefit , is a perfect recipe for a potential disaster.

While the above statement may be seen as pessimistic view , the optimistic cardiologist would vouch for the“Curious open artery hypothesis” .This theory simply states , whatever be the status of the distal myocardium ( dead or alive !) opening an obstruction in the concerened coronary artery will benefit the patient !

It is huge surprise , this concept continues to be alive even after repeatedly shot dead by number of very good clinical trials (TOAT, CTO limb of COURAGE etc ).

The REACT study (2004) concluded undisputed benefit of rescue PCI for failed thrombolysis , only if the rescue was done within 5-10 hours after the onset of symptoms.The mean time for pain-to-rescue PCI was 414 minutes (6.5hours)

Final message

It is fashionable to talk about time window for thrombolyis but not for PCI .The time window for rescue PCI is an redundant issue for many cardiologists ! . But , the fact of the matter is , it is not . . .

The concept of time window in rescue PCI , is as important as , that of thrombolysis. Please , think twice or thrice ! if some body suggest you to do a rescue PCI in a stable patient , 12hours after the index event .

Important note : This rule does not ( or need not ) apply for patients in cardiogenic shock or patient ‘s with ongoing iscemia and angina.

Posted in cardiology -ECG, Cardiology -Interventional -PCI, cardiology -Therapeutics | Tagged acute coronary syndrome, cardiogenic shock, chronic total occulusion, cto, cypher, des, door to balloon time, door to needle time, door to pci, europcr, jcc, no reflow, nstemi, react trial, repeat thrombolysis, reperfusion, rescue angioplasty, rescue pci, rescue ptca, rescue thrombolysis, reteplase, scai, stemi, streptokinase, swit trial, taxus, tct md, tenekteplase, thrombolysis, time window, timi flow, tnk tpa, toat study, tpa, unstable angina, what is recue angioplasty ?, what is rescue pci ? | 1 Comment »

Fallacies in emergency room :Why we are not risk stratifying STEMI on arrival , but do it promptly in NSTEMI ?

May 21, 2009 by dr s venkatesan

NSTEMI constitutes a very heterogeneous population .The cardiac risk can vary between very low to very high . In contrast , STEMI patients carry a high risk for electro mechanical complication including sudden death .They all need immediate treatment either with thrombolysis or PCI to open up the blood vessel and salvage the myocardium.

The above concept , may be true in many situations , but what we fail to recognize is that , STEMI also is a heterogeneous clinico pathological with varying risks and outcome !
Let us see briefly , why this is very important in the management of STEMI

Management of STEMI has undergone great change over the past 50 years and it is the standing example of evidence based coronary care in the modern era ! The mortality , in the early era was around 30-40% . The advent of coronary care units, defibrillators, reduced the mortality to around 10-15% in 1960 /70s . Early use of heparin , aspirin further improved the outcome .The inhospital mortality was greatly reduced to a level of 7-8% in the thrombolytic era. And , then came the interventional approach, namely primary PCI , which is now considered the best form of reperfusion when done early by an experienced team.

Inspite of this wealth of evidence for the superiority of PCI , it is only a fraction of STEMI patients get primary PCI even in some of the well equipped centers ( Could be as low as 15 %)

Why ? this paradox

Primary PCI has struggled to establish itself as a global therapeutic concept for STEMI , even after 20 years of it’s introduction (PAMI trial) . If we attribute , lack of infrastructure , expertise are responsible for this low utility of primary PCI , we are mistaken ! There are so many institutions , at least in developing world , reluctant to do primary PCI for varied reasons.( Affordability , support system , odd hours ,and finally perceived fear of untoward complication !)

Primary PCI may be a great treatment modality , but it comes with a inherent risk related to the procedure.

In fact the early hazard could exceed the potential benefit in many of the low risk STEMI patients !

All STEMI’s are not same , so all does not require same treatment !

Common sense and logic would tell us any medical condition should be risk stratified before applying the management protocol. This will enable us to avoid applying “high risk – high benefit” treatments in low risk patients . It is a great surprise, the cardiology community has extensively researched to risk stratify NSTEMI/UA , it has rarely considered risk stratification of STEMI before starting the treatment.

In this context , it should be emphasized most of the clinical trails on primary PCI do not address the clinical relevance and the differential outcomes in various subsets of STEMI .

Consider the following two cases.

Two young men with STEMI , both present within 3 hours after onset of symptoms

ST elevation in V1 -V6 , 1 , AVL , Low blood pressure , with severe chest pain.
ST elevation in 2 ,3, AVF , hemodynamically stable , with minimal or no discomfort .

In the above example, a small inferior MI by a distal RCA occlusion , and a proximal LAD lesion jeopardising entire anterior wall , both are categorized as STEMI !
Do you want to advocate same treatment for both ? or Will you risk stratify the STEMI and treat individually ? (As we do in NSTEMI !)

Current guidelines , would suggest PCI for both situations. But , logistic , and real world experience would clearly favor thrombolysis for the second patient .
Does that mean, the second patient is getting an inferior modality of treatment ?

Not at all . In fact there is a strong case for PCI being inferior in these patients as the risk of the procedure may far outweigh the benefit especially if it is done on a random basis by not so well experienced cath lab team.
(Note : Streptokinase or TPA does not vary it’s action , whether given by an ambulance drive or a staff nurse or even a cardiologist ! .In contrast , the infrastructure and expertise have the greatest impact on the success and failure of PCI )
Final message

So , it is argued the world cardiology societies(ACC/ESC etc) need to risk stratify STEMI (Like we do in NSTEMI ) into low risk, intermediate risk and high risk categories and advice primary PCI only for high risk patients.

Reference

https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/226907

Posted in Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, Cardiology-Coronary artery disese | Tagged acc aha, acute coronary syndrome, angina, anterior mi, cardiogenic shock, coronary care unit, emergency triaging of chestpain, high risk nstemi, high risk stemi, inferior mi, is there a low risl stemi, jacc, LAD, left main, low risk nstemi, primary pci, RCA, stemi, thrombolysis, unstable angina, vulnerable plaque | 2 Comments »

Management of Atrial septal defect : Device closure lagging behind surgical closure !

May 11, 2009 by dr s venkatesan

Atrial septal defect is one among the commonest congenital heart disease .After years of controversy, there is consensus now , all significant ASDs need to be closed , at whatever age it is detected.

This rule does not apply to small ASDs without chamber right atrial and right ventricular dilatation. These defects and PFOs need not be closed .

Over the years , the controversy has shifted from Should we close ? to How to close ?

There are two options available : Device closure , Surgical closure

The following table compares the both treatment modalities

( Personal perspective )

Final message

Device closure is a complex, costly, often difficult and error prone cardiac procedure .It needs long term follow up and may carry a life long risk of major cardiac complication.It is useful only in selected subset of ASD patients. Surgical closure prevails over device closure in most situations.

Is this article has biased view against this emerging pediatric interventional procedure of ASD closure ?

It may appear so . But that is the reality as on 2009 !.May we hope technology evolves further and take our surgeons head on .

2012 update on ASD device closure .

The hard-ware as well as the expertise has improved a lot and it is on right track to become a real challenge to surgery.

The only issue again is the availability of rims to mount the device . Another realistic and sensitive issue which have I come across is , many interventionist cardiologist do feel awkward when they experience unexpected rim shortage on table. They should realise it is not their fault.

Always be ready to abandon the procedure and refer to the surgeon , according to your true conscience

After all , improperly delivered device is a life long pain for the patient .He has come to you with a great belief isn’t !

2014 update

Device closure for most ASDs in both children and adult is now possible with high degree of success. We have crossed about 50 patient experience. And I am truly amazed , how within a short period the device closure is about to conquer the crown from the surgeons ! (Exciting new data are coming from my colleague Dr Gnanavelu from the new Super specialty hospital of Government of Tamil Nadu Chennai. )

Reference

Aortic erosion following ASD closure

http://content.onlinejacc.org/cgi/content/full/45/8/1213

Posted in cardiac surgery | Tagged amplatzer asd device, asd, asd surgery, asdos, device closure, ostium primum, ostium secundum, pfo, starflex | 8 Comments »

If ischemia is a powerful trigger for ventricular arrhythmias ,Why cardiac arrhytmias are less common in NSTEMI ?

May 10, 2009 by dr s venkatesan

Acute coronary syndrome is the commonest cardiac emergency. STEMI and NSTEMI are the two clinical limbs of ACS. Generally they have distinct clinical, ECG, angiographic features.(Ofcourse, with some degree of overlap) . It is a mystery , both clinical presentations differ so much inspite of the common denominator , namely , an injured plaque with add on thrombus within the coronary artery. The primary difference between these two entities is, in STEMI the occlusion occurs sudden and complete and in NSTEMI it occurs slow and incomplete

Cardiac arrhythmias in ACS

It is a much published factoid for many decades, that only one third of STEMI patients reach the hospital alive ! The reason being , STEMI is very much prone for primary VF. Contrary to this , most pateints with NSTEMI reach the hospital alive ! How ?

Both are ACS, if ischemia is a powerful trigger for dangerous ventricular arrhythmia’s , NSTEMI should also behave similarly .So what protects against arrhythmias in NSTEMI ?

We realise , by observational experience (Not EBM !) It is the suddenness and totality of ischemia that trigger dangerous form of arrhythmia .

Further, a balanced ischemia in two contralateral segments (or global ischemia) some how protects against development of ventricular fibrillation .This may be due to preservation of electrical homogeneity , and the spherical VT spiral waves are not sustainable.

In contrast , STEMI has a sudden focal , ischemic zone that initiates the VT and ischemia free contralateral segment welcoming and sustaining the reentrant wavelet.

The observation of primarily single vessel disese in STEMI and multivessel disease in NSTEMI also give credence to this concept.

Further , ischemic preconditioning can exert an important anti arrhythmic effect in NSTEMI as patients with unstable angina have slow, repetitive episodes of ischemia prior to the index event .

Post MI scar mediated VT/VF is independent of degree of overall ischemia

It is also established , a sub group of STEMI pateints who had preinfarction angina( ie . a brief period of UA/NSTEMI) have very low risk of SCD supporting the concept of sensitising the myocardium against ventricular arrhythmias.

Final message

Even though , there is a convincing concept of Ischemia induced cardiac arrhythmia in literature ,in real patients it is very difficult to link the two in many situations..UA/NSTEMI is the most common acute ischemic event but the incidence of VT/VF here, is far less than one would expect.In ACS , focal , total ischemia is more likely to precipitate a VT/VF than multifocal and global ischemia.

Posted in Cardiology - Clinical | Tagged bundle brancg reentry, cardiac arhhythmias, dc shock, defibrillator, ICD, ischemic vt, lvot vt, madit, madit 2, naspe, nstemi, pace, ventricular fibrillation, ventricular tachycardia, vf, vt, vt in unstable angina | Leave a Comment »

Can we advice CABG for single vessel disease ?

May 9, 2009 by dr s venkatesan

Can we advice CABG for single vessel disease ?

Yes, CABG may be indicated in

Critical , proximal , complex LAD disease with or without ostium involvement.
Many of the bifurcation lesions with large and significant side branch
Small caliber LAD with diffuse disease .

When these occur in diabetic subjects , the indication for CABG is more certain .

* Present generation cardiologists would feel every lesion is stentable and should not be referred to the surgeon .But it should be emphasized here, technical feasibility alone , does not imply PCI is superior and ideal in all coronary interventions.

Can we do a CABG in single vessel disease with normal LAD ?

CABG is very rarely indicated for isolated RCA or LCX disease. It should be consciously avoided in this patient population.

This is because the at risk myocardium supplied by these vessels are far less than that of LAD. PCI is preferred in these vessels .(Ofcourse , after considering medical management ) .

CABG is , too traumatic a surgery , to offer in this low risk coronary lesions.

Exceptions

CABG can still be done in following situations for non LAD single vessel disease.

Left dominant circulation with complex lesions in LCX /OMs.
It is common to see diffuse , long segment and severe disease of RCA with normal LAD /LCX system .PCI is not feasible in this subset.
Failed PCI
Recurrent instent restenosis.
Bail out CABG after a acute complication during PCI

One should remember , inability to do a PCI does not mean , the patient should land in surgeon’s table .We should recall , from our memory medical management is an effective and established form of treatment in single vessel disease ( Mainly for non LAD , and some cases of LAD also !)

Posted in cardiac surgery | Tagged acc.aha, ambrose, bari 2, bari satudy, cabg, cabg vs PCI, cass study, diagonal, double vessel disease, ellis, LAD, lcx, lima graft, mid lad, midcab, obtuse marginal, om 1, om 2, opcab, pci, posterior descending artery, proximal lad, ptca, RCA, single vessel disease, svg graft, syntax score, triple vessel disease, venous graft | 1 Comment »

Biochemical diagnosis of ventricular remodelling

May 7, 2009 by dr s venkatesan

Ventricular remodeling follows large myocardial infarction .This term denotes to change in size , shape and function of the ventricle due to altered myocyte geometry .It is now believed , this process begins to occur very early following a STEMI.(less than 24hours)

In which MI remodeling is more common ?

Any MI of large size , especially anterior and lateral MI. Inferior and posterior MI are less affected by adverse remodeling.The incidence is up to 20% of all myocardial infarction , if left untreated. Ventricular aneurysm formation and dyskinetic segments can be termed as the worst form of remodeling. The old terminologies of infarct extension and expansion could by synonymous with ventrilar remodeling .(Note : Every patient with STEMI undergoes some form of physiological remodeling that should not be confused with progressive pathological remodeling , we are discussing here ! )

What is the clinical impact of remodeling ? How to prevent it ?

Progressive cardiac failure and a poor outcome . It may provoke ventricular arrhythmias. ACE inhibitors (CONSENSUS study 1992 ) has since revolutionized the pharmacological prevention of adverse remodeling.

How to recognise left ventricular remodeling ?

Many methods are available .

2 D Echocardiography
Tissue doppler
LV angiogram
MRI

These imaging methods diagnose remodeling only after it manifest* .We know remodeling is a cellular and molecular process .The earliest trigger for remodeling is the mechanical stretch and wall stress on the ventricles.Large areas of necrosed myocardium and the adjacent normal myocardium sets a perfect stage for eccentric pulling of myocardial segments and unregulated slippage of myocytes.

* Diagnosing fully established ventricular remodeling serves , no great purpose as it is very difficult to reverse it by pharmacological methods.it requires complex surgery.

What is the effect of mechanical stretch on cellular function ?

It is well known myocyte granules secrete Type B -Naturetic peptide in response to stretch. It could be a very early sign of adverse remodeling. So monitoring of BNP may give us an opportunity to intensively treat those patients who are likely to land in progressive cardiac failure.

A baseline level of NT-proBNP >120 pmol/L identified patients prone for adverse remodeling .Serial measurements showed further increase. It is possible to identify adverse remodeling of LV by documenting fresh elevation of BNP following MI .

Reference :

1 )Nilsson JC, Groenning BA, Nielsen G, et al. Left ventricular remodeling in the first year after acute myocardial infarction and the predictive value of N-terminal pro brain natriuretic peptide. Am Heart J 2002;143:696-702.

2)http://content.nejm.org/cgi/content/full/352/7/666#R24

Posted in Cardiology - Clinical, cardiology -Therapeutics, Cardiology -unresolved questions, cardiology- coronary care | Tagged airex, bnp, cardiac failure, consensus, hope aire study, naturetic pepetide, nt bnp, post infarc failure, REMODELING, stemi, VENTRICUALR REMODELLING | Leave a Comment »

A new marker for transudate in pleural effusion

April 17, 2009 by dr s venkatesan

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.

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 | Leave a Comment »

Can we diagnose Infective endocarditis without vegetation ?

April 10, 2009 by dr s venkatesan

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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