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Reciprocal ST elevation in unstable Angina

August 10, 2008 by dr s venkatesan

Is reciprocal ST  segment changes  occur  only in STEMI ? Can it occur in UA/NSTEMI ?   

                           

                      Even   after   100 years of electro cardiology   the electrophysiological mechanism of ST elevation in STEMI  and ST depression in Unstable  angina is   still in the hypothetical stages. One popular theory   says that the   current of injury   as we see   as  ST  segment elevation  in surface ECG  is  actually   an illusion. It’s   apparently due to   constant negative current    pushing down the   rest of ECG segments. Ironically   the concept   of  reciprocal ST depression in patients who have  ST elevation is well debated  for over 3 decades and  is considered  a  settled issue. It   probably   represents , a  purely electrical phenomenon where the  tail end  of the  lead   picks up the opposite vector. Even   as   conflicts   continue to confront the basic electro physiological   concepts management    strategies   of   acute coronary syndromes is witnessing   great strides.
Aim
                                     We   hypothesized   if   ST depression occurs as response to ST elevation it’s logic to expect strong ST depressive forces should  possibly elevate The ST segments in the reciprocal leads .
In fact  we have seen this phenomenon in three distinct  clinical situations. 
1) ST   elevation   in posterior leads: Patients who present   with isolated   ST depression in V1,  V2 , V3  and  ST elevation in posterior chest leads V7, V8 .These patients were initially thought to have isolated posterior MI. But later the cardiac enzymes were found to be normal   indicating no myocardial necrosis   echo evaluation revealed wall motion defects in anterior segments rather than in posterior segments. CAG revealed critical   LAD disease .  This we believe a pure reciprocal ST elevation in the posterior leads to  a  ST depressive forces in anterior leads.
 2) Inferior  ST   elevation   with ST depression   in   V4- V6 : Few  patients who present with  infero    lateral STEMI   later  do not  evolve into  Q  MI but as a NSTEMI .The initial ST elevation  was found  be transient and  disappeared  much earlier,  while the  ST depression  lateral leads persisted.
 3) ST elevation in AVR   in high risk unstable angina :As   already reported in the literature,  we have seen  ST  elevation in AVR  in patients with  high risk unstable angina. This was   more often observed when there is > 3mm ST depression in V4-V6. The AVR  ST elevation  possibly   represents   the  reciprocal  vector.
    Conclusion
                                            ST elevation in certain   specific leads in   some of the patients with ACS,   could   be   a pure reciprocal   electrical phenomenon   to   dominant ST depressive forces in Opposite leads .  And hence   ST elevation in the surface ECG during early hours of ACS   should be interpreted more cautiously. The   sanctity   assocociated with ST segment   elevation   could  be  opened   for debate. 
 
                                     To down load full PPT  click on  the slide

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Posted in Cardiology - Electrophysiology -Pacemaker, cardiology -ECG, Uncategorized | Tagged , , , , , , , | Leave a Comment »

What are the angiographic correlates of lateral myocardial infarction ?

August 9, 2008 by dr s venkatesan

                    Lateral myocardial infarction is not a common site when compared to anterior and inferior MI. But the lateral MI has some unique features, since it involves free wall of the ventricle.The laplace law mediated wall stress is more as the dyskinetic segments bulge with a long radius .Due to this,  lateral MI has a distinctly high risk for free wall rupture .Further pericardial rub is more common in thse patients.Ischemic mitral regurgitation and vulnerability to LVF is also more prevalent if the lateral wall is involved.  Generally lateral MI pateints have a turbulent and complicated course than a simple inferior or anteroseptal MI.

The angiographic correlation of  lateral MI is rarely reported in literature.

The following leisons are commonly observed.

1. Proximal  LAD with large D1  involvement

2. Isolated large D1/D2 disese

3.A left dominat LCX  with large OM1 disease

4.Large ramus disease

5.LAD total and RCA to LAD/D1 collateral pattern

Final message

If we encounter a lateral MI either alone or in combination with inferior/  posterior MI , it is better to manage these patients  aggresively with early triaging for CAG and revascularisation.

Posted in cardiology- coronary care, Infrequently asked questions in cardiology (iFAQs) | Tagged , , , , , , | Leave a Comment »

“ Wave Red Flag” For Anticoagulation, When You Encounter Mobile LV Clot

August 8, 2008 by dr s venkatesan

To download complete presentation click on the slide

“ WAVE RED FLAG” FOR ANTICOAGULATION, WHEN YOU ENCOUNTER MOBILE LV CLOT !

Venkatesan Sangareddi , G. Gnanavelu ,M.A Rajasekar, V.Jaganathan

Department of cadiology , Madras medical college , Chennai.

Formation of LV mural thrombus is one of the important sequel of STEMI. The natural history of LV clot is variable. Spontaneous dissolution often occur . Stroke and peripheral embolism, are other natural events by which left ventricle get rid of the clot. The morphology and the behavior of LV clot is determined by endogenous procoagulant and fibrinolytic mechanisms. Drugs administered in the peri infarct phase also play an important role. In current thrombolytic era ,the incidence of LV clot has come down. Once the clot begins to form over the raw area adjoining a dyskinetic segment, it follows the local hemodynamic factors , that determine the shape , size of the clot which varies from linear , layered , projectile or pedunculated.

Administration of oral anticoagulants remain the standard practice in patients with LV clot. It is prescribed , in the hope that it will prevent the progression of clot and prevent thrombo embolism . Whether, long term warfarin dissolve , regress or dislodge the thrombus is not known. We have observed the incidence of CVA is high in the first few weeks following introduction of oral anticoagulants . We report our experience in 8 patients, with LV clot in Acute MI . All patients were male . Age range 22-58 .All had anterior MI. The mean EF was 38%(28-43%) the mean size of LV clot was 1.4cm (7mm -24mm) mobility was graded with reference to independent movement parallel or perpendicular to the LV. 3 had highly mobile clot. 5 had relatively fixed clot. All were put on titrated warfarin. Two patients who had large LV clot with a stalk got dislodged after starting anticoagulation. The CVA occurred on 12 th and 14 th day after starting warfarin .The pedicle is probably the vulnerable point and is exposed to greatest risk for dissolution . On the other hand the 5 patients who showed relatively stable clots are attending to our cardiology OPD without any events . One patient who had a mobile clot , which got organized at 4 weeks , incidentally this patient had discontinued anticoagulants.

We conclude, oral anticoagulation has a potential to destabilise and dislodge a mobile LV clot in the early days following STEMI .Existing anticoagulation protocol recommends, oral anticoagulation for all patients who have LV clot. This need to be redefined. If surgery is not an option , temporary withdrawal of anticoagulation may be indicated in selected patients with LV clot, to facilitate organization of clot.


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Isolated distal coronary artery disease : A newly recognised entity among CAD population.

August 6, 2008 by dr s venkatesan

Coronary artery disese  predominantly  occur in the proximal segments of coronary artery.The fact that CAD is mainly a proximal disese , implies  that  clincal impact is likely to be more . But we now recognise distal coronary artery system is equally affected .But isolated distal CAD  is a not a common finding .We describe our analysis on the topic .

distal-cad-csi-2005

Click on the slide to download

Posted in cardiology- coronary care | Tagged , , , , , , , , , | 1 Comment »

Transient ischemic attacks (TIA s) can it occur in coronary circulation?

August 6, 2008 by dr s venkatesan

Transient ischemic attacks are not exclusive to cerebral circulation.

Many such episodes can occur in coronary circulation also .

TIA of heart PPT presentation

Click here to download  tia-of-heart

Posted in cardiology- coronary care, My presentations | Tagged , , , , , , | Leave a Comment »

Is there a role for plain balloon angioplasty today ? If so where ?

August 5, 2008 by dr s venkatesan

 

Is it a crime to do a plain balloon angioplasty in 2008 ?

Plain balloon angioplasty,   the greatest  innovation in   cardiology  when it was introduced in 1977 in a Zurich cath lab , has now become an  ugly  word for most of the cardiologist !

Why this turn around ?  Has technology ,  really overtaken a great procedure and made it obsolete now ?

The answer is a definite ” No”

The restenosis which was the villian in the plain old angioplasty has never been overcome even today. Stents initally used as a bail out procedure during  abrupt closure , later it was used conditionally, followed by provisional stenting and now in 2008  we are made to believe  it is mandatory.

When we realised , bare metal stents are equally  bad (If not slightly better ) in arresting the restenosis drug eluting stents came into vogue with a big bang in 2002. It was projected as the ultimate breakthrough in interventional cardiology and  in 5 years the truth was exposed and it not only failed to prevent the restenois but also had a dreaded complication of acute stent thrombosis.

Now we know , metals  inside a coronary artery  carry  a life long  risk of sudden occulusion , and we talk about biodegradable stents (With poly lactic acid ).

 Common sense ( Unscientific truths)  would suggest

Plain balloon angioplasty still has a major role in our global  cardiovascualr population.

Since restenosis is the  only issue here, ( about 30% )  we can choose patients in whom even if restenosis is likely to happen  no major harm is done . A vast majority of chronic stable angina patients  fall in this category.

Aggressive lipid lowering with plain  balloon angioplasty has never been tested properly . In future also it is unlikely,  such trials will be done as it would be considered unethical . But that would be a premature conclusion.

The other major issue is the cost of stenting , the procedure of PCI/PTCA  has become unaffordable for most of the population in developing countries .The primary reason being the PCI without stenting is considered  ” A untouchable” . If only we remove this stigma from the cardiology community   a signiificant population will be benefited.

A patient with chronic stable angina treated with POBA ,if develop further angina after few years , he  is likely to get a recurrence of  relatively safe  stable angina.  While in a post PCI patient  any angina after the procedure becomes a unstable angina ( Braunwald classification)  and requires emergency care . Angina in a  stented patient is can not be taken lightly as  the the course of angina is unpredictable .

POBA in primary PCI ?

Many may think it is a foolish idea . It has been found many times,  when we rush the pateint to   cath lab after a STEMI  we are in for a surprise !. About 30% of times it is a very complex lesion profile  like diffuse disese,  tight bifurcation lesions , loaded with thrombus or a left main disese.

We fail to realise a basic  fact  , the  initial aim of primary PCI is to salvage the myocardium ,and the next comes the prevention of restenosis . It may even , be argued salvaging  myocardium is the only aim ! Myocardial salvage sould be done urgently . And even  removing the thrombus and opening a IRA can be suffice in a patient who is crashing on table.  Of course stenting can be done whenever possible. But for IRAs which has complex anatomy attempting a perfect stent PCI   (Some may require more than few stents)  as an emergency procedure invariably affects the outcome. One should spend  shortest possible time  inside the  illfated coronary artery. Prolonged manipulations within the coronary artery in an unstable patient  aiming at  longterm patency of an IRA  is to be avoided .The pending procedures can always planned in a next stage. 

Final message

So it is not a crime to think about plain balloon  angioplasty  in some of  our  patients  with acute or chronic coronary syndromes .  Hope Gruentzig  is listening from the heaven and hopefully agree with me !

Dr.S.Venkatesan, madras medical college, chennai, India .

Posted in Cardiology -Interventional -PCI, Infrequently asked questions in cardiology (iFAQs) | Tagged , , , , , , , , , , , , , , , , , , , , | 1 Comment »

Can we suck out left ventricular apical clots with a suction catheter device in post MI patients?

August 4, 2008 by dr s venkatesan

LV clot formation is one of the important complications of acute myocardial infarction. Preventing this is difficult and managing this problem is still more difficult.Some of these clots are linear and laminar along the shape of LV apex and carry less risk of dislodging.

 While mobile LV clots , even if it is small can cause a embolic episode. Most of these patients have a significant LV dysfunction and they are candidates for early CAG and revascularisation. Even If the coronary anatomy is very ideal for a PCI these patients are often sent for CABG and physical removal of LV clot . If  only ,we have an option to remove these LV clots by a catheter based modality, we can offer them a totally non surgical cure.

This is not impossible,  considering  we are in the era of percutaneous implantation of prosthetic valve in Aorta ! The only issue is potential embolism into carotids and periphery .A temporary distal protection at the level of aortic root will prevent that .

Device companies shall produce one such exclusive catheter system to remove LV clot.

Dr .S.Venkatesan, Madras medical college, Chennai,India

Posted in Cardiology -Interventional -PCI, Infrequently asked questions in cardiology (iFAQs), Uncategorized | Tagged , , , , , , , , , , , | Leave a Comment »

Postural diastolic dysfunction:Is it the mechanism of orthopnea in CHF ?

August 1, 2008 by dr s venkatesan

Orthopnea is a classical sign of established CHF.

While paroxysmal nocturnal dyspnea is an early sign of cardiac failure,orthopnea is a late manifestation of cardiac failure .This symptom was mainly attributed to volume displacement from systemic venous to pulmonary circulation when the patient goes to recumbent posture.The exact mechanism of this has been speculative. Now with liberal usage of bedside echocardiography, we have found out there is postural variation in the diastolic function of the failing left venticle.

Many patients develop a restrictive ventricular filling pattern in recumbent posture (Grade 3 diastolic dysfunction). While sitting up some of them revert to normal or downgrade to grade 1 diastolic dysfunctionThis observation proves another fact that every patient with severe systolic dysfunction also has significant diastolic dysfunction at some point in their course of illness.

Posted in Cardiology - Clinical, Infrequently asked questions in cardiology (iFAQs) | Tagged , , , , , , , | 2 Comments »

Journal club debates : Can a “Aim of a study” be wrong ?

July 27, 2008 by dr s venkatesan

Peer review of an article even in major journals never scrutinise the “Aim of  a study ” . However big is the journal,  they seem to bother only about the authors, materials, methods, and statistical analysis.  If only they peer review an article , right from the “Aim of the study” like ,

  • Who asks the research questions?
  • Who  defines the aim of the study ?
  • Who decides which drug to be compared with which drug ?
  • Who steers the steering commitee of a trial ?

If only , we could answer these questions without bias , pharma industry and their  regulators  would have ,  far more better image than what they have now !

A typical example for , the aim of the study  to be  wrong  , is  the “ONTARGET’ study on telmisartan.

Here they ( Who ? ) raised an inappropriate  question of     “Non inferiority” of one drug with other  without any  valid reason to compare these two drugs that will benefit the man kind !

Posted in cardiology -Therapeutics | Tagged , , , , , , , , , , , , , , , , , , | 2 Comments »

Is pulmonary artery atherosclerosis possible ? Are we under diagnosing it ?

July 26, 2008 by dr s venkatesan

Atherosclerosis is  the number one killer of mankind  .It involves all medium and large sized blood vessels.Any intima and media can be invaded by the disese process.Most common to involve are  cerebral, carotid, coronary, aortic  and it’s branches, renal, and peripheral arteries. But how pulmonary artery is missing in this list ? Is it really true (or) are we missing it ? One logical explanation is pulmonary circulation is a low pressure circulation and the maximum presssure is less than  30mmhg . This pressure may be insufficient to induce endothelial injury that predispose lipid mediated injury.

Other explanation could be a structural difference in the media and intima compared to aorta .But in patients  with primary or secondary pulmonary hypertension where,   inspite of PA pressure being high ,  still atherosclerotic changes is very uncommon . or Is it the Heath Edwards pulmonary vascular sclerosis  grading  reflects nothing but pulmonary atherosclero-thrombosis !

If this is true there could be a major role for HMG Coa reductase inhibitors in altering the natural course of pulmonary obstructive vascular  disese . Statins might be tried in PPH  a disese with no specific  treatment !

Posted in Infrequently asked questions in cardiology (iFAQs), Uncategorized | Tagged , , , , , | 1 Comment »

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