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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 »

Can medical managment save a patient with cardiogenic shock ?

July 19, 2008 by dr s venkatesan

CCU’S can also save  patients with cardiogenic shock

Many of us would say ” never” or some may say “rarely” but in reality the answer is “yes it can ” slightly lower than  Primary PCI . One could save atleast  few  lives every month by  intensive medical  management alone (Inotrope, vasodilator,pacing if needed ) in any coronary care unit.

So the message here is, not offering or doing  a primary PCI in a patient with cardiogenic shock is not  synonymous with  inferior treatment or death.  After all, in the much hyped SHOCK  trial a significant no of patients survived in medical limb .

Posted in Cardiology - Clinical, cardiology -Therapeutics, cardiology- coronary care | Tagged , , , , , , , | Leave a Comment »

Can primary neural pain originate from heart ?

July 19, 2008 by dr s venkatesan

Are we missing an entity called Primary cardiac neuralgia ?

Unexplained chestpain even after elaborate investigation is a very common clinical cardiac problem. Cardiac neural plexus has a complex network with mainly autonomic network ,with somatic projections. Neural dysfunction could occur in any organ which has rich neural network.Diabetes is the classical example of cardiac autonomic dysfunction and result in silent ischemia. The same disease can result in stimulation of type c nerve fibres that could result in cardiac neuralgic pain , which we may wrongly attribute to ischemia. One of the manifestation of this phenomenon occurs in syndrome X .

Future research is aimed at

Imaging cardiac neurons and sympathetic receptors will shed light on this . But clinical experience has taught us there should be many other sources of cardiac pain other than ischemia and neural pain definitely plays an important role.

It may take years to prove this by evidence !

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

If aortic dissection is the most painful clinical condition why coronary dissection is least painful?

July 19, 2008 by dr s venkatesan

Thousands of dissections happen in cath labs  all over the world every day  very rarely it is painful . The answer is not clear. Both have rich vasa nervorum. Aortic dissection  involves media and smooth muscle . Coronary dissection may also be a  equally painful  , probably we are not recognising it ! or we attribute   all  chest pain in ACS  to ischemia .

Deep dissections into the smooth muscle should be painful.  Type c nerve fibers carry pain signals from heart

Answers welcome.

Posted in Cardiology -Interventional -PCI | Tagged , , , , , , , , , , , , | 1 Comment »

Is plaque fissure or rupture painful ?

July 19, 2008 by dr s venkatesan

Plaque fissure ,rupture and subsequent thrombois is the hallmark of acute coronary syndrome . Are these events painful ? We always attribute any chest pain in an ACS patient to ischemia of myocardium.Is that always true? Coronary artery also has a rich vasa nervorum that could be activated by plaque disruption.

Why  we need an answer to this question ?

We are triaging patients for early invasive apporach based on chestpain .

Many patients may be subjected to revascularisation process for an non ischemic coronary pain !

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

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