Archive for July, 2008

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 !

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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 !

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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 .

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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 !

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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.

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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 !

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Salvaging lung tissue is not the aim in pulmonary embolism , Hence Time window is a myth !

There is a time window for thrombolysis in myocardial infarction ( STEMI). This time window is to salvage myocardium before it dies.The average time window in STEMI is 12 hours. When does the lung start dying in Pulmonary embolism ?.Is salvaging lung tissue an aim in the management of pulmonary embolism ?. Not really .Lung parenchymal death occurs only in minority of patients with pulmonary embolism .

The bronchial artery continue to supply the lungs.

So the aim here is to restore pulmonary circulation and oxygenation. Hence there is no strict time window in the management of pulmonary embolism.

The General consensus is , one can attempt thrombolysis up to 7 days after diagnosing pulmonary embolism.

Beyond this time, it is believed thrombus gets organised and thrombolytic agents may be ineffective.

But this is only an assumption, in an individual patient thrombolysis may be done even beyond this period if warrented by clinical intuition .

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

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Atrial septal defect is one of the common congenital heart disese. Surgical correction or device closure is indicated in all patients  with significant shunts. Statistically for every  ASD diagnosed  with  more than 2:1 shunt there must be  is atleast three pateints  with ASD with less than 2:1 shunt in general population. Do we diagnose it ? . Some may be miss diagnosed as PFO.

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Heart is a muscular pump .But it contains more of  non muscular cells than contractile cells.

The average human heart which weighs 300 -400 grams . Contrary  to the popular perception heart is not purely a muscular organ. In fact myocytes constitutes only 30% of heart mass. Rest formed by


2.Endothelial cells

3.Purkinje cells

4.Interstitial cells


6.Fibrous skeleton

7.Extracellualr matrix.

Why is this important to recognise ?

Cardiac failure is not synonymous with myocardial failure .

Many times cardiac failure is due to supporting structure failure like in connective tissue disorders.

Exceesive fibroblast proliferation and resulting in fibrosis of heart.

Cardiac interstitial failure is new emerging clincal entity.

In future individual cell based therapy will aim  at replacing specific cells that are defective or depleting.


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How is LAD angina differnt from RCA angina ?

Can we localise the “Angina related artery ”  from the  the type of chest pain ?

Patients with stable  angia  many times have  multivessel CAD. There has been some correlation with radiation of anginal pain and the culprit artery.If the angina spreads to jaw or neck it is possibleit might indicate RCA(RIGHT coronary angina) but rarely it indicates LAD/LCX lesions. if the angina radiates to left shoulder it virtually ruels out a RCA disease

Source .Braunwald 1992 Edition

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

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