Showing posts with label MYOCARDIAL ISCHAEMIA. Show all posts
Showing posts with label MYOCARDIAL ISCHAEMIA. Show all posts

Monday, 24 September 2012

Translation at its best?

The key word in science nowadays is Translation i.e. how to get something useful from a scientific discovery. There is still some merit in finding out facts just for the sake of finding out facts - after all we need to make a discovery first before one is able to extract value out of it.
The concept of Translation is now given great importance because I suppose it is that part of science that drives economic growth or in medicine leads to better outcomes. Translation has always been the main Raison d'etre for my liking of science. This is one reason I really like papers like this one  -  and it pleases me to see that the main author is a chairman of Clinical and Translational Science at the University of Colorado School of Medicine - it strikes me that Professor Wischmeyer is fulfilling his role rather well.  Another reason for appreciating this paper is its simplicity - no expensively acquired, parenterally administered complex monoclonal antibodies - just a simple inexpensive orally taken small molecule - it's nearly too good to be true.
Translating positive studies of myocardial preservation from small animal models to humans is fraught with difficulty. Some cardiac surgeons may also argue that the methods we have to preserve the human heart during iatrogenic periods of ischaemia are already very good and that we do not need anything new. That is probably true for a significant number of cases in as much as deaths from poor heart preservation are very rare.  However, they still occur and more importantly, the nonlethal effects of myocardial preservation injury cost alot to treat requiring expensive intensive or high dependancy care. Any study of an intervention that demonstrates an improvement in the markers of myocardial injury sustained in heart surgery cannot be ignored - especially when the intervention is so simple. 

Tuesday, 26 July 2011

POOR RENAL FUNCTION AND MYOCARDIAL NECROSIS


NDT
This is a very interesting study. One wonders whether if this increased level of myocardial necrosis associated with diminished renal function applies to global cardiac ischaemia that occurs in cardiac surgery. It is well known that any degree of renal dysfunction is associated with poorer outcomes after cardiac surgery. This phenomenon may explain why.
What is not known and what surely must be a good avenue for study is why does impaired renal function lead to increased myocardial necrosis?

Sunday, 1 May 2011

BAD SCIENCE (REPORTING)

New heart attack jab even more effective than statins - Telegraph
Read this story and you might think that this is a report of a new treatment for patients with coronary artery disease that was compared in a randomised controlled trial with statins and that most of the work was done in Leicester, UK.

Tuesday, 28 December 2010

TROPONIN RE-INVENTED

This and another article in a recent edition of JAMA illustrates the significance of the new, now commonly used,  high sensitivity troponin assays. With the old assay, one thought of troponin as essentially being present or not and when present, usually indicative of myocardial damage. These new assays have confirmed that troponin is and has always present in the circulating blood stream and that levels consistent with myocardial necrosis are now much higher. Does this mean that at any time there is always a 'turn over' of myocytes? These newly available assays are also good news for researchers of cardiac ischaemia re-perfusion and in the case of cardiac surgery for those who are trying to develop the 'perfect' cardioplegic solution. One is now able to detect smaller levels of myocardial damage and as confidence intervals for these assays are likely to be narrower, required number of individuals to show a significant difference will be smaller.
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