Robert Greenbaum, MD, Cardiology, Interventional, 08:38PM Nov 15, 2009
Today I went to two major sessions and took a walk around the exhibition. I was struck by the feeling that the recession was hitting the meeting. Fewer people were at the meeting compared with my last visit to the AHA two years ago. It also seemed that the exhibition was on a smaller scale. I gather from one of the officials that total registrations were down - he did not say by how much - I would guess about 10 - 15%. Interestingly foreign registrations are much the same so for whatever reason less American physicians are attending.
The morning session "Circulation Editors' Choices" was excellent. My particular favourite presentation concerned the (TIME - CHF) trial and its subsequent discussion. This trial looked at the possible benefit of drug therapy guided by N-terminal brain-type naturetic-peptide (NT-proBNP) levels, as compared with conventional symptom-guided management in patients with severe congestive cardiac failure. The trial found no significant difference to the primary end point of hospitalization-free survival at 18 months. The discussion pointed out that the trials of agents such as beta blockers, ace inhibitors / angiotensin II receptor blockers and spironolactone on which we base current treatment guidelines looked at younger patients than are often encountered in clinical practice. I would also point out that many were stopped early because they seemed to indicate such a great treatment advantage. This makes me uneasy. Older patients can and do respond differently to medication. It was pointed out that the effect of this trial design was to continue to increase the doses of therapy in patients in the guided therapy group because in spite of therapy the target NT-proBNP levels were not reached. Increasing doses of drugs in older patients might not be the optimal policy. It was felt that NT-proBNP levels were a useful diagnostic tool and indicator of prognosis but were not useful in guiding treatment. It was clear to me that there is a need for further trials of treatment for older patients with congestive cardiac failure.
Another fascinating presentation concerned the production of induced Pluripotent stem cells (iPS). Stem cell research has generated much ethical concern and debate particularly research which has used human embryonic stem cells. At medical school, I was taught that during embryonic development that as stem cells differentiated into the various tissues of the body eg neurones, cardiac muscle and liver cells this was a "one way street". There was no way to turn a liver cell into a cardiac muscle cell. This seemed to me unlikely because differentiation involves the turning off of various synthetic pathways in cells as they become more specialised. However all somatic cells have essentially the same DNA so it seemed to me that there might be ways of turning these pathways back on so returning cells to a dedifferentiated state. Happily medical science continues to question received wisdom and challenge immutable "facts". It was explained that it is now possible to take differentiated murine cells and "reprogramme" them so that they become plurpotent cells (iPs) very similar in their properties to true embryonic stem cells. It is possible to take these and then stimulate them so that collections of these cells take on many of the contractile and electrophysiological properties of cardiac myocytes. Clearly I have simplified the technique greatly. One can see that if the "donor adult cells" were from a human source such as chord blood there would be little moral objection to such a technique. Even better if we could supply our own donor cells perhaps for later use. This technique has many potential applications out side the heart eg in degenerative neurological disease such as Parkinson's. Interestingly in the discussion it was mentioned that if pluripotent cells are introduced into the myocardium they "sense" where they are and develop along the "myocyte" route. Clearly we are some way from being able to replace fibrous scar following myocardial infarction but I would like to imagine that at some stage part of the job of the interventional cardiologist would not be to simply suck out the clot and stent the coronary artery but to inject down the affected coronary cells that would populate the myocardium and with restored blood flow minimise the damage to the heart.
I did say in one of my earlier postings that I would not confine myself to discussing the latest stent technology and certainly today I think I have done that.