Large clinical trials provide invaluable information. This, combined with a
number of small studies about the pathophysiology of certain diseases, per
mits us to re-consider previously accepted pathophysiological mechanisms an
d suggests an updated theory about the definition and diagnosis of individu
al diseases. This information obtained appears to place unstable angina in
a new light. The instability of unstable angina seems to be the transient m
oment in which the previous clinical state is abandoned to pass into anothe
r clinical condition, rather than the establishment of a new diagnosis or n
osological entity. Is this then the end of unstable angina as a final diagn
osis?
The development of troponin has increased our ability to identify myocardia
l necrosis. The myocardial ischemia leading to myocardial necrosis is the m
ost important issue in atherosclerosis. In addition, immune cell activation
may also relate to the extent of necrosis. The activation of the immune/in
flammatory system in patients with acute coronary syndromes is probably not
exactly related with the presence of an unstable plaque per se, as is usua
lly inferred by inflammatory markers, but with the total atherosclerotic bu
rden in the arterial tree of these patients.
After all the new evidence of studies regarding coronary syndromes, is it n
ot the time to reconsider the definition of unstable angina?