Clearly, macrovascular complications are the prognosis limiting problem of
diabetes patients which consecutively account for the majority of socio-eco
nomic burden of the disease. The overall morbidity and mortality developmen
t does not indicate improvement hallmarking better or at least adequate car
e for these patients. Possible explanations address the late detection prob
lem of a clinically silent disease onset as well as unrecognised multiple c
omorbid conditions all of which end-up with en dothelial dysfunction as rep
resentation of the so called "functional atherosclerosis" and blood hyper r
esponsiveness. Here, we describe new experimental aspects of the early athe
rosclerosis development focussing inflammation as one driving pathogenetic
force for the evolution of the complicated lesion type in diabetes. However
, emphasis is put on the view that inflammation, atherogenesis and thrombog
enesis are severely crosslinked by soluble and cellular adhesion molecules.
From a diagnostic point of view genomic detection of risk associated genes
opens both the vision of early identification of high risk individuals and
the targetting of drug intervention based on conditioned responsiveness. B
y using available drugs and evidence based risk factor intervention strateg
ies a plea is made for a multimodal therapeutic approach fitted to the indi
vidual patient's needs aiming at endpoint reduction. This corresponds to th
e recent releases of guidelines from nearly all vascular medicine related s
cientific societies. Diabetes is a vascular disease!