While more than 6,000,000 U.S. patients have symptomatic coronary
artery disease, many more adults have some degree of asymptomatic
atherosclerosis affecting their arteries. Because individuals
with mild atherosclerosis usually experience no symptoms, the
total number of adults with asymptomatic disease is unknown. In
1998 stroke affected approximately 600,000 people, killing more
than 158,000; peripheral vascular disease resulted in 306,000
hospitalizations and 43,000 deaths. Many patients die suddenly
and unexpectedly from arteriosclerotic vascular disease, and the
therapeutic options are limited once a stroke occurs. There is
now a clear evidence that the atherosclerotic process begins in
youth. Thus, the identification of individuals with asymptomatic
disease would be of major importance to permit institution of
preventive measures.
Conventionally, atherosclerosis was presumed to be a degenerative
and slowly progressive disease that affected the vascular function
via its mechanical effects on blood flow. It was thought to most
significantly affect small arteries supplying the myocardium and
brain and was considered an end-stage disease of the elderly.
Consequently, surgical approaches have typically been implemented
during which the most significant lesions were treated mechanically
with the aim of increasing lumen diameters in the affected arterial
segments.
Recently, cellular and molecular research of the processes leading
to arterial plaque development demonstrated that the course of
atherosclerotic disease may be altered by administration of lipid
lowering drugs, particularly the statins. Clinical trials proved
that statins yield a major reduction in clinical events caused
by plaque rupture, although their affect on lesion size was minimal.
Statins therefore exhibit plaque stabilizing properties. The outcome
of these lipid-lowering trials is highly important since it calls
for a change from a quantitative characterization of arterial
narrowing to a quantitative assessment of plaque composition,
morphology, and vulnerability. New methods must be developed for
non-invasive determination of plaque composition in vivo and for
using this information in clinical decision-making as well as
for population screening.
Once non-invasive assessment of plaque vulnerability is available,
it will dramatically change the way in which atherosclerotic disease
is diagnosed, monitored, and treated. Plaque composition, its
mechanical stress consequences, as well as its hemodynamic consequences
in more developed lesions will be determined, and cardiovascular
risk will be assessed on a per-subject basis. Biochemical markers
of atherosclerosis will likely contribute as well. This will serve
as an indication for either pharmaceutical or localized interventional
treatment. Many steps remain to be accomplished and many hurdles
overcome to reach such a level of sophistication. Nevertheless,
there is no doubt that this is an extremely promising and challenging
direction of current and future cardiovascular research.
