Understanding
Atherosclerosis
Atherosclerosis is a slow, progressive, systemic disease that may
start in childhood. Pathological changes have been identified in large
arteries as early as fetal life and, by the first decade, the majority
of children are affected.1
In the landmark Pathobiological Determinants of Atherosclerosis in
Youth (PDAY) Study,2
autopsies of over 1,500 patients aged 15 to 34 demonstrated dramatic
and early differences in atherosclerosis between those with bad risk
factor profiles (i.e., high- and low-density lipoprotein-cholesterol
and evidence of smoking) versus those with good profiles. Interestingly,
significant differences were noted in subjects by the age of 15.2
Angiographic studies3
show that the progression of atherosclerosis and coronary artery disease
is neither linear nor predictable. While atherosclerosis progresses
over many decades,1,2,4,5
this condition progresses rapidly in some people in their third decade.
In others, it doesn’t become threatening until they’re in
their fifties and sixties.6
Two characteristics of atherosclerosis are:7
Artery
wall stiffness or reduced arterial compliance, due to tissue degeneration.
Arterial compliance (elasticity of arteries or arterial stiffness)
is an important property of the vascular system that provides the
smooth, continuous flow of blood, while maintaining optimal systolic
and diastolic blood pressures. It is, therefore, an important determinant
of left ventricular function and coronary blood flow.8
For more information on blood pressure as a risk factor, click
here.
Narrowing of the artery due to plaque build-up
Lipid-based lesions contribute to narrowing of the arteries and appear
to predispose the vascular walls to injury and subsequent thrombic
formation. Variable degrees of vascular injury and thrombosis lead
to periodic, but acute ischemic events in the progression of atherosclerosis.
Most of these acute events are subclinical without symptoms, but others
are clinical and include acute coronary syndromes or unstable angina,
myocardial infarction or sudden death.9
Plaque rupture that results in a significant ischemic event is often
apparent at sites with only modest luminal stenosis (blocking of an
artery). Therefore, based on the commonly accepted definition for
a clinically diseased vessel (i.e., > 50% occlusion9),
it is clear that a significant percentage of patients with subclinical
disease suffer catastrophic ischemic events.
The
Degree of Occlusion of Pre-existing Lesions in AMI9
| Patients
who developed an acute myocardial infarction |
Percent
stenosis in patients the pre-exisiting lesion in the infarct-related
artery |
| 52%
of patients |
<
50% stenotic |
| 855
of patients |
<
75% occluded |
| 15%
of patients |
76%
to 100% stenotic |
In
most patients, acute ischemic events are a complication not necessarily
of severe fibrotic and calcified lesions, but rather the disruption
associated with mildly to moderately stenotic, lipid-rich plaques.
Coronary artery plaques with positive remodeling (the size of the
arterial wall expands to accommodate the plaque and maintain blood
flow) have a higher lipid content and are associated with an inflammatory
process, which are both indicators of plaque vulnerability.10,11
Innovations in cardiac biomarkers and instrumentation have fueled
a high level of interest in using these important tools to detect
and assess existent cardiovascular disease and/or stratify cardiac
risk by identifying:
References 
