Over time, foam cells accumulate and
form atheromas or plaque. Plaque can either grow in to the lumen of the artery
where it blocks blood flow or into the wall of the artery where it does not
block blood flow. Either type can break off into the bloodstream and trigger
blood clot formation. In one histologic
study, coronary tissue from diabetics contained a greater amount of lipid –rich
atheromas and more macrophage infiltration, both of which are associated with a
greater risk for plaque rupture and a higher incidence of thrombosis (Nesto,
2009). Increased platelet adhesion and
decreased fibrinolysis also promotes thrombus formation in persons with
diabetes (Heuther & McCance, 2008).
Obesity is also associated with
chronic low grade inflammation. Obesity causes the metabolic stretching of
adipose tissue, activating inflammatory responses and macrophage recruitment.
Adipose secretes active adipokines such as C- reactive protein (CRP), tumor
necrosis factor –alpha and monocytes chemotactic protein-1 which have a
proinflammatory and atherogenic response (Arora &Chahwala, 2009). These
adipokines reduce insulin sensitivity and contribute to endothelial
dysfunction. Recent work has suggested
that free fatty acids may be the driving force behind insulin resistance and
perhaps even beta cell dysfunction (Isley &Ligaray, 2008).
Hypertension is defined as a sustained
systolic blood pressure greater than 140 and a diastolic blood pressure greater
than 90 based on two or more separate readings. (Rosendorff,
et al,2007). Hypertension can be primary, also known as essential, or
secondary. Primary hypertension accounts
for 90 to 95 percent of hypertensive cases. The cause of primary hypertension
is largely unknown but it is believed that multiple genes interact with
environmental factors. Besides genetic
predisposition other risk factors for hypertension include advancing age,
smoking, obesity, high dietary sodium intake, heavy alcohol consumption and
glucose intolerance.
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