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Christopher A. DeSouza, Ph.D., University of Colorado, Boulder, CO, USA


Hypertension (blood pressure > 140 mmHg systolic and/or 90 mmHg diastolic) is a primary risk factor for premature cardiovascular and cerebrovascular morbidity and mortality. Hypertension is estimated to cause 7.1 million premature deaths and account for ~5% of global disease burden. In 2003, the Seventh Report of the Joint National Committee on Prevention, Evaluation, and Treatment of High Blood Pressure (JNC-7) defined for the first time blood pressures of 120-139 mmHg systolic and/or 80-89 mmHg diastolic as prehypertension. The prehypertension designation was not intended to define a disease state, but rather identify individuals at significantly greater risk for progression to hypertension and development of cardiovascular disease. Indeed, prehypertension, which is prevalent in middle-aged and older adults, is not only a precursor to hypertension, increasing risk two- to threefold, but is now considered an independent risk factor for cardiovascular disease. The increased cardiovascular risk associated with prehypertension may be mediated, in part, by vascular endothelial dysfunction. Vascular endothelial dysfunction occurs early in the pathogenesis of vascular disease and contributes to the development of atherogenic lesions, thrombus formation, vasospasm, plaque rupture, intimal growth, and, in turn, coronary and cerebrovascular events. Primary deficiencies in endothelial function that precedes and predisposes to atherosclerosis and thrombosis include impaired nitric oxide-mediated endothelium-dependent vasodilation, elevated endothelin-1 vasoconstrictor tone and diminished fibrinolytic function. These vascular abnormalities are well-established characteristics of hypertension. However, this atherosclerotic endothelial phenotype associated with hypertension is already apparent in the prehypertensive state.



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