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(Hypertension. 2004;43:531.)
© 2004 American Heart Association, Inc.

Editorial Commentaries

Diastolic and Pulse Pressure: The Old and the New?

From the Department of Clinical Pharmacology, School of Medicine, Flinders University, Adelaide, Australia.

Correspondence to Dr Arduino A Mangoni, Department of Clinical Pharmacology, Flinders Medical Centre, Bedford Park, SA 5042, Australia. E-mail arduino.mangoni@flinders.edu.au

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The human aorta plays a major role in determining cardiac afterload and arterial hemodynamics. Therefore, alterations in aortic wall composition are likely to produce important circulatory changes. Aortic wall calcification, a common feature of the atherosclerotic process, is associated with reduced arterial distensibility (or increased arterial stiffness), higher systolic blood pressure, and lower diastolic blood pressure, hence an increase in pulse pressure. These hemodynamic changes impose a burden on the cardiovascular system: an increase in systolic blood pressure further increases cardiac afterload and promotes left ventricular hypertrophy whereas a reduction in diastolic blood pressure may critically reduce coronary perfusion, thus triggering ischemia.

Until recent years, the imaging of the aorta in atherosclerosis has received little attention if compared with the coronary and carotid arterial beds. Nevertheless, the burden of atherosclerosis in the aorta correlates well with the degree of atherosclerosis in other vascular beds. Moreover, aortic calcification is a strong and independent predictor of cardiovascular morbidity and mortality.¹ This should prompt studies aimed at identifying the factors responsible for the presence and progression of aortic calcification to understand the underlying pathophysiological mechanisms and identify preventive pharmacological and non-pharmacological strategies. The data published so far have demonstrated a positive relationship between systolic blood pressure, and perhaps pulse pressure, and the presence of aortic calcification.^2–5 However, the frequent coexistence of complex metabolic conditions, such as end-stage kidney failure, diabetes, and hyperlipidemia,^2–5 potentially confounding this relationship, the relative small sample size,² the lack of serial assessment of aortic calcification progression, and the retrospective . . . [Full Text of this Article]