ME 04-1 ASSESSMENT OF CENTRAL BLOOD PRESSURE FOR CLINICAL APPLICATION

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Abstract

Central Systolic Blood Pressure is lower than brachial artery blood Pressure due to reflected waves and greater augmentation at the periphery. The relationship is not consistent during life and alters with aging of the blood vessels. Increasing stiffness means that a greater component of the reflected waves returns to the central aorta during systolic contraction causing more amplification and a higher systolic blood pressure. Diastolic blood pressure on the other hand is always higher in the aorta than at the periphery allowing blood flow. The heart contracts against the central aortic pressure and it is likely that cardiac hypertrophy iis dependent on this value. Likewise damage to the larger blood vessels are more likely to be related to central rather than brachial pressure and this may reflect a greater association with stroke.

Central aortic pressure may be measured directly but not practicable in large groups of patients or indirect using tonometry and transformation equations. While the correlation is not ideal there is significant correlation. Central aortic systolic blood pressure is associated with mortality, stokes, heart attacks and cardiac hypertrophy with a higher p value than brachial artery blood pressure. The question is whether it is an independent predictor of these events and whether measurement is justifiable in clinical practice. There is a strong correlation between aortic and brachial systolic blood pressure reducing the ability of the central BP to be independent. In addition the question arises does the measurement of central systolic BP provide extra information above pulse wave velocity?

Measuring central systolic blood pressure has allowed an exploration of the effects of different drug classes on central systolic blood pressure. Thus beta blockers increase the amplification index meaning that the fall in central systolic blood pressure is not as great as the fall in brachial artery systolic BP. This may explain in part why beta blockers do not reduce cardiac hypertrophy as well as other drugs despite similar brachial artery levels. ACE Inhibitors and ARBs appear to reduce central pressure more than other agents and may explain some of their extra beneficial effects.

Measurement of central systolic blood pressure by noninvasive techniques has made a significant contribution to our understanding of the haemodynamics of the cardiovascular system. It is a worthwhile technique which has important applications in specific situations. However in routine clinical practice it probably adds little additional information over and above that available by simpler methods.

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