The cardio-ankle vascular index (CAVI) is a new arterial stiffness index of the arterial tree from the origin of the aorta to the ankle, and was essentially derived from the stiffness parameterβtheory proposed by Hayashi. The conspicuous feature of CAVI is independency from blood pressure at the time of measurement.Aim:
The purpose is to clarify the meaning of CAVI as a surrogate marker of arteriosclerosis, and also the role of CAVI in the blood pressure control system.Results:
We reported that during a prospective study on 1000 patients for 7 years, a high CAVI was shown to be a predictive factor for cardiovascular events. Among antihypertensive drugs, we observed that Olmesartan (ARB) and Efonidipine (CCB) decreased CAVI, as well as decreasing blood pressure, indicating that those depressants would improve arterial stiffness.Results:
As for a regulatory factor of blood pressure, we observed that the CAVI value increased when blood pressure decreased during blood removal in the rabbits. And, CAVI value decreased, when blood pressure recovered by blood transfusion. Heart to ankle pulse wave velocity (hsPWV) was changed associating with blood pressure.Results:
During hypotensive attacks in patients taking hemodialysis therapy, some cases increased CAVI whereas other cases decreased CAVI. The former 's hypotension is associated with a reduction in cardiac output. The latter's hypotension was not associated with a reduction in cardiac output, but was associated with an increase in the high frequency of the coefficient of variation of R-R intervals (CVRR), indicating that parasympathetic nerve stimulation might decrease blood pressure by decreasing stiffness of the muscular arteries.Results:
In patients suffering from hypotension shock by sepsis, CAVI decreased, indicating that endotoxins might dilate the muscular arteries.Conclusion:
CAVI was reflecting arterial stiffness, independently from blood pressure at mearing time, and might also reflect a part of vascular resistance. By measuring CAVI, the blood pressure control mechanism could be evaluated in several situations, as well as using it as a surrogate marker for arteriosclerosis.