» Articles » PMID: 21892740

The Correlation Between the Cardio-ankle Vascular Index (CAVI) and Serum Amyloid A in Asymptomatic Japanese Subjects

Overview
Journal Heart Vessels
Date 2011 Sep 6
PMID 21892740
Citations 5
Authors
Affiliations
Soon will be listed here.
Abstract

Chronic inflammation has received a great deal of attention due to the role it plays in cardiovascular disease (CVD). The cardio-ankle vascular index (CAVI) has recently been developed to evaluate arterial stiffness. This index is independent of blood pressure at the time that it is measured, making it a better measure for clinical studies on the prevention of CVD. Information on the association of serum amyloid A (SAA) with arterial stiffness in relatively healthy subjects is still scarce. The aim of the present study was to investigate the potential correlation between SAA and CAVI in asymptomatic Japanese subjects. In addition to SAA and CAVI, data on smoking status, body mass index, blood pressure, and serum/plasma biochemical indices such as glucose and total cholesterol were collected in 387 nonmedicated and CVD-free adult subjects during a health check examination (male/female 191/196, mean age 61.8 years). Among them, a randomly selected subgroup of 256 subjects (male/female 133/123, mean age 62.4 years) had a full dataset, including low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglyceride, and hemoglobin A1c. Among the whole population, CAVI levels were significantly higher in males than in females [mean 8.5 ± (SD 1.1) vs. 8.2 ± 1.1, p < 0.05], while SAA levels were slightly but nonsignificantly higher in females than in males [median 6.4 (interquartile range 4.0-9.3) μg/mL vs. 5.1 (3.5-8.4)]. In a multiple linear regression analysis, CAVI was weakly but significantly, independently, and positively correlated with SAA (β-coefficient 0.200, p < 0.01). The results of the same analyses for the randomly selected subgroup were relatively similar to the findings for the whole population. SAA may be a positive inflammatory factor associated with arterial stiffness, and the clinical relevance and the biological mechanism for this relationship should be established in future studies.

Citing Articles

Adipokines and Arterial Stiffness in Obesity.

Para I, Albu A, Porojan M Medicina (Kaunas). 2021; 57(7).

PMID: 34202323 PMC: 8305474. DOI: 10.3390/medicina57070653.


Relationships Between the Cardio-Ankle Vascular Index and Pulsatility Index of the Common Carotid Artery in Patients With Cardiovascular Risk Factors.

Hitsumoto T J Clin Med Res. 2019; 11(8):593-599.

PMID: 31413771 PMC: 6681855. DOI: 10.14740/jocmr3914.


Relationships Between Skin Autofluorescence and Cardio-Ankle Vascular Index in Japanese Male Patients With Metabolic Syndrome.

Hitsumoto T Cardiol Res. 2019; 10(3):172-180.

PMID: 31236180 PMC: 6575114. DOI: 10.14740/cr878.


Cardio-ankle vascular index (CAVI) as an indicator of arterial stiffness.

Sun C Integr Blood Press Control. 2013; 6:27-38.

PMID: 23667317 PMC: 3650513. DOI: 10.2147/IBPC.S34423.


Olmesartan reduces inflammatory biomarkers in patients with stable coronary artery disease undergoing percutaneous coronary intervention: results from the OLIVUS trial.

Miyoshi T, Hirohata A, Usui S, Yamamoto K, Murakami T, Komatsubara I Heart Vessels. 2013; 29(2):178-85.

PMID: 23563752 DOI: 10.1007/s00380-013-0343-0.

References
1.
Shirai K, Utino J, Otsuka K, Takata M . A novel blood pressure-independent arterial wall stiffness parameter; cardio-ankle vascular index (CAVI). J Atheroscler Thromb. 2006; 13(2):101-7. DOI: 10.5551/jat.13.101. View

2.
Miyoshi T, Doi M, Hirohata S, Kamikawa S, Usui S, Ogawa H . Olmesartan reduces arterial stiffness and serum adipocyte fatty acid-binding protein in hypertensive patients. Heart Vessels. 2010; 26(4):408-13. DOI: 10.1007/s00380-010-0060-x. View

3.
Pietri P, Vyssoulis G, Vlachopoulos C, Zervoudaki A, Gialernios T, Aznaouridis K . Relationship between low-grade inflammation and arterial stiffness in patients with essential hypertension. J Hypertens. 2006; 24(11):2231-8. DOI: 10.1097/01.hjh.0000249701.49854.21. View

4.
Libby P, Ridker P, Hansson G . Inflammation in atherosclerosis: from pathophysiology to practice. J Am Coll Cardiol. 2009; 54(23):2129-38. PMC: 2834169. DOI: 10.1016/j.jacc.2009.09.009. View

5.
Schillinger M, Exner M, Mlekusch W, Sabeti S, Amighi J, Nikowitsch R . Inflammation and Carotid Artery--Risk for Atherosclerosis Study (ICARAS). Circulation. 2005; 111(17):2203-9. DOI: 10.1161/01.CIR.0000163569.97918.C0. View