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This study was conducted in healthy Japanese subjects to examine the effects of age and gender on the relationship between the risk factors for cardiovascular disease (CVD) and augmentation index (AI), and the effects of clusters of those risk factors on AI. Radial arterial pressure wave analysis was used to obtain AI in 3675 men and 2919 women. AI was found to be higher in women than in men, and age-related increase in AI showed an attenuated curve in subjects aged X50 years. A step-wise multivariate linear regression analysis showed that mean blood pressure and smoking are independent significant variables related to AI in men regardless of age, and in women aged o50 years, but not in women aged X50 years. A general linear model univariate linear regression analysis showed that mean blood pressure and smoking had a significant interaction for their relation with AI in men, but not in women. In conclusion, among the risk factors for CVD, smoking and blood pressure were found to be independent factors related to increase in AI. Although age-related attenuation of increase in AI was confirmed in Japanese subjects, these risk factors may act to increase AI even in elderly subjects, at least in part. However, the effects of these factors on AI may differ based on gender, and these factors may act synergistically to increase AI in men. On the contrary, these factors may act independently in young women to increase AI without interaction, whereas only the blood pressure seems to increase AI in elderly women. Keywords: age; augmentation index; gender; risk factors INTRODUCTION Accumulating evidence suggest that increased arterial stiffness is an independent risk for cardiovascular disease (CVD). 1-3 The augmentation index (AI) is a marker related to systemic arterial stiffness, and some studies reported that increased AI or central blood pressure estimated by AI predicts future cardiovascular events. [4][5][6] Some studies reported that CVD risk factors affect AI. 7-11 The age-related increase in AI shows an attenuated curve in subjects aged 450 years, and AI is thought to be less sensitive in reflecting arterial stiffness in elderly subjects. 12 Although AI increases predominantly in women, the Second Australian National Blood Pressure Study (ANBP 2 study) showed that it cannot be used as a marker for predicting future CVD events in elderly women with hypertension. 13 Matsui et al. 14 examined the effects of age and gender on AI in subjects with hypertension under anti-hypertensive medication. However, their study could not avoid the influence of anti-hypertensive medication on the results. Thus, the effects of both age and gender on the relationship between the risk factors for CVD and AI in healthy individuals have not been fully clarified. Furthermore, although it is noted that a cluster of those risk factors additively or synergistically augments the progression of

EG-MYH7 [R403E], EG-HFE [Cys282Tyr+/+], EV-HCMV, EG-A-TTR [V30M], EM-sarcoidosis SA-I, SA-II *The morphofunctional phenotype description (M) may contain more information using standard abbreviations, such as AVB, atrioventricular block; WPW, Wolff-Parkinson-White syndrome; LQT, prolongation of the QT interval; AF, atrial fibrillation; ↓R, low electrocardiogram voltages; ↓PR, short PR interval. † Organ (O) involvement in addition to the H subscript (for heart) should be expanded for the involvement of M, skeletal muscle; O, ocular system; A, auditory system; K, kidney; L, liver; N, nervous system; C, cutaneous; G, gastrointestinal system, and other comorbidities, including MR, mental retardation. ‡ Genetic (G) describes the available information about inheritance of the disease. It also provides complete information if the family history is not proven or unknown, and if genetic testing has not been performed or was negative for the mutation/mutations identified in the family. § The etiologic annotation (E) provides the facility for the synthetic description of the specific disease gene and mutation, as well as description of nongenetic etiology. || The functional annotation or staging (S) allows the addition of ACC/ AHA stage and NYHA functional class.

Cardiotoxicity is a limiting factor in the treatment of cancer with adriamycin. We administered adriamycin by a method which minimizes the risk of peritonitis in an adriamycin-induced cardiomyopathy rat model. Sixty male Wistar rats were given Ž . 1 mgrkg of adriamycin intraperitoneally 15 times over a 3-week period total dose, 15 mgrkg to induce the cardiomyopathy model. Fifteen control rats received 10 mlrkg body wt. saline 15 times over 3 weeks. The animals were observed for 12 weeks and assessed for mortality, and cardiac volume and function was analyzed by echocardiography at 4, 8, and 12 weeks. In rats treated with adriamycin, the cumulative mortality was 35.8% while in the controls, none of the rats died. Left ventricular Ž . Ž . diameter of the systole LVDs was significantly increased at 4 weeks 4.5 vs. 3.3 mm; P-0.001 . Left ventricular diameter of Ž . Ž . Ž . the diastole LVDd was significantly increased at 12 weeks 7.9 vs. 7.0 mm; P-0.01 and the % fractional shortening FS Ž . was significantly decreased at 8 weeks 33.4% vs. 50.0%; P-0.01 in the adriamycin-treated rats. This administration method appears to be useful for investigating the cardiac effect of adriamycin while avoiding the influence of peritonitis typically caused by an intraperitoneal injection of higher single doses of adriamycin. ᮊ