Arterial stiffness is an age-related disorder. In the medial layer of arteries, mechanical fracture due to fatigue failure for the pulsatile wall strain causes medial degeneration vascular remodeling. The alteration of extracellular matrix composition and arterial geometry result in structural arterial stiffness. Calcium deposition and other factors such as advanced glycation end product-mediated collagen cross-linking aggravate the structural arterial stiffness. On the other hand, endothelial dysfunction is a cause of arterial stiffness. The biological molecular mechanisms relating to aging are known to involve the progression of arterial stiffness. Arterial stiffness further applies stress on large arteries and also microcirculation. Therefore, it is closely related to adverse outcomes in cardiovascular and cerebrovascular system. Cardio-ankle vascular index (CAVI) is a promising diagnostic tool for evaluating arterial stiffness. The principle is based on stiffness parameter β, which is an index intended to assess the distensibility of carotid artery. Stiffness parameter β is a two-dimensional technique obtained from changes of arterial diameter by pulse in one section. CAVI applied the stiffness parameter β to all of the arterial segments between heart and ankle using pulse wave velocity. CAVI has been commercially available for a decade and the clinical data of its effectiveness has accumulated. The characteristics of CAVI differ from other physiological tests of arterial stiffness due to the independency from blood pressure at the time of examination. This review describes the pathophysiology of arterial stiffness and CAVI. Molecular mechanisms will also be covered.

Background: Endothelial insulin resistance is insulin‐insensitivity in the vascular endothelium and can be observed in experimental models. This study aimed to investigate endothelial insulin resistance in patients with suspected coronary artery disease. To this end, a novel method of obtaining freshly isolated arterial endothelial cells from a radial catheter sheath was developed. Methods and Results: Freshly isolated arterial endothelial cells were retrieved from catheter sheaths placed in radial arteries for coronary angiography (n=69, patient age 64±12 years). The endothelial cells were divided into groups for incubation with or without insulin, vascular endothelial growth factor, or acetylcholine. The intensity of phosphorylated endothelial nitric oxide synthase at Ser1177 (p‐ eNOS ) was quantified by immunofluorescence microscopy. The percentage increase of insulin‐induced phosphorylated endothelial nitric oxide synthase correlated negatively with derivatives of reactive oxygen metabolites, an oxidative stress test ( r =−0.348, n=53, P =0.011), E/E′, an index of left ventricular diastolic dysfunction in Doppler echocardiography (ρ=−0.374, n=49, P =0.008), and log‐transformed brain natriuretic peptide ( r =−0.266, n=62, P =0.037). Furthermore, percentage increase of insulin‐induced p‐ eNOS was an independent factor for the cardio‐ankle vascular index (standardized coefficient β=−0.293, n=42, P =0.021) in the multivariate regression analysis of adaptive least absolute shrinkage and selection operator. Conclusions: Our results suggested that endothelial insulin resistance is associated with oxidative stress, left ventricular diastolic dysfunction, heart failure, and arterial stiffness.

The management of chronic disseminated intravascular coagulation (DIC) caused by aortic dissection has not yet been established. Even in cases where surgical correction is performed, therapeutic control of systemic hemorrhaging is still required. We herein report the successful treatment of a case of aortic dissection with a patent false lumen using tranexamic acid for acute exacerbation of chronic DIC. Oral administration of 1,500 mg tranexamic acid per day stabilized the coagulative and fibrinolytic parameters and relieved bleeding tendencies with no side effects. Heparin was administered periodically for the management of hemodialysis. This favorable result continued for up to 3 years.

Adjusted-dose warfarin therapy can prevent stroke in patients with atrial fibrillation. However, the quality of the warfarin control may be considered to be important for elderly patients. methods: We followed 188 patients (age > or =70 years) with atrial fibrillation (warfarin, 120 patients; non-warfarin, 68 patients) for 2 years. Their warfarin control was assessed by time in therapeutic range (TTR) for an international normalized ratio of prothrombin time of 1.6-2.6, based on the Japanese guidelines of anticoagulation for elderly patients with atrial fibrillation. Stroke occurred in 23 patients (12.2%). In warfarin-treated patients, receiver-operator characteristic (ROC) curves suggested that patients with TTR >68% had anticoagulation benefit. In the ROC curves for prediction of stroke, the area under the curve of TTR was 0.709 (95% confidence interval, 0.585 to 0.834; p=0.02). The sensitivity and specificity of TTR < or =68% were 91.7% and 54.0%, respectively. Kaplan-Meier curves showed that the event-free ratio of stroke was significantly higher in patients who achieved this cut-off of TTR. The results suggest that the quality of warfarin control is directly associated with the incidence of stroke in elderly patients.