Switching Dipeptidyl Peptidase-4 Inhibitors to Tofogliflozin, a Selective Inhibitor of Sodium-Glucose Cotransporter 2 Improve Arterial Stiffness Evaluated by Cardio-Ankle Vascular Index in Patients with Type 2 Diabetes: A Pilot Study

Bekki, Munehisa; Tahara, Nobuhiro; Tahara, Atsuko; Igata, Sachiyo; Honda, Akihiro; Sugiyama, Yoichi; Nakamura, Tomohisa; Sun, Jiahui; Kumashiro, Yuki; Matsui, Takanori; Yamagishi, Sho‐ichi

doi:10.2174/1570161116666180515154555

Cited by 22 publications

(16 citation statements)

References 53 publications

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“…Post hoc analysis of data from the EMPA‐REG BP trial showed a trend toward a reduction in the ambulatory arterial stiffness index ( P = .059) in patients with type 2 diabetes mellitus treated with empagliflozin for 24 weeks 34 . Looking specifically at CAVI, this was significantly reduced 6 months after switching from a dipeptidyl peptidase‐4 (DPP‐4) inhibitor to the SGLT2 inhibitor tofogliflozin in patients with type 2 diabetes 35 . The latter two trials had a longer duration of action than the current study, and it is possible that treatment with an SGLT2 inhibitor for longer than 12 weeks may be necessary to detect beneficial effects on arterial stiffness in patients with type 2 diabetes mellitus.…”

Section: Discussionmentioning

confidence: 99%

Effects of luseogliflozin on arterial properties in patients with type 2 diabetes mellitus: The multicenter, exploratory LUSCAR study

Kario

Okada

Murata³

et al. 2020

J of Clinical Hypertension

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Section: Discussionmentioning

confidence: 99%

Effects of luseogliflozin on arterial properties in patients with type 2 diabetes mellitus: The multicenter, exploratory LUSCAR study

Kario

Okada

Murata³

et al. 2020

J of Clinical Hypertension

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“…Nagayama et al 64) reported that glimepiride, a third generation sulfonylurea, improves CAVI and markers of insulin resistance and oxidative stress, but glibenclamide, a conventional sulfonylurea, has no such effects. A recent study shows that switching DPP-4 inhibitors to the sodium-glucose cotransporter-2 inhibitor tofogliflozin ameliorates CAVI that correlates with the level of advanced glycation end products 65) . These findings suggest that postprandial hyperglycemia, insulin resistance and oxidative stress may influence CAVI in patients with diabetes.…”

Section: (B) Diabetes Mellitusmentioning

confidence: 99%

New Horizons of Arterial Stiffness Developed Using Cardio-Ankle Vascular Index (CAVI)

Saiki

Ohira

Yamaguchi

et al. 2020

JAT

105

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Arterial stiffness is recognized mainly as an indicator of arteriosclerosis and a predictor of cardiovascular events. Cardio-ankle vascular index (CAVI), which reflects arterial stiffness from the origin of the aorta to the ankle, was developed in 2004. An important feature of this index is the independency from blood pressure at the time of measurement. A large volume of clinical evidence obtained using CAVI has been reported. CAVI is high in patients with various atherosclerotic diseases including coronary artery disease and chronic kidney disease. Most coronary risk factors increase CAVI and their improvement reduces CAVI. Many prospective studies have investigated the association between CAVI and future cardiovascular disease (CVD), and proposed CAVI of 9 as the optimal cutoff value for predicting CVD. Research also shows that CAVI reflects afterload and left ventricular diastolic dysfunction in patients with heart failure. Furthermore, relatively acute changes in CAVI are observed under various pathophysiological conditions including mental stress, septic shock and congestive heart failure, and in pharmacological studies. CAVI seems to reflect not only structural stiffness but also functional stiffness involved in acute vascular functions. In 2016, Spronck and colleagues proposed a variant index CAVI0, and claimed that CAVI0 was truly independent of blood pressure while CAVI was not. This argument was settled, and the independence of CAVI from blood pressure was reaffirmed. In this review, we summarize the recently accumulated evidence of CAVI, focusing on the proposed cutoff values for CVD events, and suggest the development of new horizons of vascular function index using CAVI. appropriate in studies that examine the effect of hypertension or the effect of antihypertensive drugs on intrinsic arterial stiffness. To overcome this problem, Hayashi 4) proposed the stiffness parameter , an index reflecting arterial stiffness of local arterial segment, which is not influenced by blood pressure at the time of measurement. Subsequently, this theory has been applied to a new arterial stiffness index called cardio-ankle vascular index (CAVI) developed in 2004 5) , and this index reflects the stiffness of the arterial tree from the origin of the aorta to the ankle. The CAVI equation was essentially derived from the stiffness parameter , and the changes of the artery caliber in the equation during the cardiac cycle were obtained Copyright©2020 Japan Atherosclerosis Society This article is distributed under the terms of the latest version of CC BY-NC-SA defined by the Creative Commons Attribution License.

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“…After 6 months of treatment, CAVI was significantly reduced, concomitantly with markers of visceral obesity, advanced glycation end products and UA. 149 Empagliflozin, a potent and highly selective SGLT-2 inhibitor, 150 was shown to reduce blood pressure and improve measures of arterial stiffness in diabetic patients. 151,152 However, the protective cardiovascular effect of SGLT-2 inhibitors has been shadowed by the results from postmarketing studies which indicate significant adverse effects, such as an increased risk of diabetic ketoacidosis and leg amputations.…”

Section: Uricosuric Medicationmentioning

confidence: 99%

<p>Uric Acid and Arterial Stiffness</p>

Albu¹,

Para²,

Porojan³

2020

TCRM

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Hyperuricemia is usually associated with hypertension, diabetes mellitus, metabolic syndrome and chronic kidney disease. Accumulating data from epidemiological studies indicate an association of increased uric acid (UA) with cardiovascular diseases. Possible pathogenic mechanisms include enhancement of oxidative stress and systemic inflammation caused by hyperuricemia. Arterial stiffness may be one of the possible pathways between hyperuricemia and cardiovascular disease, but a clear relationship between increased UA and vascular alterations has not been confirmed. The review summarizes the epidemiological studies investigating the relationship between UA and arterial stiffness and highlights the results of interventional studies evaluating arterial stiffness parameters in patients treated with UA-lowering drugs.

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Switching Dipeptidyl Peptidase-4 Inhibitors to Tofogliflozin, a Selective Inhibitor of Sodium-Glucose Cotransporter 2 Improve Arterial Stiffness Evaluated by Cardio-Ankle Vascular Index in Patients with Type 2 Diabetes: A Pilot Study

Abstract: The present study suggests that switching DPP-4 inhibitors to tofogliflozin ameliorates arterial stiffness in T2DM patients partly via improvement of liver function. Baseline serum levels of AGEs may identify patients who improve arterial stiffness more after treatment with tofogliflozin.

Cited by 22 publications

References 53 publications

Effects of luseogliflozin on arterial properties in patients with type 2 diabetes mellitus: The multicenter, exploratory LUSCAR study

Effects of luseogliflozin on arterial properties in patients with type 2 diabetes mellitus: The multicenter, exploratory LUSCAR study

New Horizons of Arterial Stiffness Developed Using Cardio-Ankle Vascular Index (CAVI)

<p>Uric Acid and Arterial Stiffness</p>

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