PS 14-04 THE EFFECTS OF THE VILDAGLIPTIN FOR CARDIAC DYSFUNCTION AFTER THE ACUTE MYOCARDIAL INFARCTION. (September 2016)

• Record Type: Journal Article
• Authors: Nishikido, Toshiyuki; Oyama, Junichi; Tanaka, Atsushi; Ohira, Hiroshi; Node, Koichi
• Is Part Of: Journal of hypertension. Volume 34:(2016) Supplement 1
• Publication Date: 2016-09
• Subjects: Hypertension -- Periodicals; Hypertension -- Periodicals; 616.132005
• DOI: 10.1097/01.hjh.0000501127.66325.bf
• Languages: English
• ISSNs: 1473-5598

Abstract

Abstract : Objective: The diabetes mellitus is one of high risk factors for the acute coronary syndrome. The dipeptidyl-peptidase 4(DPP-4) inhibitors is the antihyperglycemic agents with the possible protective effects for cardiovascular system. It was reported that Glucagon-like peptide-1 had improved left ventricular systolic function, and DPP-4 inhibitors had attenuated post-infarct myocardial remodeling. In contrast, the rate of hospitalization for heart failure was increased by saxagliptin in SAVOR-TIMI 53 trial. The purpose of this study was evaluating effects of DPP-4 inhibitors on the cardiac function by DPP-4 inhibitors in patients with myocardial infarction. Design and Method: We performed an open-label, parallel-group comparison study between vildagliptin treatment group and non-incretin treatment group. A total of 28 patients of type2 diabetes without use of insulin were enrolled and 21 patients were assigned to vildagliptin treatment group and non-incretin treatment group randomly within 48 hours after the acute myocardial infarction onset. Eleven patients had been taken 100 mg of vildagliptin per-day and/or another antihyperglycemic agent in vildagliptin treatment group, and 10 patients had been taken antihyperglycemic agents without incretin agents in non-incretin group. We evaluated the effects and safety for cardiac function by vildagliptin 6 months later. Results: The glycated hemoglobin levels were lower with vidagliptin (5.95 ± 0.94%vs 6.99 ± 1.63%; p = 0.04), and glycemic standard deviation (SD) and J-index without mean amplitude of glycemic excursions (MAGE) in glycemic variability were improved significantly in most of vildagliptin treatment group. (p < 0.05, p = 0.03) There were no serious adverse events such as hypoglycemia, pancreatitis, and the hospitalization for heart failure in either group. There were the protective tendencies but no statistically significant changes of the ejection fraction, deceleration time, E/A, E/e', and BNP levels between two groups. (p = 0.24, p = 0.10, p = 0.40, p = 0.37, and p = 0.25, respectively). Conclusions: Our results suggest that vildagliptin did not improved cardiac dysfunction statistically including the systolic and diastolic functions significantly after myocardial infarction so far.