Search

Background: Protection from lethal ventricular arrhythmias leading to sudden cardiac death (SCD) is a crucial challenge after acute myocardial infarction (AMI). Cardiac sympathetic and parasympathetic activity can be noninvasively assessed using heart rate variability (HRV) and heart rate turbulence (HRT). The EMBODY trial was designed to determine whether the Sodium–glucose cotransporter 2 (SGLT2) inhibitor improves cardiac nerve activity. Methods: This prospective, multicenter, randomized, double-blind, placebo-controlled trial included patients with AMI and type 2 diabetes mellitus (T2DM) in Japan; 105 patients were randomized (1:1) to receive once-daily 10-mg empagliflozin or placebo. The primary endpoints were changes in HRV, e.g., the standard deviation of all 5-min mean normal RR intervals (SDANN) and the low-frequency–to–high-frequency (LF/HF) ratio from baseline to 24 weeks. Secondary endpoints were changes in other sudden cardiac death (SCD) surrogate markers such as HRT. Results: Overall, 96 patients were included (46, empagliflozin group; 50, placebo group). The changes in SDANN were + 11.6 and + 9.1 ms in the empagliflozin (P = 0.02) and placebo groups (P = 0.06), respectively. Change in LF/HF ratio was – 0.57 and – 0.17 in the empagliflozin (P = 0.01) and placebo groups (P = 0.43), respectively. Significant improvement was noted in HRT only in the empagliflozin group (P = 0.01). Whereas intergroup comparison on HRV and HRT showed no significant difference between the empagliflozin and placebo groups. Compared with the placebo group, the empagliflozin group showed significant decreases in body weight, systolic blood pressure, and uric acid. In the empagliflozin group, no adverse events were observed. Conclusions: This is the first randomized clinical data to evaluate the effect of empagliflozin on cardiac sympathetic and parasympathetic activity in patients with T2DM and AMI. Early SGLT2 inhibitor administration in AMI patients with T2DM might be effective in improving cardiac nerve activity without any adverse events. Trial Registration: The EMBODY trial was registered by the UMIN in November 2017 (ID: 000030158). UMIN000030158; https://upload.umin.ac.jp/cgi-open-bin/ctr_e/ctr_view.cgi?recptno=R000034442. [ABSTRACT FROM AUTHOR]

Competing Interests: Conflict of interest: None declared.

Background: An inter-arm difference in blood pressure (IADBP) is characteristic of acute aortic dissection (AAD), but the importance of which arm exhibits lower blood pressure (BP) and the mechanism underlying IADBP are not well understood., Methods: We identified consecutive patients with chest and/or back pain and suspected acute cardiovascular disease whose BP had been measured in both arms. We retrospectively compared the characteristics of such patients with AAD (n=93) to those without AAD (non-AAD group, n=122). Additionally, we separately compared patients with type A AAD (TAAD group, n=58) or type B AAD (TBAD group, n=35) to the non-AAD group. The characteristics analyzed were patient background and IADBP-related factors, including systolic BP (SBP) in the right arm (R) and left arm (L), and R-L or L-R as IADBP. Computed tomography (CT) findings of AD extending to the brachiocephalic artery (BCA) and/or left subclavian artery (LSCA) were examined in patients with an IADBP., Results: In a comparison of the TAAD group and non-AAD group, the prevalences of R <130 mm Hg (38% vs. 19%, p=0.009), L-R >15 mm Hg (19% vs. 8%, p=0.047), L-R >20 mm Hg (14% vs. 4%, p=0.029) were higher in the TAAD group. Multivariate analysis showed that L-R >15 mm Hg with R <130 mm Hg was independently associated with TAAD (OR 25.97, 95% CI 2.45-275.67, p=0.007). However, IADBP-related factors were not associated with TBAD. AAD patients with L-R >20 mm Hg all had TAAD, and all aortic dissection extended to the BCA just before the right common carotid artery on CT., Conclusions: IADBP was characterized by R

A 54-year-old man was admitted to our hospital for evaluation of chest pain occurring at rest in the morning. ST segment depression was observed during a treadmill exercise test. Coronary angiography identified spontaneous spasm of the proximal right coronary artery, and right coronary obstruction was improved from 90% to about 50% stenosis after intracoronary administration of nitroglycerin. Myocardial iodine-123 beta-methyl-p-iodophenyl-pentadecanoic acid uptake was absent, but thallium-201 uptake during single photon emission computed tomography was normal, and neither platelet nor monocyte expression of the CD36 molecule was observed, indicating type I CD36 deficiency. High blood pressure, elevated plasma triglyceride and fasting plasma glucose levels, and low high-density lipoprotein values suggested metabolic syndrome. The final diagnosis was type I CD 36 deficiency associated with metabolic syndrome and vasospastic angina.