Clinical Impact of Perfusion Balloon for ST-segment Elevated Myocardial Infarction: RYUSEI Study.

Drug-eluting stents have significantly contributed to reducing mortality in patients with ST-segment elevation myocardial infarctions (STEMIs), but slow flow/no-reflow phenomenon (SFNR) and in-stent restenosis are still clinical problems. On the other hand, perfusion balloons (PBs) can compress thrombi and ruptured plaque for long inflation without ischemia and can be used as a delivery device for infusion of nitroprusside to distal risk area during ballooning. We conducted RYUSEI (Reduction of risk bY perfUsion balloon for ST-segment Elevated myocardial Infarction) study to evaluate whether PBs before stenting are more effective than conventional stenting for STEMIs. We divided consecutive patients with STEMIs who underwent optical coherence tomography (OCT)-guided percutaneous coronary intervention (PCI) into PB group who were treated with PBs (Ryusei®; Kaneka Medix Corporation, Osaka, Japan) before stenting and the conventional PCI (CP) group. We compared clinical results including SFNR, OCT findings, and clinical events between the two groups. We finally analyzed 34 patients in PB group and 90 in CP group. After propensity score matching, PB and CP groups consisted of 23 patients, respectively. In the propensity score-matched cohort, SFNR and maximum protrusion area detected by OCT were significantly lower (P=0.047 and P=0.019) and TIMI flow grade 3 higher (P=0.022) in the PB group than CP group. Kaplan-Meier analysis revealed a significantly better clinical outcome in PB group than CP group (p=0.038). In conclusion, the RYUSEI study revealed a pre-stent lesion modification in addition to nitroprusside infusion using PB is useful to achieve better clinical course in STEMI patients.

Prognostic Comparison of Octogenarian vs. Non-Octogenarian With Acute Decompensated Heart Failure　- AURORA Study.

BACKGROUND: Acute decompensated heart failure (ADHF) is the main cause of hospitalization and death of octogenarians, but no data on the 1-year post-discharge mortality rate. We evaluated the clinical status and predictors of 1-year mortality in octogenarians with ADHF.Methods and Results: From the AURORA (Acute Heart Failure Registry in Osaka Rosai Hospital) study, we examined 1,246 hospitalized ADHF patients. We compared the in-hospital mortality rate and the proportion of heart failure (HF) with preserved ejection fraction (HFpEF) between octogenarians and non-octogenarians. After discharge we compared the 1-year mortality rate between these groups, and we also evaluated the predictors of death in both groups. The proportion of HFpEF among the in-hospital deaths of octogenarians was significantly higher than in non-octogenarians (46.2% vs. 15.0%, P=0.031). The 1-year mortality rate after discharge was significantly higher in the octogenarians than non-octogenarians (P=0.014). Multivariable Cox regression analysis revealed that albumin ≤3.0 g/dL and antiplatelet agents were useful predictors of 1-year death after discharge of octogenarians whereas chronic kidney disease was a predictor in the non-octogenarians. CONCLUSIONS: The proportion of HFpEF among in-hospital deaths of octogenarians with ADHF was high as compared with non-octogenarians. When octogenarians with ADHF have severe hypoalbuminemia and antiplatelet agents, early nutritional and medical interventions after discharge may be important to improve the 1-year prognosis.

Prdm13 regulates subtype specification of retinal amacrine interneurons and modulates visual sensitivity.

Amacrine interneurons, which are highly diversified in morphological, neurochemical, and physiological features, play crucial roles in visual information processing in the retina. However, the specification mechanisms and functions in vision for each amacrine subtype are not well understood. We found that the Prdm13 transcriptional regulator is specifically expressed in developing and mature amacrine cells in the mouse retina. Most Prdm13-positive amacrine cells are Calbindin- and Calretinin-positive GABAergic or glycinergic neurons. Absence of Prdm13 significantly reduces GABAergic and glycinergic amacrines, resulting in a specific defect of the S2/S3 border neurite bundle in the inner plexiform layer. Forced expression of Prdm13 distinctively induces GABAergic and glycinergic amacrine cells but not cholinergic amacrine cells, whereas Ptf1a, an upstream transcriptional regulator of Prdm13, induces all of these subtypes. Moreover, Prdm13-deficient mice showed abnormally elevated spatial, temporal, and contrast sensitivities in vision. Together, these results show that Prdm13 regulates development of a subset of amacrine cells, which newly defines an amacrine subtype to negatively modulate visual sensitivities. Our current study provides new insights into mechanisms of the diversification of amacrine cells and their function in vision.