Veno-arterial extracorporeal membrane oxygenation (ECMO) through the femoral vein and artery may cause differential hypoxia, i.e., lower PaO2 in the upper body than in the lower body, because of normal cardiac output with severe impairment of pulmonary function. Hereby, we report the diagnosis and the treatment of differential hypoxia caused by veno-arterial ECMO. A 39-year-old man received cardiopulmonary resuscitation from a cardiac arrest due to acute myocardial infarction. Even after more than 30 min of resuscitation, spontaneous circulation had not resumed. Next, we performed veno-arterial ECMO through the femoral artery and vein, and the patient recovered consciousness on the second day of ECMO. On day 5 of ECMO, he lost consciousness again and presented a generalized tonic-clonic seizure, and an electroencephalogram showed delta waves suggesting diffuse cerebral cortical dysfunction. While an echocardiogram revealed improvements in myocardial function, a follow up chest radiograph showed increasing massive parenchymal infiltrations, and gas analysis of blood from the right radial artery revealed severe hypoxemia. These findings indicated a definite diagnosis of differential hypoxia, and therefore, we inserted a 17-Fr cannula into the left subclavian vein as a return cannula. The patient’s consciousness and pulmonary infiltrations were improved 2 days after veno-arterial-venous ECMO, and the electroencephalogram showed normal findings. To our knowledge, this is the first report of successful clinical management of differential hypoxia. We suggest that veno-arterial-venous ECMO could be the treatment of choice for differential hypoxia resulting from veno-arterial ECMO.

Platelet aggregation is not only an essential part of hemostasis, but also initiates acute coronary syndrome or ischemic stroke. The precise understanding of the activation mechanism of platelet aggregation is fundamental for the development of more effective agents against platelet aggregation. Adenosine diphosphate, thrombin, and thromboxane A2 activate platelet integrin αIIbβ3 through G protein-coupled receptors. G protein-mediated signaling pathways, which are initiated by Gq, G12/G13 or Gi, include phospholipase C with calcium signaling, Rho signaling, protein kinase C and phosphatidylinositol 3-kinase. Rap1b, Ca2+ and diacylglycerol-regulated guanine nucleotide exchange factor I, Rap1-GTP-interacting adaptor molecule, and Akt are important proteins involved in G protein-mediated activation of integrin αIIbβ3. Binding of talin-1 and kindlin-3 to cytoplasmic domains of β3-integrin triggers a conformational change in the extracellular domains that increases its affinity for ligands, such as fibrinogen or von Willebrand factor. Fibrinogens act as bridges between adjacent platelets to generate a platelet aggregate.

The aim of this study was to assess the feasibility, safety, and performance of a novel diagnostic catheter specifically designed for engaging both coronary arteries via the right transradial artery approach. A total of 160 patients were randomized between the standard Judkins (5F R4, L4; Cordis Corporation, Miami, FL) and the 5F Tiger II (Terumo Corporation, Tokyo, Japan) catheters. End points included the duration of various procedures and the assessments of angiographic image quality and catheter performance. The Tiger II was associated with a significantly shorter (40%) total procedure time (199.6+/-50.2 vs. 331.5+/-72.9 s, p=0.001) and a 33% shorter total fluoroscopic time (93.1+/-33.8 vs. 138.2+/-47.6 s, p=0.001) for diagnostic coronary angiography, compared with those with the Judkins catheter. There was no significant difference between the Tiger II and Judkins catheters for left coronary angiographic quality (left anterior descending, 2.82+/-0.48 vs. 2.94+/-0.29, p=0.084; left circumflex, 2.90+/-0.38 vs. 2.87+/-0.44, p=0.629). The Tiger II provided superior right coronary angiograms, compared with the Judkins catheter (2.99+/- 0.11 vs. 2.82+/-0.48, p=0.003). For the left coronary angiograms, the initial randomized catheter completed the procedure in 91% of the patients with the Tiger II and in 98% with the Judkins (p=0.167) catheters. For the right coronary angiograms, 100% were completed with the Tiger II and 95% with the Judkins (p=0.120) catheters. There were no angiographic or clinical complications in either group, so the procedural success rate was 100%. The potential of the Tiger II catheter for use as a multipurpose catheter for right transradial coronary angiography to reduce procedural and X-ray times to the level of classic transfemoral coronary angiography has to be confirmed in a randomized study.

Aims This observational study aimed to investigate the association between beta-blocker therapy and clinical outcomes in patients with acute myocardial infarction (AMI), especially with mid-range or preserved left ventricular systolic function. Methods and results Among 13 624 patients enrolled in the Korea Acute Myocardial Infarction Registry-National Institute of Health (KAMIR-NIH), 12 200 in-hospital survivors were selected. Patients with beta-blockers showed significantly lower 1-year major adverse cardiac events (MACE), which was a composite of cardiac death, MI, revascularization, and readmission due to heart failure [9.7 vs. 14.3/100 patient-year; hazard ratio (HR) 0.84, 95% confidence interval (CI) 0.72–0.97; P = 0.022). However, this association had a significant interaction with left ventricular ejection fraction (LVEF). Beta-blocker therapy at discharge was associated with lower 1-year MACE in patients with LVEF ≤40% (HR 0.63, 95% CI 0.48–0.81; P < 0.001), and 40% <LVEF < 50% (HR 0.69, 95% CI 0.51–0.94; P = 0.020), but not in patients with LVEF ≥50% (HR 1.16, 95% CI 0.91–1.48; P = 0.234). Conclusions Beta-blocker therapy at discharge was associated with better 1-year clinical outcomes in patients with reduced or mid-range LVEF after AMI, but not in patients with preserved LVEF. These data suggested that the long-term beta-blocker therapy may be guided by LVEF.