No abstract

Background Aortic stenosis ( AS ) is highly prevalent in patients with atherosclerotic cardiovascular disease. Advanced glycation end products ( AGE s) and the receptor for AGE s ( RAGE ) play a pivotal role for vascular calcification in atherosclerosis. We hypothesize that the AGEs– RAGE axis could also be involved in the pathophysiological mechanism of calcified AS . Methods and Results A total of 54 patients with calcified AS who underwent aortic valve replacement were prospectively enrolled from 2014 to 2016 (mean age 75.3±7.7 years). Aortic valve specimens were obtained from 47 patients and 16 deceased control subjects without aortic valve disease (mean age 63.2±14.5 years). The valvular expression of RAGE was evaluated by immunohistochemistry. Serum levels of AGE s and soluble RAGE were measured in 50 patients with calcified AS and 70 age‐matched and sex‐matched control subjects without heart disease. The valvular RAGE expression in patients with calcified AS was higher than controls ( P =0.004) and was significantly associated with a decreased ankle‐brachial pressure index ( P =0.007) and an increased intima‐media thickness ( P =0.026). RAGE and α–smooth muscle actin were coexpressed and were partially costained with osteocalcin and alkaline phosphatase. The serum levels of AGE s and soluble RAGE were significantly higher in the patients with calcified AS than in the controls ( P =0.013 and P <0.001, respectively). Soluble RAGE (inversely) and use of aspirin were independently correlated with changes in left ventricular systolic function after aortic valve replacement ( P =0.012 and P =0.002, respectively). Conclusions Our present study suggests that RAGE may play a role in the pathogenesis of calcified AS , which is a prognostic marker in patients with AS after aortic valve replacement.

No abstract

A 67-year-old man was admitted to our hospital following cardiopulmonary arrest CPA during work. After resuscitation, coronary angiography revealed left main coronary artery stenosis and three-vessel disease. We considered that coronary artery revascularization was required, but the neurological prognosis was unknown. Thus, an IMPELLA CP ® device was inserted and systemic management, including hypothermic therapy, was initiated. Circulatory conditions were stable during hypothermia therapy. Rewarming was initiated 24 h later, and we confirmed no abnormal neurological findings. Emergency off-pump coronary artery bypass was then performed. During the procedure, hemodynamic status was maintained using the IMPELLA CP ® device. After surgery, the patient was discharged without neurological complications. We report the management of a patient with severe three-vessel disease after resuscitation for CPA using an IMPELLA CP ® device and hypothermic therapy.

No abstract