Device based prevention of neurological events in coronary artery bypass patients with calcified ascending aorta.

Patients with severely calcified aorta undergoing conventional cardiac surgery are at increased risk for postoperative neurologic deficits. Implementation of cerebroprotective devices may substantially reduce or even eliminate the risk of adverse neurologic event, thus enabling surgical therapy, especially when interventional treatment cannot be considered an alternative option.

Ameliorative effect of allicin on vascular calcification via inhibiting endoplasmic reticulum stress

Objectives Vascular calcification (VC) is an independent predictor for cardiovascular events and mortality. However, there are currently no effective methods to reverse or prevent it. The present study aimed to determine the ameliorative effect of allicin on VC. Methods VC model of rats was induced by high-dose vitamin D3, which was valued by Alizarin Red staining, calcium contents, and alkaline phosphatase in the aorta. Systolic blood pressure, pulse pressure, and pulse wave velocity were measured to determine aortic stiffness. Protein levels were detected by Western blot. Results Allicin treatment rescued aortic VC and stiffness. The increased protein levels of RUNX2 and BMP2, two markers of osteoblastic phenotype of vascular smooth muscle cells, in the calcified aorta were attenuated by allicin, whereas the decreased levels of calponin and SM22α induced by calcification were improved. Allicin treatment significantly attenuated the increased protein levels of GRP78, GRP94, and CHOP, which are key markers of endoplasmic reticulum stress, in the calcified aorta. The activation of PERK/eIF2α/ATF4 cascades was also prevented by allicin. Conclusions Allicin could ameliorate aortic VC and stiffness. The ameliorative effect of allicin on VC might be mediated by inhibiting PERK/eIF2α/ATF4 cascades. Our results might provide a new proof for VC treatment.

Dysphagia Aortica: A Case Report and Review of Treatment Options

A 64-year-old, cachectic man with body mass index (BMI) <19 visited in clinic with the chief complaint of dysphagia for 6 months. He reported a 2-year history of reflux and heartburn, for which he has been taking pantoprazole but reported only 40% relief of reflux symptoms. He reported progressive solid food mid-chest dysphagia. Additional comorbidities included severe pulmonary bronchiectasis and bullous emphysema and a history of treated pulmonary tuberculosis 40 years prior and two previous episodes of spontaneous pneumothorax in the right-sided lung treated with a chest tube. A chest X-ray showed a calcified aorta crossing the midline (Figure 1). A CT scan done for assessment of pneumothorax showed a torturous descending thoracic aorta and a dilated mid-/proximal esophagus. The diameter of the descending aorta was 41 mm, and it crossed the midline. For evaluation of dysphagia, a barium swallow was performed, which showed a narrowing in the mid-esophagus with proximal dilation and lack of peristalsis (Figure 2). Upper gastrointestinal endoscopy showed a dilated esophagus with eccentric extraluminal compression. High-resolution manometry (HRM) showed an absence of peristalsis and a vascular pressure artifact around the mid-esophagus correlating with the external aortic compression (Figure 3). Due to alarming weight loss and a BMI <19, we recommended a feeding jejunostomy to maintain nutrition before scheduling definitive treatment.

MicroRNA profiles in calcified and healthy aorta differ: therapeutic impact of miR-145 and miR-378

Our goal was to elucidate microRNAs (miRNAs) that may repress the excess bone morphogenetic protein (BMP) signaling observed during pathological calcification in the Klotho mouse model of kidney disease. We hypothesized that restoring healthy levels of miRNAs that posttranscriptionally repress osteogenic calcific factors may decrease aortic calcification. Our relative abundance profiles of miRNAs in healthy aorta differ greatly from those in calcified mouse aorta. Many of these miRNAs are predicted to regulate proteins involved in BMP signaling and may control osteogenesis. Two differentially regulated miRNAs, miR-145 and miR-378, were selected based on three criteria: reduced levels in calcified aorta, the ability to target more than one protein in the BMP signaling pathway, and conservation of targeted sequences between humans and mice. Forced expression using a lentiviral vector demonstrated that restoring normal levels repressed the synthesis of BMP2 and other pro-osteogenic proteins and inhibited pathological aortic calcification in Klotho mice with renal insufficiency. This study identified miRNAs that may impact BMP signaling in both sexes and demonstrated the efficacy of selected miRNAs in reducing aortic calcification in vivo. Calcification of the aorta and the aortic valve resulting from abnormal osteogenesis is common in those with kidney disease, diabetes, and high cholesterol. Such vascular osteogenesis is a clinically significant feature. The calcification modulating miRNAs described here are candidates for biomarkers and “miRNA replacement therapies” in the context of chronic kidney disease and other procalcific conditions.

MicroRNA Profiles in Calcified and Healthy Aorta Differ: Therapeutic Impact of miR-145 and miR-378

Our goal was to elucidate microRNAs (miRNAs) that may repress the excess bone morphogenetic protein (BMP) signaling observed during pathological calcification in the Klotho mouse model of kidney disease. We hypothesized that restoring healthy levels of miRNAs that post-transcriptionally repress osteogenic calcific factors may decrease aortic calcification. Our relative abundance profiles of miRNAs in healthy aorta differ greatly from those in calcified mouse aorta. Many of these miRNAs are predicted to regulate proteins involved in BMP signaling and may control osteogenesis. Two differentially regulated miRNAs, miR-145 and miR-378, were selected based on three criteria: reduced levels in calcified aorta, the ability to target more than one protein in the BMP signaling pathway, and conservation of targeted sequences between humans and mice. Forced expression using a lentiviral vector demonstrated that restoring normal levels repressed the synthesis of BMP2 and other pro-osteogenic proteins and inhibited pathological aortic calcification in Klotho mice with renal insufficiency. This study identified miRNAs that may impact BMP signaling in both sexes and demonstrated the efficacy of selected miRNAs in reducing aortic calcification in vivo. Calcification of the aorta and the aortic valve resulting from abnormal osteogenesis is common in those with kidney disease, diabetes, and high cholesterol. Such vascular osteogenesis is a clinically significant feature. The calcification modulating miRNAs described here are candidates for biomarkers and “miRNA replacement therapies” in the context of chronic kidney disease and other pro-calcific conditions.

A clampless anastomosis technique using the aortic cannula mounted by a prosthetic graft for a severely calcified aorta in a patient with subclavian steal syndrome

Patients with severely calcified aorta are at high risk of embolic stroke during surgery and it is not feasible to clamp the aorta, necessitating alternative surgical strategies. We present a clampless anastomosis technique using the aortic cannula mounted by a prosthetic graft for a severely calcified aorta in a patient with subclavian–vertebral artery steal syndrome.