Novel Transcatheter Approach to Treat Primum Atrial Septal Defects.

•Degenerative common AVC defect can mimic rheumatic MV stenosis.•Closure of primum ASD can be achieved percutaneously.•Live 3D multiplanar TEE is crucial for procedural guidance.

Intracoronary snaring of the retrograde guidewire: A novel method to solve compartment mismatch in complex retrograde CTO PCI.

The retrograde approach has allowed a remarkable improvement in the success rate of chronic total occlusion (CTO) percutaneous coronary intervention (PCI). After collateral channel crossing, the most crucial aspect of retrograde CTO PCI is creating the connection between the antegrade and retrograde system. Currently, the most common technique to achieve this is reverse controlled antegrade and retrograde subintimal tracking. However, this maneuver sometimes fails due to compartment mismatch (intraplaque situation of one wire and extraplaque situation of the other). New approaches are therefore needed to overcome challenges in this important step of the procedure. Here we present an innovative solution to this problem, which involved capturing the retrograde guidewire (advanced into a side branch at the distal cap) with a microsnare that had been advanced antegradely: this severed the dissection flap separating the antegrade and retrograde system, thus allowing us to successfully recanalize the CTO.

Complex Retrograde Chronic Occlusion Percutaneous Coronary Intervention via a Gastroepiploic Artery Graft.

Surgical bypass grafts are commonly used retrograde conduits to facilitate chronic total occlusion (CTO) percutaneous coronary intervention (PCI). While extensive experience exists using saphenous vein grafts as retrograde conduits in CTO PCI, information on the utilization of arterial grafts is more limited. In particular, the gastroepiploic artery (GEA) is a very uncommonly used arterial graft in contemporary bypass surgery and its role for retrograde CTO recanalization has received little study. We describe a case of right coronary artery CTO that was recanalized using the retrograde approach via a GEA graft to the posterior descending artery and highlight the specific challenges of this approach.

Multimodality Imaging Assessment of Anomalous Aortic Origin of the Left Main Coronary Artery Presenting With Syncope and Non-ST Elevation Myocardial Infarction.

Anomalous aortic origin of a coronary artery (AAOCA) is a rare congenital abnormality associated with myocardial ischemia and sudden cardiac death. We present a case of a 20 year old previously healthy male presenting with exertional syncope and non-ST elevation myocardial infarction. Coronary computed tomography angiography showed an anomalous left main coronary artery arising from the right coronary cusp with a slit-like appearance, acute angle origin, intramural course, and a subsequent inter-arterial course between the main pulmonary artery and the proximal aorta. Cardiac magnetic resonance imaging demonstrated myocardial infarction in the distribution of the left main coronary artery. The patient underwent successful surgical correction with unroofing of the left main coronary artery. He has had no syncopal episodes or recurrence of chest pain and returned to full duty status in the United States Marine Corps. This case report demonstrates the evaluation and management of a patient with AAOCA.

Effects of Process Improvement on Guideline-Concordant Cardiac Enzyme Testing.

Easily implemented ordering practices in the electronic health record increased the rate of guideline-concordant testing, decreased cost, and furthered the goal of high-value medical care.

Chest pain in a patient with a tall R wave in V1.

An 83-year-old man 2 days postoperative from L3 to L5 laminectomy developed sudden onset of chest pain. Initial ECGs demonstrated a tall R wave in V1 and ST-segment depression in leads V2-V5. A posterior ECG was performed, but failed to demonstrate ST elevations. The patient was initially treated as an non-ST-segment elevation myocardial infarction with weight-based enoxaparin. On further review, the patient's ECG was identified as a STEMI equivalent, and he underwent cardiac catheterisation. He was noted to have a near complete occlusion of the posterior descending branch of the right coronary artery (RCA). Bare-metal stents were placed in the proximal and distal RCA, with restored flow distal to the lesions. The patient was transferred to the intensive care unit for observation, and was noted to develop atrial fibrillation. Rate control was achieved with diltiazem, and the patient was started on dabigatran. Medical therapy including aspirin and clopidogrel was initiated, and the patient was discharged home.

Integrated genomic analysis of relapsed childhood acute lymphoblastic leukemia reveals therapeutic strategies.

Despite an increase in survival for children with acute lymphoblastic leukemia (ALL), the outcome after relapse is poor. To understand the genetic events that contribute to relapse and chemoresistance and identify novel targets of therapy, 3 high-throughput assays were used to identify genetic and epigenetic changes at relapse. Using matched diagnosis/relapse bone marrow samples from children with relapsed B-precursor ALL, we evaluated gene expression, copy number abnormalities (CNAs), and DNA methylation. Gene expression analysis revealed a signature of differentially expressed genes from diagnosis to relapse that is different for early (< 36 months) and late (≥ 36 months) relapse. CNA analysis discovered CNAs that were shared at diagnosis and relapse and others that were new lesions acquired at relapse. DNA methylation analysis found increased promoter methylation at relapse. There were many genetic alterations that evolved from diagnosis to relapse, and in some cases these genes had previously been associated with chemoresistance. Integration of the results from all 3 platforms identified genes of potential interest, including CDKN2A, COL6A2, PTPRO, and CSMD1. Although our results indicate that a diversity of genetic changes are seen at relapse, integration of gene expression, CNA, and methylation data suggest a possible convergence on the WNT and mitogen-activated protein kinase pathways.