Surgical management of post-infarction ventricular septal defect, mitral regurgitation and ventricular aneurysm.

A 49-year-old diabetic male was admitted to a hospital in 2018 following a 3-week history of worsening dyspnoea and pedal oedema. Early review and investigations indicated acute heart failure. Transthoracic echocardiogram (TTE) revealed mitral regurgitation (MR), aneurysmal change of the ventricles, a ventricular septal defect (VSD) and systolic dysfunction. Coronary angiogram demonstrated a significant left anterior descending and right coronary artery disease. He was diagnosed with a late presenting myocardial infarction (MI) with secondary mechanical complications. Mechanical complications of MI frequently require surgical intervention. The patient underwent a repair of VSD, mitral valve repair, excision of aneurysmal segment and coronary artery bypass grafting. Post-operative recovery was complicated by a sternal wound infection managed in conjunction with the plastic surgeons. A post-operative TTE showed a repaired ventricular septum and no residual MR. Early recognition and appropriate medical optimisation are required to achieve good patient outcomes.

Erratum: Surgical management of post-infarction ventricular septal defect, mitral regurgitation and ventricular aneurysm.

[This corrects the article DOI: 10.1093/jscr/rjz256.].

Circulating Tumor Cells and Cell-Free DNA in Pancreatic Ductal Adenocarcinoma.

Pancreatic cancer is detected late in the disease process and has an extremely poor prognosis. A blood-based biomarker that can enable early detection of disease, monitor response to treatment, and potentially allow for personalized treatment would be of great benefit. This review analyzes the literature regarding two potential biomarkers, circulating tumor cells (CTCs) and cell-free DNA (cfDNA), with regard to pancreatic ductal adenocarcinoma. The origin of CTCs and the methods of detection are discussed and a decade of research examining CTCs in pancreatic cancer is summarized, including both levels of CTCs and analyzing their molecular characteristics and how they may affect survival in both advanced and early disease and allow for treatment monitoring. The origin of cfDNA is discussed, and the literature over the past 15 years is summarized. This includes analyzing cfDNA for genetic mutations and methylation abnormalities, which have the potential to be used for the detection and prognosis of pancreatic ductal adenocarcinoma. However, the research certainly remains in the experimental stage, warranting future large trials in these areas.

Time-course analysis of C3a and C5a quantifies the coupling between the upper and terminal Complement pathways in vitro.

An in vitro zymosan-activation of the Complement system, through the lectin and alternative pathways, was performed in pooled human serum over a 24h time-course. Activation was quantitatively monitored by measuring the concentration of the upper Complement pathway fragment, C3a and the terminal pathway fragment, C5a. Upper Complement showed a maximum activation of 39% and the time-to-maximum activation reduced 8-fold, as a highly non-linear function of the zymosan dose. The C3a:C5a molar ratio rose to a maximum of 1100:1, before terminal pathway activation was initiated; indicating a flux threshold. This threshold appears to be exceeded once more than 31% of C3 molecules are activated. Above this threshold, significant activation of terminal pathway was observed; reducing the molar ratio to 17:1. The C5a/C3a molar ratio was used to determine the terminal pathway activation relative to total Complement activation and ranged from 0.1-0.8%. This depicts upper Complement activation to be 49-fold larger than terminal activation, a figure consistent with the observed density of the membrane attack complex in the membrane of cells. Our results thus indicate that the relative activity of opsonisation is ~50-fold greater than membrane attack complex formation, in vitro, in the pooled serum phenotype. The results suggest a potential clinical application, where an in vitro analysis of a patient on admission, or prior to a surgical procedure, would indicate their upper Complement activation capacity, with activation of C3 measured thereafter, or post-operatively. A patient with an exhausted upper Complement capacity may be vulnerable to infections and complications, such as sepsis.