Tissue-specific reprogramming leads to angiogenic neutrophil specialization and tumor vascularization in colorectal cancer.

Neutrophil (PMN) tissue accumulation is an established feature of ulcerative colitis (UC) lesions and colorectal cancer (CRC). To assess the PMN phenotypic and functional diversification during the transition from inflammatory ulceration to CRC we analyzed the transcriptomic landscape of blood and tissue PMNs. Transcriptional programs effectively separated PMNs based on their proximity to peripheral blood, inflamed colon, and tumors.

Macrophage-endothelial cell crosstalk orchestrates neutrophil recruitment in inflamed mucosa.

Neutrophil (PMN) mobilization to sites of insult is critical for host defense and requires transendothelial migration (TEM). TEM involves several well-studied sequential adhesive interactions with vascular endothelial cells (ECs); however, what initiates or terminates this process is not well-understood. Here, we describe what we believe to be a new mechanism where vessel-associated macrophages through localized interactions primed EC responses to form ICAM-1 "hot spots" to support PMN TEM.

Long-term patency of rescue stenting of an anomalous left circumflex coronary artery after transcatheter aortic valve replacement.

Transcatheter aortic valve replacement (TAVR) in the setting of an anomalous left circumflex coronary artery (LCX) has had a variety of outcomes. Most commonly an anomalous LCX originates as a separate ostium arising from the right coronary sinus or is found branching off of the proximal right coronary artery. The artery courses around the aortic annulus before taking the course seen in typical anatomy.

Iatrogenic ventricular septal defects following transcatheter aortic valve implantation.

Ventricular septal defect (VSD) rarely occurs following transcatheter aortic valve implantation (TAVI). We report two patients who developed VSD following TAVI. One case was a Gerbode defect treated by percutaneous closure, and the second was a restrictive perimembranous VSD managed conservatively.

Kounis syndrome presenting as ST elevation acute myocardial infarction.

Allergic acute coronary syndrome, Kounis syndrome, is a rare cause of ST-segment elevation myocardial infarction triggered by an allergic reaction to a drug or environmental allergen, resulting in atheromatous plaque rupture or coronary artery vasospasm. We report three cases of Kounis syndrome presenting as ST-segment elevation myocardial infarction.