Plaque angiogenesis promotes the growth of atheromas, but the functions of plaque capillaries are not fully determined. Neovascularization may act as a conduit for the entry of leukocytes into sites of chronic inflammation. We observe vasa vasorum density correlates highly with the extent of inflammatory cells, not the size of atheromas in apolipoprotein E-deficient mice. We show atherosclerotic aortas contain activities that promote angiogenesis. The angiogenesis inhibitor angiostatin reduces plaque angiogenesis and inhibits atherosclerosis. Macrophages in the plaque and around vasa vasorum are reduced, but we detect no direct effect of angiostatin on monocytes. After angiogenesis blockade in vivo, the angiogenic potential of atherosclerotic tissue is suppressed. Activated macrophages stimulate angiogenesis that can further recruit inflammatory cells and more angiogenesis. Our findings demonstrate that late-stage inhibition of angiogenesis can interrupt this positive feedback cycle. Inhibition of plaque angiogenesis and the secondary reduction of macrophages may have beneficial effects on plaque stability.angiogenesis ͉ inflammation ͉ vasa vasorum ͉ endothelium

Postcardiotomy cardiogenic shock (PCCS) complicates 0.2% to 6% of cardiac operations and is a clinical entity fraught with considerable morbidity and mortality. A previous review of this topic by our group suggested that regardless of device, only 25% of patients survived to hospital discharge. In the interim, newer technologies have entered the clinical arena. Additional contributions have been made to the literature and new databases are collecting data that are likely to provide more robust guidance for the management of these very complex patients. In this review, we update the experience of mechanical support in the PCCS patient and provide a strategy to maximize survival for a patient who develops PCCS in the community cardiac surgery center.

Pericardial–esophageal fistula and/or atrial–esophageal fistula after cardiac ablation is nearly universally fatal if not detected and treated expeditiously. This condition should be assumed and ruled out in anyone with a recent history of cardiac ablation presenting with signs of sepsis, pneumomediastinum, pneumopericardium, or chest pain. Computed tomography scan of the chest is a rapid and a sensitive diagnostic modality. Tenets of treatment and repair consist of preventing an air embolism, repairing the esophageal perforation and atrial defect, and interposing autologous tissue between the esophagus and heart.