Modified dual guide catheter ("ping-pong") technique to treat left internal mammary artery graft perforation.

Perforation of a left internal mammary artery (LIMA) graft during percutaneous coronary intervention is a rare event. We report a case of mid-LIMA perforation treated by a polytetrafluoroethylene-covered stent using a modification of the dual catheter ("ping pong") technique. We propose that use of this modification when possible will further improve safety of treating a perforation.

High proportion of patients with end-stage heart failure regardless of aetiology demonstrates anti-cardiac antibody deposition in failing myocardium: humoral activation, a potential contributor of disease progression.

Aims: Various reports have raised the possibility of humoral immune responses as contributors for the progression of heart failure. Previous studies, however, have focused on the analysis of serum and documented circulating antibodies against a variety of cardiac proteins. However, there is little evidence on whether anti-cardiac antibodies are deposited in end-stage failing myocardium.

The use of continuous milrinone therapy as bridge to transplant is safe in patients with short waiting times.

Objective: The limited availability of donor organs creates a need for more effective management of heart disease when bridging a patient to cardiac transplant. Inotropic therapy is becoming more commonly used long term to maintain baseline function. The effectiveness and complications associated with their use have not been fully evaluated, and indications for mechanical versus medical therapy as a bridge have not been delineated.

Cytokines and acute heart failure.

In patients with chronic heart failure, ongoing myocardial injury partially results from activation of the inflammatory system, with production and release of proinflammatory cytokines, activation of the complement system, production of autoantibodies, overexpression of major histocompatibility complex molecules, and expression of adhesion molecules that may perpetuate the inflammatory state. Acute decompensated heart failure modifies the course of chronic heart failure and worsens outcomes via a combination of potential mechanisms, including neurohormonal activation, apoptosis, and the inflammatory cascade. Proinflammatory cytokines, including tumor necrosis factor-alpha and interleukin-6, play a pathogenetic role in chronic heart failure, and anti-inflammatory immune therapy is currently under investigation.

Mast cell-derived cathepsin g: a possible role in the adverse remodeling of the failing human heart.

Background: The role of cardiac mast cells (MCs) in the progression to heart failure has recently become increasingly evident. Cathepsin g is a neutrophil- and mast cell-derived protease, which can convert angiotensin I to angiotensin II and thereby activate the TGF-beta pathway, resulting in myocyte necrosis, hypertrophy, and increased fibrosis. This study focuses on mast cell-derived cathepsin g in the human heart during heart failure and following mechanical unloading by means of heart-assist devices (LVADs).