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. Our objective was to determine whether or not there was evidence of deposition of anti-cardiac antibodies and/or activated complement components in end-stage failing human myocardium. METHODS AND RESULTS: Myocardial samples were obtained from 100 end-stage heart failure patients and 40 donor control biopsies. Sections were cut and stained using standard fluorescent immunohistochemistry techniques with anti-human immunoglobulin G (IgG), IgG3, and C3c. Gel electrophoresis and protein identification by mass spectrometry were used to confirm the presence of IgG and its antigen. Immunoglobulin G was localized to the sarcolemma in 71% of patients, 48% of those being positive for the subtype IgG3. The proportion of patients with ischaemic heart disease that was positive for IgG was 65% and among those with non-ischaemic aetiologies was 76%. In a subgroup analysis, the presence of IgG and its subunits were confirmed by mass spectrometry and adenosine triphosphate synthase ß subunit identified as an antigen. Complement was activated in 31% of all patients. The presence of IgG, IgG3, and C3c was directly correlated with the length of disease (r = 0.451, P = 0.006). CONCLUSION: Evidence of anti-cardiac antibodies and complement activation was found in a large number of patients with end-stage cardiomyopathy regardless of the aetiology. Adenosine triphosphate synthase appears to be a new prominent antigenic stimulus; but more interestingly, the simultaneous co-existence of activated complement components suggests that this humoral mechanism may participate in disease progression.

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. In acute decompensation of chronic heart failure, the change in the inflammatory cytokine activation cascade is less clear. Larger investigational studies are needed to assess the exact roles of circulating and intracardiac cytokines in this particular patient population.

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. METHODS AND RESULTS: The purpose of this study is to evaluate the safety and efficacy of milrinone as a bridge to transplant. This was a retrospective study of 60 patients listed for a cardiac transplant and committed to home intravenous milrinone therapy. A subgroup of patients who eventually progressed to the use of a ventricular assist device were analyzed. Complications and survivals were analyzed for each group. Forty-six patients (76%) were successfully bridged to transplant with milrinone alone, and 14 patients' (24%) conditions deteriorated and required a left ventricular assist device (LVAD); 1-year survivals were 83% and 71%, respectively. The mean waiting time was 59.5 days (9-257 days) for patients receiving milrinone who did not require an LVAD and 112 days (24-270 days) for those whose conditions deteriorated to require an LVAD. CONCLUSIONS: This study suggests that chronic intravenous milrinone provides an adequate strategy as a bridge to transplant if the waiting time is short (<100 days), whereas an elective ventricular assist device implantation may be a safer strategy for patients expected to wait longer. These data provide the basis for a prospective evaluation of inotrope versus LVAD as a bridge to transplantation.

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). MATERIALS AND METHODS: Myocardial tissue was obtained from 10 patients with end-stage cardiomyopathy at the time of LVAD implantation (pre-LVAD) and following orthotopic heart transplantation (post-LAVD). In addition, biopsies of four normal hearts served as a control group. Paraffin-embedded sections were dual stained for cathepsin g and tryptase, a known marker for mast cells, using standard immunohistochemistry protocols. Total cathepsin g positive mast cells were counted. RESULTS: No cathepsin g positive MCs were found in normal hearts. However, we found evidence for cathepsin g in cardiac MCs in heart failure tissues (pre-LVAD). During heart failure, 46% of total MCs were cathepsin g positive as compared to after mechanical unloading, where only 11% of total MCs were cathepsin g positive (P<0.001). CONCLUSION: Heart failure causes an increase of myocardial MCs. We have provided evidence that cathepsin g positive MCs accumulate during heart failure and their total percentage decreases after ventricular unloading. This coincides with the decrease in myocyte necrosis, hypertrophy, and fibrosis. Thus, cathepsin g may play a role in the progression to heart failure by activating angiotensin II, leading to detrimental effects on the heart.