Predictors of inpatient outcomes in hospitalized patients after left heart catheterization.

Clinical and laboratory factors predicting inpatient outcomes, specifically in-hospital mortality and length of stay (LOS), have not been defined for hospitalized patients specifically referred for left heart catheterization and coronary angiography (LHC). The objective of the study was to determine these outcomes and their predictors in hospitalized patients after LHC. Multivariate logistic regression models were used to identify risk factors for in-hospital mortality and Cox proportional hazards models were used to identify factors determining LOS in 9,420 consecutive patients hospitalized for LHC. Odds ratio for in-hospital mortality and hazard ratio for prolonged LOS were derived. The strongest predictors of mortality were advanced age, left ventricular (LV) end-diastolic pressure (EDP), LV ejection fraction (EF), systemic blood pressure, and renal insufficiency. Predictors of prolonged LOS were LVEDP, LVEF, 3-vessel coronary artery disease, and valvular disease. Clinical and laboratory characteristics of patients with an LVEF > or =50% were also compared with those of patients with an LVEF <50%. Predictors of mortality and LOS remained the same for patients with an LVEF <50%. For an LVEF > or =50%, LVEDP also determined LOS and chronic renal insufficiency provided predictive power to mortality and LOS in this subgroup. In conclusion, several readily attainable clinical and laboratory parameters predict inpatient mortality and LOS in hospitalized patients referred for LHC.

Overexpression of tumor necrosis factor-alpha increases production of hydroxyl radical in murine myocardium.

Transgenic (TG) mice with cardiac-specific overexpression of tumor necrosis factor-alpha develop congestive heart failure with myocardial inflammation. The purpose of this study was to investigate the effects of tumor necrosis factor-alpha on reactive oxygen species (ROS) in this mouse model of cardiomyopathy. Myocardial production of hydroxyl radical detected by electron spin resonance spectroscopy was significantly increased in TG. Myocardial expression of Mn-SOD was significantly decreased in TG, whereas that of Cu,Zn-SOD was unaltered. Myocardial expression of catalase was unchanged, whereas that of glutathione peroxidase was significantly increased, in TG. Histological analysis revealed that macrophages and CD4-positive lymphocytes were increased in TG myocardium. To investigate whether these infiltrating inflammatory cells were the source of ROS, we treated TG mice with cyclophosphamide for 7 days. Although cyclophosphamide significantly suppressed the infiltration of inflammatory cells, it did not diminish the production of hydroxyl radical in TG myocardium. Damaged myocytes, but not infiltrating inflammatory cells, may be the source of ROS in TG.

MMP inhibition modulates TNF-alpha transgenic mouse phenotype early in the development of heart failure.

Myocardial extracellular matrix remodeling regulated by matrix metalloproteinases (MMPs) is implicated in the progression of heart failure. We hypothesized that MMP inhibition may modulate extracellular matrix remodeling and prevent the progression of heart failure. The effects of the MMP inhibitor BB-94 (also known as batimastat) on MMP expression, collagen expression, collagen deposition, collagen denaturation, and left ventricular structure and function in transgenic mice with cardiac-restricted overexpression of tumor necrosis factor-alpha (TNF-alpha) (TNF1.6) were assessed. The results showed that BB-94 reduced the expression of collagens, increased insoluble collagen and the ratio of undenatured to total soluble collagen, and prevented myocardial hypertrophy and diastolic dysfunction in young TNF1.6 mice. Furthermore, the treatment significantly improved cumulative survival of TNF1.6 mice. However, MMP inhibition did not have salutary effects on ventricular size and function in old mice with established heart failure. The results suggest that MMP activation may play a critical role in changes of myocardial function through the remodeling of extracellular matrix, and MMP inhibition may serve as a potential therapeutic strategy for heart failure, albeit within a narrow window during the development of heart failure.