Intravascular catheter embolization can go undiagnosed for prolonged periods. Patients might be asymptomatic or may develop severe systemic clinical signs. The mortality rate is 1.8%. There were no significant differences in clinical features of embolization between TIVD and PVC groups.

In this randomized trial addressing addition of IABP in CS patients, mechanical support was associated only with modest effects on reduction of APACHE II score as a marker of severity of disease, improvement of cardiac index, reduction of inflammatory state, or reduction of BNP biomarker status compared with medical therapy alone. However, the limitations of our present trial preclude any definitive conclusion, but request for a larger prospective, randomized, multicentered trial with mortality as primary end point.

Bacterial toxins cause cardiac dysfunction and death through an inflammatory process, but the mechanism remains unclear. Simvastatin is recognized as having anti-inflammatory properties beyond its lipid-lowering effects. We examined Staphylococcus aureus alpha-toxin in isolated heart and in vivo models and tested simvastatin's effects in sepsis. Isolated Langendorff-perfused rat hearts were exposed to a recirculating perfusate containing alpha-toxin (0.5 microg mL(-1)). Compared with controls, there was a significant increase in coronary perfusion pressure and fall in myocardial performance. Significant increases in p53 expression and apoptosis (1.3 +/- 0.5 to 7.1 +/- 1.4 terminal deoxynucleaotidyl transferase nick end labeling-positive cells; P < 0.05) compared with controls were observed, but markers of necrosis were similar. In parallel experiments, anaesthetized rats receiving alpha-toxin (40 microg kg(-1), i.v.) had in vivo hemodynamic parameters and serum markers of necrosis monitored for 4 h before the hearts were analyzed for histological change, p53 expression, and apoptosis. Over 4 h, alpha-toxin exposure produced substantial hemodynamic effects. In addition, p53 expression (0.2 +/- 0.2 to 7.1 +/- 0.5 p53-positive myocytes; P < 0.05), TNF-alpha levels, the degree of apoptosis, and markers of necrosis were all significantly increased compared with control animals. Pretreatment with simvastatin protected against alpha-toxin-induced sepsis associated with reduced p53, TNF-alpha, apoptosis, and necrosis. We found significant changes in systemic hemodynamics, coronary perfusion pressure, myocardial function, and increased p53 expression with apoptosis due to bacterial exotoxin. In vivo changes were significantly inhibited by pretreatment with simvastatin. We provide novel evidence for the mechanisms by which septicemia causes myocardial depression and hint at a potential role for simvastatin as an inhibitor of apoptosis in sepsis.

Levosimendan infusion for cardiogenic shock following acute myocardial infarction improved hemodynamic parameters of right ventricular performance. Furthermore, we describe the use of right ventricular cardiac power index as a hemodynamic parameter of right ventricular performance.

Myocardial ischemia (MI) and reperfusion (R) results in activation of the p38 MAP kinase pathway. This pathway phosphorylates transcription factors and cytoplasmic proteins leading to expression of adhesion molecules and cytokines, increased neutrophil activation, and finally, myocardial necrosis and apoptosis. We studied the effects of a p38 MAP kinase inhibitor, PD169316, on cardioprotection, protein expression, and tyrosine phosphorylation, in a rabbit model of 1 h of (MI) and 3 h of (R). PD169316 administered just before (R) significantly reduced myocardial neutrophil accumulation, necrosis area (28.4 +/- 7.9% vs. 56.4 +/- 7.9% necrosis/AAR), and CK release compared to a vehicle treated group (p<0.05). We found several proteins altered in expression following MI + R alone or with p38 inhibition including myofilament proteins, energetics proteins, heat shock proteins, and the mitochondrial porin VDAC-1. p38 MAPK inhibition significantly reduced the phosphorylation of VDAC-1 which is a known mitochondrial regulator of cell survival. Thus, p38 MAP kinase inhibition with PD169316 is cardioprotective, reduces neutrophil activation, and controls protein expression and phosphorylation in MI and reperfusion.

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Levosimendan infusion in cardiogenic shock following acute myocardial infarction improved cardiovascular hemodynamics without leading to hypotension.

Animal data strongly support a role for inflammation in myocardial ischemia reperfusion injury. Attempts at cardioprotection by immunomodulation (such as with the specific C5 antibody pexelizumab) in humans have been disappointing. We hypothesized that a broader spectrum antiinflammatory agent might yield successful cardioprotection. The serine protease inhibitor nafamostat (FUT-175), which is already in clinical use, is a potent antiinflammatory synthetic serine protease inhibitor with anticomplement activity that we tested in a well-established rabbit model of 1 hour of myocardial ischemia followed by 3 hours of reperfusion. Compared to vehicle-treated animals, nafamostat (1 mg/kg of body weight) administered 5 minutes before reperfusion significantly reduced myocardial injury assessed by plasma creatine kinase activity (38.1 +/- 6.0 versus 57.9 +/- 3.7I U/g protein; P < 0.05) and myocardial necrosis (23.6 +/- 3.1% versus 35.7 +/- 1.0%; P < 0.05) as well as myocardial leukocyte accumulation (P < 0.05). In parallel in vitro studies, Nafamostat was a significantly more potent broad spectrum complement suppressor than C1 inhibitor. Nafamostat appears to have capability as an inhibitor of both complement pathways and as a broad-spectrum antiinflammatory agent by virtue of its serine protease inhibition. Administration of nafamostat before myocardial reperfusion after ischemia produced significant, dose-dependent cardioprotection. Reduced leukocyte accumulation and complement activity seem involved in the mechanism of this cardioprotective effect.