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Background: After the introduction of antibiotics, pneumococcal pericarditis has become a rare finding. However, this severe condition with high mortality and complication rates requires rapid recognition and intervention. Herein, we describe a patient that presents with this rare disease resulting in an unusual, fatal outcome.Case Presentation: A previously healthy, 68-year-old, Caucasian male presented with progressive fatigue, dyspnea, and appetite loss since 12 days. He was diagnosed with diabetes mellitus 5 days before presentation but had not started treatment. After echocardiography revealed pericardial effusion, pericardiocentesis was performed with immediate drainage of a large volume of purulent fluid suggestive of bacterial pericarditis. On the basis of cultures showing Streptococcus pneumoniae as the causative organism, a regimen of intravenous penicillin was initiated. Additionally, antidiabetic drugs were started as his diabetes also predisposed him to invasive infectious disease. No other primary source of the infection, such as pneumonia, was found. Though the patient was found to be severely ill on admission, his clinical condition improved. A total of 1235 mL of pericardial fluid was drained, and adequate drainage was confirmed by daily, bedside echocardiography. However, 6 days post-admission, the patient suddenly developed intrapericardial bleeding with blood clot formation on the right chamber with subsequent cardiac tamponade. With the blood clot precluding adequate drainage through the catheter, the patient suffered cardiac arrest and died before surgical intervention could be attempted.Conclusions: Pneumococcal pericarditis is a very rare but life-threatening disease that necessitates immediate intervention with antibiotics and drainage of the pericardial effusion. Thus, although symptoms may be variable and aspecific, early recognition of this condition is critical. The present case illustrates the presentation, diagnosis, and clinical course of a patient presenting with pneumococcal pericarditis in current clinical practice. Through this report, we aimed to increase awareness among clinicians both of the existence of this phenomenon and of its uncertain clinical course. As is highlighted by the case, patients with pneumococcal pericarditis are at high risk for complications and should be closely monitored. [ABSTRACT FROM AUTHOR]

Abstract: Objective: To assess the safety and efficacy of the Genous™ endothelial progenitor cell (EPC) capturing stent in conjunction with HmG-CoA-reductase inhibitors (statins) to stimulate EPC recruitment, in the treatment of patients with de novo coronary artery lesions. Methods and results: The HEALING IIB study was a multi-center, prospective trial, including 100 patients. The primary efficacy endpoint was late luminal loss by QCA at 6-month follow-up (FU). Although statin therapy increased relative EPC levels by 5.6-fold, the angiographic outcome at 6 month FU was not improved in patients with an overall in-stent late luminal loss of 0.76±0.50mm. The composite major adverse cardiac events (MACE) rate was 9.4%, whereas 6.3% clinically justified target lesion revascularizations (TLRs) were observed. 2 Patients died within the first 30 days after stent implantation due to angiographically verified in-stent thrombosis. At 12 month FU, MACE and TLR increased to 15.6% and 11.5% respectively and stabilized until 24 month FU. 18 Month angiographic FU showed a significant decrease in late luminal loss (0.67±0.54, 11.8% reduction or 10% by matched serial analysis, P =0.001). Conclusion: The HEALING IIB study suggests that statin therapy in combination with the EPC capture stent does not contribute to a reduction of in-stent restenosis formation for the treatment of de novo coronary artery disease. Although concomitant statin therapy was able to stimulate EPC recruitment, it did not improve the angiographic outcome of the bio-engineered EPC capture stent. Remarkably, angiographic late loss was significantly reduced between 6 and 18 months. [Copyright &y& Elsevier]

Abstract: DNA of eukaryotic cells, including vascular cells, is under the constant attack of chemicals, free radicals, or ionizing radiation that can be caused by environmental exposure, by-products of intracellular metabolism, or medical therapy. Damage may be either limited to altered DNA bases and abasic sites or extensive like double-strand breaks (DSBs). Nuclear proteins sense this damage and initiate the attachment of protein complexes at the site of the lesion. Subsequently, signal transducers, mediators, and finally, effector proteins phosphorylate targets (e.g., p53) that eventually results in cell cycle arrest at the G1/S, intra-S, or G2/M checkpoint until the lesion undergoes repair. Defective cell cycle arrest at the respective checkpoints is associated with genome instability and oncogenesis. When cell cycle arrest is accomplished, the DNA repair machinery can become effective. Important pathways in mammalian cells are the following: base excision repair, nucleotide excision repair, mismatch repair, and DSB repair. When repair is successful, the cell cycle arrest may be lifted. If repair is unsuccessful (e.g., by high doses of DNA-damaging agents or genetic defects in the DNA repair machinery), then this may lead to permanent cell cycle arrest (cellular senescence), apoptosis, or oncogenesis. [Copyright &y& Elsevier]

Background. Novel therapies need to be evaluated in a relevant large animal model that mimics the clinical course and treatment in a reasonable time frame. To reliably assess therapeutic efficacy, knowledge regarding the translational model and the course of disease is needed. Methods. Landrace pigs were subjected to a transient occlusion of the proximal left circumflex artery (LCx) (n=6) or mid-left anterior descending artery (LAD) (n=6) for 150 min. Cardiac function was evaluated before by 2D echocardiography or 3D echocardiography and pressure-volume loop analysis. At 12 weeks of follow-up the heart was excised for histological analysis and infarct size calculations. Results. Directly following AMI, LVEF was severely reduced compared to baseline in the LAD group -17.1±1.6%, P=0.009 compared to only a moderate reduction in the LCx group -5.9±1.5%, P=0.02 and this effect remained unchanged during 12 weeks of follow-up. Conclusion. Two models of chronic MI, representative for different patient groups, can reproducibly be created through clinically relevant ischemia-reperfusion of the mid-LAD and proximal LCx. [ABSTRACT FROM AUTHOR]