Novel dry pericardiocentesis: Transvenous puncture of the right ventricle with the back end of a 0.014-inch PTCA guidewire and a 1.8 Fr microcatheter.

Background: Dry transthoracic pericardiocentesis is challenging and carries the risk of right ventricle (RV) or coronary artery injury. The RV can usually control bleeding automatically. For example, most perforations of the RV caused by pacemaker leads are treated without open surgery. Thus, we performed a transvenous puncture of the RV for dry pericardiocentesis with the back end of a 0.014-inch percutaneous transluminal coronary angioplasty (PTCA) guidewire and a 1.8 Fr microcatheter. Methods: The back end of a 0.014-inch PTCA guidewire within a 1.8 Fr microcatheter was used to transvenously punctured through the middle of the acute margin of the RV into the pericardial space in 12 Yorkshire swine and 5 beagles. PTCA balloons of different diameters were used to dilate the puncture holes for 15 min under anticoagulation in all the animals to assess the ability of the RV to control the bleeding. Then, for 3 days, the puncture hole was dilated by a 6 Fr catheter in 9 swine and 5 dogs. Results: The puncture was successful in all the animals. After withdrawal of the 2.5-mm balloon or the 6 Fr catheter, none of the animals exhibited pericardial effusion, as observed by echocardiography. There was no sustained ventricular arrhythmia or other complications. All the animals survived. Conclusion: Transvenous puncture of the right ventricle with the back end of a 0.014-inch PTCA guidewire and 1.8 Fr microcatheter may be feasible and have a good safety margin.

Hypercholesterolemia increases the production of leukotriene B4 in neutrophils by enhancing the nuclear localization of 5-lipoxygenase.

AIMS: Neutrophils can synthesize leukotriene B4 (LTB4) by activating the 5-lipoxygenase (5-LO)signaling pathway. LTB4 is a pro-inflammatory mediator associated with the etiology and progression of atherosclerosis. It can increase function and number of neutrophils in an autocrine manner. Since hypercholesterolemia is associated with an increase in the number and function of neutrophils, we hypothesized that this effect could be mediated through increased production of LTB4 in neutrophils. METHODS/RESULTS: Hypercholesterolemia was modeled in Wistar rats by feeding them with a high cholesterol diet. The induction of hypercholesterolemia caused an increase in the plasma levels of LTB4, following lipopolysaccharide stimulation. This effect was recapitulated in vitro, both in the presence and absence of stimulation with the activator of 5-LO, A23187. Neutrophils in hypercholesterolemia rats expressed similar total levels of 5-LO as control rats, but displayed increased nuclear localization of 5-LO, as well as elevated levels of phosphorylated 5-LO and ERK1/2. In vitro, MßCD/cholesterol complexes enriched cholesterol in neutrophils, resulted in similar changes in 5-LO/LTB4. In addition, these alterations could be inhibited with the ERK inhibitor PD98059. CONCLUSION: Hypercholesterolemia increases LTB4 production in neutrophils by increasing the nuclear localization of 5-LO, which is the result of its phosphorylation by activated ERK1/2.