[Biophysical study of coronary stents: which factors influence the dilatation and recoil behavior?]. / Biophysikalische Prüfung koronarer Stents: Welche Faktoren beeinflussen das Dilatations- und Recoilverhalten?

In Europe more than fifty stents are currently available for the therapy of coronary artery disease. Nonetheless it is unknown whether material and design influence the stent's behavior. We have studied the recoil and dilatation behavior of five currently available stainless steel (316L) stents compared to stent prototypes made of pure titanium. Furthermore we have investigated how the behavior is influenced by the process of crimping. The aim of this work was to determine material and design characteristics, which influence the recoil and dilatation behavior. The 316L stents showed a homogeneous behavior (plateau pressure min. 1.15 +/- 0.01 atm, max. 0.26 +/- 0.03 atm, recoil min. 0.15 +/- 0.03%, max. 0.26 +/- 0.03%). The titanium stent showed a linear response to the balloon expansion. This was seen in a significantly lower plateau pressure (0.43 +/- 0.15 atm, p < 0.001). Despite the material characteristics of titanium, there were no significant differences in the recoil behavior (0.28 +/- 0.02%). Crimping leads to stent alterations which result in a significantly higher plateau pressure (1.9 +/- 0.07 atm vs. 2.7 +/- 0.58 atm, p < 0.001) and a reduced end-diameter (3.6 +/- 0.02 mm vs. 3.54 +/- 0.05 mm, p < 0.005). The presented data show that the dilatation behavior is relying on the stent material while the recoil is strongly influenced by the stent design.

Left ventricular hemodynamic parameters in the course of acute experimental coxsackievirus B 3 myocarditis.

In susceptible DBA/2 mice coxsackievirus B 3-induced myocarditis leads to inflammatory and necrotic lesions in the myocardium 7-10 days after virus inoculation. The purpose of this study was to determine whether hemodynamic changes occur in murine coxsackievirus B 3 myocarditis and whether they are correlated to histological cardiac lesions throughout the infection. Left ventricular function was determined by open chest puncture of the left ventricle in the course of acute coxsackievirus B 3 infection. Histological cross sections of the heart were stained with hematoxylin/eosin and scored blindly for myocarditic lesions. Left ventricular function was preserved until day 7 post-virus inoculation Left ventricular systolic pressure, +dP/dtmax and -dP/dtmax and heart rate declined significantly from day 7 to day 10. The decrease in these parameters did not correlate with viral concentrations in the heart on the day of hemodynamic measurements. The decrease was related to histological changes on day 10, but not on day 7 of the infection. The data suggest (a) that a cumulative loss of cardiac myofibers, induced either by the virus and/or by immune reactions to the heart, is likely to lead to a late depression of cardiac function, and (b) that there is a weak and only temporary structure-function relationship in the heart in coxsackievirus B 3 myocarditis. Therefore, in addition to an analysis of histological changes, the measurement of cardiac function appears to be very important in order to completely evaluate the severity of myocarditis and the usefulness of any therapy.

Extramural vessel wall hematoma causing a reduced vessel diameter after coronary stenting: diagnosis by intravascular ultrasound and treatment by stent implantation.

An extramural vessel wall hematoma occurred immediately after implanting a coronary stent in an in-stent-restenosis of the intermedius branch. Angiography showed a significant luminal reduction distal to the intervention site. Intravascular ultrasound revealed an extramural echolucent zone compressing the vessel lumen. Stent implantation compressed the hematoma and allowed adequate myocardial perfusion. This demonstrates the value of intravascular ultrasound (IVUS) in cases of unusual angiographic results which can help to manage complications after coronary intervention.

Left ventricular haemodynamics in murine viral myocarditis.

In susceptible DBA/2 mice infection with coxsackievirus B3 leads to severe inflammatory and necrotic lesions in the heart. There is a temporal discrepancy of peak concentrations of replicative virus in the heart and maximal cardiac inflammation. Aims of this study were, first, to determine whether haemodynamic changes occur in coxsackievirus B3-induced murine myocarditis and, second, the time frame in which those alterations may be apparent. By puncture of the left ventricle, pressures and the first derivative dp/dt as parameters of left ventricular function could be obtained on several days of the infection. Haematoxylin-eosin stains of cross-sections of the heart showed the course of inflammatory lesions in the heart; a plaque forming assay assessed virus titres in the heart. Cardiac concentrations of replicative virus peaked on day 3, inflammatory lesions in the heart were maximal on day 7. Left ventricular function was almost preserved until day 5 of the infection, then dropped significantly until day 10. The study suggests that either a cumulative virus-mediated destruction of the myofibres or virally triggered immune reactions to heart cells lead to impairment of left ventricular function.

A central role for cohesins in sister chromatid cohesion, formation of axial elements, and recombination during yeast meiosis.

A multisubunit complex, called cohesin, containing Smc1p, Smc3p, Scc1p, and Scc3p, is required for sister chromatid cohesion in mitotic cells. We show here that Smc3p and a meiotic version of Scc1p called Rec8p are required for cohesion between sister chromatids, for formation of axial elements, for reciprocal recombination, and for preventing hyperresection of double-strand breaks during meiosis. Both Rec8p and Smc3p colocalize with chromosome cores independently of synapsis during prophase I and largely disappear from chromosome arms after pachytene but persist in the neighborhood of centromeres until the onset of anaphase II. The eukaryotic cell's cohesion apparatus is required both for the repair of recombinogenic lesions and for chromosome segregation and therefore appears to lie at the heart of the meiotic process.