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Invasive mycoses are rare in non-neutropenic ICU patients, even after a longer stay in the intensive care unit; fungal colonization, on the other hand, is frequently detectable. The mortality of invasive mycosis--even with systemic antimycotic therapy--was high; the mortality in patients with fungal colonization was not significantly increased compared to that in noncolonized patients. The serological test procedures, Candida HAT, Candida IFT, and the Candida Ramco Antigen Test, had a low specificity and were not helpful in diagnosing relevant invasive mycosis.

Our data show that the prevalence of smoking after heart transplantation may be relatively high, especially in former smokers. Repeated measurements of CO-Hb could be helpful in its detection. Despite a relatively low cigarette count, smoking is a major risk factor of morbidity and mortality after heart transplantation (HTx). Approximately 4 years of exposure time is needed to uncover its negative influence. These findings should lead to aggressive smoking screening and weaning programs in every HTx center.

In human heart failure the positive inotropic and cAMP-elevating effects of both beta-adrenoceptor agonists and phosphodiesterase inhibitors are diminished. This has been explained at least in part by an increase in the inhibitory signal-transducing G protein (Gi) and unchanged stimulatory G protein (Gs). In the present study we determined the mRNA expression pattern of the alpha subunits of Gi-1, Gi-2, Gi-3, and Gs in myocardial tissue samples of patients undergoing heart transplantation. Northern blot analysis of total RNA extracted from left ventricles with 32P-labeled cDNAs demonstrated expression of Gi alpha-2, Gi alpha-3, and Gs alpha mRNA. In contrast, Gi alpha-1 mRNA was not detectable. To investigate whether the increased ratio of Gi/Gs might be due to altered gene expression, we compared mRNA levels of Gi alpha-2, Gi alpha-3, and Gs alpha in left ventricular myocardium from failing hearts with idiopathic dilated cardiomyopathy (n = 8) and ischemic cardiomyopathy (n = 6) and from nonfailing hearts from transplant donors (n = 8). Compared with nonfailing control hearts, the Gi alpha-2 mRNA was increased by 75 +/- 26% (p less than 0.05) in idiopathic dilated cardiomyopathy hearts and 90 +/- 26% (p less than 0.05) in ischemic cardiomyopathy hearts. Gi alpha-3 and Gs alpha mRNA levels were similar in the three groups. The results suggest that as in other mammalian species, Gi alpha-2 and Gi alpha-3 mRNA are the predominant Gi alpha mRNA subtypes in human ventricular myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)

These data demonstrate the feasibility and safety of using a robotic-assisted platform for performing peripheral arterial revascularization.

In dialysis access fistulas and grafts, percutaneous transluminal angioplasty (PTA) is frequently followed by restenosis development, which results in repeated periodical re-interventions. The technique of drug-eluting balloon (DEB) angioplasty has shown promising results in the treatment of femoropopliteal arteriosclerotic lesions. In contrast to arteriosclerotic arteries, dialysis access vessels host unfavorable hemodynamics due to the direct conduction of high-pressure fluid into a low-pressure system. Hence, the beneficial effect of DEB angioplasty may be limited in this system. However, a first prospective randomized trial on 40 patients with arteriovenous fistula or graft stenoses exhibited a significantly higher 6-month primary patency of the treated lesions after DEB angioplasty than after uncoated balloon angioplasty. Despite such a positive reference, general recommendations regarding the value of DEBs in dialysis access vessels cannot be considered as serious unless large randomized controlled trials have been performed.

and tKlinik fur Herz-, Thorax-und Gefdii3chirurgie, Medizinische Hochschule Hannover, Konstanty-Gutschow-Strape 8, 3000 Hannover 61, Germany 1 a1-Adrenoceptor (phenylephrine in the presence of propranolol) andf/2-adrenoceptor (fenoterol)-mediated positive inotropic effects were investigated in human ventricular preparations isolated from five nonfailing (prospective organ donors) and from eight explanted failing hearts with end-stage idiopathic dilative cardiomyopathy (NYHA IV).2 For comparison, the nonselective fJ-adrenoceptor agonist isoprenaline, the phosphodiesterase (PDE) inhibitor 3-isobutyl-1-methylxanthine (IBMX), the cardiac glycoside dihydroouabain, and calcium were studied. 3 Furthermore, the influence of IBMX on adenosine 3': 5'-cyclic monophosphate (cyclic AMP) PDE activity as well as total #-adrenoceptor density, /J,-andfi2-adrenoceptor subtype distribution, and xl-adrenoceptor density were compared in nonfailing and failing human heart preparations. The radioligands (_)-j[j25I]-iodocyanopindolol for fJ-adrenoceptor binding and [3H]-prazosin for o1-adrenoceptor binding were used. 4 The inotropic responses to calcium and dihydroouabain in failing human hearts were unchanged, whereas the maximal cl-and /12-adrenoceptor-mediated positive inotropic effects were greatly reduced. The inotropic effects of the other cyclic AMP increasing compounds, i.e. isoprenaline and IBMX, were also reduced to about 60% of the effects observed in nonfailing controls. The potency of these compounds was decreased by factors 4-10. 5 The basal PDE activity and the PDE inhibition by IBMX were similar in nonfailing and failing preparations.6 The total fJ-adrenoceptor density in nonfailing hearts was about 70 fmol mg-' protein. In failing hearts the total number of,-adrenoceptors was markedly reduced by about 60%. The l/2-adrenoceptor ratio was shifted from about 80/20% in nonfailing to approximately 60/40% in failing hearts which was due to a selective reduction of /11-adrenoceptors. The 2-adrenoceptor population remaining unchanged. ac-Adrenoceptor density was increased from about 4 fmol mg-' protein in nonfailing to 10 fmol mgprotein in failing hearts. 7 Changes in PDE activity and adrenoceptor downregulation cannot completely explain the reduced positive inotropic effects of ax-and f12-adrenoceptor agonists in failing human hearts. This supports the hypothesis that impairment of other processes such as the coupling between receptor and effector system, i.e. the respective G-proteins, are equally important in end-stage heart failure.

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