Valvular surgery in octogenarians is a safe and low risk procedure compared to functional benefit and long-term survival. Our data how that logistic Euroscore overestimates the mortality in this high-risk group of patients.

Mitochondria-related oxidative stress is a pathomechanism causally linked to coronary heart disease (CHD) and diabetes mellitus (DM). Recently, mitochondrial monoamine oxidases (MAOs) have emerged as novel sources of oxidative stress in the cardiovascular system and experimental diabetes. The present study was purported to assess the mitochondrial impairment and the contribution of MAOs-related oxidative stress to the cardiovascular dysfunction in coronary patients with/without DM. Right atrial appendages were obtained from 75 patients randomized into 3 groups: (1) Control (CTRL), valvular patients without CHD; (2) CHD, patients with confirmed CHD; and (3) CHD-DM, patients with CHD and DM. Mitochondrial respiration was measured by high-resolution respirometry and MAOs expression was evaluated by RT-PCR and immunohistochemistry. Hydrogen peroxide (H2O2) emission was assessed by confocal microscopy and spectrophotometrically. The impairment of mitochondrial respiration was substrate-independent in CHD-DM group. MAOs expression was comparable among the groups, with the predominance of MAO-B isoform but no significant differences regarding oxidative stress were detected by either method. Incubation of atrial samples with MAOs inhibitors significantly reduced the H2O2 in all groups. In conclusion, abnormal mitochondrial respiration occurs in CHD and is more severe in DM and MAOs contribute to oxidative stress in human diseased hearts with/without DM.

Monoamine oxidases (MAOs) are mitochondrial enzymes with 2 isoforms that have emerged as important contributors to cardiovascular oxidative stress via the constant generation of hydrogen peroxide. The present study was purported to assess whether MAO-derived H 2 O 2 contributes to the endothelial dysfunction in mammary arteries harvested from coronary heart disease patients with/without diabetes mellitus subjected to coronary artery bypass grafting.To this aim the effects of MAO inhibition on vascular contractility to phenylephrine and endothelial-dependent relaxation (EDR) in response to acetylcholine were studied in vascular segments. Clorgyline (irreversible MAO A inhibitor), selegiline (irreversible MAO B inhibitor), and moclobemide (reversible MAO A inhibitor) were applied in the organ bath (10µmol/L). MAO expression was assessed by immunohistochemistry. We found a constant impairment of EDR that has been significantly attenuated in the presence of the MAO A and B inhibitors in both groups of coronary heart disease patients. MAO B was the dominant isoform in all human diseased vessels. In conclusion, in vitro inhibition of MAO significantly improved endothelium-dependent relaxation in human mammary arteries, regardless the presence of diabetes. These data suggest that MAO inhibitors might be useful in restoring endothelial response in clinical conditions associated with increased oxidative stress, such as coronary artery disease and diabetes.Key words: monoamine oxidases, coronary artery disease, diabetes mellitus, endothelial dysfunction, MAO inhibitors IntroductionCoronary heart disease (CHD) is currently the leading cause of morbidity due to heart failure and its evolution is aggravated by the presence of diabetes mellitus (DM) whose prevalence is increasing at an alarming rate worldwide. Nowadays, it is widely accepted that A large body of experimental evidence showed that under physiological conditions the amount of H 2 O 2 generated via MAO is reduced but in cardiac pathologies (such as myocardial ischemia/reperfusion and heart failure) the increased activity of the MAO-A isoform becomed deleterious (Bianchi et al. 2005a; Kaludercic et al. 2011; Kaludercic et al. 2010).Accordingly, in the rodent heart, MAO-A activation contributes to the ischemia/reperfusion injury in the in vivo model of regional ischemia (Bianchi et al. 2005a,b; Carpi et al. 2009) and to the maladaptive ventricular remodeling in the transverse aortic constriction-induced model of heart failure, respectively (Kaludercic et al. 2010;Villeneuve et al. 2013).Furthermore, an elegant study has unequivocally proven the role of MAO-B activation in triggering mitochondrial dysfunction besides the cardiac structural and functional alterations in mice with experimentally induced heart failure (Kaludercic et al. 2014). Recently, we described the role of MAOs as mediators of endothelial dysfunction and the beneficial effect of MAO inhibition in murine diseased vessels (Sturza et al. 2013), and in experimental diabetes mellitus, respec...

We retrospectively reviewed the files of 19 extracorporeal life support (ECLS) applications performed after cardiac surgery in 15 patients from January 2002 to December 2004. We placed 16 arteriovenous ECLS applications with oxygenator, 2 venovenous ECLS applications with oxygenator, and 1 biventricular ECLS application without oxygenator (graft dysfunction after heart transplant). Mean age was 4.9 +/- 7 years (median 5.9 months, range 11 days to 21 years). All patients underwent surgery for congenital heart disease, except for one patient who had a heart transplant. Indications were hemodynamic failure in 12 cases, respiratory failure in 5 cases, and mixed failure in 2 cases. Four patients were undergoing cardiopulmonary resuscitation during ECLS placement (no deaths). Mean delay between surgery and ECLS placement was 3.2 +/- 3.4 days (median 2 days). Mean ECLS duration was 3.4 +/- 5.8 days (mean 6 days, range 3-16 days). Three patients had further surgery for residual lesions. Thirteen patients (86.7%) survived to ECLS weaning; 12 patients survived to hospital discharge (80%). No survivor presented obvious neurologic damage. Specific morbidity included reentry for bleeding, multiple transfusions, and mediastinitis. These results support early placement of ECLS in children whenever a severe postoperative hemodynamic or respiratory failure, refractory to medical treatment, is present.

Seronegative women are susceptible to primary rubella virus (RV) infection during pregnancy, which can cause fetal damage. Vaccination represents the main strategy in rubella prevention. The aim of this study was to analyze changes in the rubella seroprevalence and identify populations with a high susceptibility to RV. A cross-sectional study was performed on 6914 Caucasian fertile women who had Toxoplasma gondii, other viruses, Rubella, Cytomegalovirus, and the herpes simplex virus (TORCH) screening in two distinct periods—1452 at the Timișoara Municipal Hospital, Romania (Group 1: 2008–2010) and 5462 at the laboratory Bioclinica S.A., Timișoara, Romania (Group 2: 2015–2018). The RV seroprevalence decreased (Group 1 versus Group 2; 94.1% (92.7–95.2) versus 91.4% (90.6–92.1), OR = 0.76 (p = 0.0007)). According to the year of birth and eligibility to vaccination program, RV seroprevalence rates were 82.4% (76.8–86.8)/1997–2004, 85.4% (80.5–89.3)/1995–1996, 90.1% (89.0–91.1)/<1989, and 95.8% (94.7–96.6)/1989–1994. No significant difference in the RV seropositivity according to the place of residence was found. The overall RV susceptibility increased from 2008–2010 to 2015–2018. The highest susceptibility was found in women born between 1997–2004 eligible for measles-mumps-rubella (MMR) vaccine through the family practice system and the lowest in women born between 1989–1994 eligible for monovalent rubella vaccine conducted in schools.