Effect of gallium on in vitro aortic homograft valve cusp mineralization.
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Biomedical subjects
Publications and source records attributed to Jerzy Sadowski.
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BACKGROUND: Chemokines are important mediators of inflammatory cell recruitment that play a significant role in atherosclerosis. Fractalkine (CX3CL1) is an unusual membrane-bound chemokine that mediates chemotaxis through the CX3CR1 receptor. Recently, functional polymorphisms in the human CX3CR1 gene have been described that are associated with coronary artery disease. METHODS AND RESULTS: We investigated the expression of the CX3C chemokine fractalkine and its receptor CX3CR1 in human coronary artery plaques by immunocytometry. We show that a subset of mononuclear cells expresses high levels of fractalkine in human coronary atherosclerotic plaques and that smooth muscle cells within the neointima express the fractalkine receptor CX3CR1. There is a positive correlation between the number of fractalkine-expressing cells and the number of CX3CR1-positive cells in human atherosclerotic plaques (r=0.70, n=15 plaques). Furthermore, we demonstrate that cultured vascular smooth muscle cells express the CX3CR1 receptor and undergo chemotaxis to fractalkine that can be inhibited by G protein inactivation by pertussis toxin. CONCLUSIONS: These results suggest that in human atherosclerosis, fractalkine, rather than mediating inflammatory cell recruitment, can act as a mediator of smooth muscle cell migration.
OBJECTIVE: Through a retrospective study on the use of fresh homografts in 655 aortic valve replacement patients over a period of 23 years, we aimed to assess the reasons for eventual reoperation and causes of valve dysfunction. METHODS: Between January 1980 and December 2002, 655 patients received fresh homografts. All homografts were antibiotic sterilized and stored at 4 degrees C. During this time, 139 patients (116 male and 23 female) with a mean age of 46.7 years (range 18-72) required reoperation. RESULTS: The 30-day hospital overall mortality was 2.87%. The mean durability for all homografts was 12.4+/-4.54 years (1 month to 23 years). The cumulative rates for freedom from reoperation for any cause were 94.09+/-2% at 5 years and 87.9%+/-4% at 10 years, 76.6 at 15 years, 49.55 at 20 years. The major cause of valve dysfunction and indication for reoperation was degeneration in 111 patients (79.8%). Predominant aortic valve insufficiency in 87 patients (62.5%) and predominant stenosis in 24 patients (17.26%). Endocarditis occurred in 21 patients (15.1%). Early endocarditis was diagnosed in five patients (3.59%), late endocarditis in 16 patients (11.5%). Additional causes for reoperation included ascending aortic aneurysm, mitral valve insufficiency and congestive cardiomyopathy. Seventeen patients (12.2%) required concomitant procedures. Coronary artery bypass grafting was performed in six cases (4.3%), mitral valve replacement in five cases (3.59%), mitral valve annuloplasty in six (4.3%). The primary reoperative procedure was artificial/mechanical aortic valve implantation. In five cases, St. Jude Medical conduit grafts were implanted due to ascending aortic aneurysms. Homograft reimplantation was performed in four cases. One patient underwent mitral valve replacement and one patient received a heart transplant. CONCLUSION: The results of the study suggest that reoperation in patients with aortic homografts is a low-risk procedure as compared to alternative therapies. Primary allograft aortic valve replacement can give acceptable results for up to 23 years. The major cause of valve dysfunction and indication for reoperation was degeneration. Cumulative rates for freedom from reoperation for any cause in age groups suggest careful selection and indications in homograft implantation in the younger patients. Young age is a risk factor for an early homograft structural deterioration (degeneration).
BACKGROUND: As Chlamydia pneumoniae (Cp), a common cause of respiratory infection, is of vasotropic character, chronic infection may be associated with the development of coronary disease, although there have been few reports on the impact of Cp infection on the post-orthotopic heart transplantation (OHT) survival rate. MATERIAL/METHODS: A total of 41 patients (4 females) were followed up for one year after OHT. Serology investigations for IgM, IgG and IgA antibodies against Cp were performed using the enzyme immunoassay (EIA) method. Univariate and multivariate analyses were carried out with respect to IgA, IgG, gender and type of cardiomyopathy. The IgA-IgG joint effect was also studied. RESULTS: The one-year survival rate was reported for patients with IgA < 8 EIU to be 72.2%, whereas those with IgA >or= 8 EIU accounted for only 43.5% (Kaplan-Meier analysis, p = 0.0548). In multivariate analysis IgA /IgG status proved to be a highly significant factor in survival. IgA positive outcome combined with IgG negative outcome showed that the relative risk of death equaled 12.08 versus other combinations of IgA/IgG status. In the Cox multivariate model ischemic cardiomyopathy showed a relative risk of 2.79 (p=0.0594), although it was not significant in univariate CONCLUSIONS: Chronic Cp infection, as expressed through a high IgA level, seems to have adverse impact on the survival rate in one-year follow-up after OHT. IgA titers against Cp in heart transplant recipients should therefore be assessed, as the high values might be a predictive risk factor within the first post-operative year.
BACKGROUND: The aim of this study is to evaluate the risk of accepting cardiac donors after an episode of cardiopulmonary resuscitation. MATERIALS AND METHODS: Since 1997, 13 resuscitated donor hearts (10 M, 3 F, age 15-54 years) after sudden cardiac arrest have been transplanted. The retrospective analysis was used. RESULTS: Allografts after resuscitation episode were implanted in 13 patients (6 M, 7 F, age 31-65 years). 11 patients were on the urgency list and two of them required periodically intravenous inotropic therapy. Two patients (P.A, B.J) died in the first 24 hours after procedure (cause of death: pulmonary embolism, extensive cardiac ischemia). During follow up (6-48 months, avg. 25.1 +/- 15.9 months) none of the 11 patients died. All patients are NYHA functional class I or I/II. Total time of cardiopulmonary resuscitation did not influence the time of reperfusion (p > 0.05). Analysis of cardiac index Cl (l/min/m2) at 2, 4, 6, 8, 12, 24, 72 hours after heart transplantation showed correct values during following days. Echocardiographic and invasive examinations (8 patients) do not show any abnormalities. CONCLUSION: These results suggest that acceptance of cardiac donors after cardiopulmonary resuscitation may not increase the risk of heart transplantation.
BACKGROUND: Percutaneous coronary intervention (PCI) in patients with non ST segment elevation acute coronary syndrome (NSTEACS) is regarded as a procedure which carries a high risk of immediate and long-term adverse cardiac events. This may potentially limit the use of PCI in catheterisation laboratories which do not have on-site surgical back up. However, stents and GP IIb/IIIa receptor inhibitors improved safety of interventional procedures. AIM: To analyse the immediate and long-term outcome of patients with NSTEACS in whom PCI was performed in a catheterisation laboratory without on-site surgical back-up in. METHODS: In a cohort of 479 consecutive patients (160 with NSTEACS - group A, 319 with stable angina - group B) we analysed short and long-term clinical outcome of PCI performed in our catheterisation laboratory which is located several kilometres from a cardiac surgery department, with an effective transfer time <30 minutes. RESULTS: Stent implantation rate and the usage of GP IIb/IIIa blockers were higher in group A than in group B (61.3% vs 50.2%, p=0.04, and 17.5% vs 6.3%; p<0.001, respectively). The in- hospital outcome was similar in both groups (death: 0.6 vs 0.6%; myocardial infarction (MI): 2.5 vs 1.6%; and urgent reintervention (rePCI): 1.9 vs 1.3%, all differences NS). Acute PCI complications requiring urgent surgical operation occurred in 1 (0.6%) patient from group A and in 1 (0.3%) patient from group B (NS). Both patients were successfully transferred for cardiac surgery. During a long-term follow-up the incidence of death (2.0 vs 2.0%), MI (0.7 vs 0.7%), rePCI (21.8 vs 25.2%), CABG (1.4 vs 1.4%) or coronary rehospitalisation (5.4 vs 7.7%) was similar in both groups. The Kaplan-Meier survival and event-free curves were parallel. CONCLUSIONS: In the era of coronary stents and platelet GP IIb/IIIa receptor inhibitors the short and long-term outcome after PCI in patients with NESTACS and stable angina is similar. The early aggressive approach to patients with NESTACS is feasible and safe in a catheterisation laboratory without on-site cardiac surgery. Surgical back-up is still necessary for only few PCI complications.
Carotid angioplasty and stenting (CAS) has been introduced as an alternative to carotid endarterectomy (CEA) for treatment of carotid atherosclerosis. This paper summarizes benefits and limitations of CAS and CEA, describes the main technical points of CAS procedure, use of protection devices and adjunctive pharmacotherapy to reduce procedure related incidents.
The most frequent arrhythmia is an atrial fibrillation, which involves 10% of population over 70. The mortality in this group is 2 times higher than in general population. Moreover, if the atrial fibrillation co-exists with the rheumatic disease, the risk of the brain embolism is growing up 17 times. In the many European medical centers, intraoperative ablation is the obligatory procedure performed during mitral valve replacement/mitral valvuloplasty or coronary artery bypass grafting. Results of that procedure (in experienced centers) are evaluated on 75%. It reduces significantly the cost of the farther pharmacological treatment and improves the quality of life of the patients. In our Clinic ablation is performed in patients qualified to the mitral valve replacement or mitral valvuloplasty. All procedures are performed in extracorporeal circulation, in general and local hypothermia, with using crystal cardioplegine. Before the clumping of the aorta, on the beating heart ablation in the right atrium is performed. After that, the aorta is being clumped and the heart is being stopped. The left cardiac auricle is being cut off. Then the ablation around the ostia of the pulmonary veins is being done. After that, mitral valve replacement or mitral valvuloplasty procedure is being performed. Changes in the heart wall are transmural through the full wall. From the December 2001 till today 4 ablation procedures were done. Units Cobra (Boston Scientific) and Cardioblate Surgical Ablation System (Medtronic) were used. Both units are based on the unipolar energy with frequency similar to the radio-waves. After this procedure, regular rhythm came back in our 4 patients. Advantages of the intraoperative ablation are: simultaneous procedure with open heart operation, reduction of the price of the treatment, minimal risk of complication.
BACKGROUND: Increased superoxide production contributes to reduced vascular nitric oxide (NO) bioactivity and endothelial dysfunction in experimental models of diabetes. We characterized the sources and mechanisms underlying vascular superoxide production in human blood vessels from diabetic patients with coronary artery disease compared with nondiabetic patients. METHODS AND RESULTS: Vascular superoxide production was quantified in both saphenous veins and internal mammary arteries from 45 diabetic and 45 matched nondiabetic patients undergoing coronary artery bypass surgery. NAD(P)H-dependent oxidases were important sources of vascular superoxide in both diabetic and nondiabetic patients, but both the activity of this enzyme system and the levels of NAD(P)H oxidase protein subunits (p22phox, p67phox, and p47phox) were significantly increased in diabetic veins and arteries. In nondiabetic vessels, endothelial NO synthase produced NO that scavenged superoxide. However, in diabetic vessels, the endothelium was an additional net source of superoxide production because of dysfunctional endothelial NO synthase that was corrected by intracellular tetrahydrobiopterin supplementation. Furthermore, increased superoxide production in diabetes was abrogated by the protein kinase C inhibitor chelerythrine. CONCLUSIONS: These observations suggest important roles for NAD(P)H oxidases, endothelial NO synthase uncoupling, and protein kinase C signaling in mediating increased vascular superoxide production and endothelial dysfunction in human diabetes mellitus.