Reduced Permanent Pacemaker Implantation in Patients With Stentless Freedom SOLO Compared With Stented Perimount Magna Aortic Bioprostheses: A Propensity Score Weighted Analysis.

OBJECTIVES: Postoperative permanent pacemaker implantation (PPI) after conventional aortic valve replacement (AVR), due to new-onset severe conduction system disorders, is required in approximately 7% of patients. This study investigated the need for PPI after AVR with conventional stented Perimount Magna compared with the Freedom SOLO (FS) stentless valve (Sorin Group, Saluggia, Italy), now LivaNova plc (London, UK) that uses a strictly supra-annular, subcoronary running suture implantation technique, sparing the vulnerable interleaflet triangles in the region of the septum membranaceum. METHODS: A total of 413 consecutive patients (71.4±9.2 yrs, 178 [43.1%] female) underwent isolated AVR using the stented Perimount Magna (n=264) or the stentless FS (n=149) bioprosthesis. Propensity score weighted analysis was used to account for patient-specific and procedural-specific variables, and to identify the prosthesis-specific need for early postoperative PPI within 30 days of AVR. RESULTS: Twenty (20) patients required PPI, which was associated with longer intensive care unit (2.1±1.7 vs 1.5±3.0 days, p<0.001) and overall hospital stays (13.8±5.2 vs 10.7±5.3 days, p<0.001) compared with no PPI. Propensity weighted logistic regression including cross-clamp times identified that use of the stented Perimount Magna was associated with increased need for PPI, as compared with the FS, with an odds ratio 5.8 (95% CI, 1.09-30.76; p=0.039). CONCLUSIONS: After corrections for all plausible confounders, AVR with the stented Perimount valve was associated with an odds ratio of almost 6 for an increased early postoperative need for pacemaker implantation compared with the FS stentless valve. This finding can be explained by the conventional implantation technique, which is potentially associated with mechanical trauma to the conducting system.

[Traumatic aortic rupture - diagnosis and managment]. / Die traumatische Aortenruptur.

Road traffic accidents are the main cause of traumatic aortic ruptures, mostly in combination with other severe injuries. The pre-hospital mortality rate is high. Suspected aortic trauma, following a high traumatic aortic injury score, is an indication for computer tomography. Injuries are triaged and the treatment priority of the aortic trauma is ascertained based on the severity of the aortic and concomitant injuries and the condition of the patient. Until definitive treatment of the aortic lesion is completed, the blood pressure of the patient must be kept low. Grade I and II lesions can be managed under strict monitoring with initial conservative treatment in individual cases. Grade III (contained perforation) and grade IV (open rupture) lesions need surgical or interventional treatment as swiftly as possible. In selected cases, a delayed treatment can also be advantageous.The endovascular stent graft therapy has established itself as the preferred form of treatment.

Freedom SOLO-Associated Thrombocytopaenia is Valve-Dependent and Not Due to In Vitro Pseudothrombocytopaenia.

BACKGROUND: Use of the Freedom SOLO (FS) stentless aortic bioprosthesis is limited by a unique and as yet unexplained severe decrease in postoperative platelet count in the absence of FS-related excess bleeding or thromboembolism. We investigated whether anticoagulant-associated pseudothrombocytopaenia could explain this complication. METHODS: Thirty consecutive patients (mean age 75.4±7.7 years, 11 [36.7%] female) underwent elective aortic valve replacement (AVR) with either the stented bovine Mitroflow (MF, n=18) or the stentless bovine FS (n=12) aortic valve bioprostheses. Serial platelet counts were performed simultaneously with sampling tubes containing tripotassium (K3-)-EDTA, trisodium (Na3)-citrate, or novel alternative magnesium sulfate (MgSO4, ThromboExact™)-based anticoagulant, respectively. RESULTS: Postoperative platelet counts decreased compared with preoperative values in all patients (p<0.001), but were significantly lower in patients receiving FS compared to MF at all measurement time points until the end of observation (day 9). Lowest platelet counts were seen on the first postoperative day for MF (mean reduction: -41.5%) and on the second postoperative day for FS (mean reduction: -59.9%). Postoperative platelet counts did not correlate with any of the anticoagulants, thereby indicating no pseudothrombocytopaenia in the study population. There was no interaction between anticoagulant and type of valve. Only 1% of variance in platelet counts was caused by the anticoagulant, 46% by the day of measurement relative to baseline, and 20% was caused by the type of valve. CONCLUSIONS: The platelet-lowering effect in patients receiving the FS is valve-dependent and is not caused by systemic preanalytical (laboratory) measurement error such as anticoagulant-dependent pseudothrombocytaemia, particularly with EDTA and citrate.

Type A aortic dissection after nonaortic cardiac surgery.

BACKGROUND: Cardiac surgery with cardiopulmonary bypass is associated with mechanical manipulation of the ascending aorta that occasionally leads to type A aortic dissection (AAD). METHODS AND RESULTS: One hundred three patients with surgical repair for AAD following nonaortic cardiac surgery were identified. With the use of logistic regression modeling, coronary artery bypass surgery (CABG), either isolated or combined with another procedure in the initial operation, was associated with significantly higher operative mortality in comparison with patients with non-CABG procedures at the time of AAD repair both for all patients (odds ratio, 2.90; 95% confidence interval, 1.09-7.72; P=0.033) and for patients with acute and chronic AAD≥30 days after the initial operation (odds ratio, 3.62; 95% confidence interval, 1.13-11.54; P=0.03). In patients who developed AAD late after the initial operation, operative mortality was highest in patients without preoperative coronary angiography and appropriate management of their native coronary artery disease and graft disease (odds ratio, 5.36; 95% confidence interval, 1.68-17.0; P=0.002). Nearly all the intimal dissection tears were located at sites of previous surgical trauma. Most of the ascending aortas that had dissected initially had a diameter≥40 mm with histological evidence of medial degeneration in resected tissue samples. CONCLUSIONS: In patients who have undergone previous cardiac surgery, preexisting aortic wall pathology contributes to AAD with typical intimal damage at sites of mechanical trauma. The operative mortality was the highest in patients with previous CABG in comparison with patients with non-CABG procedures. Preoperative coronary angiography and operative management of native coronary and graft disease were significantly associated with outcome in patients with previous CABG.

Antioxidant supplementation attenuates oxidative stress in patients undergoing coronary artery bypass graft surgery.

Ischemia-reperfusion has been reported to be associated with augmented oxidative stress in the course of surgery, which might be causally involved in the onset of atrial fibrillation (AF), the most common arrhythmia after cardiac surgery. We hypothesized that supplementation of antioxidants and n-3 polyunsaturated fatty acids (n-3 PUFAs) might lower the incidence of AF following coronary artery bypass graft (CABG) surgery. In the present study, by monitoring oxidative stress in the course of CABG surgery, we analyzed the efficacy of vitamins (ascorbic acid and α-tocopherol) and/or n-3 PUFAs (eicosapentaenoic acid and docosahexaenoic acid). Subjects (n = 75) were divided into 4 subgroups: control, vitamins, n-3 PUFAs, and a combination of vitamins and n-3 PUFAs. Fluorescent techniques were used to measure the antioxidative capacity, i.e. ability to inhibit oxidation. Total peroxides, endogenous peroxidase activity, and antibodies against oxidized LDL (oLAb) were used as serum oxidative stress biomarkers. Post-operative increase in oxidative stress was associated with the consumption of antioxidants and a simultaneous onset of AF. This was confirmed through an increased peroxide level and a decreased oLAb titer in control and n-3 PUFAs groups, indicating the binding of antibodies to oxidative modified epitopes. In both subgroups that were supplemented with vitamins, total peroxides decreased, and the maintenance of a constant IgG antibody titer was facilitated. However, treatment with vitamins or n-3 PUFAs was inefficient with respect to AF onset and its duration. We conclude that the administration of vitamins attenuates post-operative oxidative stress in the course of CABG surgery.

Enzymatic and non-enzymatic antioxidative effects of folic acid and its reduced derivates.

A great part of the population appears to have insufficient folate intake, especially subgroups with higher demand, as determined through more sensitive methods and parameters currently in use. As the role of folate deficiency in congenital defects, e.g. in cardiovascular and neurodegenerative diseases, and in carcinogenesis has become better understood, folate has been recognized as having great potential to prevent these many disorders through folate supplementation or fortification for the general population. Folates are essential cofactors in the transfer and utilization of one-carbon groups in the process of DNA-biosynthesis with implications for genomic repair and stability. Folate acts indirectly to lower homocysteine levels and insures optimal functioning of the methylation cycle. Homocysteine was shown to be an independent risk factor for neurodegenerative and cardiovascular disease, which includes peripheral vascular disease, coronary artery disease, cerebrovascular disease and venous thrombosis. In fact, it was long believed that the beneficial effects of folate on vascular function and disease are related directly to the mechanism of homocysteine-diminution. Recent investigations have, however, demonstrated beneficial effects of folates unrelated to homocysteine-diminution, suggesting independent properties. One such mechanism could be free radical scavenging and antioxidant activity, as it is now recognized that free radicals play an important role in the oxidative stress leading to many diseases. It was found that folic acid and, in particular, its reduced derivates act both directly and indirectly to produce antioxidant effects. Folates interact with the endothelial enzyme NO synthase (eNOS) and, exert effects on the cofactor bioavailability of NO and thus, on peroxynitrite formation. Folate metabolism provides an interesting example of gene-environmental interaction.

Reduction of nuclear encoded enzymes of mitochondrial energy metabolism in cells devoid of mitochondrial DNA.

Mitochondrial DNA (mtDNA) depletion syndromes are generally associated with reduced activities of oxidative phosphorylation (OXPHOS) enzymes that contain subunits encoded by mtDNA. Conversely, entirely nuclear encoded mitochondrial enzymes in these syndromes, such as the tricarboxylic acid cycle enzyme citrate synthase (CS) and OXPHOS complex II, usually exhibit normal or compensatory enhanced activities. Here we report that a human cell line devoid of mtDNA (HEK293 ρ(0) cells) has diminished activities of both complex II and CS. This finding indicates the existence of a feedback mechanism in ρ(0) cells that downregulates the expression of entirely nuclear encoded components of mitochondrial energy metabolism.

Mitochondrial DNA haplogroup T is associated with coronary artery disease and diabetic retinopathy: a case control study.

BACKGROUND: There is strong and consistent evidence that oxidative stress is crucially involved in the development of atherosclerotic vascular disease. Overproduction of reactive oxygen species (ROS) in mitochondria is an unifying mechanism that underlies micro- and macrovascular atherosclerotic disease. Given the central role of mitochondria in energy and ROS production, mitochondrial DNA (mtDNA) is an obvious candidate for genetic susceptibility studies on atherosclerotic processes. We therefore examined the association between mtDNA haplogroups and coronary artery disease (CAD) as well as diabetic retinopathy. METHODS: This study of Middle European Caucasians included patients with angiographically documented CAD (n = 487), subjects with type 2 diabetes mellitus with (n = 149) or without (n = 78) diabetic retinopathy and control subjects without clinical manifestations of atherosclerotic disease (n = 1527). MtDNA haplotyping was performed using multiplex PCR and subsequent multiplex primer extension analysis for determination of the major European haplogroups. Haplogroup frequencies of patients were compared to those of control subjects without clinical manifestations of atherosclerotic disease. RESULTS: Haplogroup T was significantly more prevalent among patients with CAD than among control subjects (14.8% vs 8.3%; p = 0.002). In patients with type 2 diabetes, the presence of diabetic retinopathy was also significantly associated with a higher prevalence of haplogroup T (12.1% vs 5.1%; p = 0.046). CONCLUSION: Our data indicate that the mtDNA haplogroup T is associated with CAD and diabetic retinopathy in Middle European Caucasian populations.

A Randomized Pilot Trial to Evaluate the Bioavailability of Natural versus Synthetic Vitamin B Complexes in Healthy Humans and Their Effects on Homocysteine, Oxidative Stress, and Antioxidant Levels.

The vitamin B complex comprises 8 different water-soluble constituents that humans must sequester from the diet. This pilot study compared natural versus synthetic vitamin B complexes for their bioavailability, accumulation, and their impact on antioxidants, homocysteine levels, and oxidative stress. We conducted a double-blind randomized clinical trial with thirty healthy participants. They were randomly assigned to group N (natural) and group S (synthetic). Vitamin B was ingested daily for 6 weeks in the range of about 2.5 times above the recommended daily allowance. Blood samples were taken at baseline, 1.5 h, 4 h, 7 h (diurnal), 6 w (discontinuation of supplements), and 8 w (washout). Blood levels of thiamine (B1), riboflavin (B2), pyridoxine (B6), folic acid (B9), cobalamin (B12), homocysteine, total antioxidants, peroxidase activity, polyphenols, and total peroxides were determined. Compared to initial values, serum levels of each B vitamin increased at the end of the supplementation period: i.e., B1 (+23% N; +27% S), B2 (+14% N; +13% S), B6 (+101% N; +101% S), B9 (+86% N; +153% S), and B12 (+16% N) (p < 0.05). Homocysteine (-13% N) decreased, while peroxidase activity (+41% S) and antioxidant capacity increased (+26% N). Short-term effects were already observed after 1.5 h for B9 (+238% N; +246% S) and after 4 h for vitamin B2 (+7% N; +8% S), B6 (+59% N; +51% S), and peroxidase activity (+58% N; +58% S). During the washout period, serum levels of B vitamins decreased except for thiamine and peroxidase activity, which increased further. This clinical pilot study revealed comparable bioavailability for both natural and synthetic B vitamins but did not show statistically noticeable differences between groups despite some favourable tendencies within the natural vitamin group, i.e., sustained effects for cobalamin and endogenous peroxidase activity and a decrease in homocysteine and oxidative stress levels.

The methylenetetrahydrofolate reductase 677C>T gene polymorphism is not associated with chronic plaque psoriasis.

BACKGROUND: Methylenetetrahydrofolate reductase (MTHFR) is involved in the formation of methyl donors, which contribute to DNA methylation. DNA methylation is an essential epigenetic feature playing a critical role in gene regulation and cellular differentiation. In addition, MTHFR activity affects plasma homocysteine levels. A functional polymorphism in the MTHFR gene (677C>T, rs1801133) leading to reduced enzyme activity has been associated with chronic plaque psoriasis in a Chinese population. This finding, however, has not yet been either confirmed or refuted in other populations. The purpose of the present study was to investigate a hypothesized association between the MTHFR 677C>T polymorphism and the presence of chronic plaque psoriasis in a Caucasian population. METHODS: Genotypes for the MTHFR 677C>T polymorphism were determined in 310 patients and 247 control subjects. In a subgroup of 33 patients and 33 sex- and age-matched control subjects, fasting plasma homocysteine concentrations were determined by high-performance liquid chromatography and immunological assays were used for the measurement of folate and vitamin B(12). RESULTS: Prevalence of the homozygous MTHFR 677TT genotype did not significantly differ between patients and controls (15.2% vs 11.7%, P = 0.24). Mean plasma homocysteine concentrations were significantly higher in psoriasis patients than among control subjects (13.5 +/- 5.3 micromol/l vs 11.0 +/- 2.2 micromol/l, P = 0.026). No significant differences between either mean plasma folate or vitamin B(12) concentrations were observed between both groups. CONCLUSION: Our data suggest that the MTHFR 677C>T gene polymorphism is not associated with chronic plaque psoriasis among Caucasians.

Immunohistochemical detection of N-homocysteinylated proteins in humans and mice.

N-homocysteinylation of epsilon-amino group of protein lysine residues by homocysteine (Hcy) thiolactone has been implicated in vascular disease in humans. We have previously generated polyclonal rabbit anti-N-Hcy-protein IgG antibodies that specifically recognize the Nepsilon-Hcy-Lys epitope on N-homocysteinylated proteins. The present work was undertaken to examine the utility of these antibodies for the immunohistochemical detection of N-homocysteinylated proteins in biological samples. We found that the rabbit antibody specifically detected N-Hcy-protein in a dot-blot assay, that the signal resulting from the reaction of the antibody with N-Hcy-protein depended on the amount of the antigen, and that the sensitivity of the assay was protein-dependent. The rabbit anti-N-Hcy-protein IgG also specifically detected Nepsilon-Hcy-Lys epitopes in human tissues, as shown by positive immunohistochemical staining of myocardium and aorta samples from cardiac surgery patients, and a lack of staining when the antibody was pre-adsorbed with N-Hcy-albumin. We also observed increased immunohistochemical staining for N-Hcy-proteins in aortic lesions from ApoE-/- mice with hyperhomocysteinemia induced by a high methionine diet, relative to ApoE-/- mice fed a control chow diet. In conclusion, polyclonal rabbit anti-N-Hcy-protein antibody can detect and monitor N-homocysteinylated proteins in human and mouse tissues with good sensitivity and specificity.

Methylenetetrahydrofolatereductase (MTHFR) 677C>T polymorphism and open angle glaucoma.

PURPOSE: Increased plasma homocysteine levels have been found in patients with primary open angle glaucoma (POAG) and glaucoma secondary to pseudoexfoliation syndrome (PEXG). A common polymorphism of the methylenetetrahydrofolatereductase (MTHFR 677C>T) leads to moderately elevated plasma homocysteine levels particularly under conditions of impaired folate status. It was the aim of this study to investigate a hypothesized association between this polymorphism and the presence of either POAG or PEXG. METHODS: The present retrospective case-control study included a total of 553 participants comprising 204 patients with POAG, 138 patients with PEXG, and 211 control subjects. Genotyping for the MTHFR 677C>T polymorphism was performed by polymerase chain reaction (PCR). RESULTS: No significant difference in the genotype distribution of the MTHFR 677C>T polymorphism was found between control subjects and patients with POAG or PEXG. The prevalence of the MTHFR 677TT genotype was 6.9% in patients with POAG, 11.6% in patients with PEXG, and 9.5% in control subjects. CONCLUSIONS: The present data suggest that the MTHFR 677C>T polymorphism itself is not a major genetic risk factor for POAG and PEXG in a central European population.

Folate supplementation does not affect biochemical markers of bone turnover.

BACKGROUND: Recently, increased plasma homocysteine (HCY) has been suggested as a novel independent risk factor for osteoporotic fractures. This study aimed to analyze the effect of a HCY lowering therapy by folic acid (FA) supplementation on biochemical bone markers in healthy subjects. MATERIAL AND METHODS: We treated 61 healthy individuals (mean age: 58+/-8 years) with placebo, 0.4, 1 or 5 mg FA daily for 2 months. Fasting blood samples were taken after 0, 4 and 8 weeks. Serum HCY, folate, vitamin B12, osteocalcin (OC), procollagen type I N-terminal propeptide (PINP) and C-terminal telopeptides of human collagen type I (CTX) were studied. RESULTS: Overall baseline HCY and folate levels were 13.4 +/- 3.6 micromol/L and 5.7 +/- 3.0 microg/L, respectively. Participants exhibited normal baseline OC, PINP and CTX levels. Serum folate increased during supplementation (4 weeks of placebo, 0.4, 1 and 5 mg of FA: -7, +160, +162 and +436 %; 8 weeks: -6, +305, +340 and +216 %) and HCY decreased (4 weeks of placebo, 0.4, 1 and 5 mg of FA: +2, -14, -21 and -17 %; 8 weeks: +2, -8, -20 and -17 %) in the treatment groups, but not in the placebo group. OC (placebo: 22.8 vs. 23.0 vs. 23.6; 0.4 mg FA: 21.6 vs. 22.1 vs. 24.1; 1 mg FA: 23.7 vs. 22.6 vs. 23.4; 5 mg FA: 24.1 vs. 20.5 vs. 20.9 microg/L), PINP (placebo: 43.5 vs. 51.3 vs. 46.5; 0.4 mg FA: 34.0 vs. 34.1 vs. 39.5; 1 mg FA: 43.6 vs. 39.7 vs. 43.2; 5 mg FA: 41.1 vs. 38.7 vs. 37.4 microg/L) and CTX (placebo: 258 vs. 360 vs. 321; 0.4 mg FA: 229 vs. 290 vs. 315; 1 mg FA: 319 vs. 325 vs. 301; 5 mg FA: 293 vs. 321 vs. 304 ng/L) did not change throughout the study. CONCLUSION: Short-term FA supplementation does not affect biochemical bone markers in non-osteoporotic subjects with a low folate status.

Asymmetric dimethyl-L-arginine (ADMA): a possible link between homocyst(e)ine and endothelial dysfunction.

Hyperhomocyst(e)inemia is associated with an increased risk for atherosclerotic disease and venous thromboembolism. The impact of elevated plasma homocysteine levels seems to be clinically relevant, since the total cardiovascular risk of hyperhomocyst(e)inemia is comparable to the risk associated with hyperlipidemia or smoking. There is substantial evidence for impairment of endothelial function in human and animal models of atherosclerosis, occurring even before development of overt plaques. Interestingly endothelial dysfunction appears to be a sensitive indicator of the process of atherosclerotic lesion development and predicts future vascular events. NO is the most potent endogenous vasodilator known. It is released by the endothelium, and reduced NO bioavailability is responsible for impaired endothelium-dependent vasorelaxation in hyperhomocyst(e)inemia and other metabolic disorders associated with vascular disease. Substances leading to impaired endothelial function as a consequence of reduced NO generation are endogenous NO synthase inhibitors such as ADMA. Indeed there is accumulating evidence from animal and human studies that ADMA, endothelial function and homocyst(e)ine might be closely interrelated. Specifically elevations of ADMA associated with impaired endothelium-dependent relaxation were found in chronic hyperhomocyst(e)inemia, as well as after acute elevation of plasma homocyst(e)ine following oral methionine intake. The postulated mechanisms for ADMA accumulation are increased methylation of arginine residues within proteins, as well as reduced metabolism of ADMA by the enzyme DDAH, but they still need to be confirmed to be operative in vivo. Hyperhomocyst(e)inemia, as well as subsequent endothelial dysfunction can be successfully treated by application of folate and B vitamins. Since ADMA seems to play a central role in homocyst(e)ine-induced endothelial dysfunction, another way of preventing vascular disease in patients with elevated homocyst(e)ine concentrations could be supplementation with L-arginine to reverse the detrimental effects of ADMA.

Role of thrombophilic gene polymorphisms in branch retinal vein occlusion.

OBJECTIVE: Branch retinal vein occlusion (BRVO) is a common cause of severe visual loss. Numerous risk factors, including arterial hypertension, diabetes mellitus, and arteriosclerosis, have been identified. Gene polymorphisms affecting hemostasis may also play a role in the pathogenesis of BRVO. The present study was therefore done to determine the prevalence of genetic polymorphisms in factors implicated in hypercoagulability among patients with BRVO. DESIGN: Retrospective case-control study. PARTICIPANTS: The study cohort consisted of 294 patients with BRVO and 294 control subjects, matched for age and gender. METHODS: Determination of genotypes was done by allele-specific digestion of polymerase chain reaction products, or by 5' exonuclease assay (TaqMan). MAIN OUTCOME PARAMETERS: Genotypes of factor V R506Q (factor V Leiden), prothrombin 20210G>A, fibrinogen beta -455G> A, factor XII (FXII) 46C>T, and ITGA2 807C>T (platelet glycoprotein Ia [GPIa] 807C>T) and ITGB3 L59P (platelet GPIIIa PlA1/PlA2) polymorphisms. RESULTS: Genotype distributions of the investigated gene polymorphisms did not differ significantly between patients and control subjects. In contrast, significantly increased prevalences of arterial hypertension and hypercholesterolemia were found among patients with BRVO. In a logistic regression analysis, the presence of arterial hypertension was associated with an odds ratio (OR) of 2.32 (95% confidence interval [CI], 1.62-3.32), whereas hypercholesterolemia yielded an OR of 2.54 (95% CI, 1.74-3.70) for BRVO. CONCLUSION: Our data indicate that the prevalences of the investigated gene polymorphisms do not differ significantly in patients with BRVO and control subjects. This suggests that these polymorphisms are not major risk factors for BRVO.

Pitfalls and premature failure of the Freedom SOLO stentless valve.

OBJECTIVES: This study reports a series of pitfalls, premature failures and explantation of the third-generation Freedom SOLO (FS) bovine pericardial stentless valve. METHODS: A total of 149 patients underwent aortic valve replacement using the FS. Follow-up was 100% complete with an average observation time of 5.5 ± 2.3 years (maximum 8.7 years) and a total of 825 patient-years. Following intraoperative documentation, all explanted valve prostheses underwent histological examination. RESULTS: Freedom from structural valve deterioration (SVD) at 5, 6, 7, 8 and 9 years was 92, 88, 80, 70 and 62%, respectively. Fourteen prostheses required explantation due to valve-independent dysfunction (n = 5; i.e. thrombus formation, oversizing, aortic dilatation, endocarditis and suture dehiscence) or valve-dependent failure (acute leaflet tears, n = 4 and severe stenosis, n = 5). Thus, freedom from explantation at 5, 6, 7, 8 and 9 years was 95, 94, 91, 81 and 72%, respectively. An acute vertical tear along the non-coronary/right coronary commissure to the base occurred at a mean of 6.0 years (range 4.3-7.3 years) and affected size 25 and 27 prostheses exclusively. Four FS required explantation after a mean of 7.5 years (range 7.0-8.3 years) due to severe functional stenosis and gross calcification that included the entire aortic root. CONCLUSIONS: The FS stentless valve is safe to implant and shows satisfying mid-term results in our single institution experience. Freedom from SVD and explantation decreased markedly after only 6-7 years, so that patients with FS require close observation and follow-up. Exact sizing, symmetric positioning and observing patient limitations are crucial for optimal outcome.

The Freedom Solo pericardial stentless valve: Single-center experience, outcomes, and long-term durability.

OBJECTIVES: To report our institutional experience and long-term results with the Freedom Solo bovine pericardial stentless bioprosthesis (Sorin Group, Saluggia, Italy). METHODS: Between January 2005 and November 2009, 149 patients (mean age, 73.6 ± 8.7 years; 68 [45.6%] female) underwent isolated (n = 75) or combined (n = 74) aortic valve replacement (AVR) using the Solo in our institution. Follow-up was 100% complete with an average follow-up time of 5.9 ± 2.6 years (maximum, 9.6 years) and a total of 885.3 patient years. RESULTS: Operative (30-day) mortality was 2.7% (1.3% for isolated AVR [n = 1] and 4.0% for combined procedures [n = 3]). All causes of death were not valve-related. Preoperative peak (mean) gradients of 74.2 ± 23.0 mm Hg (48.6 ± 16.3 mm Hg) decreased to 15.6 ± 5.4 mm Hg (8.8 ± 3.0 mm Hg) after AVR, and remained low for up to 9 years. The postoperative effective orifice area was 1.6 ± 0.57 cm(2), 1.90 ± 0.45 cm(2), 2.12 ± 0.48 cm(2), and 2.20 ± 0.66 cm(2) for the valve sizes 21, 23, 25, and 27, respectively, with absence of severe prosthesis-patient mismatch and 0.7% (n = 1) experienced moderate prosthesis-patient mismatch. During follow-up, 26 patients experienced structural valve deterioration (SVD) and 14 patients underwent explantation. Kaplan-Meier estimates for freedom from death, explantation, and SVD at 9 years averaged 0.57 (range, 0.47-0.66), 0.82 (range, 0.69-0.90), and 0.70 (range, 0.57-0.79), respectively. CONCLUSIONS: The Freedom Solo stentless aortic valve is safe to implant and shows excellent early and midterm hemodynamic performance. However, SVD was observed in a substantial number of patients after only 5-6 years and the need for explantation increased markedly, suggesting low durability.