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Objective: To assess the results of tricuspid annuloplasty performed with the Edwards MC3 remodeling ring. Methods: From 2005 to 2007, 140 patients with tricuspid regurgitation (TR) secondary to left-sided valve disease (mean age 63.8 +/- 11.6, permanent pacemaker in 7.8%, LVEF 56.4 +/- 10.1%, LVEDD 54.1 +/- 8 mm, SPAP 52.5 +/- 14.4 mmHg) underwent tricuspid annuloplasty using the MC3 ring. Dilatation of the tricuspid annulus was present in all patients. Other concomitant mechanisms of TR (moderate leaflet prolapse, pacemaker wires, leaflets' retraction) were documented in 21 cases (15%). All patients underwent concomitant left-sided valve surgery. Ring size was between 28 and 32 in 84.3% of patients. Results: Hospital mortality was 3.5% and actuarial survival at 3 years 94.8 +/- 2.1%. Mean follow-up of the 135 hospital survivors was 22 +/- 9.5 months (median 23 months). Echocardiography at hospital discharge documented no or mild TR in 119 patients (87%), moderate TR (2+/4+) in 15 (11%) and moderate-to-severe (3+/4+) in 1 patient (0.7%). At echocardiographic follow-up moderate TR was present in 14 patients (10.3%) and moderate-to-severe TR in 2 (1.4%). At 3 years freedom from TR >= 2+ was 88.1 +/- 2.78% and freedom from TR >= 3+ was 94.3 +/- 4.89. Predictors of TR >= 2+ at hospital discharge and at follow-up were preoperative LVEF (OR:0.8; p = 0.001 at discharge; HR:0.9; p = 0.003 at follow-up) and the presence of other mechanisms of TR besides annular dilatation (OR:10.8; p = 0.007 at discharge; HR:6.1; p = 0.003 at follow-up). Conclusion: Tricuspid annuloplasty with the MC3 ring provides satisfactory early results which remain stable at mid-term follow-up. The presence of other mechanisms besides annular dilatation leads to residual valve insufficiency after ring annuloplasty alone. doi: 10.1111/j.1540-8191.2012.01443.x (J Card Surg 2012;27:288-294)

Objectives: To describe results from a novel percutaneous technique designed to minimize the risk of hemorrhage in the event of a major complication during transcatheter aortic valve implantation. Background: Vascular access management is a major challenge in transfemoral TAVI due to the large introducer sheathes required. Methods: Fifty-two pts underwent TAVI between November 2007 and March 2009. Of these, 37 received an Edwards-Sapien Valve (23 mm valve: 17/37; 26 mm valve: 20/37) whilst 15 patients received a CoreValve (26 mm valve: 6/15; 29 mm valve: 9/15). Using a crossover technique, the opposing femoral artery was cannulated with a 7Fr long sheath. This allowed contralateral passage of a balloon and inflation in the proximal iliac. The sheath was then removed and Prostar sutures tied in a dry field. Balloon optimization of the puncture site was performed as required. Results: In three subjects, elective surgical repair was undertaken due to excessive femoral arterial calcification. In the remaining 49, the crossover technique was employed and closed with two Prostar devices (Edwards-Sapien) or one (CoreValve). There were serious “on-table” complications in seven patients, six due to the large introducer sheathes used in the TAVI procedure—iliac avulsion, two iliac dissections, iliac perforation, common femoral perforation and scrotal hematoma. All were repaired safely by combined surgical and endovascular techniques, using the crossover technique to ensure patient stability. All made a good recovery and were independently ambulant at discharge. Conclusion: Using crossover balloon inflation as an adjunct to Prostar closure may be helpful for managing TAVI vascular access sites. © 2009 Wiley-Liss, Inc.

Objective: Despite its efficacy and swiftness, bipolar radiofrequency is generally not used on the left isthmus for concern of injuring a coronary branch. Incomplete lesion sets or use of an additional unipolar device are often considered. We report a technique to perform a full left lesion set involving the mitral line using a standard bipolar radiofrequency device. Methods: An innovative complete left atrial lesion set was performed using only bipolar radiofrequency in 70 consecutive patients (study group). In 67/70 patients (96%) mitral valve disease was the main indication to surgery. Atrial fibrillation was permanent in 42 patients (60%), persistent in 25 (36%) and paroxysmal in three patients (4%). After beating-heart pulmonary vein isolation on-pump, the coronary-free area of the AV groove was marked epicardially by sticking a needle into the left atrial wall, behind the coronary sinus. The projection of the needle marker on the mitral annulus was then identified through the atriotomy and an endo-epicardial ablation was performed with the bipolar device involving the atrial wall, the coronary sinus, up to the annulus. The lesion set was then completed by connecting the encirclings and the left appendage, which was then sutured. Follow-up was 100% complete. Results were compared with those of a control group of 33 patients receiving bipolar radiofrequency left atrial ablations and a mitral connecting line with a second unipolar device. Results: All patients survived. No major complication occurred. Haematoma of the AV groove was observed during retrograde cardioplegia in one case. No myocardial ischaemia or re-exploration for bleeding (median 325 cc, interquartile range 250-442) occurred. Two out of 70 patients required a permanent pacemaker for AV block. Freedom from atrial fibrillation was 84% (95% CI: 75%, 93%) at 6 months and 81% (95% CI: 70%, 93%) at 1 year. One patient had left flutter. Comparison with the control group did not show any difference in clinical outcomes, but revealed bipolar ablation to the mitral annulus to abate the per patient cost of the ablation devices (1245 ± 50 ∈ vs 2403 ± 17 ∈; p < 0.0001). Conclusions: Performing the mitral line with bipolar radiofrequency is safe and cost-effective. A complete left atrial ablation with a single bipolar radiofrequency device yields excellent clinical mid-term results.

Atrial fibrillation becomes a self-perpetuating arrhythmia as a consequence of electrophysiologic and structural remodeling involving the atrium. Oxidative stress may be a link between this rhythm disturbance and electrophysiologic remodeling. The aim of this study was to evaluate whether the heme oxygenase-1 (HO-1) marker of oxidative stress was more expressed in left atrial sites with stronger structural remodeling in patients affected by chronic atrial fibrillation (CAF) and mitral valve disease (MD). Myocardial samples were taken from the left atrial posterior wall (LAPW) and left atrial appendage (LAA) of 24 patients with CAF-MD in addition to 10 autopsy controls. The levels of HO-1 messenger RNA (mRNA) and HO-1 protein in each pathologic LAPW and LAA were quantified using reverse transcriptase polymerase chain reaction and enzyme-linked immunosorbent assay. Furthermore, light microscopy was used to morphometrically evaluate the differential myocyte and interstitial changes in the same CAF-MD LAPW and LAA samples. In controls, HO-1 protein was quantified using enzyme-linked immunosorbent assay. Unlike controls, patients with CAF-MD had higher levels of HO-1 mRNA and its protein product, expressed as LAPW/LAA ratios, in the LAPW (2.18 +/- 1.18, P.0001, and 1.55 +/- 0.67, P.005), and their LAPW also showed greater histologic changes in myocytolytic myocytes (15.1% +/- 3.1% versus 6.9% +/- 3.3%, P.0001), interstitial fibrosis (8.2% +/- 2.2% versus 2.8% +/- 1.2%, P.0001), and capillary density (816 +/- 120 number/mm(2) versus 1114 +/- 188 number/mm(2); P.05). In addition, markers of oxidative stress were immunohistochemically studied with antinitrotyrosine and anti-iNOS antibodies. In patients with CAF-MD, the inducible enzyme HO-1 is more expressed in the left atrial areas that show greater structural remodeling. This finding strongly suggests a pathogenetic relationship between oxidative stress and the degree of histologic change.

All patients undergoing heart surgery experience a certain amount of nonspecific myocardial injury documented by the release of cardiac biomarkers and associated with poor outcome. We investigated the role of unipolar radiofrequency ablation of atrial fibrillation on the release of cardiac biomarkers in 71 patients undergoing mitral valve surgery and concomitant left atrial ablation case-matched with 71 patients undergoing isolated mitral surgery. The study was powered to detect a 3 ng/mL difference. There was no difference between the 2 groups in terms of cardiac troponin 1 (10 +/- 5.3 versus 12 + 10.4 ng/mL; P = 0.7) or creatine kinase-MB (50 +/- 21.8 versus 57 +/- 62.0 ng/mL; P = 0.5) release. Postoperative peak cardiac troponin I levels had univariate associations with the duration of cardiopulmonary bypass (P = 0.002) and aortic cross-clamping (P = 0.001) and with the surgical technique (15 +/- 12 ng/mL for mitral valve replacement versus 9 +/- 14.8 for mitral valve repair; P = 0.0007) at univariate analysis. Mitral valve replacement was the only independent predictor of postoperative peak release of cardiac troponin I identified with multivariate analysis (P = 0.005). Radicifrequency ablation of atrial fibrillation does not significantly increase cardiac biomarker release compared with isolated mitral surgery; mitral valve repair is associated with less release of cardiac biomarkers compared with mitral valve replacement.

It has been found that the pulmonary veins and adjacent left atrial posterior wall (LAPW) are deeply involved in both the initiation and maintenance of atrial fibrillation (AF), and the identification of these high-risk sites has aroused great interest in investigating their histopathologic substrate. We used light and conventional electron microscopy to evaluate the differential myocyte and interstitial changes in LAPW and left atrial appendage (LAA) samples from 28 patients with chronic AF undergoing mitral valve surgery and from 12 autoptic controls. There were always more myocytes with loss of sarcomeres in the LAPW than in the LAA (19.9% +/- 7.7% versus 8.2% +/- 5.0%; P < .0001), and the LAPW showed more marked immunohistochemical evidence of dedifferentiation, characterized by the reexpression of smooth muscle actin. In pathological left atria, myocyte diameter in the LAPW and LAA was comparable (19.0 +/- 1.5 versus 18.5 +/- 2.0 microm; not significant) but larger than in the controls (11.9 +/- 0.8 and 12.1 +/- 1.3 microm, respectively; P < .0001). A terminal deoxynucleotidyltransferase assay did not reveal any myocyte apoptosis. The LAPW also showed more interstitial fibrosis than the LAA (7.49% +/- 3.34% versus 2.80% +/- 1.35%; P < .0001). Ultrastructural examination confirmed the presence of myocyte myocytolysis in the perinuclear area and showed changes in mitochondrial shape. In conclusion, the LAPW in patients with chronic AF related to mitral valve disease seems to be a particular anatomical site in which major myocyte and interstitial changes are concentrated, whereas the LAA is more protected. This remodeling may increase the heterogeneity of LAPW electrical conduction, thus confirming this location as an elective target for the ablation treatment of AF.

The degeneration of a previously surgically implanted aortic bioprosthesis is an increasing etiology of aortic stenosis in the elderly, but reoperative surgery may present prohibitive risks. The feasibility of transcatheter aortic valve implantation into a conventional bioprosthesis (valve-in-valve concept) has been evaluated to decrease the reoperative risk for patients with a failed bioprosthesis. There have been several reports of valve-in-valve procedures using the self-expandable prosthesis CoreValve (Medtronic Inc.), whereas the feasibility of this procedure with the Sapien balloon expandable valve (Edwards Lifesciences Inc.) is still not well established. Here we report the case of a patient submitted to balloon-expandable aortic valve-in-valve implantation in an emergency setting to treat a severe aortic stenosis due to the premature failure of a surgical bioprosthesis.

Luting fiber posts to intraradicular dentin remains an unpredictable goal due to various clinical factors influencing the clinical procedure. Primarily differences can be found between bonding to coronal or to intraradicular dentin due to the different histological characteristics of the substrates, the high C-factor of the endodontic space, the presence of smear layer due to the post preparation technique, incompatibility between some adhesive systems and resin-based cements, and finally the limited access of the post space that may lead the clinician to different mistakes. Thus this article critically evaluates all aspects that may jeopardize the adhesion of luted fiber posts within the endodontic space, suggesting the use of standardized techniques that improve immediate adhesion and stabilize the adhesive interface over time. The review of the data currently available in peer-reviewed journals suggests that a strict following of a step-by-step clinical standardized technique allows the clinician to minimize bond failure and obtain a clinically reliable durable bond. (C) Koninklijke Brill NV, Leiden, 2009