Use of tissue welding technology to obliterate left atrial appendage--novel use of Ligasure.

The left atrial appendage is one source of thromboemobolus. Complete occlusion of this appendage is required to sever communication with the left atrium; however, current ligation techniques can potentially leave residual communication. A novel technique of occluding the appendage has been developed using a bipolar device and radiofrequency energy. Twelve patients underwent an off-pump, epicardial Maze procedure using radiofrequency ablation. As an adjunct to the procedure, ligation of the left atrial appendage was completed using the LigaSure Xtd (Valleylab, Tyco Healthcare, Boulder, CO) with a modified application technique. Patients were followed to ensure sinus or paced rhythm. All twelve patients are in sinus or paced rhythm upon follow-up. Four patients required pacemakers for sick sinus syndrome. To date there have been no incidents of strokes, thromboembolic events, postoperative bleeding or deaths in all patients. Complete occlusion of the left atrial appendage is necessary to eliminate communication, which is accomplished by this radiofrequency, bipolar device. Extensive studies are necessary to verify the efficacy of this novel occluding technique.

Current state of intraoperative echocardiography.

Intraoperative use of echocardiography is becoming more prevalent and is now considered an essential part of modern cardiac surgery. Echocardiography can be performed intraoperatively using transesophageal, epicardial or epiaortic, and substernal approaches. These techniques have a variety of applications in evaluating myocardial and valvular function, assessing aortic atheroma, and determining adequacy of various kinds of repair and reconstruction. Future applications will most likely involve more compact equipment, the implementation of epicardial and transesophageal real-time three-dimensional echocardiography, and better use of provocative methods of intraoperative testing.

Single dose of glutamine enhances myocardial tissue metabolism, glutathione content, and improves myocardial function after ischemia-reperfusion injury.

BACKGROUND: Myocardial ischemia and reperfusion (I/R) injury causes significant morbidity and mortality. Protection against I/R injury may occur via preservation of tissue metabolism and ATP content, preservation of reduced glutathione, and stimulation of heat shock protein (HSP) synthesis. Supplementation with glutamine (GLN) has been reported to have beneficial effects on all of these protective pathways. Thus, we hypothesized that GLN pretreatment given to the rat in vivo would protect the myocardium against I/R-induced dysfunction. METHODS: GLN (0.52 g/kg, intraperitoneally, given as alanine-glutamine dipeptide), alanine alone (0.23 g/kg), or a Ringer's lactate solution (control) was administered to Sprague-Dawley rats 18 hours before heart excision, perfusion, exposure to global ischemia (15 minutes) and reperfusion (1 hour). Tissue metabolites were analyzed via magnetic resonance spectroscopy. RESULTS: In control and alanine-treated animals, I/R injury resulted in cardiac dysfunction, indicated by a decrease in cardiac output. Administration of GLN 18 hours before I/R injury preserved cardiac output after reperfusion. Metabolic analysis of the myocardial tissue revealed that [/R injury led to significant diminution of myocardial tissue glutamate, ATP content, accumulation of myocardial lactate, and a reduction in reduced glutathione content in control animals. GLN significantly reduced the deleterious changes in myocardial metabolism and improved reduced glutathione content. No changes in pre- or post-I/R injury HSP expression were observed after GLN administration. CONCLUSIONS: These observations demonstrate that remote in vivo administration of GLN before cardiac I/R injury can improve post-I/R cardiac function. This effect may be mediated via improved myocardial metabolism and enhanced reduced glutathione content.

Brief hypoxia conditions monocytes to protect reperfused cardiocytes against cell death via the CD11b receptor.

BACKGROUND: Traditionally leukocytes have been viewed as the mediators and effectors of cell injury after tissue ischemia and reperfusion through the indiscriminate release of toxic cytokines and oxygen free radicals. This can be detrimental to functioning of the transplanted heart when reperfused after implantation. Paradoxically, evidence now suggests that certain cytotoxic cytokines and even oxygen free radicals can be cytoprotective in smaller concentrations. This study sought to determine whether cultured human monocytes can be pre-conditioned by brief hypoxia to protect cardiomyocytes from cell death after hypoxia and re-oxygenation. METHODS: Cultured human monocytes were exposed to transient hypoxia (10 minutes), after which we determined CD11b expression using flow cytometry. The 3 control groups comprised immunoglobulin G-negative controls, fMLP-positive controls, and virgin monocyte (VM) controls. We studied chick embryonic ventricular myocytes in a flow-through chamber while controlling flow rate, pH, O(2), and CO2 tension. We quantified cardiomyocyte viability using propidium iodide (5 micromol/liter). Cell systems of cardiomyocytes alone, cardiomyocytes and VM, human monocytes exposed to transient hypoxia before coculture with cardiomyocytes (PCHM-cardiomyocyte), and PCHM cocultured with anti-CD11b antibodies for 30 minutes before coculture with cardiomyocytes (CDHM-cardiomyocyte) were subjected to 1 hour of hypoxia and 3 hours of re-oxygenation, and cell death was determined. The experiment was repeated and the cell systems fixed, stained, and examined for monocytes adhering to cardiomyocytes. RESULTS: CD11b expression increased significantly with both transient hypoxia and fMLP (18.39% +/- 4.116%, n = 5, and 37.04% +/- 7.783%, n = 5, respectively, p < 0.05 vs VM 100%, n = 5). Coculture of cardiomyocytes with VM had no effects on cardiocyte death (40.6% +/- 6.1%, n = 6) compared with controls (46.5% +/- 4.0%, n = 10). The PCHM cocultured with cardiomyocytes significantly decreased cardiomyocyte death (25.2% +/- 4.7%, n = 6, p < 0.05). This protection was abrogated by the addition of CD11b-blocking antibodies to PCHM before coculture with cardiomyocytes (51.0% +/- 6.1%, n = 6, p < 0.05). The PCHM showed increased adhesion to cardiomyocytes (5.4 +/- 0.38/high-power [HP] field vs 0.67 +/- 0.24/HP field in VM, p < 0.05). The increased adhesion was abolished by CD11b-blocking antibody (0.78 +/- 0.28 vs 0.67 +/- 0.24 cells/HP field, p < 0.05). CONCLUSIONS: These results suggest that monocytes activated by transient hypoxia protect cardiomyocytes during hypoxia and re-oxygenation through expression of CD11b receptors. These cells seem to adhere to myocytes through this receptor to achieve this effect. The exact mechanism is unclear and requires further study. Autologous recipient monocytes may be pre-conditioned to protect the donor heart during reperfusion.

Dynamic three-dimensional color flow Doppler: an improved technique for the assessment of mitral regurgitation.

BACKGROUND: Prior studies have reconstructed mitral regurgitant flow in three dimensions displaying gray scale renditions of the jets, which were difficult to differentiate from surrounding cardiac structures. Recently, a color-coded display of three-dimensional (3D) regurgitant flow has been developed. However, this display was unable to integrate cardiac anatomy, thereby losing spatial information, which made it difficult to determine the jet origin and its spatial trajectory. To overcome this limitation, an improved method of 3D color reconstruction of regurgitant jets obtained from color flow Doppler using a transesophageal approach was developed to allow the combined display of both color flow and gray scale information. OBJECTIVES: To demonstrate the feasibility of 3D reconstruction of regurgitant mitral flow jets using an improved method of color encoding digital data acquired by transesophageal echocardiography (TEE). METHODS: We studied 46 patients undergoing a clinically indicated TEE study. All subjects had mitral regurgitation detected on a previous transthoracic study. Atrial fibrillation or poor image quality were not used as exclusion criteria. The 3D study was performed using a commercial ultrasound imaging system with a TEE probe (Sonos 5500, Agilent Technologies). A rotational mode of acquisition was used to collect two-dimensional (2D) color flow images at 3-degree intervals over 180 degrees. Images were processed off line using the Echo-View Software (TomTec Imaging Systems). Volume-rendered 3D color flow jets were displayed along with gray scale information of the adjacent cardiac structures. RESULTS: Mitral regurgitant flow, displayed in left atrial and two longitudinal orientations, was successfully reconstructed in all patients. The time for acquisition, post-processing, and rendering ranged between 10 and 15 minutes. There were 28 centrally directed jets and 15 eccentric lesions. Eight patients in the study had periprosthetic mitral regurgitant flow. CONCLUSIONS: Three-dimensional imaging of mitral regurgitant jets is feasible in the majority of patients. This improved technique provides additional information to that obtained from the 2D examination. Particularly, in patients with paravalvular leaks 3D color flow Doppler provides information on the origin and the extent of the dehiscence, as well as insight into the jet direction. In addition, in patients with eccentric mitral regurgitation, this new modality overcomes the inherent limitations of 2D echo Doppler by depicting the full extent of the jet trajectory.

Surgical treatment for chronic heart failure.

Advances in the surgical treatment of chronic heart failure including ventricular re-modeling, artificial heart technology and bridge to recovery have revolutionized cardiac surgical management. This article summarizes the most popular surgical treatment of heart failure with experiences from various institutes.

Differential mechanical activation of mitogen-activated protein kinases in intact human blood vessels.

BACKGROUND: Vascular tissue remodels in response to a variety of hemodynamic factors, often transduced through activation of mitogen-activated protein kinases such as extracellular signal-related kinase (ERK1/2) and c-jun N-terminal kinase (JNK). This study tests the hypothesis that these kinases are involved in mechanical signal transduction in intact human arteries and veins. METHODS: Unused portions of human saphenous vein and radial artery were obtained fresh at the time of peripheral or coronary bypass. A sample of the vessel was immediately snap frozen (control(0)) and the remainder separated into three segments. One segment was placed in sterile medium and left undisturbed for 2 h (control(2)), one was perfused with sterile medium for 2 h at a steady rate of 150 ml/min, yielding shear stress values of 8-20 dyne/cm(2) (flow), and one was statically pressurized without flow at 110 mm Hg for 2 h (pressure). After treatment, samples were tested for phosphorylated ERK1/2 and JNK using Western blot. RESULTS: Two hours of culture produced mild increases in ERK1/2 activity in both vessel types. Stimulation with continuous rapid flow produced significantly increased ERK1 activity and a nearly 100% increase in ERK2 in veins. Static pressurization also stimulated ERK1/2, although slightly less than continuous flow. ERK1/2 phosphorylation was only mildly increased in flow-stimulated radial arteries, and exposure to normal systemic pressure showed no appreciable effect. Significant phosphorylation of JNK was not observed in either vessel. CONCLUSION: ERK1/2 phosphorylation is increased in human saphenous veins and radial arteries exposed to the hemodynamic conditions of arterial grafting. This pathway may be involved in the transduction of external stimuli leading to remodeling.

Circulatory assistance with a permanent implantable IABP: initial human experience.

PURPOSE: The Kantrowitz CardioVAD (KCV) is an electrically powered, pneumatically driven circulatory assist device which provides diastolic augmentation and systolic unloading to the failing heart. It consists of a 60cc-pumping chamber, a percutaneous access device (PAD), and an external controller. The pumping chamber, is surgically implanted in the descending thoracic aorta with the patient on cardiopulmonary bypass. Its physiologic function is analogous to that of the intra-aortic balloon pump (IABP). METHODS: Between 1997 and 2000, 5 men (age 59 to 73) with end-stage cardiomyopathy refractory to maximal drug treatment and with documented hemodynamic improvement on an IABP were enrolled in a feasibility study. RESULTS: Mean bypass time was 157 minute (range 120 to 196 minute); mean cross-clamp time was 101 minute (range 69 to 144). Patient 1 died intra-operatively. Compared with preoperative values, at 1 month, cardiac index increased (1.7 to 2.6 L/min/m(2)) and there were significant decreases in creatinine (2.6 to 1.5 mg/dL), pulmonary capillary wedge pressure (PCWP) (32 to 14 mm Hg), and right atrial pressure (RA) (19 to 9 mm Hg). NYHA class improved (IV to II). The mean increase in cardiac index with the KCV OFF to ON was 0.53 L/min/m(2) (36%). Two patients were discharged home. The device was used intermittently without thromboembolic complications. The only device related complications were attributed to PAD design and have been corrected. CONCLUSION Our initial human trial demonstrates successful implantation of the KCV in end-stage patients, the ability of the device to be used intermittently without anticoagulation, and documents hemodynamic and functional improvement in the status of these patients.

Papillary fibroelastoma of the aortic valve.

We hereby report the case of a patient with a papillary fibroelastoma involving the right coronary cusp of the aortic valve that was diagnosed with the use of transesophageal echocardiography after workup for recurrent transient ischemic attacks.

Acetylcholine attenuates cardiomyocyte oxidant stress during simulated ischemia and reoxygenation.

We wanted to determine whether oxygen radicals open the mitochondrial ATP-dependent potassium channels (K(ATP)) during an ischemic period to reduce cell death and oxidant stress. Chick embryonic cardiomyocytes were used. Cell viability was quantified with propidium iodide (5 microM), and free radicals was measured using 2',7'-dichlorofluorescein diacetate. Preconditioning was produced by 10 min of simulated ischemia followed by 10 min of reoxygenation. Acetylcholine (1 mM), infused for 10 min instead of preconditioning, reduced cell death similarly (24 +/- 5%, n = 7 and 18 +/- 2%, n = 7, respectively, vs. controls, 49 +/- 6%, n = 8). In control series, 60 min of simulated ischemia and 3 h of reoxygenation generated free radicals more than 300% above the baseline (ischemia: 3.63 +/- 0.58, reoxygenation: 3.66 +/- 0.47, n = 8). Preconditioning and acetylcholine markedly attenuated the oxidant stress during simulated ischemia (1.18 +/- 0.41, n = 6 and 1.34 +/- 0.60, n = 7 vs. controls 3.63 +/- 0.58, n = 8) and re-oxygenation (1.23 +/- 0.36, n = 6 and 1.50 +/- 0.59, n = 7 vs. controls 3.66 +/- 0.47, n = 8). The protection of acetylcholine was abolished with pretreatment with the antioxidant thiol reductant 2-mercaptopropionyl glycine and posttreatment with 5-hydroxydecanoate, a selective mitochondrial K(ATP) channel antagonist (37 +/- 7%, n = 7). These results demonstrate that oxygen radicals open mitochondrial K(ATP) channels, which mediates the acetylcholine-induced preconditioning effect, and that stimulation of this signaling pathway attenuates oxidant stress.