Novel Biomaterial for Artery Patch in Swine Model With High-Fat Diet.

OBJECTIVE: We evaluated swine and bovine pulmonary visceral pleura (PVP) in artery patch-angioplasty in swine model of high-fat diet. BACKGROUND: Arterial patch-angioplasty is frequently used for repair or reconstruction of arteries. An autologous patch is often limited by the number and dimension of donor tissue and can result in donor complications. Furthermore, mechanical mismatch is a cause of poor performance of vascular reconstruction. Here, we introduce a readily available patch biomaterial with similar compliance as native arteries. METHODS: The PVP was peeled from swine and bovine lungs by hydro-dissection. The swine and bovine PVPs were crosslinked with glutaraldehyde and then sterilized. The swine PVP (sPVP) patches were implanted in the carotid and femoral arteries of six Yorkshire pigs that were fed a regular diet and euthanized at 2 and 4 months postoperative. The bovine PVP (bPVP) patches were implanted in the carotid artery of six Yucatan pigs that were fed a high-fat diet and euthanized at 4 months postoperative. Patency was evaluated by ultrasound and angiography. Neo-endothelium and media were evaluated by histologic examination. RESULTS: All arteries in patch-angioplasties remained patent with no adhesions, inflammation, or aneurysms. Biomarkers of endothelial cells (e.g., Factor VIII and eNOS) were detected in the neo-endothelial cells. We observed endothelial cell-cell junctions in the confluent neo-endothelium in the PVP patches. Neo-media composed of vascular smooth muscle developed similar as native arteries. In the hypercholesterolemic model, we observed the accumulation of cholesterol in both arterial tissues and in the neo-vascular tissues in the PVP patches. Protein expressions of lipid transport and metabolism (e.g., APOE-1, ABCA, and PACK9) were also observed in both arterial and neo-vascular tissues. CONCLUSION: The PVP patch-angioplasty overcomes the pitfalls of compliance mismatch of synthetic patches and has a non-thrombogenic surface. The proliferation of vascular cells assembled to generate the neo-endothelium and media in the patch-angioplasties to support long-term patency. The neo-vascular tissue in PVP patch-angioplasty also developed similar cellular functions for lipid transport and metabolism compared with native arteries in hypercholesterolemia.

Bilateral Brachiocephalic Vein and Superior Vena Cava Reconstruction With an Aortic Allograft.

Malignant thymoma can be invasive and may require radical resection. Here we present a case with phrenic nerve, right upper lobe, bilateral brachiocephalic vein, and superior vena cava involvement. Total venous reconstruction was performed with a cryopreserved aortic allograft by using the aortic root, ongoing transverse arch, and innominate arterial branch. The patient then had postoperative radiotherapy for a total of 63 Gy over 35 treatment days. Follow-up imaging demonstrated no evidence of recurrence and intermediate-term patency but with homograft calcification developing at 4 years.

Homologous and heterologous assessment of a novel biomaterial for venous patch.

OBJECTIVE: This study evaluated swine and bovine pulmonary visceral pleura (PVP) as a vascular patch. Venous patches are frequently used in surgery for repair or reconstruction of veins. Autologous patches are often limited by the number and dimension of donor tissue and can result in donor complications. Bovine pericardium is the most common heterologous patch used by vascular surgeons. Researchers, however, are continually seeking to improve heterologous and synthetic patches for improved outcome. METHODS: The PVP was peeled from swine and bovine lungs and cross-linked with glutaraldehyde. After sterilization and rinsing, the PVP patches were implanted in the jugular vein (10 × 35 mm) of pigs and dogs. Patency was evaluated by ultrasound, and animals were euthanized at 2 and 4 months. Neoendothelium and neomedia were evaluated by histologic analysis. RESULTS: The jugular vein patched by PVP in pigs and dogs remained patent at 2 and 4 months with no adhesions, inflammation, or aneurysm in the patches. The biomarkers of endothelial cells-factor VIII, platelet/endothelial cell adhesion molecule 1, and endothelial nitric oxide synthase-were detected in the neoendothelial cells. The expression of vascular smooth muscle cell (VSMC) α-actin was robust in the neomedia at 2 and 4 months. Neomedia composed of VSMCs developed to nearly double the thickness of adjacent jugular vein. The circumferential orientation of VSMCs in neomedia further increased in the 4-month group. CONCLUSIONS: The cross-linked swine and bovine PVP patch has a nonthrombogenic surface that maintains patency. The PVP patch may overcome the pitfall of compliance mismatch of synthetic patches. The proliferation of vascular cells assembled in the neoendothelium and neomedia in the patches may support long-term patency.

Emergency physician-initiated extracorporeal cardiopulmonary resuscitation.

CONTEXT: Extracorporeal cardiopulmonary resuscitation (ECPR) refers to emergent percutaneous veno-arterial cardiopulmonary bypass to stabilize and provide temporary support of patients who suffer cardiopulmonary arrest. Initiation of ECPR by emergency physicians with meaningful long-term patient survival has not been demonstrated. OBJECTIVE: To determine whether emergency physicians could successfully incorporate ECPR into the resuscitation of patients who present to the emergency department (ED) with cardiopulmonary collapse refractory to traditional resuscitative efforts. DESIGN: A three-stage algorithm was developed for ED ECPR in patients meeting inclusion/exclusion criteria. We report a case series describing our experience with this algorithm over a 1-year period. RESULTS: 42 patients presented to our ED with cardiopulmonary collapse over the 1-year study period. Of these, 18 patients met inclusion/exclusion criteria for the algorithm. 8 patients were admitted to the hospital after successful ED ECPR and 5 of those patients survived to hospital discharge neurologically intact. 10 patients were not started on bypass support because either their clinical conditions improved or resuscitative efforts were terminated. CONCLUSION: Emergency physicians can successfully incorporate ED ECPR in the resuscitation of patients who suffer acute cardiopulmonary collapse. More studies are necessary to determine the true efficacy of this therapy.

Clinical strategies and outcomes in advanced heart failure patients older than 70 years of age receiving the HeartMate II left ventricular assist device: a community hospital experience.

OBJECTIVES: The primary objective of this study was to determine outcomes in left ventricular assist device (LVAD) patients older than age 70 years. BACKGROUND: Food and Drug Administration approval of the HeartMate II (Thoratec Corporation, Pleasanton, California) LVAD for destination therapy has provided an attractive option for older patients with advanced heart failure. METHODS: Fifty-five patients received the HeartMate II LVAD between October 5, 2005, and January 1, 2010, as part of either the bridge to transplantation or destination therapy trials at a community hospital. Patients were divided into 2 age groups: ≥ 70 years of age (n = 30) and < 70 years of age (n = 25). Outcome measures including survival, length of hospital stay, adverse events, and quality of life were compared between the 2 groups. RESULTS: Pre-operatively, all patients were in New York Heart Association functional class IV refractory to maximal medical therapy. Kaplan-Meier survival for patients ≥ 70 years of age (97% at 1 month, 75% at 1 year, and 70% at 2 years) was not statistically different from patients <7 0 years of age (96% 1 month, 72% at 1 year, and 65% at 2 years, p = 0.806). Average length of hospital stay for the ≥ 70-year age group was 24 ± 15 days, similar to that of the < 70-year age group (23 ± 14 days, p = 0.805). There were no differences in the incidence of adverse events between the 2 groups. Quality of life and functional status improved significantly in both groups. CONCLUSIONS: The LVAD patients ≥ 70 years of age have good functional recovery, survival, and quality of life at 2 years. Advanced age should not be used as an independent contraindication when selecting a patient for LVAD therapy at experienced centers.

Aortic valve closure associated with HeartMate left ventricular device support: technical considerations and long-term results.

BACKGROUND: Aortic valve integrity is crucial for optimal left ventricular assist device (LVAD) support. Pre-existing native aortic insufficiency, aortic valve incompetence acquired during support, as well as previously placed prosthetic aortic valves present unique problems for these patients. METHODS: We reviewed and analyzed data for 28 patients who underwent left ventricular outflow tract closure associated with HeartMate I (n =12) and HeartMate II (n = 16) LVAD insertion or exchange. Indications for valve closure, surgical technique, LVAD function, survival rates and complications were retrospectively analyzed. Survival rates were compared with those of HeartMate LVAD patients (n = 104) who did not undergo aortic valve closure. RESULTS: Indications for closure included native aortic valve insufficiency (10 patients), aortic valve deterioration after prolonged LVAD support (8 patients) and previously placed mechanical (9 patients) or bioprosthetic aortic prostheses (1 patient). There were 2 operative and 5 late deaths (mean 227 days post-operatively). Of the deaths, none were due to aortic valve closure. Actuarial survival was 78% at 1 year and 53% at 3 years, which was statistically better than for our patients with an intact aortic outflow (61% at 1 year, 45% at 3 years; p < 0.05). Five patients had transplants, 1 patient was successfully bridged to recovery, and 15 patients remain on LVAD support. No patient with outflow closure developed regurgitation, embolization or compromised LVAD support. CONCLUSION: Outflow tract closure in LVAD-supported patients is safe, often necessary and well tolerated.

HeartMate left ventricular assist system exchange: results and technical considerations.

The duration times of left ventricular assist system (LVAS) support have increased because of prolonged wait times for transplant and the more frequent use of devices for destination therapy. The HeartMate LVAS, the only device approved for bridge to transplant and destination therapy, has limited durability, making replacement increasingly necessary. Since 1996, we have exchanged 19 left ventricular assist devices in 15 patients (11 men: mean age, 57.1 years; range, 33-77 years). Most of the devices (14) were replaced with the HeartMate vented electric/extended-lead vented electric pump; five devices were exchanged for a HeartMate II LVAS. Bearing failure was the most frequent reason for exchange (15 of 19 pumps); four of the 19 pumps also had active device-related infections at the time of exchange. There were no early deaths (30 days). Overall survival (Kaplan-Meier) was 85% at 1 year, 67% at 2 years, and 56% at 3 years. Three patients had transplants (mean, 518 days); six patients died during support (mean, 934 days), and six patients remain on LVAS support (mean, 1,219 days). One patient has been on device for over 6 years. Left ventricular assist devices exchange is becoming increasingly likely and can be associated with acceptably low-operative mortality rates and good intermediate-term survival.

Case series: clinical management of persistent mechanical assist device driveline drainage using vacuum-assisted closure therapy.

Percutaneous driveline lead and pocket sites are potential sources of drainage that can lead to infection. Some patients experience a slower closure of tissue growth into the driveline. The management of chronically open and or draining driveline wounds is a challenge. The KCI vacuum-assisted closure (VAC) device is a noninvasive negative-pressure therapy that promotes the healing of wounds not responding to conventional treatment. Vacuum-assisted closure therapy has proven safe, effective, and cost efficient by decreasing the number of dressing changes and length of stay. The left ventricular assist device (LVAD) team initiated VAC therapy in 3 patients. The tunneling method allowed the wound to heal from the inside out. The dressing was changed every 3 days, and the size and depth of the wound was monitored. Patients may be sent home using a portable VAC device until wound closure is obtained, which decreases the hospital length of stay. Our experience with three patients suggests the VAC device can be used for draining and tunneling LVAD driveline-site wounds and may prevent fistula formation. It is especially useful for patients with ascites that may be draining along the driveline tract. The sites showed increased granulation, decreased drainage, and a reduced bacterial burden after having the device in place.

Assessment of recurrent heart failure associated with left ventricular assist device dysfunction.

BACKGROUND: Patients with advanced heart failure may require long-term support with an intracorporeal left ventricular assist device (LVAD) before cardiac transplant, while awaiting myocardial recovery, or during destination therapy. Compared with the diagnosis of native heart dysfunction, there is less experience with the assessment of recurrent heart failure after LVAD placement. METHODS: Ten patients (9 men, 1 woman; age, 58 +/- 11 years) were studied after LVAD placement. Six patients were studied because of recurrent heart failure; the remaining 4 had other indications for study and are reported here as controls. Cardiac catheterization, including LVAD and cannulae catheterization, and angiography were performed. RESULTS: Inflow cannula valve regurgitation by LVAD angiography was found in 3 cases. Patients with regurgitation had a mean increased resting LVAD rate of 105 beats/min (range, 90-120); LVAD output exceeded forward cardiac output (LVAD - thermodilution cardiac output = +3.7 liters/min [0.6-6.4]). Inflow cannula obstruction identified with a filling phase pressure gradient between the left ventricle and the LVAD was found in 3 additional patients. Patients with obstruction had decreased resting LVAD rates (50 beats/min, all patients); LVAD output was less than the forward cardiac output (LVAD - thermodilution cardiac output = -2.3 liters/min [-0.8 to -3.5]). Compared with those with inflow valve regurgitation, patients with cannula obstruction had higher pulmonary capillary wedge pressures; phasic left ventricular pressure variation was reduced. Patients with cannula dysfunction underwent surgical intervention, and 4 of 6 were long-term survivors. CONCLUSIONS: When heart failure recurs after LVAD placement, abnormalities of the inflow cannula are common. Cardiac catheterization can confirm the diagnosis before surgical intervention. Hemodynamic coupling between the left ventricle and the LVAD is increased with inflow valve regurgitation and reduced with cannula obstruction.

Left ventricular outflow tract obstruction associated with chronic ventricular assist device support.

Favorable long-term patient outcome after insertion of a left ventricular assist device (LVAD) as a bridge to recovery or destination therapy for the treatment of end-stage cardiomyopathy is adversely affected by pathophysiologic changes affecting the heart. Alterations in the native aortic valve apparatus, specifically aortic valve cusp fusion, is an example of such a phenomenon and may especially affect patients in cases of bridge to recovery, a rare but reported event. A retrospective review of the last 33 LVAD placements at our institution was conducted, including reviews of operative reports and pathologic examinations of the native hearts. Seven hearts were found to have varying degrees of aortic valve cusp fusion after chronic LVAD support (63-1, 339 days). Five of these patients had native aortic valves, and two had bioprosthetic valves. The left ventricular outflow tracts in two patients were surgically occluded at the time of LVAD insertion. Aortic valve cusp fusion occurs in roughly 25% of patients on chronic LVAD support. This phenomenon may prove to be clinically significant by creating a potential source of emboli and infection. In addition, in the case of myocardial recovery, left ventricular outflow tract obstruction could limit parallel flow and produce suprasystemic ventricular pressures that in turn would elevate left ventricular end diastolic pressures. The latter may contribute to further myocardial injury, ultimately limiting the ability of an otherwise recovered heart to be weaned from LVAD support.