Biomedical subjects
Publications and source records attributed to Y Naka.
We report a rare cause of trigger finger related to an anatomical variation of an intertendinous connection between the flexor digitorum superficialis and flexor digitorum profundus tendons in the palmar region.
OBJECTIVE: The HeartMate VE left ventricular assist system (LVAS) has supported more than 2300 patients and has been shown to be effective for bridge to cardiac transplantation and has demonstrated improved outcomes in survival as a destination therapy. Improvements in device durability are needed as bridge to transplant times increase and as we move into the era of LVAD as destination therapy. The purpose of this study is to determine if design enhancements to the HeartMate LVAS have improved device reliability and durability. METHODS: A retrospective analysis of serious mechanical failures was performed in 1865 devices (1458 VE, 407 XVE). The analysis of data included devices used to support patients from September 1998 for bridge to transplantation and destination therapy. Serious mechanical failures were defined as inflow valve dysfunction, percutaneous lead breaks, diaphragm fractures or punctures, bearing failures, outflow graft erosion and pump disconnects. RESULTS: Median device duration for the VE was 97 days (max 1206 days), and 85 days (max 517 days) for the XVE. A total of 134 serious mechanical failures occurred and included inflow valve dysfunction (5.3% VE, 2.4% XVE) (P = 0.853) percutaneous lead breaks (1.9% VE, 0% XVE) (P < 0.001) diaphragm fractures (0.1% VE, 0% XVE) (P = 0.134) outflow graft erosion (0.2% VE, 0% XVE) (P = 0.1096), pump disconnects (0.1% VE, 0% XVE) (P = 0.1336) and bearing failures (0.6% VE, 0.2% XVE) (P = 0.5538). Of the XVEs 97% were free of serious mechanical failures at 6 months and 82% at 1 year compared to 92 and 73% for the VE, respectively. The 6-month difference between the devices was statistically significant (P = 0.0063) and there was no statistically significant difference at 1 year (P = 0.1492). CONCLUSIONS: Preliminary experience with the HeartMate XVE LVAS demonstrated a significant reduction in percutaneous lead breaks. Early trends indicate positive impact of recent design modifications on XVE performance. These design modifications may improve device durability and reliability, which is crucial as we enter the era of LVADs as an alternative to medical therapy.
BACKGROUND: Endotoxaemia, caused by splanchnic ischaemia during surgery, is believed to trigger systemic inflammation and cause postoperative organ dysfunction. A relationship between the plasma concentration of endotoxin during surgery and known risk factors for postoperative morbidity and mortality (e.g. age, abnormal gastric tonometric variables) and adverse outcome after surgery has not been demonstrated. METHODS: In a prospective study, the plasma concentration of endotoxin was measured in 12 patients undergoing implantation of a left ventricular assist device. Automated air gastric tonometry was performed in all patients. The relationship between plasma endotoxin concentration, risk factors, and postoperative outcome was explored. RESULTS: Carbon dioxide gap increased from 0.7 (0.3) to 3.6 (1.6) kPa at the end of surgery. Endotoxin was detected in one of 12 patients at baseline and in nine of 12 patients at the end of surgery (P=0.003). A high plasma concentration of endotoxin at the end of surgery was associated with a higher carbon dioxide gap (r=0.59, P<0.05), and a higher postoperative multiple organ dysfunction score (r=0.7, P=0.01). CONCLUSIONS: The finding of an association between high intraoperative plasma concentrations of endotoxin, abnormal gastric tonometric variables and adverse outcome supports the view that endotoxaemia is caused by gut hypoperfusion during surgery and is associated with postoperative organ dysfunction.
OBJECTIVE: To assess the accuracy of a continuous cardiac output (CCO) monitor against an independent, intravascular measurement of flow as can be performed in patients fitted with a left ventricular assist device (LVAD). DESIGN: A prospective cohort study. SETTING: Academic tertiary-care center. PARTICIPANTS: Adult patients (n = 15) presenting for LVAD placement. INTERVENTIONS: Consenting patients presenting for LVAD placement for end-stage cardiac failure were anesthetized, and a CCO pulmonary artery catheter was placed (OptiQ, CCO/SvO(2); Abbott Critical Care, North Chicago, IL). Patients were monitored with transesophageal echocardiography and excluded from analysis if aortic regurgitation was found. Cardiac output was determined using a Q-Vue, CCO/SvO(2) computer with digital readout (Abbott Critical Care, North Chicago, IL). The LVAD was placed in standard fashion during cardiopulmonary bypass. The Thoratec vented electric Heartmate (Thoratec Co, Pleasanton, CA) incorporates an LVAD flow console, which computes LVAD flow within +/- 5% (range, 1.8 to 10 L/min). MEASUREMENTS AND MAIN RESULTS: Cardiac output flow measurements were made from both systems at the following time points: 5 minutes and 30 minutes after protamine administration, at chest closure, and after skin closure. Mean cardiac output for each device did not differ at any time point. Regression analysis (Pearson's) showed acceptable correlation (r(2) = 0.79, p < 0.0001), whereas a bias of 529 mL with limits of agreement of 1,208 mL were shown for CCO measurement compared with LVAD flow. CONCLUSION: The data indicate that the CCO system tends to overestimate cardiac output by approximately 500 mL/min when compared with LVAD flow. Nevertheless, this bias is within the range found by other less-invasive studies done to assess the accuracy of this system and further serves to confirm its relative accuracy.
BACKGROUND: Allicin is a sulfur-containing compound extracted from garlic, with antiaggregatory, anti- migratory, anti-oxidant and pulmonary vasodilator actions. We hypothesized that allicin might be beneficial in lung ischemia-reperfusion. METHODS: A non-nothermic rat lung ischemia-reperfusion model was established by clamping left pulmonary artery (PA) for 1 hr, followed by reperfusion for 2 hrs by clamping right PA to reflect solely the function of left lung. Groups were control (n=7), allicin 0.1 mg (n=8) and allicin 0.01 mg (n=4). In the beginning of reperfusion allicin/saline were injected. Pulmonary artery pressures (PAP), pulmonary artery flow (PAF), left atrial pressure (LAP) were monitored. At the end of reperfusion period arterial blood gas (ABG) analysis was done. RESULTS: Six of 7 control and 3 of 8 group 2 animals died before completing the experiment. In group 1 all animals completed the experiment (p=0.015 vs control). PAF was significantly increased after 30, 60 and 120 min of reperfusion in group 1 (p=0.0028, 0.0009, 0.0003 respectively vs control) and after 60 and 120 minutes in group 2 (p=0.0453, 0.018 respectively vs control). Pulmonary vascular resistance was lower at 30 min in allicin 0.01 mg group (p=0.0017 vs control). PAP was increased after 60 and 120 min of reperfusion in group 1 (p=0.016, 0.0029 respectively vs control) and after 120 min in group 2 (p=0.0104 vs control). CONCLUSIONS: This study shows that allicin improves postischemic PAF in this model. Allicin needs further investigation of potential utility and mechanism(s) of action.
BACKGROUND: Left ventricular assist devices (LVAD) reverse ventricular, myocardial, and systemic abnormalities characteristic of severe heart failure (reverse remodeling). The relative contributions of hemodynamic unloading and normalized biochemical milieu to reverse remodeling are unknown. METHODS AND RESULTS: Structural and functional characteristics were measured from 53 hearts of patients undergoing transplantation without LVAD support (medical support) and 33 hearts from patients receiving a median of 46 days of LVAD support (range, 8 to 360 days). Compared with medical support alone, patients receiving LVAD support for >/=30 days had higher central venous pressures (11+/-6 versus 8+/-5 mm Hg, P=0.04), lower pulmonary artery diastolic pressures (14+/-9 versus 21+/-9 mm Hg, P=0.01), and higher cardiac outputs (5.1+/-1.6 versus 3.7+/-1.0 L/min, P<0.001). In LVAD versus transplantation hearts, V(30) (ex vivo volume yielding ventricular pressure of 30 mm Hg) was decreased in the left ventricle (LV) (179+/-75 versus 261+/-118 mL, P=0.005) but not in the right ventricle (RV) (140+/-59 versus 148+/-52 mL, P=NS). LV myocyte diameter decreased more significantly after LVAD support (17%, P=0.05) than in the RV (11%, P=NS). Compared with transplantation, LVAD support increased normalized SERCA2a content in the LV (0.51+/-0.26 versus 1.04+/-0.34, P<0.001) but not in the RV (0.48+/-34 versus 0.67+/-0.55, P=NS). Finally, LVAD support improved force-frequency relations of isolated superfused LV trabeculae (P=0.01) but not RV trabeculae. CONCLUSIONS: Reduction of hemodynamic load is a primary factor underlying several important features of reverse remodeling. These findings do not preclude a possible primary role of neurohormonal factors underlying other facets of reverse remodeling during LVAD support.
BACKGROUND: Extremes in body weight are a relative contraindication to cardiac transplantation. METHODS: We retrospectively reviewed 474 consecutive adult patients (377 male, 97 female, mean age 50.3+/-12.2 years), who received 444 primary and 30 heart retransplants between January of 1992 and January of 1999. Of these, 68 cachectic (body mass index [BMI]<20 kg/m2), 113 overweight (BMI=>27-30 kg/m2), and 55 morbidly obese (BMI>30 kg/m2) patients were compared with 238 normal-weight recipients (BMI=20-27 kg/m2). We evaluated the influence of pretransplant BMI on morbidity and mortality after cardiac transplantation. Kaplan-Meier survival distribution and Cox proportional hazards model were used for statistical analyses. RESULTS: Morbidly obese as well as cachectic recipients demonstrated nearly twice the 5-year mortality of normal-weight or overweight recipients (53% vs. 27%, respectively, P=0.001). An increase in mortality was seen at 30 days for morbidly obese and cachectic recipients (12.7% and 17.7%, respectively) versus a 30-day mortality rate of 7.6% in normal-weight recipients. Morbidly obese recipients experienced a shorter time to high-grade acute rejection (P=0.004) as well as an increased annual high-grade rejection frequency when compared with normal-weight recipients (P=0.001). By multivariable analysis, the incidence of transplant-related coronary artery disease (TCAD) was not increased in morbidly obese patients but cachectic patients had a significantly lower incidence of TCAD (P=0.05). Cachectic patients receiving oversized donor hearts had a significantly higher postoperative mortality (P=0.02). CONCLUSIONS: The risks of cardiac transplantation are increased in both morbidly obese and cachectic patients compared with normal-weight recipients. However, the results of cardiac transplantation in overweight patients is comparable to that in normal-weight patients. Recipient size should be kept in mind while selecting patients and the use of oversized donors in cachectic recipients should be avoided.
A series of 1-phenylpyrazoles was evaluated for inhibitory activity against xanthine oxidase in vitro. Of the compounds prepared, 1-(3-cyano-4-neopentyloxyphenyl)pyrazole-4-carboxylic acid (Y-700) had the most potent enzyme inhibition and displayed longer-lasting hypouricemic action than did allopurinol in a rat model of hyperuricemia induced by the uricase inhibitor potassium oxonate.
BACKGROUND: Infection remains as the most serious complication and represents a significant threat to patients during long-term mechanical circulatory support. Fungal infection is a particularly worrisome complication and left ventricular assist device (LVAD) endocarditis does pose a serious threat. METHODS: One hundred and sixty-five patients underwent TCI Heartmate LVAD implantation between July 1991 and December 1999 at our institution. Detailed medical records were kept prospectively for all patients, and a variety of infection-related endpoints were analyzed on patients with fungal LVAD endocarditis. RESULTS: Thirty-seven patients (22%) developed fungal infections during LVAD support. Five (3%) of those met our criteria for the diagnosis of fungal LVAD endocarditis. Microbial portals of entry were identifiable in all cases. Infections were managed successfully in 4 patients (80%). CONCLUSIONS: The successful management of fungal LVAD endocarditis currently requires early recognition of potentially nonspecific signs and symptoms, and timely institution of antifungal therapy. In some cases with device-specific manifestations of LVAD endocarditis, device removal and replacement is necessary. In patients with clinical manifestations of sepsis and fungal driveline site or pocket infections without positive blood culture, urgent transplantation may be the appropriate management. In the setting of shortage in the donor supply, device removal and replacement is necessary.
The need for right ventricular support as an adjunct to left ventricular assistance is uncommon. When required, the insertion of a right ventricular assist device may be complicated by preexisting hepatic dysfunction, coagulation abnormalities, and renal failure, all of which are exacerbated by cardiopulmonary bypass. We report a technique for insertion of a right ventricular assist device without the need for cardiopulmonary bypass.
BACKGROUND: Success with long-term implantable left ventricular assist devices (LVAD) has led to increased use in patients previously thought to be unsuitable for mechanical circulatory assistance. Patients with preexisting or newly diagnosed valvular disease have been traditionally excluded from device placement. The purpose of this study was to review our experience with LVAD support in patients with valvular disease and to develop a management algorithm for these difficult patients. METHODS: We reviewed the clinical records of 199 consecutive patients who received the ThermoCardiosystems, Inc, HeartMate Pneumatic or Vented Electric LVAD. There were 18 patients (9%) who required surgical management of native or prosthetic valvular disease during LVAD implantation. RESULTS: Suture or patch closure of the aortic valve was performed in 6 patients, aortic valve plication and repair in 1 patient, mitral valve repair in 4 patients, and tricuspid valve annuloplasty in 5 patients. Two patients with mechanical mitral valve prostheses were treated with postoperative warfarin anticoagulation. Fifteen of the 18 patients with valvular pathology survived the immediate postoperative period (17% mortality). Eleven patients have either undergone transplantation or continue to be supported with an LVAD (61%). Operative mortality in LVAD patients without concomitant valve repair was 18% (n = 33) with a late mortality of 7% (n = 13). Seven of these late deaths occurred in patients who received a device as destination therapy. In the remaining 6 patients, the cause of death was sepsis (n = 2), multisystem organ failure (n = 2), driveline rupture (n = 1), and massive gastrointestinal bleed (n = 1). CONCLUSIONS: Preexisting native or prosthetic valve pathology does not increase the immediate perioperative risk of LVAD insertion; however, these patients continue to pose a challenge for postoperative management while awaiting transplantation.
BACKGROUND: Constantly changing practices in heart transplantation have improved posttransplant survival in patients with end-stage heart disease. The objective of this study was to evaluate long-term outcomes in different eras of immunosuppressive therapy after cardiac transplantation at a single center during a two-decade period. METHODS: A retrospective review of 1,086 consecutive cardiac allograft recipients who underwent transplantation between 1977 to 1999 was performed. Patients were divided into four eras based on type of immunosuppressive therapy: era 1 = steroids, azathioprine (n = 26, February 1977 to March 1983), era II = steroids, cyclosporine (n = 43, April 1983 to April 1985), era III = cyclosporine, steroids, azathioprine (n = 752, April 1985 to December 1995), era IV = cyclosporine, steroids, mycophenolate mofetil (n = 315, January 1996 to October 1999). RESULTS: The actuarial survival of the entire cohort of 1,086 patients undergoing cardiac transplantation was 79%, 66%, and 49% at 1, 5, and 10 years, respectively. There were significant trends in recipient age and gender distribution among the four eras with increasing proportion of older age (> 60 years) and female recipients in eras III and IV (p = 0.001 and 0.02). Early mortality and long-term survival improved significantly over all eras (p < 0.001). Rejection as a cause of death decreased over time (era I, 24%; era II, 21%; era III, 15%; era IV, 9%; p = 0.02), whereas the contribution of transplant coronary artery disease as a cause of death remained unchanged. CONCLUSIONS: Cardiac transplantation provides satisfactory long-term survival for patients with end-stage heart failure. The improving outcomes in survival correlate with improved immunosuppressive therapy in each era. Although the reasons for improvement in survival over time are multifactorial, we believe that changes in immunosuppressive therapy have had a major impact on survival as evidenced by the decreasing number of deaths due to rejection.
Acute type A aortic dissection is an uncommon complication with left ventricular assist device insertion, but is often fatal even if successfully repaired with conventional techniques including aortic valve repair. Residual aortic insufficiency is common because this valve is now subjected to systolic pressure. We present a novel technique for the repair of type A acute aortic dissection in patients with a left ventricular assist device with no chance of residual aortic insufficiency.
OBJECTIVES: Hemodilution induced by cardiopulmonary bypass (CPB) often prevents open heart operations without blood transfusion because of a large CPB-priming volume. A vacuum-assisted venous drainage system appears to overcome this problem and our previous experimental study demonstrated the beneficial effect of a vacuum-assisted CPB with a pressure relief valve. In this study, we clinically applied this novel system, and evaluated its efficacy by comparing it with the results of a conventional siphon-dependent drainage system. METHODS: Sixty patients undergoing open heart operation were divided into Group V (vacuum-assisted system, n=30) and Group S (siphon-dependent system, n=30). The vacuum-assisted system contains a powerful vacuum generator and a pressure relief valve to keep the negative pressure in the reservoir constant when the blood suction is used. RESULTS: The CPB-priming volume was significantly smaller in Group V (V vs. S: 1071+/-88 vs. 1405+/-137 ml; P<0.01), resulting in the lower hemodilution in Group V evidenced by the minimum hemoglobin level (V vs. S: 6.83+/-1.06 vs. 5.78+/-0.79 mg/dl; P<0.01) and blood transfusion rate (V vs. S: 9 vs. 20%; P<0.01). There were no significant differences in the plasma free hemoglobin level and the reduction ratio of plasma haptoglobin between the groups. CONCLUSIONS: These data demonstrate that this vacuum-assisted CPB can provide simplification of the CPB circuit, resulting in a smaller CPB-priming volume and lower hemodilution. This vacuum-assisted CPB may attenuate the negative effect of CPB by minimizing hemodilution and appears to be a useful modification to accomplish no blood-requiring open heart operations.
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Carbon monoxide (CO) can arrest cellular respiration, but paradoxically, it is synthesized endogenously by heme oxygenase type 1 (Ho-1) in response to ischemic stress. Ho-1-deficient (Hmox1-/-) mice exhibited lethal ischemic lung injury, but were rescued from death by inhaled CO. CO drove ischemic protection by activating soluble guanylate cyclase and thereby suppressed hypoxic induction of the gene encoding plasminogen activator inhibitor-1 (PAI-1) in mononuclear phagocytes, which reduced accrual of microvascular fibrin. CO-mediated ischemic protection observed in wild-type mice was lost in mice null for the gene encoding PAI-1 (Serpine1). These data establish a fundamental link between CO and prevention of ischemic injury based on the ability of CO to derepress the fibrinolytic axis. These data also point to a potential therapeutic use for inhaled CO.
Little is known about interactions between endogenous anti-inflammatory paradigms and microvascular thrombosis in lung ischemia/reperfusion (I/R) injury. Interleukin (IL)-10 suppresses macrophage activation and down-regulates proinflammatory cytokine production, but there are no available data to suggest a link between IL-10, thrombosis, and fibrinolysis in the setting of I/R. We hypothesized that hypoxia/ischemia triggers IL-10 production, to dampen proinflammatory cytokine and adhesion receptor cascades and to restore vascular patency by fibrinolytic potentiation. Studies were performed in a mouse lung I/R model. IL-10 mRNA levels in lung were increased 43-fold over base line by 1 h of ischemia/2 h of reperfusion, with a corresponding increase in plasma IL-10. Expression was prominently localized in bronchial epithelial cells and mononuclear phagocytes. To study the link between IL-10 and fibrinolysis in vivo, the induction of plasminogen activator inhibitor-1 (PAI-1) was evaluated. Northern analysis demonstrated exaggerated pulmonary PAI-1 expression in IL-10 (-/-) mice after I/R, with a corresponding increase in plasma PAI/tissue-type plasminogen activator activity. In vivo, IL-10 (-/-) mice showed poor postischemic lung function and survival after I/R compared with IL-10 (+/+) mice. Despite a decrease in infiltration of mononuclear phagocytes in I/R lungs of IL-10 (-/-) mice, an increased intravascular pulmonary fibrin deposition was observed by immunohistochemistry and Western blotting, along with increased IL-1 expression. Recombinant IL-10 given to IL-10 (-/-) mice normalized the PAI/tissue-type plasminogen activator ratio, reduced pulmonary vascular fibrin deposition, and rescued mice from lung injury. Since recombinant hirudin (direct thrombin inhibitor) also sufficed to rescue IL-10 (-/-) mice, these data suggest a preeminent role for microvascular thrombosis in I/R lung injury. Ischemia-driven IL-10 expression confers postischemic pulmonary protection by augmenting endogenous fibrinolytic mechanisms.