Telemedicine platforms and their use in the coronavirus disease-19 era to deliver comprehensive vascular care.

Implementation of telemedicine for patient encounters optimizes personal safety and allows for continuity of patient care. Embracing telehealth reduces the use of personal protective equipment and other resources consumed during in-person visits. The use of telehealth has increased to historic levels in response to the coronavirus disease 2019 (COVID-19) pandemic. Telehealth may be a key modality to fight against COVID-19, allowing us to take care of patients, conserve personal protective equipment, and protect health care workers all while minimizing the risk of viral spread. We must not neglect vascular health issues while the coronavirus pandemic continues to flood many hospitals and keep people confined to their homes. Patients are not immune to diseases and illnesses such as stroke, critical limb ischemia, and deep vein thrombosis while being confined to their homes and afraid to visit hospitals. Emerging from the COVID-19 crisis, incorporating telemedicine into routine medical care is transformative. By leveraging digital technology, the authors discuss their experience with the implementation, workflow, coding, and reimbursement issues of telehealth during the COVID-19 era.

Multiple duplications of the superficial femoral artery - Case report and review of the literature.

OBJECTIVES: Lower extremity arterial anatomic variations are rare, with duplication of the superficial femoral artery being an extremely uncommon variant with few prior reports in the literature.Methods/Results: We report the case of a 68-year-old male with calf claudication who underwent angiography and was found to have two separate areas of vessel duplication along the superficial femoral artery, which has not previously been described in the literature. CONCLUSION: Although uncommon, recognition of a duplicated superficial femoral artery is important to avoid difficulties and complications that may arise during open or endovascular procedures.

Dissection of left iliac artery during anterior lumbar interspace fusion: Report of a case.

Vascular injury is an uncommon complication of spine surgery. Among the different approaches, anterior lumbar interbody fusion has increased potential for vascular injuries, since the great vessels and their branches overly the disc spaces to be operated on, and retraction of these vessels is necessary to gain adequate surgical exposure. The reported incidence for anterior lumbar interbody fusion-associated vascular injuries ranges from 0% to 18.1%, with venous laceration as the most common type. We report a case of anterior lumbar interbody fusion-associated left common iliac artery dissection leading to delayed acute limb ischemia developing in early post-operative period.

Current applications of artificial intelligence in vascular surgery.

Basic foundations of artificial intelligence (AI) include analyzing large amounts of data, recognizing patterns, and predicting outcomes. At the core of AI are well-defined areas, such as machine learning, natural language processing, artificial neural networks, and computer vision. Although research and development of AI in health care is being conducted in many medical subspecialties, only a few applications have been implemented in clinical practice. This is true in vascular surgery, where applications are mostly in the translational research stage. These AI applications are being evaluated in the realms of vascular diagnostics, perioperative medicine, risk stratification, and outcome prediction, among others. Apart from the technical challenges of AI and research outcomes on safe and beneficial use in patient care, ethical issues and policy surrounding AI will present future challenges for its successful implementation. This review will give a brief overview and a basic understanding of AI and summarize the currently available and used clinical AI applications in vascular surgery.

A novel physiologic model for the study of abdominal compartment syndrome (ACS).

BACKGROUND: : Current abdominal compartment syndrome (ACS) models rely on intraperitoneal instillation of fluid, air, and other space-occupying substances. Although this allows for the study of the effects of increased abdominal pressure, it poorly mimics its pathogenesis. We have developed the first reported large animal model of ACS incorporating hemorrhagic shock/resuscitation. METHODS: : Hemorrhagic shock was induced and maintained (1 hour) in 12 Yorkshire swine by bleeding to a mean arterial pressure (MAP) of 50 mm Hg. The collected blood plus two additional volumes of crystalloid was then reinfused. Mesenteric venous hypertension was induced by tightening a previously placed portal vein snare in a nonocclusive manner to mimic the effects of abdominal packing. Crystalloids were infused to maintain MAP. Hemodynamic measurements, abdominal pressure, peak inspiratory pressures, urine output, and blood chemistries were measured sequentially. Animals were studied for 36 hours after decompression. RESULTS: : ACS (intra-abdominal pressure of > or =20 mm Hg with new organ dysfunction) developed in all animals. There were significant increases in peak inspiratory pressure, central venous pressure, and pulmonary artery pressure and decreases in MAP upon development of ACS. Urine output was significantly decreased before decompression. Mean blood lactate decreased and base excess increased significantly after decompression. CONCLUSIONS: : We have created the first reported physiologic animal ACS model incorporating hemorrhagic shock/resuscitation and the effects of damage control surgery.

Myocardial function after gut ischemia/reperfusion: does NF kappaB play a role?

BACKGROUND: Mesenteric ischemia/reperfusion (I/R) is a common problem in critically ill patients and is frequently associated with myocardial dysfunction. Several potential mechanisms have been proposed to be involved in the myocardial dysfunction associated with mesenteric I/R, including nuclear factor kappa B (NF kappaB)-mediated tumor necrosis factor alpha (TNF-alpha) release leading to cardiodepression. Thus, we sought to investigate the effect of NF kappaB inhibition on mesenteric I/R-associated myocardial dysfunction in a large animal model (dog). MATERIALS AND METHODS: A total of 21 mongrel dogs were anesthetized and mechanically ventilated. Animals were instrumented with a Swan-Ganz Catheter, left ventricle (LV) pressure manometer, and ultrasonic crystals. Mesenteric I/R consisted of 60 min of ischemia followed by 180 min of reperfusion. Seven animals received pyrrolidine dithiocarbamate (PDTC, 100 mg/kg) prior to mesenteric I/R (I/R PDTC). Another group of animals (n = 7) without mesenteric ischemia received PDTC following baseline measurements and served as control for the effect of PDTC alone (PDTC). Preload recruitable stroke work, +/-dp/dt(max), isovolumic relaxation (tau), and cardiac output were measured. Myocardial tissue was analyzed for NF kappaB activity, TNF-alpha production, and myocardial apoptosis. RESULTS: Mesenteric I/R impaired both LV systolic and diastolic function. Administration of PDTC worsened LV function impairment following I/R. In addition, PDTC resulted in decreased LV function even without mesenteric I/R. NF kappaB, TNF-alpha, and myocardial apoptosis were not different among the groups. CONCLUSIONS: Mesenteric I/R affects LV function independent of NF kappaB and TNF-alpha pathways. PDTC acts as a cardiac depressant through a thus far unknown mechanism. Therefore, evaluation of cardiac and hemodynamic function in experimental setups using PDTC has to be carefully interpreted.

Intravenous mesenchymal stem cell therapy for traumatic brain injury.

OBJECT: Cell therapy has shown preclinical promise in the treatment of many diseases, and its application is being translated to the clinical arena. Intravenous mesenchymal stem cell (MSC) therapy has been shown to improve functional recovery after traumatic brain injury (TBI). Herein, the authors report on their attempts to reproduce such observations, including detailed characterizations of the MSC population, non-bromodeoxyuridine-based cell labeling, macroscopic and microscopic cell tracking, quantification of cells traversing the pulmonary microvasculature, and well-validated measurement of motor and cognitive function recovery. METHODS: Rat MSCs were isolated, expanded in vitro, immunophenotyped, and labeled. Four million MSCs were intravenously infused into Sprague-Dawley rats 24 hours after receiving a moderate, unilateral controlled cortical impact TBI. Infrared macroscopic cell tracking was used to identify cell distribution. Immunohistochemical analysis of brain and lung tissues 48 hours and 2 weeks postinfusion revealed transplanted cells in these locations, and these cells were quantified. Intraarterial blood sampling and flow cytometry were used to quantify the number of transplanted cells reaching the arterial circulation. Motor and cognitive behavioral testing was performed to evaluate functional recovery. RESULTS: At 48 hours post-MSC infusion, the majority of cells were localized to the lungs. Between 1.5 and 3.7% of the infused cells were estimated to traverse the lungs and reach the arterial circulation, 0.295% reached the carotid artery, and a very small percentage reached the cerebral parenchyma (0.0005%) and remained there. Almost no cells were identified in the brain tissue at 2 weeks postinfusion. No motor or cognitive functional improvements in recovery were identified. CONCLUSIONS: The intravenous infusion of MSCs appeared neither to result in significant acute or prolonged cerebral engraftment of cells nor to modify the recovery of motor or cognitive function. Less than 4% of the infused cells were likely to traverse the pulmonary microvasculature and reach the arterial circulation, a phenomenon termed the "pulmonary first-pass effect," which may limit the efficacy of this therapeutic approach. The data in this study contradict the findings of previous reports and highlight the potential shortcomings of acute, single-dose, intravenous MSC therapy for TBI.

Distribution of NOS isoforms in a porcine endotoxin shock model.

Sepsis is a major cause of morbidity and mortality. NO, an endogenous vasodilator, has been associated with the hypotension, catecholamine hyporesponsiveness, and myocardial depression of septic shock. Although iNOS is thought to be responsible for the hypotension and loss of vascular tone occurring several hours after endotoxin administration, little is known on the effects of constitutive eNOS on LPS-induced organ dysfunction. This study assessed the distribution of eNOS and iNOS in various vascular beds in conscious pigs challenged with LPS. Cardiac and regional hemodynamic parameters were recorded over 8 h in the presence and absence of aminoguanidine, a rather selective inhibitor of iNOS activity, and N-methyl-L-arginine, a nonspecific NOS inhibitor. Our data show that LPS-induced cardiac depression was associated with coronary, renal, and mesenteric vasoconstrictions and a hepatic vasodilatation. LPS also induced increases in eNOS in the heart and lungs, whereas iNOS was mostly detected in the liver. Nitrotyrosine formation was mainly detected in the lungs, with traces in the kidney, liver, and gut. Accordingly, our results suggest that the early decrease in blood pressure and cardiac depression are likely due to activated eNOS, whereas both isoforms are involved in the hepatic vasodilation. In contrast, carotid, coronary, mesenteric, and renal vasoconstrictions were significant at 5 and/ or 6 h after LPS infusion, suggesting that NO is not the primary mediator, facilitating and/or unmasking the release of vasoconstrictor mediators. Consequently, developing newer tissue- or isoform-specific NOS inhibitors can lead to novel therapeutic agents in septic shock.

Pneumocyte apoptosis induction during cardiopulmonary bypass: effective prevention by radical scavenging using N-acetylcysteine.

Cardiopulmonary bypass (CPB) and cardioplegic arrest are associated with pulmonary dysfunction. We sought to investigate whether pulmonary ischemia/reperfusion during standard CPB and cardioplegic arrest is associated with reactive oxygen species (ROS)-mediated pulmonary tissue injury and pneumocyte apoptosis induction, and whether ROS scavenging using N-acetylcysteine (NAC) attenuates these alterations. Twelve pigs (41 +/- 8 kg) were randomized to receive either NAC (100 mg/kg prior to CPB; n = 7) or placebo (n = 5) and subjected to CPB and 60 min of cold (4 degrees C) crystalloid cardioplegic arrest. We collected lung biopsies prior to CPB, at 60 min CPB, as well as at 30, 60, and 120 min post CPB. Lung specimens were immunocytochemically stained against nitrotyrosine, 8-isoprostaglandin-F(2)alpha, and 8-hydroxy-2'-deoxyguanosine (8-OH-dG) as indicators for ROS-mediated tissue injury and active caspase-3, an apoptosis signal pathway key enzyme. Oxidative stress markers were judged using a scale from 1 to 4 (low to intensive staining), and caspase-3-positive pneumocytes were counted per view field. In placebo, the number of caspase-3-positive pneumocytes significantly increased over time to reach a maximum at 120 min post CPB (p = .03 vs baseline). NAC significantly prevented caspase-3 activation in pneumocytes (p = .001 vs Placebo). Pneumocyte nitrotyrosine and 8-OH-dG staining significantly increased over time (p = .003) in the placebo group, but decreased in the NAC group (p = .004). In both groups staining for 8-isoprostaglandin-F(2)alpha showed no significant changes. This yields the conclusion that standard CPB and cardioplegic arrest initiate ROS-mediated tissue injury and apoptosis in pneumocytes that can be reduced by NAC. Thus, ROS scavenging using NAC may represent a novel approach to minimize lung injury associated with CPB.

First year changes of myocardial lymphatic endothelial markers in heart transplant recipients.

OBJECTIVE: The lymphatic system plays an important role in interstitial fluid balance, lipid metabolism, and immune response. The recent introduction of specific lymphatic endothelial cell markers has made the investigation of lymphangiogenesis under various conditions and from small tissue samples feasible. It was the purpose of the study to investigate the changes of myocardial lymphatic endothelial markers during the first 12 months after heart transplantation and to analyze if a correlation between lymphatic markers and rejection can be found. METHODS: Right ventricular endomyocardial biopsies taken for routine rejection monitoring from 26 heart transplant recipients were investigated. Selected time points were 0.5, 1, 1.5, 6, and 12 months after human heart transplantation (HTX). Immunohistostaining was performed for VEGFR-3, the receptor for lymphangiogenic vascular endothelial growth factors C and D, for LYVE-1, a novel hyaluronan receptor, restricted to lymphatic vessels, and PROX-1, a homeobox gene product, which plays a key role in lymph vessel development and differentiation. RESULTS: Density of VEGFR-3 positive lymphatics did not change during the first 12 months after transplantation. However, in comparison to the 0.5-month biopsy, density of LYVE-1 and PROX-1 positive lymphatics was significantly decreased at 1 month after transplantation (p<0.03) and at the subsequent time points (p<0.01). Patients with only moderate rejection during the first 12 months (ISHLT

Impact of acute myocardial edema on left ventricular function.

Studies of the impact of myocardial edema on left ventricular (LV) systolic function show conflicting results. We sought to evaluate the impact of increased myocardial water content (MWC) on LV systolic and diastolic function. Anesthetized dogs (n = 12) were instrumented with myocardial ultrasonic crystals and an LV micromanometer. Systolic function was measured by preload recruitable stroke work (PRSW) and dP/dt(max). Diastolic function was measured by -dP/dt(max) and the isovolumic relaxation constant tau (t). Myocardial water content (MWC) was determined using microgravimetry. In six dogs (coronary sinus hypertension, CSH group) we produced myocardial edema by inflating a coronary sinus balloon for 2 h (30-40 mm Hg). In six other dogs (Plegisol, PLEG group) cardiopulmonary bypass (CPB) was initiated (12.3 +/- 0.8 min), the aorta was cross-clamped (117 +/- 19 s), and 700 mL 4 degrees C crystalloid, hyperkalemic cardioplegic solution (Plegisol) was administered into the aortic root (62 +/- 4 mm Hg). After declamping and reperfusion (7.2 +/- 1.0 min), the dogs were separated from CPB. Myocardial function parameters and MWC were measured for 2 h after edema generation. In the CSH group, MWC significantly increased from 75.9 +/- 0.3% to 77.6 +/- 0.3% (p < .05). In the PLEG group, MWC increased from 75.8 +/- 0.3% to 77.7 +/- 0.3% (p < .05). PRSW and dP/dt(max) did not decrease in either group. Diastolic parameters did not change significantly. We conclude that acute myocardial edema without myocardial injury does not impair LV function.

Renal protection by radical scavenging in cardiac surgery patients.

OBJECTIVE: Renal function impairment is a common complication in cardiac surgery patients. Because cardiopulmonary bypass and cardioplegic arrest are associated with formation of free radicals, which have been shown to impair various organs including the kidneys, radical scavenging may protect renal function. Therefore, the purpose of our study was to evaluate the impact of the radical scavenger N-acetylcysteine (NAC) versus placebo on peri-operative renal function in cardiac surgery patients. RESEARCH DESIGN AND METHODS: We reanalyzed the data of our previous study in which 40 coronary artery surgery patients (66 +/- 9 [SD] years, 9 women and 31 men) with normal pre-operative renal function had been randomized in a double-blind fashion to receive either NAC (100 mg/kg into the cardiopulmonary bypass prime followed by infusion at 20 mg/kg/h; n = 20) or placebo (n = 20). We determined serum creatinine levels as an indicator for renal function pre- and at 1 day post-surgery as well as peri-operative urinary output and diuretic medication. Creatinine clearance was calculated according to Cockcroft and Gault. RESULTS: Biometric and intra-operative patient data were similar between both groups. In the placebo group, serum creatinine increased from 93.1 +/- 35.4 micromol/L pre-operatively to 115.9 +/- 47.2 micromol/L on post-op day 1 (p < 0.001). In contrast, serum creatinine in the NAC group remained unchanged (92.3 +/- 31.3 micromol/L pre-op; 99.3 +/- 25.4 micromol/L on post-op day 1; p = 0.084). Accordingly, creatinine clearance decreased by 16.9 +/- 14.3 mL/min in the placebo group as compared to 7.5 +/- 17.7 mL/min in the NAC group (p = 0.039). Urinary output and diuretic medication were similar between NAC and placebo. CONCLUSIONS: Our data suggest that free radical-scavenging using NAC protects renal function in patients subjected to cardiac surgery on cardiopulmonary bypass.

Mild hypothermia impairs left ventricular diastolic but not systolic function.

Hypothermia is a component of myocardial protection during cardiopulmonary bypass (CPB) and cardioplegic arrest (CA). Patients in the early post CPB period often show mild hypothermia and cardiac dysfunction. We sought to investigate the impact of hypothermia on left ventricular (LV) function. Anesthetized dogs (n = 12) were instrumented with myocardial ultrasonic crystals and LV micromanometer. Systolic function was measured by preload recruitable stroke work (PRSW). Diastolic function was measured by -dP/dt(max) and tau. In six dogs (Norm group), body temperature was maintained at baseline levels. In another six dogs (Hypo group), body temperature dropped gradually over the time course of the experiment. The body temperature in the Hypo group decreased from 37.0 +/- 0.3 degrees C to 35.2 +/- 1.0 degrees C. -dP/dt(max) decreased and tau increased significantly with hypothermia but were stable in the Norm group. Both tau and -dP/dt(max) showed a linear relationship to the body temperature (r =.91 and r = .93, respectively). PRSW did not change and cardiac output decreased with hypothermia. Thus, even mild hypothermia impairs LV diastolic but not systolic function. Cardiac output is temperature sensitive and therefore rewarming of patients post-CPB has priority.

Case Report: En Bloc Resection of Pancoast Tumor with Adjuvant Aortic Endograft and Chemoradiation.

"Pancoast" tumors frequently require a multidisciplinary approach to therapy and are still associated with high morbidity and mortality. Due to their sensitive anatomic location, complex resections and chemoradiation regimens are typically required for treatment. Those with signs of aortic invasion pose an even greater challenge, given the added risks of cardiopulmonary bypass for aortic resection and interposition. Placement of an aortic endograft can facilitate resection if the tumor is in close proximity to or is invading the aorta. Prophylactic endografting to prevent radiation-associated aortic rupture has also been described. This case describes a 60-year-old female who presented with a stage IIIa left upper lobe undifferentiated non-small-cell carcinoma encasing the subclavian artery with thoracic aorta and bony invasion. Following carotid-subclavian bypass with Dacron, en bloc resection of the affected lung, ribs, and vertebral bodies was performed. The aorta was prophylactically reinforced with a Gore TAG thoracic endograft prior to adjuvant chemoradiation. The patient remains disease-free at more than 5 years follow-up after completing her treatment course. Endovascular stenting with subsequent chemoradiation may prove to be a viable alternative to palliation or open operative management and prevention of aortic injury during tumor resection and/or adjuvant therapy in select patients with aortic involvement.

Myocardial apoptosis prevention by radical scavenging in patients undergoing cardiac surgery.

BACKGROUND: Reactive oxygen-derived species, including those generated during myocardial ischemia and reperfusion induced by cardioplegia, have been suggested to be involved in myocardial apoptosis induction. The purpose of our study was to investigate (1) whether cardioplegic arrest initiates apoptosis in the hearts of cardiac surgery patients and (2) whether reactive oxygen-derived species scavenging with N-acetylcysteine attenuates myocardial apoptosis initiation. METHODS: In transmural left ventricular biopsy samples collected before and at the end of cardiopulmonary bypass, we densitometrically determined cardiac myocyte staining intensity for active caspases-3 and -7, the apoptosis signal pathway central effector enzymes. The left ventricular biopsy samples had been obtained from 36 coronary artery bypass graft patients randomized in a double-blind fashion to receive either N-acetylcysteine (100 mg/kg into cardiopulmonary bypass prime followed by infusion at 20 mg.kg(-1).h(-1); n = 18) or placebo (n = 18). RESULTS: The change in left ventricular cardiac myocyte staining (end of cardiopulmonary bypass minus before cardiopulmonary bypass) differed significantly between groups for both measures: caspase-3, -3.1 +/- 4.5 gray units (mean +/- SD; N-acetylcysteine group) versus 7.1 +/- 8.1 gray units (placebo); 95% confidence interval, 6.4 to 14.4; P <.0001; caspase-7, -5.1 +/- 6.1 gray units (N-acetylcysteine) versus 5.1 +/- 5.7 gray units (placebo); 95% confidence interval, 6.3 to 15.0; P <.0001. Clinical outcome did not differ between N-acetylcysteine and placebo. CONCLUSIONS: Our data show that cardioplegic arrest initiates the apoptosis signal cascade in human left ventricular cardiac myocytes. This apoptosis induction can effectively be prevented by N-acetylcysteine.

Nitrotyrosine and 8-isoprostane formation indicate free radical-mediated injury in hearts of patients subjected to cardioplegia.

OBJECTIVE: Myocardial ischemia and reperfusion induced by cardioplegic arrest subjects the heart to free radical-mediated stress. The purpose of our study was to investigate the effect of cardioplegia-induced ischemia and reperfusion on myocardial formation and distribution of (1) nitrotyrosine as an indicator for peroxynitrite-mediated tissue injury resulting from increased nitric oxide release and (2) 8-isoprostane as an indicator for oxygen-derived free radical-mediated lipid peroxidation. METHODS: In 10 patients undergoing coronary artery operations (64 +/- 6 [mean +/- SD] years, 3 women and 7 men) subjected to cardiopulmonary bypass and intermittent cold blood cardioplegia, we collected transmural left ventricular biopsy specimens before and at the end of cardiopulmonary bypass. Specimens were cut at 10 micro m and subjected to immunocytochemical staining against the nitric oxide-producing enzyme constitutive nitric oxide synthase, cyclic guanosine monophosphate (intracellular second messenger of nitric oxide), nitrotyrosine, and 8-isoprostane by using polyclonal antibodies. For global left ventricular function determination, we measured the fractional area of contraction using transesophageal echocardiography. RESULTS: Nitric oxide synthase activity in cardiac myocytes increased from 34 +/- 10 gray units before cardiopulmonary bypass to 47 +/- 12 gray units at the end of bypass (P =.015), and all hearts showed increased cyclic guanosine monophosphate content in both myocytes and endothelial cells at the end of bypass. The number of nitrotyrosine-positive capillaries increased from 36 +/- 29/mm(2) before bypass to 82 +/- 47/mm(2) at the end of bypass (P =.012), and 8-isoprostane-positive capillaries increased from 92 +/- 72/mm(2) before bypass to 209 +/- 108/mm(2) at the end of bypass (P =.005). The fractional area of contraction was 53% +/- 12% before bypass and 56% +/- 12% after bypass (P =.47) but was slightly decreased to 45% +/- 14% at 4 hours after bypass (P =.121). CONCLUSIONS: Our data show that cardioplegia-induced myocardial ischemia and reperfusion is associated with nitrotyrosine and 8-isoprostane formation mainly in the coronary endothelium, indicating injury mediated by both peroxynitrite and oxygen-derived free radicals. Because nitric oxide synthase activation was accompanied with increased cyclic guanosine monophosphate, these data suggest that direct effects of nitric oxide on cardiac myocytes, as well as nitric oxide-mediated coronary endothelial injury, might contribute to injury associated with cardioplegia and cardiopulmonary bypass.

The antioxidant N-acetylcysteine preserves myocardial function and diminishes oxidative stress after cardioplegic arrest.

OBJECTIVE: Oxidative stress contributes to myocardial ischemia-reperfusion injury. We hypothesized that administration of the antioxidant N-acetylcysteine would have beneficial effects on myocardial function after cardiopulmonary bypass and cardioplegic arrest. METHODS: Anesthetized dogs (n = 18) were instrumented with myocardial ultrasonic crystals and a left ventricular micromanometer. Systolic function was measured by preload recruitable stroke work. Myocardial tissue water was determined by microgravimetry. Treated animals received 100 mg.kg(-1) N-acetylcysteine 10 minutes before initiation of cardiopulmonary bypass followed by 20 mg.kg(-1).h(-1) continuous infusion until 1 hour after cardiopulmonary bypass. After baseline, cardiopulmonary bypass and 2-hour crystalloid cardioplegic arrest was initiated, then reperfusion/rewarming for 40 minutes and separation from cardiopulmonary bypass. Myocardial function parameters and myocardial tissue water were measured at 30, 60, and 120 minutes after cardiopulmonary bypass. Oxidative stress was measured by 8-isoprostane concentrations in the coronary sinus plasma. RESULTS: Preload recruitable stroke work did not decrease from baseline in the N-acetylcysteine group and was significantly greater in N-acetylcysteine group compared with controls at 30 (104% +/- 9% vs 80% +/- 4%; P <.05) and 120 minutes (98% +/- 7% vs 79% +/- 4%; P <.05) after cardiopulmonary bypass. Concentrations of 8-isoprostane in the coronary sinus plasma of the control dogs were significantly higher 30 minutes after cardiopulmonary bypass compared with baseline but were unchanged in the N-acetylcysteine group. Myocardial edema resolution was significantly greater in the N-acetylcysteine group at 30 minutes after cardiopulmonary bypass compared with control (-2.5% +/- 0.7% vs -0.3% +/- 0.5% myocardial tissue water; P <.05). CONCLUSIONS: Administration of the antioxidant N-acetylcysteine preserves systolic function and enhances myocardial edema resolution after cardiopulmonary bypass/cardioplegic arrest. Furthermore, oxidative stress was significantly reduced in the treated animals. Therefore, our findings support the hypothesis that oxidative stress is the main cause for myocardial dysfunction after ischemia-reperfusion.

Effect of the Na+/H+ exchange inhibitor eniporide on cardiac performance and myocardial high energy phosphates in pigs subjected to cardioplegic arrest.

BACKGROUND: Pharmacologic Na(+)/H(+) exchange inhibition has been suggested to ameliorate cardiac performance depression associated with myocardial ischemia/reperfusion. The purpose of our experimental study was to investigate the impact of the novel Na(+)/H(+) exchange inhibitor Eniporide (EMD 96785) on cardiac performance and high energy phosphate content in a clinically relevant pig model of cardioplegic arrest. METHODS: We subjected 21 pigs (47 +/- 12 [SD] kg) to cardiopulmonary bypass (CPB) and 60 minutes cold (4 degrees C) crystalloid cardioplegic arrest (Bretschneider). The pigs were randomized to receive either systemic infusion of 3 mg/kg Eniporide before cardioplegia with added 2 micromol/L Eniporide (ENI-CP+iv; n = 7); 3 mg/kg Eniporide in cardioplegia only (ENI-CP; n = 7); or no Eniporide (control; n = 7). For cardiac performance determination we measured preload recruitable stroke work and Tau, the time constant of left ventricular (LV) isovolumic relaxation using sonomicrometry and micromanometry before CPB as well as 30, 60, and 120 minutes after weaning off CPB. LV and right ventricular myocardial adenine nucleotides (ATP, ADP, and AMP), glycogen, and water content were determined at the end of the experiments. RESULTS: Neither for standard hemodynamics including vascular pressures and cardiac index nor for cardiac performance factors did we find statistically significant differences between the groups. Similarly, myocardial adenine nucleotides, glycogene, and water content did not differ significantly between the groups. CONCLUSIONS: In this acute study we did not find significant effects of the Na(+)/H(+) exchange inhibitor Eniporide on cardiac performance and high energy phosphate content in healthy pig hearts subjected to ischemia/reperfusion induced by crystalloid cardioplegic arrest.

Cardioplegic arrest induces apoptosis signal-pathway in myocardial endothelial cells and cardiac myocytes.

OBJECTIVE: Myocardial ischemia-reperfusion is associated with free radical-mediated injury and may be involved in cardiac apoptosis. The purpose of our study was to investigate (1) if cardioplegia-induced ischemia-reperfusion initiates cardiac apoptosis signal pathway, and (2) if this is mediated by free radicals. METHODS: We subjected 13 pigs (56+/-10 kg) to 1 h of cold crystalloid cardioplegic arrest (CA) on cardiopulmonary bypass (CPB), and collected five transmural LV biopsies: prior to CPB (baseline), at 60 min CA, at 15 and 30 min reperfusion on CPB, and at 120 min post CPB. Two additional pigs were subjected to CPB but not CA and two further pigs were neither subjected to CPB nor CA and served as sham-operated time controls. LV specimens were cut at 7 microm and immunocytochemically stained against active caspase-3 and 85 kDa poly(ADP-ribose) polymerase (PARP) as apoptosis signal-pathway key enzymes, nitrotyrosine as indicator for peroxynitrite (ONOO(-))-mediated tissue injury, and 8-iso-prostaglandin-F(2)alpha as indicator for oxygen free radical-mediated lipid peroxidation. Specimen were assessed using a scale of 0 (negative) to 3 (highly positive), and cardiomyocytes were quantitatively investigated using TV densitometry. RESULTS: At 60 min CA, caspase-3 was increased by 9.2+/-3.7 gray units and remained on this level until 2 h post CPB (P

Bouveret syndrome.

Gastric outlet obstruction secondary to an impacted duodenal gallstone, or Bouveret syndrome, is a rare variant of gallstone ileus. It is most common in elderly women and frequently requires endoscopic or surgical management. We present the case of an 80-year-old woman with multiple medical comorbidities who presented to our service with 2 weeks of abdominal pain and nausea. MRI revealed a 4.4-cm gallstone impacted in the duodenum with associated cholecystoduodenal fistula. She required operative exploration to remove the impacted stone and had an unremarkable post-operative course. This case demonstrates the presentation and workup of this rare disorder and the various options for treatment, which can sometimes be difficult given the typical age and associated comorbidities of the patient.