Case report Evidence of leaflet injury during percutaneous aortic valve deployment

Abstract It has been suggested that valved stent deployment during transcatheter aortic valve implantation may be responsible for traumatic injury to pericardial leaflets, especially with balloon expandable valved stents. However, such an injury has not been described nor reported so far. We here report the microscopic analysis of 4 Sapien-Edwards prostheses, 2 of which have been implanted in humans. There was no macroscopic evidence of traumatic injury to the pericardial leaflets of the percutaneous valves. However, pathological microscopic findings were observed in all of them. These mainly consisted of collagen fibers fragmentation and disruption. Areas of non-or mildly affected tissue were adjacent to areas of severely damaged tissue. The entire thickness of the leaflets might be involved. The severity of the lesions also differed among leaflets from a same prosthesis. Areas of plasmatic insudation were identified in one case. The disruption index was significantly higher in the Sapien group in comparison to the control group: 42.4% (14-63.5%) versus 17.5% (9.2-31%) ( p < 0.001). Although of limited size sample, this study does prove that traumatic injury to leaflets occurs during percutaneous valves implantation. This should prompt physicians to wait for the long-term results of this new technology before extending the indications to low-risk patients.

The induction of heme oxygenase 1 decreases contractility in human internal thoracic artery and radial artery grafts

ObjectiveSpasm remains a potential problem encountered during the use of arterial grafts in coronary artery bypass surgery. Heme oxygenase plays a role in the control of arterial vasoreactivity. Heme oxygenase exists in 2 constitutive isoforms (heme oxygenase 2 and 3) and an inducible isoform (heme oxygenase 1). The aim of our study was to induce heme oxygenase 1 by using hemin in human internal thoracic and radial arteries and to evaluate the effect of this induction on the contractility of these arterial grafts.MethodsSegments of human arterial grafts obtained from patients undergoing isolated coronary artery bypass surgery were incubated in organ chambers for 4 hours in the presence of 10−4 mol/L hemin. Concentration-response curves to norepinephrine were obtained in control and hemin-treated arterial rings. Heme oxygenase 1 expression was evaluated by using enzyme-linked immunosorbent assays and immunohistochemical staining.ResultsThe contractility of the arterial rings to norepinephrine was significantly reduced after incubation with hemin. Zinc protoporphyrin (an inhibitor of heme oxygenase) reversed the effect of hemin, whereas the inhibitor of nitric oxide synthase had no effect. The inhibitor of soluble guanylate cyclase blocked the decrease in contractility induced by hemin. Immunohistochemical staining revealed a large expression of heme oxygenase 1 in all vascular layers of hemin-treated internal thoracic artery and radial artery rings. Enzyme-linked immunosorbent assay studies showed a significant increase in heme oxygenase 1 levels in hemin-treated internal thoracic artery and radial artery rings.ConclusionHemin caused in vitro induction of heme oxygenase 1 in human internal thoracic artery and radial artery grafts. This induction resulted in a reduced contractility to norepinephrine, partially through the cyclic guanosine monophosphate–dependent pathway. This effect was independent from nitric oxide synthesis

ULtrasonographic diagnostic criterion for severe diaphragmatic dysfunction after cardiac surgery

Background: Severe diaphragmatic dysfunction can prolong mechanical ventilation after cardiac surgery. An ultrasonographic criterion for diagnosing severe diaphragmatic dysfunction defined by a reference technique such as transdiaphragmatic pressure measurements has never been determined.Methods: Twenty-eight patients requiring mechanical ventilation > 7 days postoperatively were studied. Esophageal and gastric pressures were measured to calculate transdiaphragmatic pressure during maximal inspiratory effort and the Gilbert index, which evaluates the diaphragm contribution to respiratory pressure swings during quiet ventilation. Ultrasonography allowed measuring right and left hemidiaphragmatic excursions during maximal inspiratory effort. Best E is the greatest positive value from either hemidiaphragm. Twenty cardiac surgery patients with uncomplicated postoperative course were also evaluated with ultrasonography preoperatively and postoperatively. Measurements were performed in semirecumbent position.Results: Transdiaphragmatic pressure during maximal inspiratory effort was below normal value in 27 of the 28 patients receiving prolonged mechanical ventilation (median, 39 cm H2O; interquartile range [IQR] 28 cm H2O). Eight patients had Gilbert indexes ≤ 0 indicating severe diaphragmatic dysfunction. Best E was lower in patients with Gilbert index ≤ 0 than > 0 (30 mm; IQR, 10 mm; vs 19 mm; IQR, 7 mm, respectively; p = 0.001). Best E < 25 mm had a positive likelihood ratio of 6.7 (95% confidence interval [CI], 2.4 to 19) and a negative likelihood ratio of 0 (95% CI, 0 to 1.1) for having a Gilbert index ≤ 0. None of the patients with uncomplicated course had Best E < 25 mm either preoperatively or postoperatively.Conclusions: Ultrasonographic-based determination of hemidiaphragm excursions in patients requiring prolonged mechanical ventilation after cardiac surgery may help identify those with and without severe diaphragmatic dysfunction as defined by the Gilbert index

Role of computed tomography imaging for transcatheter valvular repair/insertion

During the last decade, the development of transcatheter based therapies has provided feasible therapeutic options for patients with symptomatic severe valvular heart disease who are deemed inoperable. The promising results of many nonrandomized series and recent landmark trials have increased the number of percutaneous transcatheter valve procedures in high operative risk patients. Pre-procedural imaging of the anatomy of the aortic or mitral valve and their spatial relationships is crucial to select the most appropriate device or prosthesis and to plan the percutaneous procedure. Multidetector row computed tomography provides 3-dimensional volumetric data sets allowing unlimited plane reconstructions and plays an important role in pre-procedural screening and procedural planning. This review will describe the evolving role of multidetector row computed tomography in patient selection and strategy planning of transcatheter aortic and mitral valve procedures

Exhaled carbon monoxide in asthmatics: a meta-analysis

<p>Abstract</p> <p>Background</p> <p>The non-invasive assessment of airway inflammation is potentially advantageous in asthma management. Exhaled carbon monoxide (eCO) measurement is cheap and has been proposed to reflect airway inflammation and oxidative stress but current data are conflicting. The purpose of this meta-analysis is to determine whether eCO is elevated in asthmatics, is regulated by steroid treatment and reflects disease severity and control.</p> <p>Methods</p> <p>A systematic search for English language articles published between 1997 and 2009 was performed using Medline, Embase and Cochrane databases. Observational studies comparing eCO in non-smoking asthmatics and healthy subjects or asthmatics before and after steroid treatment were included. Data were independently extracted by two investigators and analyzed to generate weighted mean differences using either a fixed or random effects meta-analysis depending upon the degree of heterogeneity.</p> <p>Results</p> <p>18 studies were included in the meta-analysis. The eCO level was significantly higher in asthmatics as compared to healthy subjects and in intermittent asthma as compared to persistent asthma. However, eCO could not distinguish between steroid-treated asthmatics and steroid-free patients nor separate controlled and partly-controlled asthma from uncontrolled asthma in cross-sectional studies. In contrast, eCO was significantly reduced following a course of corticosteroid treatment.</p> <p>Conclusions</p> <p>eCO is elevated in asthmatics but levels only partially reflect disease severity and control. eCO might be a potentially useful non-invasive biomarker of airway inflammation and oxidative stress in nonsmoking asthmatics.</p

Effects of Biliverdin Administration on Acute Lung Injury Induced by Hemorrhagic Shock and Resuscitation in Rats

Hemorrhagic shock and resuscitation induces pulmonary inflammation that leads to acute lung injury. Biliverdin, a metabolite of heme catabolism, has been shown to have potent cytoprotective, anti-inflammatory, and anti-oxidant effects. This study aimed to examine the effects of intravenous biliverdin administration on lung injury induced by hemorrhagic shock and resuscitation in rats. Biliverdin or vehicle was administered to the rats 1 h before sham or hemorrhagic shock-inducing surgery. The sham-operated rats underwent all surgical procedures except bleeding. To induce hemorrhagic shock, rats were bled to achieve a mean arterial pressure of 30 mmHg that was maintained for 60 min, followed by resuscitation with shed blood. Histopathological changes in the lungs were evaluated by histopathological scoring analysis. Inflammatory gene expression was determined by Northern blot analysis, and oxidative DNA damage was assessed by measuring 8-hydroxy-2' deoxyguanosine levels in the lungs. Hemorrhagic shock and resuscitation resulted in prominent histopathological damage, including congestion, edema, cellular infiltration, and hemorrhage. Biliverdin administration prior to hemorrhagic shock and resuscitation significantly ameliorated these lung injuries as judged by histopathological improvement. After hemorrhagic shock and resuscitation, inflammatory gene expression of tumor necrosis factor-alpha and inducible nitric oxide synthase were increased by 18- and 8-fold, respectively. Inflammatory gene expression significantly decreased when biliverdin was administered prior to hemorrhagic shock and resuscitation. Moreover, after hemorrhagic shock and resuscitation, lung 8-hydroxy-2' deoxyguanosine levels in mitochondrial DNA expressed in the pulmonary interstitium increased by 1.5-fold. Biliverdin administration prior to hemorrhagic shock and resuscitation decreased mitochondrial 8-hydroxy-2' deoxyguanosine levels to almost the same level as that in the control animals. We also confirmed that biliverdin administration after hemorrhagic shock and resuscitation had protective effects on lung injury. Our findings suggest that biliverdin has a protective role, at least in part, against hemorrhagic shock and resuscitation-induced lung injury through anti-inflammatory and anti-oxidant mechanisms