Excessive Stretch Research Articles

Role of Integrin β4 in Lung Endothelial Cell Inflammatory Responses to Mechanical Stress.

Simvastatin, an HMG-CoA reductase inhibitor, has lung vascular-protective effects that are associated with decreased agonist-induced integrin β4 (ITGB4) tyrosine phosphorylation. Accordingly, we hypothesized that endothelial cell (EC) protection by simvastatin is dependent on these effects and sought to further characterize the functional role of ITGB4 as a mediator of EC protection in the setting of excessive mechanical stretch at levels relevant to ventilator-induced lung injury (VILI). Initially, early ITGB4 tyrosine phosphorylation was confirmed in human pulmonary artery EC subjected to excessive cyclic stretch (18% CS). EC overexpression of mutant ITGB4 with specific tyrosines mutated to phenylalanine (Y1440, Y1526 Y1640, or Y1422) resulted in significantly attenuated CS-induced cytokine expression (IL6, IL-8, MCP-1, and RANTES). In addition, EC overexpression of ITGB4 constructs with specific structural deletions also resulted in significantly attenuated CS-induced inflammatory cytokine expression compared to overexpression of wildtype ITGB4. Finally, mice expressing a mutant ITGB4 lacking a cytoplasmic signaling domain were found to have attenuated lung injury after VILI-challenge (VT = 40 ml/kg, 4 h). Our results provide mechanistic insights into the anti-inflammatory properties of statins and may ultimately lead to novel strategies targeted at ITGB4 signaling to treat VILI.

A modified virtual multi-dimensional internal bonds model for geologic materials

This article presents a modified version of the vir-tual multi-dimensional internal bonds model. In this modi-fied model, a different approach for virtual internal bond’ strain energy is proposed, which uses the spherical stretch strain and the shear strain to calculate the bonds’ stretch energy and shear energy respectively, so as to overcome the excessive stretch energy in the virtual multi-dimensional internal bonds model. And the modified model successfully extends the limit Poisson ratio to 0.5. This new model could be applied to simulate material non-linearity behavior. DOI: http://dx.doi.org/10.5755/j01.mech.21.5.10956

Oesophageal injury

Oesophageal injury

Application of neuroendoscopy in primary hemifacial spasm surgery

Objective To investigate the application value of neuroendoscope techniques in primary hemifacial spasm of the local complex anatomy aiming to the difficulties of primary hemifacial spasm surgery. Methods Forty-two patients with hemifacial spasm of the local complex anatomy were treated with neuroendoscope-assisted microvascular decompression at the Department of Neurosurgery, Wuxi No. 2 Hospital Affiliated to Nanjing Medical University from January 2008 to January 2012. When the blind area appeared during the operation, a neuroendoscope was used to perform comprehensive observation of the surgical area, exploring the facial nerves from the brain stem area and distal end, and carefully distinguishing the relationship between the nerves and the blood vessels. The offending vessels were confirmed. After decompression, a neuroendoscope was use to reexamine whether there were omission of offending vessels and vascular excessive stretch, twisting in an angular shape, or formation of a new compression. The clinical and imaging data of all patients were analyzed retrospectively and were followed up after procedure. Results All patients were followed for 18-30 months (mean 25 months). Forty-one patients had complete remission after procedure without recurrence (98%), 3 recovered from Shorr grade Ⅰ to grade 0 at discharge, 1 with hearing loss was fully restored within 6 months, and 1 with Shorr grade Ⅱ did not obviously aggravate at the end of follow-up. Conclusions Neuroendoscopy is an useful complement to microvascular decompression for the treatment of hemifacial spasm, particularly in patients with local anatomical complex or unusual hemifacial spasm, such as combining the advantages of neuroendoscopy may improve the operation effect under the conditions of small posterior fossa volume, full cerebellum pompoms, rock bone block, local arachnoid adhesions and thickening, and identifying offending vessels with difficulty. Key words: Facia1 spasm; Neuroendoscope; Microvascular decompression

Bariatric Surgery and Urinary Incontinence.

About one-quarter of adults in the United States are obese.1 Among itsmyriadadverseeffectsonhealth, obesity affects the support and function of the pelvic floor. As obesity increases, the pelvic floor disorders of urinary incontinence, anal incontinence, and (forwomen) pelvic organ prolapse become more prevalent. More than half of the women who are morbidly obese have pelvic floor disorders.2 Obesity may cause or aggravate pelvic floor disorders throughmechanisms such as chronic strain on ligaments and nerves, leading to excessive stretch and increased abdominal pressure. Using an indwelling urinary catheter in 63morbidly obese patients about to undergo bariatric surgery, Varela and colleagues3 demonstrated elevated intra-abdominal pressure in 48 patients (77.0%). Increased intra-abdominal pressure has also been found in obese women with stress urinary incontinence, which is involuntary leakage on effort or exertion, sneezing, or coughing, and in urge urinary incontinence, which is involuntary leakage accompanied by or immediately preceded by urgency.4 Epidemiological investigationshave shown that obesity is a strong independent risk factor for urinary incontinence.5 Obesewomen undergoing surgery for stress incontinence report more incontinence episodes, greater symptom distress, andworsequalityof lifecomparedwithnormal-weightwomen. Formen andwomen, the probability of having urinary incontinence increases with increasing weight.5 Although urinary incontinence ismore common in severely obesewomen than men, it occurs frequently in both sexes. Thewide rangeof treatments forurinary incontinenceand other pelvic floor disorders include pelvic muscle exercises, vaginal devices knownas continence rings or dishes, anticholinergicandbeta-agonistmedications, andbehavioral changes. Weight loss is one of the best-studied behavioral treatments. In the 2009 PRIDE (Program to Reduce Incontinence by Diet and Exercise) study,6 a total of 338 overweight and obese womenwith urinary incontinencewere randomized to an intensive intervention to lose weight or to a control intervention. The intensive weight loss program met in groups of 10 to 15personsweekly for 6months for 1-hour sessions. The sessions were led by experts in nutrition and exercise. The control interventionwasa structurededucationprogram inwhich groups met monthly for 4 months. All participants received self-help information on pelvic muscle exercises and methods for improving bladder control. The intensive group had a greater reduction in the mean weekly number of urinary incontinence episodes than the control group. The effects of bariatric surgery on pelvic floor disorders have also been studied, but typically with small cohorts or in single-site studies.Outcomeshavebeenassessedwithin 1year after surgery and are assessed with a proxy measure of urinary incontinence such as International Classification of Diseases, Ninth Revision, codes.7 In this issue of JAMA Internal Medicine, Subak et al8 report a large multicenter observational cohort study of urinary incontinencebefore andafter bariatric surgerywithmultiple direct assessments of incontinence symptoms and longtermfollow-up.Amongwomenandmen,bariatric surgerywas associated with substantial reductions in urinary incontinence over 3 years. For both sexes, the largest improvements occurred in the first year after surgery. Men and women had reductions in any typeof urinary incontinence, aswell as urge urinary incontinence. Forwomen, the study founda trend toRelated article page 1378 Urinary Incontinence Before and After Bariatric Surgery Original Investigation Research

Loss of the mechanotransducer zyxin promotes a synthetic phenotype of vascular smooth muscle cells.

BackgroundExposure of vascular smooth muscle cells (VSMCs) to excessive cyclic stretch such as in hypertension causes a shift in their phenotype. The focal adhesion protein zyxin can transduce such biomechanical stimuli to the nucleus of both endothelial cells and VSMCs, albeit with different thresholds and kinetics. However, there is no distinct vascular phenotype in young zyxin-deficient mice, possibly due to functional redundancy among other gene products belonging to the zyxin family. Analyzing zyxin function in VSMCs at the cellular level might thus offer a better mechanistic insight. We aimed to characterize zyxin-dependent changes in gene expression in VSMCs exposed to biomechanical stretch and define the functional role of zyxin in controlling the resultant VSMC phenotype.Methods and ResultsDNA microarray analysis was used to identify genes and pathways that were zyxin regulated in static and stretched human umbilical artery–derived and mouse aortic VSMCs. Zyxin-null VSMCs showed a remarkable shift to a growth-promoting, less apoptotic, promigratory and poorly contractile phenotype with ≈90% of the stretch-responsive genes being zyxin dependent. Interestingly, zyxin-null cells already seemed primed for such a synthetic phenotype, with mechanical stretch further accentuating it. This could be accounted for by higher RhoA activity and myocardin-related transcription factor-A mainly localized to the nucleus of zyxin-null VSMCs, and a condensed and localized accumulation of F-actin upon stretch.ConclusionsAt the cellular level, zyxin is a key regulator of stretch-induced gene expression. Loss of zyxin drives VSMCs toward a synthetic phenotype, a process further consolidated by exaggerated stretch.

The impact of channel gap distance on flame splitting limit of H2/air mixture in microchannels with wall cavities

We recently confirmed the “tip open phenomenon” of lean H 2 /air flame in a microchannel with cavities. The critical inlet velocity when fuel conversion ratio drops to 80% was defined as “flame splitting limit”. In the present work, we numerically studied the impact of channel gap distance. Results showed that corresponding limits for 1.0-mm, 0.8-mm and 0.6-mm channels are 26 m/s, 33 m/s and 16 m/s respectively, exhibiting a non-monotonic dependence. The analysis reveals that when the gap distance is decreased from 1.0 mm to 0.8 mm, the proportion of fuel that involved into the cavities is increased, flame length is reduced simultaneously, and better preheating of the fresh mixture is attained. These positive effects lead to an increase in flame splitting limit. As the gap distance is further reduced to 0.6 mm, the excessive stretch effect results in complete extinction of downstream flame, causing a decrease of the splitting limit. • Flame splitting limits of 0.6-mm, 0.8-mm and 1.0-mm channels were numerically studied. • Variation of flame splitting limit versus channel gap distance is non-monotonic. • Combined effects lead to the largest flame splitting limit of the 0.8-mm channel. • Dominant factor for the 0.6-mm channel is the extinction of downstream flames.

High Mechanical Strain of Intervertebral Disc Cells Promotes Secretion of Inflammatory Factors Associated with Disc Degeneration and Pain

IntroductionLow back pain is a debilitating disorder affecting a multitude of people and is currently ranked sixth among costliest treatable chronic illnesses.1 Low back pain is often attributed to...

The Super-Convergence in Rheological Flow

To estimate the solution of the coupled first-order hyperbolic partial differential equations, we use both the boundary-layer method and numeric analysis to study the Cauchy fluid equations and P-T/T stress equation. On the macroscopic scale the free surface elements generate flow singularity and stress uncertainty by excessive tensile stretch. A numerical super-convergence semi-discrete finite element scheme is used to solve the time dependent equations. The coupled nonlinear solutions are estimated by boundary-layer approximation. Its numerical super convergence is proposed with the a priori and a posteriori error estimates.

Lung Metabolism During Ventilator-Induced Lung Injury

Concerns about pulmonary complications of positive pressure ventilation (1) are at least as old as the description of the Acute Respiratory Distress Syndrome (ARDS) (2). Yet, it took about a decade until experimental findings (3) shifted the focus from air leaks and oxygen toxicity to the biological effects of large excursions of the lung parenchyma (4). The demonstration that mechanical ventilation with high peak inspiratory pressures and low positive end-expiratory pressure (PEEP) could produce edema, increased alveolo-capillary permeability, leukocyte infiltration, and inflammation in normal lungs established the current understanding of ventilator-induced lung injury (VILI) (4, 5). The clinical relevance of VILI was confirmed by the demonstration of a 22% decrease in mortality of ARDS patients when lung stretch was reduced through lower tidal volumes (VT). (6). In addition to excessive lung stretch due to large VT, it has been recognized that VILI can also be caused by low end-expiratory lung volumes, even at low airway pressures. Mechanisms proposed to explain such injury include concentration of stresses in the heterogeneously expanding lung parenchyma (7), and propagation and rupture of liquid plugs producing injurious fluid mechanical stresses during cyclic recruitment-derecruitment of distal lung units (8, 9). Mitigation of these low-volume phenomena by optimizing lung recruitment with higher PEEP levels (10) and proning (11) has been beneficial in patients with moderate and severe ARDS. However, despite the large number of experimental and clinical studies, uncertainty persists about the relative contribution of overdistension versus low-volume injury to the ultimate lung damage produced by VILI (12). Topographically, in supine patients, nondependent (ventral) injury would be expected if overdistension would predominate (13), whereas dependent (dorsal) damage would be expected for predominant low-volume injury (14). The clinical relevance of the topic has been emphasized by the suggestion that the mass of opening-closing lung is an independent risk factor for death in patients with ARDS (15), and that regional forces during mechanical ventilation determine lung parenchyma abnormalities found in ARDS survivors (16).

Bilateral variation in origin of pectoralis minor

Bilateral variation in origin of pectoralis minor is not reported commonly. Higher origin would likely to restrict the movement of shoulder especially abduction and lateral rotation. Origin of pectoralis minor from 2 nd to 4 th ribs and costochondral junction is recognized in 15% cases. This could press on excessive stretch to the neurovascular structures, thereby giving rise to neurological and vascular symptoms in the arm. This case report is demonstrating need for continued reporting of anatomical variation and ongoing discussion of their functional and clinical significance.

STAG2 promotes error correction in mitosis by regulating kinetochore-microtubule attachments.

Mutations in the STAG2 gene are present in ∼20% of tumors from different tissues of origin. STAG2 encodes a subunit of the cohesin complex, and tumors with loss-of-function mutations are usually aneuploid and display elevated frequencies of lagging chromosomes during anaphase. Lagging chromosomes are a hallmark of chromosomal instability (CIN) arising from persistent errors in kinetochore-microtubule (kMT) attachment. To determine whether the loss of STAG2 increases the rate of formation of kMT attachment errors or decreases the rate of their correction, we examined mitosis in STAG2-deficient cells. STAG2 depletion does not impair bipolar spindle formation or delay mitotic progression. Instead, loss of STAG2 permits excessive centromere stretch along with hyperstabilization of kMT attachments. STAG2-deficient cells display mislocalization of Bub1 kinase, Bub3 and the chromosome passenger complex. Importantly, strategically destabilizing kMT attachments in tumor cells harboring STAG2 mutations by overexpression of the microtubule-destabilizing enzymes MCAK (also known as KIF2C) and Kif2B decreased the rate of lagging chromosomes and reduced the rate of chromosome missegregation. These data demonstrate that STAG2 promotes the correction of kMT attachment errors to ensure faithful chromosome segregation during mitosis.

Unilateral Acid Aspiration Augments the Effects of Ventilator Lung Injury in the Contralateral Lung

Mechanical ventilation is necessary during acute respiratory distress syndrome, but it promotes lung injury because of the excessive stretch applied to the aerated parenchyma. The authors' hypothesis was that after a regional lung injury, the noxious effect of mechanical ventilation on the remaining aerated parenchyma would be more pronounced. Mice, instilled with hydrochloric acid (HCl) in the right lung, was assigned to one of the following groups: mechanical ventilation with tidal volumes (VT) 25 ml/kg (HCl-VILI25, n = 12), or VT 15 ml/kg (HCl-VILI15, n = 9), or spontaneous breathing (HCl-SB, n = 14). Healthy mice were ventilated with VT 25 ml/kg (VILI25, n = 11). Arterial oxygenation, lung compliance, bronchoalveolar lavage inflammatory cells, albumin, and cytokines concentration were measured. After 7 h, oxygenation and lung compliance resulted lower in HCl-VILI25 than in VILI25 (P < 0.05, 210 ± 54 vs. 479 ± 83 mmHg, and 32 ± 3.5 vs. 45 ± 4.1 µl/cm H2O, mean ± SD, respectively). After right lung injury, the left lung of HCl-VILI25 group received a greater fraction of the VT than the VILI25 group, despite an identical global VT. The number of total and polymorphonuclear cells in bronchoalveolar lavage resulted significantly higher in HCl-VILI25, compared with the other groups, in not only the right lung, but also in the left lung. The albumin content in the left lung resulted higher in HCl-VILI25 than in VILI25 (224 ± 85 vs. 33 ± 6 µg/ml; P < 0.05). Cytokines levels did not differ between groups. Aggressive mechanical ventilation aggravates the preexisting lung injury, which is noxious for the contralateral, not previously injured lung, possibly because of a regional redistribution of VT.

Human Mesenchymal Stem Cells Suppress the Stretch–Induced Inflammatory miR-155 and Cytokines in Bronchial Epithelial Cells

Current research in pulmonary pathology has focused on inflammatory reactions initiated by immunological responses to allergens and irritants. In addition to these biochemical stimuli, physical forces also play an important role in regulating the structure, function, and metabolism of the lung. Hyperstretch of lung tissues can contribute to the inflammatory responses in asthma, but the mechanisms of mechanically induced inflammation in the lung remain unclear. Our results demonstrate that excessive stretch increased the secretion of inflammatory cytokines by human bronchial epithelial cells (hBECs), including IL-8. This increase of IL-8 secretion was due to an elevated microRNA-155 (miR-155) expression, which caused the suppression of Src homology 2 domain–containing inositol 5-phosphatase 1 (SHIP1) production and the subsequent activation of JNK signaling. In vivo studies in our asthmatic mouse model also showed such changes in miR-155, IL-8, and SHIP1 expressions that reflect inflammatory responses. Co-culture with human mesenchymal stem cells (hMSCs) reversed the stretch-induced hBEC inflammatory responses as a result of IL-10 secretion by hMSCs to down-regulate miR-155 expression in hBECs. In summary, we have demonstrated that mechanical stretch modulates the homeostasis of the hBEC secretome involving miR-155 and that hMSCs can be used as a potential therapeutic approach to reverse bronchial epithelial inflammation in asthma.

Impairment of autophagy decreases ventilator-induced lung injury by blockade of the NF-κB pathway

Excessive lung stretch triggers lung inflammation by activation of the NF-κB pathway. This route can be modulated by autophagy, an intracellular proteolytic system. Our objective was to study the impact of the absence of autophagy in a model of ventilator-induced lung injury. Mice lacking Autophagin-1/ATG4B (Atg4b-/-), a critical protease in the autophagic pathway, and their wild-type counterparts were studied in baseline conditions and after mechanical ventilation. Lung injury, markers of autophagy, and activation of the inflammatory response were evaluated after ventilation. Mechanical ventilation increased autophagy and induced lung injury in wild-type mice. Atg4b-/- animals showed a decreased lung injury after ventilation, with less neutrophilic infiltration than their wild-type counterparts. As expected, autophagy was absent in mutant animals, resulting in the accumulation of p62 and ubiquitinated proteins. Activation of the canonical NF-κB pathway was present in ventilated wild-type, but not Atg4b-deficient, animals. Moreover, these mutant mice showed an accumulation of ubiquitinated IκB. High-pressure ventilation partially restored the autophagic response in Atg4b-/- mice and abolished the differences between genotypes. In conclusion, impairment of autophagy results in an ameliorated inflammatory response to mechanical ventilation and decreases lung injury. The accumulation of ubiquitinated IκB may be responsible for this effect.

Mechanical induction of group V phospholipase A2causes lung inflammation and acute lung injury

Ventilation at high tidal volume may cause lung inflammation and barrier dysfunction that culminates in ventilator-induced lung injury (VILI). However, the mechanisms by which mechanical stimulation triggers the inflammatory response have not been fully elucidated. This study tested the hypothesis that onset of VILI is triggered by activation of secretory group V phospholipase A(2) (gVPLA2) in pulmonary vascular endothelium exposed to excessive mechanical stretch. High-magnitude cyclic stretch (18% CS) increased expression and surface exposure of gVPLA2 in human pulmonary endothelial cells (EC). CS-induced gVPLA2 activation was required for activation of ICAM-1 expression and polymorphonuclear neutrophil (PMN) adhesion to CS-preconditioned EC. By contrast, physiological CS (5% CS) had no effect on gVPLA2 activation or EC-PMN adhesion. CS-induced ICAM-1 expression and EC-PMN adhesion were attenuated by the gVPLA2-blocking antibody (MCL-3G1), general inhibitor of soluble PLA2, LY311727, or siRNA-induced EC gVPLA2 knockdown. In vivo, ventilator-induced lung leukocyte recruitment, cell and protein accumulation in the alveolar space, and total lung myeloperoxidase activity were strongly suppressed in gVPLA2 mouse knockout model or upon administration of MCL-3G1. These results demonstrate a novel role for gVPLA2 as the downstream effector of pathological mechanical stretch leading to an inflammatory response associated with VILI.

Spinal neuronal plasticity is evident within 1 day after a painful cervical facet joint injury

Excessive stretch of the cervical facet capsular ligament induces persistent pain and spinal plasticity at later time points. Yet, it is not known when such spinal modifications are initiated following this painful injury. This study investigates the development of hyperalgesia and neuronal hyperexcitability in the spinal cord after a facet joint injury. Behavioral sensitivity was measured in a model of painful C6/C7 facet joint injury in the rat, and neuronal hyperexcitability in the spinal cord was evaluated at 6h and 1 day after injury or a sham procedure, in separate groups. Extracellular recordings of C6/C7 dorsal horn neuronal activity (229 neurons) were used to quantify spontaneous and evoked firing. Rats exhibited no change in sensitivity to mechanical stimulation of the forepaw at 6h, but did exhibit increased sensitivity at 1 day after injury (p=0.012). At 6h, both spontaneous neuronal activity and firing evoked by light brushing, pinch, and von Frey filaments (1.4–26g) applied at the forepaw were not different between sham and injury. At 1 day, spontaneous firing was noted in a greater number of neurons after injury than sham (p<0.04). Evoked firing was also increased 1 day after injury compared to normal and sham (p<0.03). Dorsal horn hyperexcitability and increased spontaneous firing developed between 6 and 24h after painful facet injury, suggesting that the development of hyperalgesia parallels dorsal horn hyperexcitability following mechanical facet joint injury, and these spinal mechanisms are initiated as early as 1 day after injury.

Mechanical Forces Stimulate Endothelial Microparticle Generation via Caspase‐Dependent Apoptosis‐Independent Mechanism

Microparticle release by vascular endothelium has been implicated in various cardiovascular pathologies. Ventilator-induced lung injury (VILI) is a life-threatening complication of mechanical ventilation at high tidal volumes associated with excessive mechanical stretch of pulmonary vascular endothelial cells. However, a role of VILI-relevant levels of cyclic stretch in microparticle generation by vascular endothelium remains unknown. We report microparticle formation by human pulmonary endothelial cells exposed to pathologic, but not physiologic, levels of mechanical stress. Stretch-induced microparticle generation was not affected by cell co-treatment with inflammatory agents thrombin or bacterial wall lipopolysacharide. Neither the basal nor the pathologic cyclic stretch-induced microparticle production was affected by Rho kinase and calpain inhibitors, but were instead abolished by caspase inhibitor. In contrast to lipopolysacharide, pathologic mechanical strain did not significantly induce apoptosis in pulmonary endothelial cells. These results show for the first time that mechanical strain of pulmonary endothelial cells at levels relevant to high tidal volume mechanical ventilation is a potent activator of microparticle formation, which requires caspase activity; however, this mechanism is independent of apoptosis. These results suggest a novel mechanism that may contribute to VILI-associated vascular dysfunction.

Anomalous blow-off behavior of laminar inverted flames of ultra-lean hydrogen–methane–air mixtures

An experimental study of rod-stabilized laminar inverted flames of ultra-lean hydrogen–methane–air mixtures has been performed. For mixtures with high hydrogen content, anomalous stabilization and blow-off behavior has been observed. Flames in those mixtures could be stabilized at equivalence ratios below the lean flammability limit for a zero-stretch planar flame. Stabilization of such flames was possible only when the mixture velocity exceeded some critical value. Flames were blown off when the mixture velocity was reduced below this value. The stand-off distance above the flame holder for those flames decreased and heat transfer from the flame base to the flame holder became more intense when the mixture velocity was increased. This is opposite to the regular behavior of inverted flames. These observed unusual phenomena were attributed to the combination of a strong flame stretch and preferential diffusion effects and to the negative value of the Markstein length in mixtures with high hydrogen content. According to the suggested explanation, increasing the velocity results in an increase of the flame stretch rate at the flame base. This, in turn leads to higher flame temperatures and higher burning velocities, making the survival of the flame below the flammability limits possible. Along with the anomalous blow-off behavior, normal blow-off occurring at increased velocity was observed for mixtures with high hydrogen content at the lowest tested equivalence ratios. The observation of the flame shape evolution showed that, when the normal blow-off limit is approached, a flame narrows slightly above the flame base, forming a “neck”. The flame fronts merge at the “neck” location and flame breaks there, leading to complete flame extinction or leaving a very small flamelet near the flame holder. It is suggested that the flame local extinction in that case occurs as the result of the excessive flame stretch at the flame “neck” which leads to the flame fronts merging and to the incomplete reaction.

Uncommon Cause of Ventricular Tachycardia in a Patient with a Giant Pseudoaneurysm of the Ascending Aorta

Ventricular arrhythmias occur predominantly in patients with structural heart disease. The most common substrate is scarring due to ischemic heart disease. We present an uncommon cause of ventricular tachycardia due to excessive right coronary artery stretch in a patient with a giant pseudoaneurysm of the ascending aorta years after aortic root repair.