Novel Surgical Technique to Prevent Left Ventricular Rupture After Mitral Valve Replacement.

Left ventricular rupture, also called atrioventricular disruption, remains a rare but lethal complication of mitral valve replacement. Available measures for preventing such a complication are limited to preservation of the posterior mitral leaflet and avoidance of overzealous decalcification of the annulus. Moreover, these strategies are not always feasible when annular calcifications prevent proper suture placement or when an abscess involves the mitral annulus. This report describes a surgical technique practiced in our clinic (Department of Cardiothoracic Surgery, University Hospital, Otto-von-Guericke-University, Magdeburg, Germany) that can be used in such high-risk patients to avoid left ventricular rupture.

Factors associated with physician decision making on withholding cardiopulmonary resuscitation in prehospital medicine.

This study seeks to identify factors that are associated with decisions of prehospital physicians to start (continue, if ongoing) or withhold (terminate, if ongoing) CPR in patients with OHCA. We conducted a retrospective study using anonymised data from a prehospital physician response system. Data on patients attended for cardiac arrest between January 1st, 2010 and December 31st, 2018 except babies at birth were included. Logistic regression analysis with start of CPR by physicians as the dependent variable and possible associated factors as independent variables adjusted for anonymised physician identifiers was conducted. 1525 patient data sets were analysed. Obvious signs of death were present in 278 cases; in the remaining 1247, resuscitation was attempted in 920 (74%) and were withheld in 327 (26%). Factors significantly associated with higher likelihood of CPR by physicians (OR 95% CI) were resuscitation efforts by EMS before physician arrival (60.45, 19.89-184.29), first monitored heart rhythm (3.07, 1.21-7.79 for PEA; 29.25, 1.93-442. 51 for VF / pVT compared to asystole); advanced patient age (modelled using cubic splines), physician response time (0.92, 0.87-0.97 per minute) and malignancy (0.22, 0.05-0.92) were significantly associated with lower odds of CPR. We thus conclude that prehospital physicians make decisions to start or withhold resuscitation routinely and base those mostly on situational information and immediately available patient information known to impact outcomes.

Loss of Protease-Activated Receptor 4 Prevents Inflammation Resolution and Predisposes the Heart to Cardiac Rupture After Myocardial Infarction.

BACKGROUND: Cardiac rupture is a major lethal complication of acute myocardial infarction (MI). Despite significant advances in reperfusion strategies, mortality from cardiac rupture remains high. Studies suggest that cardiac rupture can be accelerated by thrombolytic therapy, but the relevance of this risk factor remains controversial. METHODS: We analyzed protease-activated receptor 4 (Par4) expression in mouse hearts with MI and investigated the effects of Par4 deletion on cardiac remodeling and function after MI by echocardiography, quantitative immunohistochemistry, and flow cytometry. RESULTS: Par4 mRNA and protein levels were increased in mouse hearts after MI and in isolated cardiomyocytes in response to hypertrophic and inflammatory stimuli. Par4-deficient mice showed less myocyte apoptosis, reduced infarct size, and improved functional recovery after acute MI relative to wild-type (WT). Conversely, Par4-/- mice showed impaired cardiac function, greater rates of myocardial rupture, and increased mortality after chronic MI relative to WT. Pathological evaluation of hearts from Par4-/- mice demonstrated a greater infarct expansion, increased cardiac hemorrhage, and delayed neutrophil accumulation, which resulted in impaired post-MI healing compared with WT. Par4 deficiency also attenuated neutrophil apoptosis in vitro and after MI in vivo and impaired inflammation resolution in infarcted myocardium. Transfer of Par4-/- neutrophils, but not of Par4-/- platelets, in WT recipient mice delayed inflammation resolution, increased cardiac hemorrhage, and enhanced cardiac dysfunction. In parallel, adoptive transfer of WT neutrophils into Par4-/- mice restored inflammation resolution, reduced cardiac rupture incidence, and improved cardiac function after MI. CONCLUSIONS: These findings reveal essential roles of Par4 in neutrophil apoptosis and inflammation resolution during myocardial healing and point to Par4 inhibition as a potential therapy that should be limited to the acute phases of ischemic insult and avoided for long-term treatment after MI.

Acupuncture-Related Cardiac Complications: A Systematic Review.

BACKGROUND: The objective of this study is to review acupuncture-related cardiac complications, such as infective endocarditis (IE), cardiac tamponade (CT), pericarditis, and cardiac rupture, as there is no known reported literature to determine the burden of cardiac adverse events due to acupuncture. METHODS: Structured computerized databases were searched using the special Medical Subject Heading (MeSH). Manual search using the references of relevant articles was also performed. RESULTS: A total of 133 articles were initially retrieved, but careful reading resulted in only 30 cases of relevant cardiac adverse events. There were 8 articles of infective complications (mostly IE), while 22 articles of CT have been reported to date. The diagnoses were made with echocardiography and patients were treated with intravenous antibiotics. The source of the infection was mostly localized to acupuncture needle prick sites, such as earlobes and legs. Mortality rate for post-acupuncture CT was not significantly higher than infective cardiac complication (Pearson's Chi-square = 0.559; likelihood ratio = 0.553). However, the weighted percentage of death was about 80% in CT vs only 20% mortality for infective cardiac complications. On the other hand, CT was the most common presentation when the needle pricks were close to the heart, and had a clinical presentation of hypotension and venous distention. CONCLUSIONS: Although the universally reported complications of acupuncture are low, and the procedure itself has been deemed low risk in acupuncture-related literature, these cardiac complications are alarming. To avoid these potentially catastrophic consequences, more education needs to be done for adopting safer techniques.

IRAK3 gene silencing prevents cardiac rupture and ventricular remodeling through negative regulation of the NF-κB signaling pathway in a mouse model of acute myocardial infarction.

Cardiac rupture and ventricular remodeling are recognized as the severe complications and major risk factors of acute myocardial infarction (AMI). This study aims to evaluate the regulatory roles of interleukin-1 receptor-associated kinase 3 (IRAK3) and nuclear factor-κB (NF-κB) signaling pathway in cardiac rupture and ventricular remodeling. Microarray analysis was performed to screen AMI-related differentially expressed genes and IRAK3 was identified. The models of AMI were established in male C57BL/6 mice to investigate the functional role of IRAK3. Afterwards, lentivirus recombinant plasmid si-IRAK3 was constructed for IRAK3 silencing. Next, cardiac function parameters were measured in response to IRAK3 silencing. The regulatory effects that IRAK3 had on myocardial infarct size and the content of myocardial interstitial collagen were analyzed. The regulation of IRAK3 silencing on the NF-κB signaling pathway was further assayed. The obtained results indicated that highly expressed IRAK3 and activated NF-κB signaling pathway were observed in myocardial tissues of mouse models of AMI, accompanied by increased expression of matrix metalloproteinase (MMP)-2/9 and tissue inhibitor of metalloproteinase 2 (TIMP-2). Notably, IRAK3 gene silencing inhibited the activation of NF-κB signaling pathway. Furthermore, IRAK3 gene silencing led to the decreased thickness of infarct area and collagen content of myocardial interstitium, alleviated diastolic, and systolic dysfunctions, as well as, facilitated cardiac functions in mice with AMI, corresponding to decreased expression of MMP-2/9 expression and increased expression of TIMP-2. Taken together, silencing of IRAK3 inactivates the NF-κB signaling pathway, and thereby impeding the cardiac rupture and ventricular remodeling, which eventually prevents AMI progression.

Ac-SDKP decreases mortality and cardiac rupture after acute myocardial infarction.

The natural peptide N-Acetyl-Seryl-Aspartyl-Lysyl-Proline (Ac-SDKP) decreases inflammation in chronic diseases such as hypertension and heart failure. However, Ac-SDKP effects on acute inflammatory responses during myocardial infarction (MI) are unknown. During the first 72 hours post-MI, neutrophils, M1 macrophages (pro-inflammatory), and M2 macrophages (pro-resolution) and release of myeloperoxidase (MPO) and matrix metalloproteinases (MMP) are involved in cardiac rupture. We hypothesized that in the acute stage of MI, Ac-SDKP decreases the incidence of cardiac rupture and mortality by preventing immune cell infiltration as well as by decreasing MPO and MMP expression. MI was induced by ligating the left descending coronary artery in C57BL/6 mice. Vehicle or Ac-SDKP (1.6 mg/kg/d) was infused via osmotic minipump. Cardiac immune cell infiltration was assessed by flow cytometry, cardiac MPO and MMP levels were measured at 24-48 hrs post-MI. Cardiac rupture and mortality incidence were determined at 7 days post-MI. In infarcted mice, Ac-SDKP significantly decreased cardiac rupture incidence from 51.0% (26 of 51 animals) to 27.3% (12 of 44) and mortality from 56.9% (29 of 51) to 31.8% (14 of 44). Ac-SDKP reduced M1 macrophages in cardiac tissue after MI, without affecting M2 macrophages and neutrophils. Ac-SDKP decreased MMP-9 activation in infarcted hearts with no changes on MPO expression. Ac-SDKP prevents cardiac rupture and decreases mortality post-acute MI. These protective effects of Ac-SDKP are associated with decreased pro-inflammatory M1 macrophage infiltration and MMP-9 activation.

Autotransplantation for Threatened Cardiac Rupture After Left Ventricular Repair.

A 26-year-old Japanese woman experienced threatened cardiac rupture after mitral valve replacement and debridement of a left ventricular (LV) posterior wall abscess caused by infectious endocarditis. We performed cardiac autotransplantation using the bicaval technique to allow bench repair of the recurrent abscess. A balloon catheter was inflated in the inferior vena cava to obtain a bloodless anastomotic field. This is the first report of autotransplantation for threatened LV rupture after posterior wall repair.

Bone marrow transplantation modulates tissue macrophage phenotype and enhances cardiac recovery after subsequent acute myocardial infarction.

BACKGROUND: Bone marrow transplantation (BMT) is commonly used in experimental studies to investigate the contribution of BM-derived circulating cells to different disease processes. During studies investigating the cardiac response to acute myocardial infarction (MI) induced by permanent coronary ligation in mice that had previously undergone BMT, we found that BMT itself affects the remodelling response. METHODS AND RESULTS: Compared to matched naive mice, animals that had previously undergone BMT developed significantly less post-MI adverse remodelling, infarct thinning and contractile dysfunction as assessed by serial magnetic resonance imaging. Cardiac rupture in male mice was prevented. Histological analysis showed that the infarcts of mice that had undergone BMT had a significantly higher number of inflammatory cells, surviving cardiomyocytes and neovessels than control mice, as well as evidence of significant haemosiderin deposition. Flow cytometric and histological analyses demonstrated a higher number of alternatively activated (M2) macrophages in myocardium of the BMT group compared to control animals even before MI, and this increased further in the infarcts of the BMT mice after MI. CONCLUSIONS: The process of BMT itself substantially alters tissue macrophage phenotype and the subsequent response to acute MI. An increase in alternatively activated macrophages in this setting appears to enhance cardiac recovery after MI.

Asymptomatic Regional Thinning of Left Ventricle After Mitral Valve Replacement.

We report the successful repair of a rare case of regional thinning of the left ventricle after mitral valve replacement. An 80-year-old woman underwent prosthetic mitral valve replacement for mitral valve stenosis. Her postoperative course was uneventful; however, regional thinning of the left ventricular wall was detected on transthoracic echocardiography on postoperative day 7. We repaired the thinned area with a patch by using the felt sandwich technique. Postoperative echocardiography and computed tomography showed a successfully repaired left ventricular wall.

[Left Ventricular Rupture following Mitral Valve Replacement].

Left ventricular rupture is a rare but lethal complication after mitral valve replacement (MVR). Between 1989 and 2014, of 850 patients who underwent MVR, 6 developed left ventricular rupture in Saitama Medical Center, Jichi Medical University. Treasure type I rupture occurred in 5 patients and Miller type III in 1. Four cases developed ventricular rupture right after declamping of the ascending aorta, and the remaining 2 after the transfer to the intensive care unit( ICU). Prompt surgical therapy was achieved for the instant closure of the muscular wall defect under the cardiopulmonary bypass and cardiac arrest, however, leading to the disappointing result of 66.7% of hospital death. It is the most important to relieving the stress of the posterior wall of the left ventricle during mitral surgery by using the modification techniques with the preservation of posterior mitral leaflet and avoiding pre and afterload of the left ventricle right after the MVR.

Attenuation of ER stress prevents post-infarction-induced cardiac rupture and remodeling by modulating both cardiac apoptosis and fibrosis.

Endoplasmic reticulum (ER) stress is implicated in the pathophysiology of various cardiovascular diseases, but the role of ER stress in cardiac rupture and/or remodeling after myocardial infarction (MI) is still unclear. Here we investigated whether ER stress plays a major role for these processes in mice. We ligated the left coronary artery (LCA) without reperfusion in mice and administered either NaCl or 4-phenylbutyric acid (4-PBA, 20 mg/kg/d) intraperitoneally for 4 weeks. Cardiac rupture rates during the first week of MI were 37.5% and 18.2% in the control and 4-PBA groups, respectively. The extent of ventricular aneurysm and fibrosis was less, and the cardiac function better, in the 4-PBA group compared with the control group. The protein levels of ER stress markers in the heart tissues of the control group remained elevated during the entire 4-week period after MI, while pro-apoptotic proteins mainly increased in the early phase, and the pro-fibrotic proteins markedly increased in the late phase post MI; 4-PBA decreased all of these protein levels. In the primary cultured neonatal rat cardiomyocytes or fibroblasts, hypoxia (3% O2) increased the number of apoptotic cardiomyocytes and promoted the proliferation and migration of fibroblasts, all of which were attenuated by 4-PBA (0.5 mM). These findings indicate that MI induces ER stress and provokes cardiac apoptosis and fibrosis, culminating in cardiac rupture and remodeling, and that the attenuation of ER stress could be an effective therapeutic target to prevent post-MI complications.

C-reactive protein and leucocyte counts drop faster using the HeartShield® device in patients with DSWI.

Right ventricular heart rupture is a devastating complication associated with negative pressure wound therapy (NPWT) in cardiac surgery. The use of a rigid barrier disc (HeartShield™) has been suggested to offer protection against this lethal complication by preventing the heart from being drawn up by the negative pressure and damaged by the sharp sternum bone edges. Seven patients treated with conventional NPWT and seven patients treated with NPWT with a protective barrier disc (HeartShield) were compared with regard to bacterial clearance and infection parameters including C-reactive protein levels and leucocyte counts. C-reactive protein levels and leucocyte counts dropped faster and bacterial clearance occurred earlier in the HeartShield® group compared with the conventional NPWT group. Negative biopsy cultures were shown after 3·1 ± 0·4 NPWT dressing changes in the HeartShield group, and after 5·4 ± 0·6 NPWT dressing changes in the conventional NPWT group (P < 0·001). All patients were followed up with clinical check-up after 3 months. None of the patients in the HeartShield group had any signs of reinfection such as deep sternal wound infection (DSWI) or sternal fistulas, whereas in the conventional NPWT group, two patients had signs of sternal fistulas that demanded hospitalisation. HeartShield hinders the right ventricle to come into contact with the sharp sternal edges during NPWT and thereby protects from heart damage. This study shows that using HeartShield is beneficial in treating patients with DSWI. Improved wound healing by HeartShield may be a result of the efficient drainage of wound effluents from the thoracic cavity.

Optimal contact forces to minimize cardiac perforations before, during, and/or after radiofrequency or cryothermal ablations.

BACKGROUND: Catheter perforations remain a major clinical concern during ablation procedures for treatment of atrial arrhythmias and may lead to life-threatening cardiac tamponade. Radiofrequency (RF) ablation alters the biomechanical properties of cardiac tissue, ultimately allowing for perforation to occur more readily. Studies on the effects of cryoablation on perforation force as well as studies defining the perforation force of human tissue are limited. OBJECTIVE: The purpose of this study was to investigate the required force to elicit perforation of cardiac atrial tissue after or during ablation procedures. METHODS: Effects of RF or cryothermal ablations on catheter perforation forces for both swine (n = 83 animals, 530 treatments) and human (n = 8 specimens, 136 treatments) cardiac tissue were investigated. RESULTS: Overall average forces resulting in perforation of healthy unablated tissue were 406g ± 170g for swine and 591g ± 240g for humans. Post-RF ablation applications considerably reduced these forces to 246g ± 118g for swine and 362 ± 185g for humans (P <.001). Treatments with cryoablation did not significantly alter forces required to induce perforations. Decreasing catheter sizes resulted in a reduction in forces required to perforate the atrial wall (P <.001). Catheter perforations occurred over an array of contact forces with a minimum of 38g being observed. CONCLUSION: The swine model likely underestimates the required perforation forces relative to those of human tissues. We provide novel insights related to the comparative effects of RF and cryothermal ablations on the potential for inducing undesired punctures, with RF ablation reducing perforation force significantly. These data are insightful for physicians performing ablation procedures as well as for medical device designers.

Olmesartan prevents cardiac rupture in mice with myocardial infarction by modulating growth differentiation factor 15 and p53.

BACKGROUND AND PURPOSE: Cardiac rupture is a catastrophic complication that occurs after acute myocardial infarction (MI) and, at present, there are no effective pharmacological strategies for preventing this condition. Here we investigated the effect of the angiotensin II receptor blocker olmesartan (Olm) on post-infarct cardiac rupture and its underlying mechanisms of action. EXPERIMENTAL APPROACH: C57Bl/6 mice with MI were treated with Olm, aldosterone (Aldo) or vehicle. Cultured neonatal cardiomyocytes and fibroblasts were exposed to normoxia or anoxia and treated with angiotensin II (Ang II), RNH6270 (active ingredient of Olm) or Aldo. KEY RESULTS: The mortality rate and incidence of cardiac rupture in MI mice during the first week in the Olm-treated group were significantly lower than in the vehicle-treated group. Olm or RNH6270 reduced myeloperoxidase staining in the infarcted myocardium, decreased apoptosis in cultured cardiomyocytes and fibroblasts, as assessed by Hoechst staining and TUNEL assay, attenuated the accumulation of p53 and phosphorylated p53 and cleaved caspase 3 induced by MI or Ang II, as assessed by Western blotting, and up-regulated growth differentiation factor-15 (GDF-15). In cultured cardiomyocytes and fibroblasts, treatment with Ang II, Aldo or anoxia significantly down-regulated the expression of GDF-15. CONCLUSIONS AND IMPLICATIONS: Olm prevents cardiac rupture through inhibition of apoptosis and inflammation, which is attributable to the down-regulation of p53 activity and up-regulation of GDF-15. Our findings suggest that early administration of an AT1 receptor anatagonist to patients with acute MI is a potential preventive approach for cardiac rupture.

Innovations and novel technologies in TAVI. Second generation transcatheter heart valves.

Transcatheter aortic valve implantation (TAVI) is the new standard-of-care for inoperable patients with superior outcome compared to conservative management including balloon valvuloplasty. In high-risk patients, TAVI has shown non-inferiority compared with surgical aortic valve replacement. Although data from national multi-centre registries are very encouraging and use of TAVI in intermediate risk patients has been discussed, it is of note that the commercially available and currently used transcatheter heart valves (THV) have not yet been assessed by randomized clinical trials in those patients. New technology advances promise to simplify TAVI and to improve outcome by reducing the rate of TAVI-specific issues such as paravalvular aortic regurgitation (PAR), annular rupture, and conduction disturbances. A reduction in the incidence and severity of PAR represents an obvious target for technical improvements in the design of upcoming "next generation" THVs and of implantation techniques including repositioning/recapturing features, paravalvular sealing techniques, and precise peri-interventional imaging modalities.

Cardiac rupture in takotsubo cardiomyopathy: a systematic review.

BACKGROUND: Takotsubo cardiomyopathy (TSC) and its complications, such as cardiac rupture (CR), are increasingly being reported in the literature. CR is associated with rapid clinical decline and is uniformly fatal if not surgically repaired. To identify patients who developed CR we performed an analysis of all available indexed cases in the literature and compared them with a control group of patients with TSC without rupture. HYPOTHESIS: Takotsubo cardiomyopathy patients with cardiac rupture do not differ significantly from those without rupture. METHODS: MEDLINE (2009) was searched for all TSC case reports with CR. Eleven case reports were identified. Using a random sampling method, we selected 12 case reports of TSC without rupture (control). We included our patient with TSC with rupture as the 12th case of TSC cohort with CR (CR group). Demographic and clinical characteristics were compared between CR group and control. RESULTS: All patients in the TSC group with rupture were female and were significantly older than controls. TSC group with rupture had significantly higher frequency of ST elevation in lead II and absence of T-wave inversion in lead V5 on hospital admission than controls. Mean ejection fraction, systolic blood pressure, and double product, a measure of oxygen demand, was significantly higher in the rupture group compared to controls. The CR group was associated with less frequent use of ß-blocker as compared to controls. CONCLUSIONS: CR as a complication of TSC could be more common than recognized. Higher double product and ejection fraction suggest higher fluctuation of intracardiac pressure and may cause CR in TSC. Use of ß blockers in TSC may provide protection against CR.

Effects on drainage of the mediastinum and pleura during negative pressure wound therapy when using a rigid barrier to prevent heart rupture.

Right ventricular heart rupture is a devastating complication associated with negative pressure wound therapy (NPWT) following cardiac surgery. The use of a rigid disc has been suggested to offer protection against this lethal complication by preventing the heart from being drawn up towards, and damaged by, the sharp sternum edges. The aim of the present study was to compare the wound fluid evacuation from the pericardium and the left pleura when using NPWT with such a disc between the sternal edges and the heart, and when using conventional NPWT. Six pigs underwent median sternotomy followed by NPWT at -120 mmHg, using foam, with or without a rigid plastic disc between the heart and the sternal edges. A 250 ml saline was infused into the pericardium, and the time required for fluid evacuation was measured. A 500 ml saline was infused into the left pleura and the time for fluid evacuation measured. The pericardium was effectively drained of 250 ml fluid in both cases [conventional NPWT: 24 ± 0·7 seconds, NPWT with the disc: 25 ± 1·1 seconds (n.s.)]. The left pleura was effectively drained when using NPWT with the disc, but was not drained at all when using conventional NPWT. The left pleura could be effectively drained of 500 ml fluid when a rigid perforated plastic disc was inserted between the sternal edges and the heart during NPWT. Significantly less drainage of the left pleura was possible when using conventional NPWT without the disc. The pericardium was equally good drained using NPWT with or without the disc.

Haemodynamic effects of negative pressure wound therapy when using a rigid barrier to prevent heart rupture.

Right ventricular heart rupture is a devastating complication associated with negative pressure wound therapy (NPWT) in cardiac surgery. The use of a rigid barrier has been suggested to offer protection against this lethal complication by preventing the heart from being drawn up and damaged by the sharp sternum bone edges. The aim of this study was to investigate the haemodynamic effects of placing a rigid barrier over the heart to protect it from rupture during NPWT. Eight pigs underwent median sternotomy followed by NPWT at --70 and --120 mmHg, using foam, with or without a rigid plastic disc between the heart and the sternal edges. The heart frequency, cardiac output, mean systemic arterial pressure, mean pulmonary artery pressure, central venous pressure and left atrial pressure were recorded. Cardiac output was not affected by NPWT, regardless of whether a rigid barrier was used. Heart frequency decreased during NPWT without a disc, and showed a tendency towards a decrease when using a rigid disc. The blood pressure decreased during NPWT without a disc, and showed only a tendency towards a decrease when a disc was inserted between the heart and the sternum. In conclusion, the results of this haemodynamic study show that a rigid disc can safely be placed over the heart during NPWT, to prevent heart rupture. The haemodynamic effects of NPWT in sternotomy wounds are slightly reduced by the presence of the rigid disc.

Sternum wound contraction and distension during negative pressure wound therapy when using a rigid disc to prevent heart and lung rupture.

BACKGROUND: There are increasing reports of deaths and serious complications associated with the use of negative pressure wound therapy (NPWT), of which right ventricular heart rupture is the most devastating. The use of a rigid barrier has been suggested to offer protection against this lethal complication by preventing the heart from being drawn up against the sharp edges of the sternum. The aim of the present study was to determine whether a rigid barrier can be safely inserted over the heart with regard to the sternum wound edge movement. METHODS: Sternotomy wounds were created in eight pigs. The wounds were treated with NPWT at -40, -70, -120 and -170 mmHg in the presence and absence of a rigid barrier between the heart and the edges of the sternum. Wound contraction upon NPWT application, and wound distension under mechanical traction to draw apart the edges of the sternotomy were evaluated. RESULTS: Wound contraction resulting from NPWT was similar with and without the rigid barrier. When mechanical traction was applied to a NPWT treated sternum wound, the sternal edges were pulled apart. Wound distension upon traction was similar in the presence and absence of a the rigid barrier during NPWT. CONCLUSIONS: A rigid barrier can safely be inserted between the heart and the edges of the sternum to protect the heart and lungs from rupture during NPWT. The sternum wound edge is stabilized equally well with as without the rigid barrier during NPWT.