Contraction Band Research Articles

Cardiomyopathies and Adrenal Diseases.

Cardiomyopathies are myocardial disorders in which heart muscle is structurally and/or functionally abnormal. Previously, structural cardiomyocyte disorders due to adrenal diseases, such as hyperaldosteronism, hypercortisolism, and hypercatecholaminism, were misunderstood, and endomyocardial biopsy (EMB) was not performed because was considered dangerous and too invasive. Recent data confirm that, if performed in experienced centers, EMB is a safe technique and gives precious information about physiopathological processes implied in clinical abnormalities in patients with different systemic disturbances. In this review, we illustrate the most important features in patients affected by primary aldosteronism (PA), Cushing’s syndrome (CS), and pheochromocytoma (PHEO). Then, we critically describe microscopic and ultrastructural aspects that have emerged from the newest EMB studies. In PA, the autonomous hypersecretion of aldosterone induces the alteration of ion and water homeostasis, intracellular vacuolization, and swelling; interstitial oedema could be a peculiar feature of myocardial toxicity. In CS, cardiomyocyte hypertrophy and myofibrillolysis could be related to higher expression of atrogin-1. Finally, in PHEO, the hypercontraction of myofilaments with the formation of contraction bands and occasional cellular necrosis has been observed. We expect to clear the role of EMB in patients with cardiomyopathies and adrenal disease, and we believe EMB is a valid tool to implement new management and therapies.

MiR-29a is a potential protective factor for fibrogenesis in gluteal muscle contracture.

Circulating miRNAs have been proposed as the effective diagnostic biomarkers for muscular fibrosis-associated diseases. However, circulating biomarkers for early diagnosis of contracture muscles are limited in gluteal muscle contracture (GMC) patients. Here we sought to explore the abnormally expressed miRNAs in plasma and contraction bands of GMC patients. The results showed miR-29a-3p expression in plasma and contraction bands tissue was significantly reduced in GMC patients compared with normal control. Cell viability and levels of proliferation-associated protein cyclin D1 and cyclin-dependent-kinase 2 (CDK2) were powerfully inhibited by miR-29a mimics and enhanced by miR-29a inhibitor compared with negative control. Furthermore, miR-29a mimics effectively impeded, while miR-29a inhibitor enhanced the expression of collagen I and collagen III, followed by the secretion of transforming growth factor beta1 (TGF-beta1), TGF-beta3 and connective tissue growth factor (CTGF) in primary human contraction bands (CB) fibroblasts. The miR-29a-3p negatively regulated the expression of TGF-beta1 through binding to the 3´ UTR region of SERPINH1 (encoding heat shock protein HSP47), but had no effect on Smad2 activity. The miR-29a-3p was inversely correlated with HSP47 in contraction bands tissue from GMC patients. Collectively, miR-29a was notably depressed and regulated cell viability and fibrosis by directly targeting HSP47 in GMC, which suggest that circulating miR-29a might be a potential biomarker for early diagnosis and provides a novel therapeutic target for GMC.

Porcelain Heart: A Case of Diffuse Myocardial Calcification.

The pathophysiology of myocardial calcifications is variable and may have potentially fatal consequences if undiagnosed and untreated.

Comparison of in vivo pathogenicity of four Candida auris clades in a neutropenic bloodstream infection murine model

ABSTRACT Candida auris is an emerging worldwide concern, but comparative data about the virulence of different C. auris lineages in mammalian hosts is lacking. Different isolates of the four prevalent C. auris clades (South Asian n = 5, East Asian n = 4, South African n = 5, and South American n = 5) were compared to assess their virulence in a neutropenic murine bloodstream infection model with C. albicans as reference. C. auris, regardless of clade, proved to be less virulent than C. albicans. Highest overall mortality at day 21 was observed for the South American clade (96%), followed by the South Asian (80%), South African (45%) and East Asian (44%) clades. Fungal burden results showed close correlation with lethality. Histopathological examination revealed large aggregates of blastoconidia and budding yeast cells in the hearts, kidneys and livers but not in the spleens. The myocardium of apparently healthy sacrificed mice as well as of mice found moribund showed contraction band necrosis in case of all lineages. Regardless of clade, the heart and kidneys were the most heavily affected organs. Isolates of the same clade showed differences in virulence in mice, but a markedly higher virulence of the South American clade was clearly demonstrated.

A myogenic motor pattern in mice lacking myenteric interstitial cells of Cajal explained by a second coupled oscillator network.

The interstitial cells of Cajal associated with the myenteric plexus (ICC-MP) are a network of coupled oscillators in the small intestine that generate rhythmic electrical phase waves leading to corresponding waves of contraction, yet rhythmic action potentials and intercellular calcium waves have been recorded from c-kit-mutant mice that lack the ICC-MP, suggesting that there may be a second pacemaker network. The gap junction blocker carbenoxolone induced a "pinstripe" motor pattern consisting of rhythmic "stripes" of contraction that appeared simultaneously across the intestine with a period of ~4 s. The infinite velocity of these stripes suggested they were generated by a coupled oscillator network, which we call X. In c-kit mutants rhythmic contraction waves with the period of X traveled the length of the intestine, before the induction of the pinstripe pattern by carbenoxolone. Thus X is not the ICC-MP and appears to operate under physiological conditions, a fact that could explain the viability of these mice. Individual stripes consisted of a complex pattern of bands of contraction and distension, and between stripes there could be slide waves and v waves of contraction. We hypothesized that these phenomena result from an interaction between X and the circular muscle that acts as a damped oscillator. A mathematical model of two chains of coupled Fitzhugh-Nagumo systems, representing X and circular muscle, supported this hypothesis. The presence of a second coupled oscillator network in the small intestine underlines the complexity of motor pattern generation in the gut.NEW & NOTEWORTHY Physiological experiments and a mathematical model indicate a coupled oscillator network in the small intestine in addition to the c-kit-expressing myenteric interstitial cells of Cajal. This network interacts with the circular muscle, which itself acts as a system of damped oscillators, to generate physiological contraction waves in c-kit (W) mutant mice.

Sudden death in a case of recurrent Takotsubo syndrome.

Herein we report an unusual case of sudden death occurring in a 65 year old woman during a minor oral surgery. The subject, who had a medically treated anxiety, had a history of two reversible left ventricle dysfunction episodes consistent with recurrent Takotsubo Syndrome that had occurred seven and six years before, respectively. She also suffered from moderate, well treated post-menopausal systemic hypertension. Post-mortem examination showed apical biventricular ballooning of the heart with no cardiac rupture, coronary artery lesion or other cardiac/extra-cardiac disease. Toxicological tests and forensic investigations excluded unnatural causes of death, including pharmacological or iatrogenic causes related to medical malpractice. Only non-specific contraction bands and mild hypertrophy were observed by histology in the left ventricle myocytes. Takotsubo syndrome is usually an acute and reversible heart failure syndrome with acute left ventricle apex ballooning, no coronary artery disease or other macroscopic or microscopic cardiac changes; physical or emotional stress are well known triggering factors. Nevertheless, recurrent forms, major cardiac adverse events and even sudden death may occur in a minority of cases, meaning that a diagnosis of Takotsubo syndrome must be considered in cases of sudden death and in forensic investigations.

CaMKII mediates myocardial ischemia/reperfusion injury‑induced contracture in isolated rat heart.

Contracture or diastolic dysfunction is a primary cause of injury following ischemia/reperfusion (IR). The present study examined whether Ca2+/calmodulin‑dependent kinaseII (CaMKII) is involved in contracture. Isolated rat hearts were subjected to either global IR or Ca2+ paradox(CaP), which is characterized by contracture. Left ventricular end‑diastolic pressure, electron microscopy and troponinI TnI) in coronary effluent were examined to indicate the extent of contracture. Compared with control hearts, both the IR and CaPgroups exhibited an increase in necrosis and apoptosis, and a marked depression in contractile function. Western blot analysis showed that IR stimulated the phosphorylation (Thr287) and oxidation (Met281/282) of CaMKII, and the phosphorylation of phospholamban (PLN), a substrate of CaMKII. By contrast, only the phosphorylation of CaMKII was increased in the CaPgroup. Treatment with either 3µM KN‑62, an inhibitor of CaMKII, or 5µM KB‑R7943, an inhibitor of the Na+/Ca2+ exchanger, mitigated the damage and the post‑translational modification of both CaMKII and PLN. Similar to the effect of the negative inotropic agent 2,3‑butanedione‑monoxime, the increased cell survival after treatment with KN‑62 was associated with improved diastolic function. Examination using electron microscopy and a biochemical test showed the development of contraction bands, disruption of the sarcolemmal membrane and an increase in the release of TnI in both IR and CaP hearts; these results indicated the occurrence of contracture. Furthermore, these changes were inhibited by either KN‑62 or KB‑R7943. Taken together, these data provided evidence that CaMKII mediates reperfusion‑elicited contracture, and that the activation of CaMKII via phosphorylation is involved in this process.

Unfolding the Restrained Encountered in Hyperspectral Images

The content of the natural scenes needs to be interpreted which is the primary concern in computer vision. In the advancement of the systems focusing on the intelligent image understanding, the most powerful key is the degree to which meaningful information is extracted by the computer. Moreover with this advancement in the field of image processing, precise and huge information capturing images are desired. The hyperspectral images find its place in such fields of applications. For a single scene, the hyperspectral images (HSI) are composed of hundreds of channels of spectral data. For different materials, with the availability of detailed spectral information, hundreds of contracted bands are collected by hyperspectral sensors. However, with the dimensional complexity, its impact varies from field to field. We reiterate our main focus in this article on providing the various challenges existing relating to HSI and a case study of the current solutions provided for each. A clear depiction of the current issues and approaches in the field of compression as well as some general issues are also discussed towards the end section.

Histopathological Characterization ofRadiofrequency Ablation in VentricularScar Tissue.

This study sought to characterize the histopathological features of radiofrequency ablation (RFA) in heterogeneous ventricular scar in comparison to those in healthy myocardium. The histopathological features of RFA have been studied largely in normal myocardium. However, itseffect on clinically relevant heterogeneous scar is not well understood. Five swine with chronic infarction underwent RFA using 35-W, 45-s, 10-20g (Biosense Webster, Irwindale, California) in heterogenous scar tissue (voltage≤1.5mV) and healthy myocardium (≥3.0mV). The location of each application was marked using the electroanatomical mapping system. Histological sections at intervals of 0.5mm with hematoxylin and eosin and Masson's trichrome stained intervals were created. A pathologist blinded to the myocardium type characterized the extent of RF injury in cellular, extracellular, and vascular structures. In healthy myocardium, 23 of 23 lesions (100%) were well demarcated and could be precisely measured (width: 11.3 ± 3.3mm; depth: 7.3 ± 2.0mm). In scar tissue, only 3 of 30 lesions (10%) were identified, and none could be measured due to a lack of defined borders. Lesions in healthy myocardium had a distinctive architecture showing a coagulative necrosis core surrounded by an outer rim of contraction band necrosis. Lesions in scar had ill-defined tissue injury without a distinct architecture. In all ablated regions, viable myocytes remained interspersed between necrotic myocytes exhibiting characteristics of both coagulative and contraction band necrosis. Connective tissue was more resistant to thermal injury in comparison to cardiomyocytes. RFA in scarred myocardium results in irregular tissue injury and unpredictable effect on survivingcardiomyocytes. This may be related to biophysical differences between healthy and scarred myocardium.

Septic myocardial calcification: A case report

The histological findings in the heart in cases of fatal sepsis can show myocytolysis, interstitial fibrosis, necrotic contraction band, mononuclear infiltrates, and interstitial edema, which can be used in post mortem diagnosis of sepsis. Septic myocardial calcification is a very rare condition, and only a few cases have been reported in the literature. In general, the pathogenesis of the myocardial calcification has not been well clarified, but two pathogenic mechanisms have been universally recognized: metastatic or dystrophic. We present a rare case of sepsis-related myocardial calcification.Here we report a case involving a 72-year-old white male who was admitted to a hospital for a polytrauma caused by a motorbike accident. On the 110th day of hospitalization, the patient was diagnosed with a septic process and a subsequent transesophageal echocardiogram revealed the presence of a calcification on the right atrial wall. According to the medical history of the patient there were no systemic factors predisposing to calcium crystals deposition in tissues. Patient died due to multi-organ failure in the course of multimicrobial septic shock during the 149th day. The autopsy revealed both the presence of a greenish-brown formation and a greater consistency of the right atrial wall. The histological investigation of the right atrium wall showed a wide calcification area localized at subendocardial level, which contained fibrin deposition and was surrounded by fibrotic tissue.

Prevalence, determinants, and correlates of coagulation necrosis and contraction band necrosis in donor hearts.

Exploration of pathologic changes in donor hearts and finding the association of pathologic findings with potentially reversible cardiac condition may result in allowing such hearts to recover and be used for transplantation. We enrolled consecutive donors from one federally designated Organ Procurement Organization for one calendar year. Hearts rejected for transplantation underwent pathological examination. We studied the association of pathologic findings with the mechanism of death. A total of 81 hearts were rejected for transplantation. The most common pathologic findings were coagulation necrosis (CN) in 17.3% and contraction band necrosis (CBN) in 34.6%. Anoxic brain injury was present in 78.6% of the donors who had CN, and only in 29.9% of those without CN (P=0.002). CBN was more commonly associated with subarachnoid hemorrhage (17.9% vs 1.9% of donors with and without CBN, P=0.017). Only hearts with CBN had significantly lower LVEF (P=0.017). Coagulation necrosis and CBN are the most common pathologic findings in the hearts rejected for transplantation. While CN is more prevalent in anoxic brain injury, CBN is more often present in subarachnoid hemorrhage. This may be clinically important because CBN is a pathologic hallmark of catecholamine-induced cardiomyopathy which is potentially reversible.

Bromine inhalation mimics ischemia-reperfusion cardiomyocyte injury and calpain activation in rats.

Halogens are widely used, highly toxic chemicals that pose a potential threat to humans because of their abundance. Halogens such as bromine (Br2) cause severe pulmonary and systemic injuries; however, the mechanisms of their toxicity are largely unknown. Here, we demonstrated that Br2 and reactive brominated species produced in the lung and released in blood reach the heart and cause acute cardiac ultrastructural damage and dysfunction in rats. Br2-induced cardiac damage was demonstrated by acute (3-24 h) increases in circulating troponin I, heart-type fatty acid-binding protein, and NH2-terminal pro-brain natriuretic peptide. Transmission electron microscopy demonstrated acute (3-24 h) cardiac contraction band necrosis, disruption of z-disks, and mitochondrial swelling and disorganization. Echocardiography and hemodynamic analysis revealed left ventricular (LV) systolic and diastolic dysfunction at 7 days. Plasma and LV tissue had increased levels of brominated fatty acids. 2-Bromohexadecanal (Br-HDA) injected into the LV cavity of a normal rat caused acute LV enlargement with extensive disruption of the sarcomeric architecture and mitochondrial damage. There was extensive infiltration of neutrophils and increased myeloperoxidase levels in the hearts of Br2- or Br2 reactant-exposed rats. Increased bromination of sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA) and increased phosphalamban after Br2 inhalation decreased cardiac SERCA activity by 70%. SERCA inactivation was accompanied by increased Ca2+-sensitive LV calpain activity. The calpain-specific inhibitor MDL28170 administered within 1 h after exposure significantly decreased calpain activity and acute mortality. Bromine inhalation and formation of reactive brominated species caused acute cardiac injury and myocardial damage that can lead to heart failure. NEW & NOTEWORTHY The present study defines left ventricular systolic and diastolic dysfunction due to cardiac injury after bromine (Br2) inhalation. A calpain-dependent mechanism was identified as a potential mediator of cardiac ultrastructure damage. This study not only highlights the importance of monitoring acute cardiac symptoms in victims of Br2 exposure but also defines calpains as a potential target to treat Br2-induced toxicity.

Functional recovery after dantrolene-supplementation of cold stored hearts using an ex vivo isolated working rat heart model.

The ryanodine receptor antagonist dantrolene inhibits calcium release from the sarcoplasmic reticulum and reduces cardiac ischaemia-reperfusion injury (IRI) in global warm ischaemia models however the cardioprotective potential of dantrolene under hypothermic conditions is unknown. This study addresses whether the addition of dantrolene during cardioplegia and hypothermic storage of the donor heart can improve functional recovery and reduce IRI. Using an ex vivo isolated working heart model, Wistar rat (3 month and 12 month) hearts were perfused to acquire baseline haemodynamic measurements of aortic flow, coronary flow, cardiac output, pulse pressure and heart rate. Hearts were arrested and stored in Celsior preservation solution supplemented with 0.2–40 μM dantrolene for 6 hours at 4°C, then reperfused (15 min Langendorff, 30 min working mode). In 3-month hearts, supplementation with 1 μM dantrolene significantly improved aortic flow and cardiac output compared to unsupplemented controls however lactate dehydrogenase (LDH) release and contraction bands were comparable. In contrast, 40 μM dantrolene-supplementation yielded poor cardiac recovery, increased post-reperfusion LDH but reduced contraction bands. All 3-month hearts stored in dantrolene displayed significantly reduced cleaved-caspase 3 intensities compared to controls. Analysis of cardioprotective signalling pathways showed no changes in AMPKα however dantrolene increased STAT3 and ERK1/2 signaling in a manner unrelated to functional recovery and AKT activity was reduced in 1 μM dantrolene-stored hearts. In contrast to 3-month hearts, no significant improvements were observed in the functional recovery of 12-month hearts following prolonged storage in 1 μM dantrolene. Conclusions: Dantrolene supplementation at 1 μM during hypothermic heart preservation improved functional recovery of young, but not older (12 month) hearts. Although the molecular mechanisms responsible for dantrolene-mediated cardioprotection are unclear, our studies show no correlation between improved functional recovery and SAFE and RISK pathway activation.

Mitochondrial transplantation prolongs cold ischemia time in murine heart transplantation.

Cold ischemia time (CIT) causes ischemia‒reperfusion injury to the mitochondria and detrimentally effects myocardial function and tissue viability. Mitochondrial transplantation replaces damaged mitochondria and enhances myocardial function and tissue viability. Herein we investigated the efficacy of mitochondrial transplantation in enhancing graft function and viability after prolonged CIT. Heterotopic heart transplantation was performed in C57BL/6J mice. Upon heart harvesting from C57BL/6J donors, 0.5 ml of either mitochondria (1 × 108 in respiration buffer; mitochondria group) or respiration buffer (vehicle group) was delivered antegrade to the coronary arteries via injection to the coronary ostium. The hearts were excised and preserved for 29 ± 0.3 hours in cold saline (4°C). The hearts were then heterotopically transplanted. A second injection of either mitochondria (1 × 108) or respiration buffer (vehicle) was delivered antegrade to the coronary arteries 5 minutes after transplantation. Grafts were analyzed for 24 hours. Beating score, graft function, and tissue injury were measured. Beating score, calculated ejection fraction, and shortening fraction were significantly enhanced (p < 0.05), whereas necrosis and neutrophil infiltration were significantly decreased (p < 0.05) in the mitochondria group as compared with the vehicle group at 24 hours of reperfusion. Transmission electron microscopy showed the presence of contraction bands in vehicle but not in mitochondria grafts. Mitochondrial transplantation prolongs CIT to 29 hours in the murine heart transplantation model, significantly enhances graft function, and decreases graft tissue injury. Mitochondrial transplantation may provide a means to reduce graft failure and improve transplantation outcomes after prolonged CIT.

Histologic Changes In Recreational Drug Misuse.

Use of recreational drugs is associated with a number of histologic changes. These may be related to the method of administration or due to systemic effects of the drugs. This paper reviews the histopathological features seen following recreational drug use. With injection, there may be local effects from abscess formation and systemic effects may result in amyloidosis. Injections have been associated with necrotizing fasciitis, anthrax, and clostridial infections. Systemic effects include infective endocarditis, with the risk of embolization, and abscesses may be seen in organs in the absence of infective endocarditis. Viral complications of injection include hepatitis and human immunodeficiency virus (HIV) infection. Injecting crushed tablets can result in intravascular granulomata in the lungs. Smoking drugs is associated with intraalveolar changes, including blackand brown-pigmented macrophages in crack cocaine and cannabis smoking, respectively. Snorting may result in intraalveolar granulomata forming when crush tablets are used and there may be systemic granulomata. Stimulants are associated with cardiovascular and cerebrovascular pathology, including contraction band necrosis and myocardial fibrosis, as well as coronary artery dissection. Stimulants may cause hyperpyrexia and rhabdomyolysis, which may be associated with changes in multiple organs including myoglobin casts in the kidney. Opioids cause respiratory depression and this can be associated with inhalational pneumonia and hypoxia in other organs if there is resuscitation and a period of survival. Ketamine use has been associated with changes in the urothelium and the liver. This paper reviews histology changes that may be seen in drug-related deaths using illustrative cases.

The Case for Takotsubo Cardiomyopathy (Syndrome) as a Variant of Acute Myocardial Infarction

The Case for Takotsubo Cardiomyopathy (Syndrome) as a Variant of Acute Myocardial Infarction

Morphological and histopathological heart changes in autopsies of heroin abusers

Backround/Aim. Heroin is a semisynthetic opioid that may cause morphological and histopathological changes in heart: ventricular hypertrophy, myocardial fibrosis, hypertrophy of cardiomyocytes, myofibrils contraction band necrosis, loss of myocytes nuclei and cross-striation, perivascular bleeding, inflammatory cells infiltrate. The aim of the study was to show morphological and histopathological heart changes in autopsies of the long-time heroin abusers with positive toxicological analysis for 6-monoacetylmorphine (6-MAM) and morphine in blood and urine. Methods. Retrospective study was done at the Institute of Pathology and Forensic of the Medicine Military Medical Academy in Belgrade between 2010 and 2014 and included forensic autopsies of 27 examinees aged between 18 and 60. Heart ventricles thicknesses was analysed and histopathological myocard findings from processed material stained by hematoxyline-eosine (H&amp;E) and trichrome stains (Masson) were examined. 6-MAM and morphine concentration in blood and urine using high-performance liquid chromatography coupled with photodiode (HPLC-PDA) and ultraviolet (UV) detector were analysed. Results. Heart ventricles thickness was increased in all persons (27/27; 100%) left 1.74 ? 0.17 cm and right 0.6 ? 0.09 cm. Myocardial fibrosis affected 27/27 (100%) of the examined persons including perivascular one in 24/27 (88.89%) and interstitial focal fibrosis in 3/27 (11.11%); hypertrophy of cardiomyocytes was present in 22/27 (81.48%); myofibril contraction band necrosis in 22/27 (81.48%); loss of myocytes nuclei and cross-striation in 10/27 (37.04%); fresh perivascular bleeding in 23/27 (85.19%); focal inflammatory cells infiltrate in 14/27 (51.85%). In toxicological findings, in 27/27 (100%), 6-MAM and morphine were found in urine. Both 6-MAM and morphine in blood were found in 3/27 (11.11%) and only morphine in blood in 16/27 (59.26%) persons subjected to an autopsy. Conclusion. Our results indicate both morphological (left and right ventricle hypertrophy) and histopathological heart changes (myocardial fibrosis, hypertrophy of cardiomyocytes, contraction-band necrosis, loss of myocytes nuclei and cross-striation, fresh perivascular bleeding and focal inflammatory infiltrate) in long-term heroin obusers. These changes are non-specific and could be caused either by long-term heroin abuse or by other factors. Having in mind a lack of medical histories of examined we could not exclude other factors besides long-term heroin abuse as cause of heart changes.

TELETHONIN AS AN EARLY IMMUNOHISTOCHEMICAL MARKER IN LIGATION-INDUCED ISCHEMIC MYOCARDIAL INJURY

In this study, acute myocardial injuries or necrosis were experimentally induced in calves and pigs by ligation of either the left anterior descending coronary artery or left circumflex branch for 30[Formula: see text]min without reperfusion. Various antibodies directed to structural and functional proteins of the sarcomere, as well as activated proteinases, were employed in immunohistochemistry to compare for their potentials to detect early myocardial injury. For comparison, the histological criteria (designated as “Method A”) of cardiomyocyte necrosis such as nuclear pyknosis, sarcoplasmic fragmentation, flocculation, and/or the presence of a contraction band, and inflammatory infiltration were also scored. Additional criteria (designated “Method B”) of changes in late reversible stage of cell injury such as irregular nuclear shape or hyperchromasia, sarcomplasmic hypereosinophilia with either swelling or atrophy in diameter, and perinuclear vacuolation likely of swollen organelles, were also scored. In this setting, telethonin (T-cap), cardiac troponin I (cTnI), the current gold standard, and Method B, were superior to others in detecting ligation-induced ischemic injury. Other markers were either less specific, or less sensitive, or inconclusive for the current application. In conclusion, telethonin may serve as an early immunohistochemical marker in ligation-induced ischemic myocardial injury due to a combination of biomechanical stress, hypoxia, and possibly additional factor as matrix metalloproteinase activation.

Non-contrast-enhanced T1 -weighted MRI of myocardial radiofrequency ablation lesions.

To demonstrate imaging of radiofrequency ablation lesions with non-contrast-enhanced T1 -weighted (T1w) MRI. Fifteen swine underwent left ventricular ablation followed by MRI using different preparations: endocardial or epicardial ablation of naïve animal, or endocardial ablation of animal with myocardial infarction. Lesion imaging was performed using free-breathing, non-contrast-enhanced, T1w sequence with long inversion time (TI). Also acquired were T1 maps and delayed contrast-enhanced (DCE) imaging. Hearts were excised for ex vivo imaging, and sliced for gross pathology and histology. All ablations were visibly enhanced in non-contrast-enhanced T1w imaging using TI = 700 ms. T1w enhancement agreed with regions of necrosis in gross pathology and histology. Enhanced lesion cores were surrounded by dark bands containing contraction band necrosis, hematoma, and edema. In animals with myocardial infarction, chronic scar was hypointense in T1w, whereas acute ablations were enhanced, allowing discrimination between chronic scar and acute lesions, unlike DCE. Contrast was sufficient to create 3D volume renderings of lesions after minor postprocessing. Non-contrast-enhanced T1w imaging with long TI promises to be an effective method for visualizing necrosis within radiofrequency ablation lesions. Enhancement is more specific and stationary than that from DCE. The imaging can be repeated as needed, unlike DCE, and may be especially useful for assessing ablations during or after a procedure. Magn Reson Med 79:879-889, 2018. © 2017 International Society for Magnetic Resonance in Medicine.

Abstract: 11.00 Oxygenated Perfusion Of Free Flaps Using A Modified Heart-Lung Machine To Minimize Tissue Damage During Ischemia Time: A Feasibility Study In A Porcine Model And Initial Results

INTRODUCTION: At the moment there is no reliable method to minimize tissue damage occurring during the ischemia time in free flap reconstructive surgery. In the current pilot study the feasibility of a novel extracorporal preservation method was explored aimed at minimizing tissue damage during ischemia time in free flap transfer. Initial results are presented. MATERIALS AND METHODS: A modified heart-lung machine was assembled to allow semi-closed extra-corporal oxygenated perfusion of free flaps. Porcine rectus abdominis flaps pedicled on the superior epigastric artery were harvested. Different test groups were created aimed at testing various preservation methods of flaps: I continuous perfusion with normothermic oxygenated heparinized autologous blood; II continuous perfusion with cooled (7 degrees Celcius) and oxygenated histidine-tryptophan-ketoglutarate (HTK) or University of Wisconsin (UW) solution; III short flush (eight minutes) with HTK, UW or saline and heparin solution after which cooled (4 degrees Celsius) preservation. Muscle biopsies were taken for histological analysis at various timepoints during the 24 hour experiments. RESULTS: Flaps from groups I and II were successfully attached to the modified heart-lung machine while maintaining stable flow and pressure. After three hours flaps from groups I and III already showed signs of cell death (contraction band necrosis) increasing throughout the experiment. Flaps from group II showed minimal (UW) or no such signs (HTK) throughout the 24-hour experiments. CONCLUSIONS: The use of a modified heart-lung machine to allow oxygenated perfusion of free flaps provides new possibilities to minimize tissue damage during ischemia time and further study of its use is warranted. 11.10–12.10 SESSION 8 – OUTCOME / CLINICAL (PART 2) Moderators Philip BLONDEEL Rene LARGO