Cardiac Tissue Specimens Research Articles

Cardioprotective Effect of Eugenol Against Cd-Induced Inflammation, Oxidative Stress, and Dyslipidemia in Male Rats: An In Vivo and Molecular Docking Study.

Cadmium, a highly toxic heavy metal, can cause severe damage to several vital organs including the kidney, liver, and brain. Many of the natural compounds found in aromatic plants have beneficial pharmacological properties. Eugenol is one such compound reported to have anti-inflammatory and antioxidant properties. The aim of this study is to investigate whether eugenol, a natural compound found in aromatic plants known for its anti-inflammatory and antioxidant properties, can mitigate the detrimental effects of cadmium exposure on cardiac inflammation, oxidative stress, and dyslipidemia. Male albino rats were subjected to randomization into four groups, each comprising six animals, to investigate the potential of eugenol in mitigating cadmium-induced toxicity. All groups received oral gavage treatment for 21days. Following the treatment regimen, cardiac tissue specimens were collected for analysis. The assessment of cardiac antioxidant status entailed the determination of enzymatic activities including catalase, SOD, GST, and GPx. Additionally, levels of lipid peroxidation, reduced glutathione, protein carbonyl oxidation, and thiol levels were quantified in the cardiac tissue samples. To evaluate cardiac damage, marker enzymes such as LDH and CK-MB were measured. Furthermore, the inflammatory response in the cardiac tissue induced by cadmium exposure was assessed through the quantification of NO, TNF-α, and IL-6 levels. Additionally, molecular docking and dynamics studies were conducted utilizing autodock and GLIDE methodologies. Cadmium administration markedly enhanced the activities of LDH and CK-MB, prominent cardiac markers. Furthermore, cadmium treatment also demonstrated a significant decrease in the reduced glutathione levels and antioxidant enzyme activities. Significant elevation of the inflammatory markers was also observed in the cadmium-treated group. Eugenol treatment effectively ameliorates cadmium-induced biochemical changes. This study underscores the potent anti-inflammatory and antioxidant attributes of eugenol. Co-administration of eugenol alongside cadmium exhibited remarkable protective efficacy against cadmium-induced cardio-toxicity. Eugenol demonstrated the capability to reinstate the cellular redox equilibrium of rats subjected to cadmium treatment to levels akin to those of the normal control group.

Molecular epidemiology of Bartonella quintana endocarditis in patients from Israel and Eastern Africa

BackgroundBartonella quintana is an important cause of culture-negative endocarditis. Although humans have been considered as its only reservoir, recent studies showed that macaque species are also reservoirs of B. quintana. Based on multi-locus sequence typing (MLST) B. quintana strains have been classified into 22 sequence types (STs), with 7 STs exclusively found in humans. Data regarding the molecular epidemiology of B. quintana endocarditis is limited to only 3 STs identified in 4 patients from Europe and Australia. We studied B. quintana endocarditis acquired in Eastern Africa or Israel to investigate the genetic diversity and clinical relatedness of B. quintana from distinct geographic regions.MethodsEleven patients with B. quintana endocarditis, 6 from Eastern Africa and 5 from Israel, were studied. DNA was extracted from cardiac tissue or blood specimens and analyzed by MLST based on 9 genetic loci. An evolutionary relationship between STs was visualized by a minimum spanning tree. A phylogenetic tree was constructed with the concatenated sequences (4271 bp) of the 9 loci using the maximum-likelihood method.ResultsSix strains were classified into previously described STs while 5 strains were identified for the first time and classified into new STs 23–27 which clustered with the previously reported STs 1–7 from human strains found in Australia, France, Germany, the USA, Russia, and the former Yugoslavia, without indication of geographical structuring. ST2 was the most prevalent ST, found in 5 of 15 patients with endocarditis (33.3%). ST26 appears to be a primary founder of the human lineage.ConclusionsThe new and previously reported human STs form a single human lineage, clearly separated from the other 3 B. quintana lineages of cynomolgus, rhesus, and Japanese macaques. From evolutionary perspectives, these findings support the assumption that B. quintana has co-evolved with host species to form a host-speciation pattern. ST26 is suggested herein as a primary founder of the human lineage and may be key to explore where B. quintana had first originated; ST2 is a dominant genetic type associated with B. quintana endocarditis. To confirm these findings, additional worldwide molecular epidemiological studies are required.

The histopathological and molecular diagnosis of myocardial sarcocystosis in sheep, and the immunohistochemical correlation of parasitic lesions with MMP - 2 and MMP - 9

This study was aimed at the histopathological and immunohistochemical level investigate cardiac tissue lesions caused by Sarcocystis spp. in sheep, and thereby, to collect detailed information on the presence of these parasites and the pathogenesis of sarcocystosis in ovine animals. PCR, a molecular diagnostic method, was used for the identification of the parasite species. Microscopic examination revealed that out of the 45 ovine cardiac tissue samples examined 23 contained Sarcocystis spp. cysts. The PCR analysis results showed that out of the 23 cardiac tissue specimens infected with sarcocysts, 7 were determined to be infected with Sarcocystis gigantea and 16 with Sarcocystis tenella. Immunohistochemical examination demonstrated that, semiquantitatively, MMP - 9 staining was stronger than MMP - 2 staining in the periphery of the parasite cysts.

Association of Complement and MAPK Activation With SARS-CoV-2–Associated Myocardial Inflammation

Myocardial injury is a common feature of patients with SARS-CoV-2 infection. However, the cardiac inflammatory processes associated with SARS-CoV-2 infection are not completely understood. To investigate the inflammatory cardiac phenotype associated with SARS-CoV-2 infection compared with viral myocarditis, immune-mediated myocarditis, and noninflammatory cardiomyopathy by integrating histologic, transcriptomic, and proteomic profiling. This case series was a cooperative study between the Ludwig Maximilian University Hospital Munich and the Cardiopathology Referral Center at the University of Tübingen in Germany. A cohort of 19 patients with suspected myocarditis was examined; of those, 5 patients were hospitalized with SARS-CoV-2 infection between March and May 2020. Cardiac tissue specimens from those 5 patients were compared with specimens from 5 patients with immune-mediated myocarditis, 4 patients with non-SARS-CoV-2 viral myocarditis, and 5 patients with noninflammatory cardiomyopathy, collected from January to August 2019. Endomyocardial biopsy. The inflammatory cardiac phenotypes were measured by immunohistologic analysis, RNA exome capture sequencing, and mass spectrometry-based proteomic analysis of endomyocardial biopsy specimens. Among 19 participants, the median age was 58 years (range, 37-76 years), and 15 individuals (79%) were male. Data on race and ethnicity were not collected. The abundance of CD163+ macrophages was generally higher in the cardiac tissue of patients with myocarditis, whereas lymphocyte counts were lower in the tissue of patients with SARS-CoV-2 infection vs patients with non-SARS-CoV-2 virus-associated and immune-mediated myocarditis. Among those with SARS-CoV-2 infection, components of the complement cascade, including C1q subunits (transcriptomic analysis: 2.5-fold to 3.6-fold increase; proteomic analysis: 2.0-fold to 3.4-fold increase) and serine/cysteine proteinase inhibitor clade G member 1 (transcriptomic analysis: 1.7-fold increase; proteomic analysis: 2.6-fold increase), belonged to the most commonly upregulated transcripts and differentially abundant proteins. In cardiac macrophages, the abundance of C1q was highest in SARS-CoV-2 infection. Assessment of important signaling cascades identified an upregulation of the serine/threonine mitogen-activated protein kinase pathways. This case series found that the cardiac immune signature varied in inflammatory conditions with different etiologic characteristics. Future studies are needed to examine the role of these immune pathways in myocardial inflammation.

CARDIOPROTECTIVE EFFECT OF CYANIDIN-3-O-GLUCOSIDE IN ISCHEMIC HEART IS MEDIATED VIA INHIBITION OF AUTOPHAGY

Abstract It is elevated proves that the polyphenolic compounds of natural origin, such as anthocyanins, being cyanidin-3-O-glucoside (Cy3G) one of the most widely distributed anthocyanins, may control ischemia/reperfusion (I/R) injury although how much sheltering occurs is not obvious. In the present study, the role of cyanidin-3-O-glucoside pretreatment of cardiac ischemia and dysfunction was studied. Cyanidin-3-O-glucoside in 3 doses (5, 10, and 15 mg/kg body weight), was introduced in vivo 5 min before a 45 min closure of the left anterior descending artery, followed by a 120 min reperfusion in male Wistar rats. Blood samples and cardiac tissue specimens were obtained for studying the cardiac markers and the expression of lncRNA-CTC-448F2.4, miR1273a, and mRNA-DCN (Decorin), Specimens of left ventricles were obtained and prepared for histopathological criteria. Specimens of pretreated rats showed minimal cardiac edema, hemorrhage, cellular inflammatory infiltration, and fibrosis in cardiac tissue samples. Notably, this protective administration of cyanidin-3-O-glucoside also produced a dose-dependent downregulation in lncRNA- CTC-448F2.4 and mRNA-DCN (Decorin, an important gene involved in the regulation of autophagy) with elevation in miR-1273a expressions. Cyanidin-3-O-glucoside pretreatment leads to improvements in cardiac function tests, enzymes, and myocytes. In conclusion, Cyanidin-3-O-glucoside is promising for the protection of the heart from injury following ischemia-reperfusion in the rat examination.

Potential functions of embryonic cardiac macrophages in angiogenesis, lymphangiogenesis and extracellular matrix remodeling

The role of cardiac tissue macrophages (cTMs) during pre- and postnatal developmental stages remains in many aspects unknown. We aimed to characterize cTM populations and their potential functions based on surface markers. Our in situ studies of immunostained cardiac tissue specimens of murine fetuses (from E11to E17) revealed that a significant number of embryonic cTMs (phenotyped by CD45, CD68, CD64, F4/80, CD11b, CD206, Lyve-1) resided mostly in the subepicardial space, not in the entire myocardial wall, as observed in adult individuals. cTMs accompanied newly developed blood and lymphatic vessels adhering to vessel walls by cellular processes. A subpopulation of CD68-positive cells was found to form accumulations in areas of massive apoptosis during the outflow tract remodeling and shortening. Flow cytometry analysis at E14 and E17 stages revealed newly defined three subpopulations:CD64low, CD64highCD206-and CD64highCD206+. The levels of mRNA expression for genes related to regulation of angiogenesis (VEGFa, VEGFb, VEGFc, bFGF), lymphangiogenesis (VEGFc) and extracellular matrix (ECM) remodeling (MMP13, Arg1, Ym1/Chil3, Retlna/FIZZ1) differed among the selected populations and/or embryonic stages. Our results demonstrate a diversity of embryonic cTMs and their tissue-specific locations, suggesting their various potential roles in regulating angiogenesis, lymphangiogenesis and ECM remodeling.

Identification of the miRNA-3185/CYP4A11 axis in cardiac tissue as a biomarker for mechanical asphyxia

Death by mechanical asphyxia is one of the most difficult conclusions to make in forensic science, especially in corpses displaying slight or no trauma to the surface of the body. Therefore, death by mechanical asphyxia is difficult to prove in medico-legal practice. MicroRNAs (miRNAs) are a class of small, non-coding RNAs involved in the regulation of numerous physiological and pathological cellular processes. In the present study, we demonstrate that significantly increased expression of miR-3185 in cardiac tissues was detected among cases of mechanical asphyxia compared to case of craniocerebral injury, hemorrhagic shock, sudden cardiac death and poisoning. We observed no correlation between the expression of miR-3185 and postmortem interval, age or temperature. Further work indicated that CYP4A11 is a putative target gene of miR-3185 and expressed at a relatively low level in cardiac tissue specimens from cases of mechanical asphyxia compared with specimens from cases of craniocerebral injury, hemorrhagic shock, sudden cardiac death and poisoning. Our results suggest that the miRNA-3185/CYP4A11 axis is associated with mechanical asphyxia-induced death and may provide new insight into asphyxial death investigations.

Thanatogenomic Investigation of the Hydroxymethylome and Mitochondrial Genome of Cadaveric Cardiomyocytes: Proposal for a Proof-of-Concept Study.

BackgroundCardiovascular disease (CVD) remains the leading cause of death in the United Arab Emirates (UAE). One of the common CVDs is hypertrophic cardiomyopathy (HCM). Recent studies conducted in heart cells of mice have shown that this condition involves a chemical modification called hydroxymethylation of the DNA of heart cells.ObjectiveObjectives of the proposed research are to profile the distribution of 5-hydroxymethylation in the cardiomyocyte (CMC) genome of cadaveric cardiac tissue and cardiac biopsy specimens; to compare the hydroxymethylome of cadaveric CMCs with that of cardiac biopsy specimens from HCM patients and/or cardiac transplant patients (control) undergoing cardiac catheterization; to histologically appraise sarcomere distribution and mitochondrial morphology of CMCs in the presence of HCM; to correlate the mitochondrial genome with the HCM phenotype; and to integrate anatomy with biochemistry and genetics into the instructional design of HCM in the core medical curriculum at Mohammed Bin Rashid University of Medicine and Health Sciences (MBRU).MethodsNormal and hypertrophic heart specimens will be obtained from 8 whole-body cadavers (2/8, 25% control and 6/8, 75% HCM). Myocardial biopsy specimens will be obtained from cardiothoracic and transplant units at the Cleveland Clinic in Abu Dhabi, UAE. As this is a proof-of-concept study, we plan to recruit 5 patients with HCM, where HCM has been diagnosed according to the guidelines of the 2014 European Society of Cardiology Guidelines. Patients with valvular heart disease, history of myocarditis, regular alcohol consumption, or cardiotoxic chemotherapy will be excluded. The control biopsy specimens will be obtained from patients who had received heart transplants. Three investigational approaches will then be employed: (1) gross anatomical evaluation, (2) histological analysis, and (3) profiling and analysis of the hydroxymethylome. These investigations will be pursued with minor modifications, if required, to the standard protocols and in accordance with institutional policy. The objective associated with the education of health professionals will be addressed through a strategy based on Graham’s knowledge translation model.ResultsThis study is at the protocol-development stage. The validated questionnaires have been identified in relation to the objectives. The MBRU and the Cleveland Clinic Abu Dhabi Institutional Review Board (IRB) are reviewing this study. Further clarification and information can be obtained from the MBRU IRB. There is funding in place for this study (MBRU-CM-RG2019-08). Currently, we are in the process of standardizing the protocols with respect to the various molecular techniques to be employed during the course of the study. The total duration of the proposed research is 24 months, with a provision for 6 months of a no-cost extension.ConclusionsThe spectrum of CVDs has recently received significant focus from the public health sector in the UAE. HCM is a common familial heart disease, contributing to the sudden increase in the mortality rate of young Emiratis in the UAE. Incorporating artificial intelligence into the identification of epigenetic risk factors associated with HCM will promote accurate diagnosis and lead to the development of improved management plans, hence, positive patient outcomes. Furthermore, integration of these findings into the instructional design of undergraduate, postgraduate, and continuous professional development medical curricula will further contribute to the body of knowledge regarding HCM.International Registered Report Identifier (IRRID)PRR1-10.2196/17241

Bacterial Infections Associated With Substance Use Disorders, Large Cohort of United States Hospitals, 2012-2017.

Rises in the incidence of bacterial infections, such as infective endocarditis (IE), have been reported in conjunction with the opioid crisis. However, recent trends for IE and other serious infections among persons with substance use disorders (SUDs) are unknown. Using the Premier Healthcare Database, we identified hospitalizations from 2012 through 2017 among adults with primary discharge diagnoses of bacterial infections and secondary SUD diagnoses, using International Classification of Diseases, Clinical Modification Ninth and Tenth Revision codes. We calculated annual rates of infections with SUD diagnoses and evaluated temporal trends. Blood and cardiac tissue specimens were identified from IE hospitalizations to describe the microbiology distribution and temporal trends among hospitalizations with and without SUDs. Among 72 481 weighted IE admissions recorded, SUD diagnoses increased from 19.9% in 2012 to 39.4% in 2017 (P < .0001). Hospitalizations with SUDs increased from 1.1 to 2.1 per 100 000 persons for IE, 1.4 to 2.4 per 100 000 persons for osteomyelitis, 0.5 to 0.9 per 100 000 persons for central nervous system abscesses, and 24.4 to 32.9 per 100 000 persons for skin and soft tissue infections. For adults aged 18-44 years, IE-SUD hospitalizations more than doubled, from 1.6 in 2012 to 3.6 in 2017 per 100 000 persons. Among all IE-SUD hospitalizations, 50.3% had a Staphylococcus aureus infection, compared with 19.4% of IE hospitalizations without SUDs. Rates of hospitalization for serious infections among persons with SUDs are increasing, driven primarily by younger age groups. The differences in the microbiology of IE hospitalizations suggest that SUDs are changing the epidemiology of these infections.

The Protective Effect of The Interleukin 1 Receptor Antagonist on Chronic Thromboembolic Pulmonary Hypertension Model

Chronic thromboembolic pulmonary hypertension (CTEPH) is one of the main reasons of severe pulmonary hypertension and has significantly higher morbidity and mortality rates. The pathogenesis of the disease is characterized by the incomplete resolution of acute embolisms. The elevated inflammatory conditions after the acute embolism are one of the critical factors. Therefore, we aimed to investigate whether or not anakinra is an option for treating CTEPH in an animal model. We studied twenty-one rats in this study They were randomly divided into three groups containing seven animals: the control group: saline-treated control; the embolism group: CTEPH + normal saline; the anakinra group: CTEPH + anakinra. We have observed that the layers of the segmental arteries and the alveolar were normal in the control group. In the cardiac tissue it was observed that muscular tissues and connective tissue were normal in the right ventricle. In embolism group, we detected a widening of the alveolar septum, a surrounding the alveolar infiltrates and a thickening of the segmental arteries in the muscular layer and a hypertrophy in the right ventricle tissues. We have determined that the lung and cardiac tissue specimens in the anakinra group are similar to control group. We have showed that anakinra was useful option for the CTEPH model in rats. Anakinra may be considered as protective effect and the regression of the increased inflammation in CTEPH. The effectiveness of anakinra will continue to be subject to the further experimental and clinical studies.

Metformin Reduces Radiation-Induced Cardiac Toxicity Risk in Patients Having Diabetes and Breast Cancer: Results from the Taiwan National Cohort and Basic Research

Background: To analyze the effects of metformin in reducing radiation-induced cardiac toxicity (RICT) risk during adjuvant radiotherapy (RT) after surgery for early-stage breast cancer among diabetic women. Methods: A retrospective national cohort study was conducted using the Taiwan Cancer Registry of 2004-2014. This study included 6,993 diabetic women with early-stage breast cancer who received adjuvant breast RT. An inverse probability of treatment weighting (IPTW) Cox hazards model was used to estimate metformin effects on the occurrence of major heart events. To investigate the effects of Metformin on the cardio-protective, primary culture of human cardiomyocytes were first used as the radiation induced cardiac toxicity experimental model. We also compared RICT in cardiac tissue specimens obtained from irradiated (10 Gy/shot) C57BL/6 mice with or without metformin administration. Results: Among diabetic women with breast cancer status post-surgery under adjuvant breast RT, 2,062 were prescribed metformin and 4,931 were not prescribed metformin. Cox proportional hazard regression analysis, with adjustment using IPTW, indicated that metformin use during adjuvant breast RT significantly reduces the risk of major heart events (adjusted hazard ratio [aHR], 0.789; 95% confidence interval [CI], 0.645-0.965; p = 0.021). The basic research results demonstrated that RT significantly reduced mitochondria membrane potential; meanwhile, metformin co-treatment significantly rescued the death of mitochondria in Human cardiomyocytes. In vivo, metformin administration attenuated RT-induced fibrosis in cardiac tissues. Conclusion: Our results suggest that metformin use during adjuvant breast RT was associated with reduced RICT risk in diabetic women with early-stage breast cancer. Funding Statement: Taipei Medical University and Wan Fang Hospital Declaration of Interests: The authors have no potential conflicts of interest to declare. Ethics Approval Statement: Our protocols were reviewed and approved by the Institutional Review Board of Taipei Medical University (TMU-JIRB No. 201712019).

DUSP1 and KCNJ2 mRNA upregulation can serve as a biomarker of mechanical asphyxia-induced death in cardiac tissue.

The incidence of death by asphyxia is second to the incidence of death by mechanical injury; however, death by mechanical asphyxia may be difficult to prove in court, particularly in cases in which corpses do not exhibit obvious signs of asphyxia. To identify a credible biomarker of asphyxia, we first examined the expression levels of 47,000 mRNAs in human cardiac tissue specimens from individuals who died of mechanical asphyxia and compared the expression levels with the levels of the corresponding mRNAs in specimens from individuals who died of craniocerebral injury using microarray. We selected 119 differentially expressed mRNAs, examined the expression levels of these mRNAs in 44 human cardiac tissue specimens of individuals who died of mechanical asphyxia, craniocerebral injury, hemorrhagic shock, or other causes. That the expression of dual-specificity phosphatase 1 (DUSP1) and potassium voltage-gated channel subfamily J member 2 (KCNJ2) was upregulated in human cardiac tissues from the mechanical asphyxia group compared with control tissues, regardless of age, environmental temperature, and postmortem interval (PMI), indicating that DUSP1 and KCNJ2 may be associated with mechanical asphyxia-induced death and can thus serve as useful biomarkers of death by mechanical asphyxia.

Detection and differentiation of early acute and following age stages of myocardial infarction with quantitative post-mortem cardiac 1.5 T MR

Recently, quantitative MR sequences have started being used in post-mortem imaging. The goal of the present study was to evaluate if early acute and following age stages of myocardial infarction can be detected and discerned by quantitative 1.5T post-mortem cardiac magnetic resonance (PMCMR) based on quantitative T1, T2 and PD values.In 80 deceased individuals (25 female, 55 male), a cardiac MR quantification sequence was performed prior to cardiac dissection at autopsy in a prospective study. Focal myocardial signal alterations detected in synthetically generated MR images were MR quantified for their T1, T2 and PD values. The locations of signal alteration measurements in PMCMR were targeted at autopsy heart dissection and cardiac tissue specimens were taken for histologic examinations. Quantified signal alterations in PMCMR were correlated to their according histologic age stage of myocardial infarction.In PMCMR seventy-three focal myocardial signal alterations were detected in 49 of 80 investigated hearts. These signal alterations were diagnosed histologically as early acute (n=39), acute (n=14), subacute (n=10) and chronic (n=10) age stages of myocardial infarction. Statistical analysis revealed that based on their quantitative T1, T2 and PD values, a significant difference between all defined age groups of myocardial infarction can be determined. It can be concluded that quantitative 1.5T PMCMR quantification based on quantitative T1, T2 and PD values is feasible for characterization and differentiation of early acute and following age stages of myocardial infarction.

Saffold virus infection associated with human myocarditis

BackgroundSaffold virus was described in 2007 as one of the first human viruses within the genus cardioviruses. Cardioviruses may cause severe infections of the myocardium in animals, and several studies have associated saffold virus with human disease. As a result, saffold virus has been isolated from different anatomical compartments, including the myocardium, but, until now, it has not been possible to demonstrate the accompanying histopathological signs of inflammation. ObjectivesThe aim of the study was to examine if saffold virus is capable of causing invasive infection in the human myocardium. Study designUsing real-time PCR, we retrospectively examined formalin-fixed paraffin embedded cardiac tissue specimens from 150 deceased individuals diagnosed with myocarditis at autopsy. The results were compared with histological findings. Results and conclusionsSaffold virus was detected in the myocardium, lung tissue and blood of one child and was accompanied by histopathological inflammation in the heart and lungs, which was supportive of a viral infection. These findings suggest that cardioviruses may be associated with myocarditis in humans.

Calibration and Evaluation of Ultrasound Thermography Using Infrared Imaging

Real-time monitoring of the spatiotemporal evolution of tissue temperature is important to ensure safe and effective treatment in thermal therapies including hyperthermia and thermal ablation. Ultrasound thermography has been proposed as a non-invasive technique for temperature measurement, and accurate calibration of the temperature-dependent ultrasound signal changes against temperature is required. Here we report a method that uses infrared thermography for calibration and validation of ultrasound thermography. Using phantoms and cardiac tissue specimens subjected to high-intensity focused ultrasound heating, we simultaneously acquired ultrasound and infrared imaging data from the same surface plane of a sample. The commonly used echo time shift-based method was chosen to compute ultrasound thermometry. We first correlated the ultrasound echo time shifts with infrared-measured temperatures for material-dependent calibration and found that the calibration coefficient was positive for fat-mimicking phantom (1.49 ± 0.27) but negative for tissue-mimicking phantom (−0.59 ± 0.08) and cardiac tissue (−0.69 ± 0.18°C-mm/ns). We then obtained the estimation error of the ultrasound thermometry by comparing against the infrared-measured temperature and revealed that the error increased with decreased size of the heated region. Consistent with previous findings, the echo time shifts were no longer linearly dependent on temperature beyond 45°C–50°C in cardiac tissues. Unlike previous studies in which thermocouples or water bath techniques were used to evaluate the performance of ultrasound thermography, our results indicate that high-resolution infrared thermography is a useful tool that can be applied to evaluate and understand the limitations of ultrasound thermography methods.

Prolonged Outbreak of Mycobacterium chimaera Infection After Open-Chest Heart Surgery.

Invasive Mycobacterium chimaera infections were diagnosed in 2012 in 2 heart surgery patients on extracorporeal circulation. We launched an outbreak investigation to identify the source and extent of the potential outbreak and to implement preventive measures. We collected water samples from operating theaters, intensive care units, and wards, including air samples from operating theaters. Mycobacterium chimaera strains were characterized by randomly amplified polymorphic DNA polymerase chain reaction (RAPD-PCR). Case detection was performed based on archived histopathology samples and M. chimaera isolates since 2006, and the patient population at risk was prospectively surveyed. We identified 6 male patients aged between 49 and 64 years with prosthetic valve endocarditis or vascular graft infection due to M. chimaera, which became clinically manifest with a latency of between 1.5 and 3.6 years after surgery. Mycobacterium chimaera was isolated from cardiac tissue specimens, blood cultures, or other biopsy specimens. We were able also to culture M. chimaera from water circuits of heater-cooler units connected to the cardiopulmonary bypass, and air samples collected when the units were in use. RAPD-PCR demonstrated identical patterns among M. chimaera strains from heater-cooler unit water circuits and air samples, and strains in 2 patient clusters. The epidemiological and microbiological features of this prolonged outbreak provided evidence for the airborne transmission of M. chimaera from contaminated heater-cooler unit water tanks to patients during open-heart surgery.

Circulation: Clinical Summaries.

Circulation: Clinical Summaries.

Effect and mechanisms of zinc supplementation in protecting against diabetic cardiomyopathy in a rat model of type 2 diabetes.

Diabetic cardiomyopathy is a prominent cause of heart failure in patients with diabetes mellitus. Currently, there is no specific treatment for diabetic cardiomyopathy. This study aimed to investigate the effect and underlying mechanisms of Zinc (Zn) supplementation in the protection against diabetic cardiomyopathy in a rat model of type 2 diabetes mellitus (T2DM). T2DM-like lesions in male Wistar rats were induced by introducing the high-fat diet and by administration of streptozocin (STZ). After STZ induction, animals with fasting plasma glucose level ≥16.7 mM were considered as diabetic, and randomly assigned to the group receiving physiological saline (control) or ZnSO4 for 56 days. On days 0, 7, 28 and 56 of treatment, animals were weighed, and their blood samples were analyzed. On day 56, hemodynamic assessment was performed right before the sacrifice of animals. Cardiac tissue specimens were collected and subjected to pathologic assessment, metallothionein (MT) concentration measurement and Western blot analysis of microtubule-associated protein light chain 3 (LC3), the marker of autophagy, and glucose-regulated protein-78 (GRP78), an oxidative stress marker. High-fat diet feeding followed by STZ administration resulted in weight loss, hyperglycemia, polydipsia, polyphagia, hemodynamic anomalies and a significant increase in the myocardial content of LC3 and GRP78 proteins, but not in MT protein. Zn supplementation effectively attenuated all these aberrations induced by high-fat diet and STZ. These findings suggest that Zn might be a protective factor in diabetic cardiomyopathy, acting in two ways: at least partially, through inhibiting autophagy and by endoplasmic reticulum stress.

Correlations Between CCN1 Immunoexpression and Myocardial Histologic Lesions in Sudden Cardiac Death

CCN1 (CYR61) is a member of the CCN family of secreted matricellular proteins; it can regulate the expression of genes involved in angiogenesis and matrix remodeling. The latter mechanisms seem to be of vital importance in the pathophysiology of sudden cardiac death. We performed an immunohistochemical analysis on 62 cardiac tissue specimens derived from individuals of young and middle age who had died of sudden cardiac death. CCN1 immunopositivity was detected in 80.6% of all specimens. Semiquantitative statistical analysis of the staining results revealed that CCN1 immunoreactivity was significantly associated with ischemic morphology and hypertrophy of myocardial fibers, interstitial edema, and atheromatosis of coronary arteries in more than 10% of the myocardial fibers. Taking the previously mentioned correlations into account, ischemia seems to induce myocardial expression of CCN1; therefore, CCN1 immunostaining could be evaluated as a complementary tool in the assessment of ischemic areas when no tissue evidence of necrosis is available.

High-frequency rapid B-mode ultrasound imaging for real-time monitoring of lesion formation and gas body activity during high-intensity focused ultrasound ablation

The goal of this study was to examine the ability of high-frame-rate, high-resolution imaging to monitor tissue necrosis and gas-body activities formed during high-intensity focused ultrasound (HIFU) application. Ex vivo porcine cardiac tissue specimens (n = 24) were treated with HIFU exposure (4.33 MHz, 77 to 130 Hz pulse repetition frequency (PRF), 25 to 50% duty cycle, 0.2 to 1 s, 2600 W/cm(2)). RF data from B-mode ultrasound imaging were obtained before, during, and after HIFU exposure at a frame rate ranging from 77 to 130 Hz using an ultrasound imaging system with a center frequency of 55 MHz. The time history of changes in the integrated backscatter (IBS), calibrated spectral parameters, and echo-decorrelation parameters of the RF data were assessed for lesion identification by comparison against gross sections. Temporal maximum IBS with +12 dB threshold achieved the best identification with a receiver-operating characteristic (ROC) curve area of 0.96. Frame-to-frame echo decorrelation identified and tracked transient gas-body activities. Macroscopic (millimeter-sized) cavities formed when the estimated initial expansion rate of gas bodies (rate of expansion in lateral-to-beam direction) crossed 0.8 mm/s. Together, these assessments provide a method for monitoring spatiotemporal evolution of lesion and gas-body activity and for predicting macroscopic cavity formation.