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The Purkinje system is a heart structure responsible for transmitting electrical impulses through the ventricles in a fast and coordinated way to trigger mechanical contraction. Estimating a patient-specific compatible Purkinje Network from an electro-anatomical map is a challenging task, that could help to improve models for electrophysiology simulations or provide aid in therapy planning, such as radiofrequency ablation. In this study, we present a methodology to inversely estimate a Purkinje network from a patient's electro-anatomical map. First, we carry out a simulation study to assess the accuracy of the method for different synthetic Purkinje network morphologies and myocardial junction densities. Second, we estimate the Purkinje network from a set of 28 electro-anatomical maps from patients, obtaining an optimal conduction velocity in the Purkinje network of 1.95 ± 0.25 m/s, together with the location of their Purkinje-myocardial junctions, and Purkinje network structure. Our results showed an average local activation time error of 6.8±2.2 ms in the endocardium. Finally, using the personalized Purkinje network, we obtained correlations higher than 0.85 between simulated and clinical 12-lead ECGs.

Purpose: To investigate the influence of bexarotene (Bex) on cardiac structure and function in streptozotocin (STZ)-induced diabetes mellitus (DM) rats, and the mechanism of action involved. Methods: Four groups of Sprague Dawley rats (n = 40) were used: normal control, DM, DM+ Bex (10 mg/kg/day), and DM+ Bex (20 mg/kg/day) (n = 10). The DM rat model was established by intraperitoneal injection of STZ. Cardiac structure and function of rats were determined and compared. Whole heart and left ventricle were weighed. The protein expressions of Bcl2 and Bax in rat myocardial tissue were determined using Western blotting. Results: Compared to control group, there was significant reduction in the levels of IVSd (inlet ventricular septal defect) and LVPWd (left ventricle posterior wall in diastole) in DM group, but significant increase in these parameters in DM +Bex (20 mg/kg/day) group, relative to DM-treated rats (p < 0.05). Moreover, there were higher expression levels of Bcl2 and Bax in DM group, when compared with normal control, but Bcl2/Bax ratio was significantly lower (p < 0.05). Furthermore, Bcl2 and Bax levels in DM + Bex (20 mg/kg/day) group were significantly lower than those in DM group, while Bcl2/Bax ratio increased significantly (p < 0.05). Conclusion: Bexarotene improves the cardiac structure of DM rats by lowering blood glucose, and by inhibiting ventricular remodeling and cardiomyocyte apoptosis. These findings may be beneficial in the development of new anti-DM drugs.

Cardiovascular disease (CVD) is one of the critical diseases and the most common cause of morbidity and mortality worldwide. Therefore, early detection and prediction of such a disease is extremely essential for a healthy life. Cardiac imaging plays an important role in the diagnosis of cardiovascular disease but its role has been limited to visual assessment of heart structure and its function. However, with the advanced techniques and tools of big data and machine learning, it become easier to clinician to diagnose the CVD. Stenosis with in the Coronary Arteries (CA) are often determined by using the Coronary Cine Angiogram (CCA). It comes under the invasive image modality. CCA is the effective method to detect and predict the stenosis. In this paper a coronary analysis automation method is proposed in disease diagnosis. The proposed method includes pre-processing, segmentation, identifying vessel path and statistical analysis.

With research progress on longevity, we have gradually recognized that cardiac aging causes changes in heart structure and function, including progressive myocardial remodeling, left ventricular hypertrophy, and decreases in systolic and diastolic function. Elucidating the regulatory mechanisms of cardiac aging is a great challenge for biologists and physicians worldwide. In this review, we discuss several key molecular mechanisms of cardiac aging and possible prevention and treatment methods developed in recent years. Insights into the process and mechanism of cardiac aging are necessary to protect against age-related diseases, extend lifespan, and reduce the increasing burden of cardiovascular disease in elderly individuals. We believe that research on cardiac aging is entering a new era of unique significance for the progress of clinical medicine and social welfare.

Background: Atrial fibrillation is still a most common arrhythmia. The incidence increases according to each remodeling of the heart chamber. Valvular and non valvular heart diseases have differences in hemodynamic adaptations that trigger a certain remodeling. However, until now it is not known whether there is a difference between the left heart structure and valvular and non valvular atrial fibrillation. Method: There were 60 patients with atrial fibrillation hospitalized from August 2018 to December 2018. The samples were then divided into 2 groups, namely the valvular and non valvular groups, each with 30 samples. All samples that met the criteria underwent echocardiography. Then comparative statistics were carried out with p values ​​

IntroductionPost-contrast delayed-enhancement MRI helps to show the extent of myocardial infarction (MI), as well as allowing the morphometric analysis of the heart structure, e.g., left ventricular volume (LVV). Here the author deployed Bayesian implementation of statistical inference to determine the difference between the LVV in MI cases and in normal controls.MethodsSixty-seven MI patients and thirty-three controls from the EMIDEC dataset challenge were used. These were acquired at the University Hospital of Dijon (France). A cardiologist with 10 years of experience in cardiology and MRI and a biophysicist with 20 years of experience of cardiovascular MRI supervised the acquisition and annotated the images. ITK-Snap was used to extract the LVV and Bayesian inference were used to investigate the data.ResultsPatients with MI were younger than the controls (58.3 ± 11.5 vs. 66.5 ± 12.9 years; BF10 = 17.9). With age taken into consideration, the patients showed larger LVV relative to the controls (128.1 ± 46.3 vs. 83.4 ± 24.4 cm3; post-hoc BF10 = 12663.8).SummaryUsing Bayesian approach, we can conclude decisively that there is volumetric difference or remodeling in individuals with MI.

According to own data, 74% of patients with hemorrhagic vasculitis have sonographic signs of liver steatosis, but its influence on clinical and laboratory parameters of vasculitis is not established yet. The aim – to reveal the pathogenetic links of liver steatosis influence using correlation analysis, which could help in the planning of management strategy. Matherial and methods. We retrospectively analyzed the data of 50 inpatients with the help of Pearson’s correlation analysis. Results. In patients with hemorrhagic vasculitis, liver steatosis was more prominent in older ones and in higher body weight patients. Liver steatosis was accompanied by more significant changes in the right ventricle, left atrium, and aorta. It was also associated with systemic inflammation activity, serum proteolytic and thrombotic activity. In patients with liver steatosis, their age – a non-modifiable cardiovascular risk factor – was strongly associated with the deterioration of heart condition and changes of serum proteolytic and thrombotic activity, which, in turn, creates the background for adverse cardiovascular events. Liver steatosis was accompanied by the activation of systemic inflammation, which led to the transformation into steatohepatitis. Conclusion. The influence onto the liver steatosis is the only way of prevention of cardiovascular events and steatohepatitis in patients with hemorrhagic vasculitis., По нашим данным, у 74% пациентов с геморрагическим васкулитом наблюдаются сонографические признаки стеатоза печени, хотя его влияние на клинические и лабораторные проявления до сих пор точно не встановлены. Цель – определение патогенетических звеньев влияния стеатоза печени по корреляционному анализу для планирования стратегии и тактики ведення таких пациентов.Материал и методы. Ретроспективно проанализированы результаты обследования 50 стационарных пациентов с корреляционным анализом Пирсона.Результаты. У пациентов с геморрагическим васкулитом стеатоз печени был более выраженным у старших по возрасту и с большей массой тела лиц с более выраженными изменениями правого желудочка, левого предсердия и аорты и ассоциировался с активностью системного воспаления, протеолитической и тромботической активностью сыворотки крови. При стеатозе печени немодифицированный фактор риска – возраст - четко ассоциировался с ухудшением состояния сердца и изменениями протеолитической и тромботической активности сыворотки крови, что создает основу для кардиоваскулярных событий. Стеатоз печени сопровождался активацией системного воспалення, что приводит к переходу в стеатогепатит., За нашими даними, у 74% пацієнтів із геморагічним васкулітом спостерігалися сонографічні ознаки стеатозу печінки, однак його вплив на клінічні та лабораторні прояви дотепер точно не встановлений. Мета - визначення патогенетичних ланок впливу стеатозу печінки за кореляційним аналізом для планування стратегії та тактики ведення таких пацієнтів.Матеріал і методи. Ретроспективно проаналізовано результати обстеження 50 стаціонарних пацієнтів за кореляційним аналізом Пірсона.Результати. У пацієнтів із геморагічним васкулітом стеатоз печінки був більш вираженим у старших за віком та більших за масою осіб із вираженішими змінами правого шлуночка, лівого передсердя та аорти й асоціювався з активністю системного запалення, протеолітичною та тромботичною активністю сироватки. За умов стеатозу печінки немодифікований фактор ризику – вік - чітко асоціювався з погіршенням стану серця та змінами протеолітичної та тромботичної активності сироватки крові, що створює підґрунтя для кардіоваскулярних подій. Стеатоз печінки супроводжується активацією системного запалення, що призводить до переходу у стеатогепатит. Висновок. Єдиним шляхом профілактики кардіоваскулярних подій та стеатогепатиту є вплив на стадії стеатозу печінки.

The QRS-T angle, as an index of non-invasive cardioelectric vector, is closely related to the change of heart structure and function. There are different methedologies to measure the QRS-T angle, which can be roughly dividedinto two types: plane angle and space angle. Studies show that the influence factors include two aspects of physiology and pathology of the angle, in pathological ways, the disease such as myocardial hypertrophy, myocardial ischemia, hypertension, ventricular arrhythmia has larger clinical significance. In recent years, the research on the risk stratification of the QRS-T angle on sudden death has made great progress, but there are still some disputes about whether the space angle can be replaced by the plane angle and the range of normal value and so on.

This study aimed to investigate the effects of the basic treatment for heart failure and sequential treatment with rh-brain natriuretic peptide (rhBNP) alone or the combination of rhBNP and sacubitril/valsartan. Cardiac structure, pulmonary artery pressure, inflammation and oxidative stress in patients with acute heart failure were evaluated. Three hundred patients with acute heart failure were included. According to the random number table method, the patients were divided into 3 groups of 100 patients per group: the standard treatment group (treated with an angiotensin-converting enzyme inhibitor, β receptor blocker, and corticosteroid antagonist), rhBNP group (basic treatment combined with rhBNP) and sequential treatment group (basic treatment for heart failure combined with rhBNP followed by sacubitril/valsartan). The changes in NT-probrain natriuretic peptide (BNP) levels, cardiac troponin T (cTnT) levels, cardiac structure, pulmonary artery pressure, and the levels inflammatory factors and oxidative stress factors were compared among the 3 groups at 1, 4, 12, and 36 weeks after treatment. The sequential treatment group displayed superior outcomes than the standard treatment group and the rhBNP group in terms of left atrium diameter, left ventricular end diastolic volume, left ventricular ejection fraction, pulmonary artery pressure, NT-proBNP levels, and cTnT levels, which respond to damage to the heart structure and myocardium. This result may be related to the decreased levels of inflammatory factors and the correction of oxidative stress imbalance. Sacubitril/valsartan significantly reduce the serum levels of inflammatory factors in patients with acute heart failure while decreasing the levels of oxidizing factors and increasing the levels of antioxidant factors. These changes may be one of the explanations for the better cardiac structure and better pulmonary artery pressure observed in the sequential treatment group.

Cardiac regeneration is an ancestral trait in vertebrates that is lost both as more recent vertebrate lineages evolved to adapt to new environments and selective pressures, and as members of certain species developmentally progress towards their adult forms. While higher vertebrates like humans and rodents resolve cardiac injury with permanent fibrosis and loss of cardiac output as adults, neonates of these same species can fully regenerate heart structure and function after injury – as can adult lower vertebrates like many teleost fish and urodele amphibians. Recent research has elucidated several broad factors hypothesized to contribute to this loss of cardiac regenerative potential both evolutionarily and developmentally: an oxygen-rich environment, vertebrate thermogenesis, a complex adaptive immune system, and cancer risk trade-offs. In this review, we discuss the evidence for these hypotheses as well as the cellular participators and molecular regulators by which they act to govern heart regeneration in vertebrates.

This study evaluated the effects of the herbal medicine red orange (Citrus sinensis (L.) Osbeck) and swimming for 84 days on the animal, heart, and abdominal fat weight and the histomorphometric aspects of heart and total cholesterol of Wistar rats. The rats were divided into seven experimental groups of 12 animals each, consisting of a normocaloric diet (Dn), hypercaloric diet (Dh), normocaloric diet and herbal medicine (DnH), hypercaloric diet and herbal medicine (DhH), normocaloric diet and swimming (DnS), hypercaloric diet and swimming (DhS), and hypercaloric diet, swimming, and herbal medicine (DhSH). The data were analyzed statistically by the Tukey test and considered significant when p

The extracellular matrix (ECM) is the non-cellular component in the cardiac microenvironment, and serves essential structural and regulatory roles in establishing and maintaining tissue architecture and cellular function. The patterns of molecular and biochemical ECM alterations in developing and adult hearts depend on the underlying injury type. In addition to exploring how the ECM regulates heart structure and function in heart development and repair, this review conducts an inclusive discussion of recent developments in the role, function, and epigenetic guidelines of the ECM. Moreover, it contributes to the development of new therapeutics for cardiovascular disease.

The left atrial appendage (LAA) is a heart structure with known prothrombogenic and pro-arrhythmogenic properties.The aim of this study was to evaluate the specific anatomy of the LAA and to create a simple classification system based on the shape of its body.This study investigated 200 randomly selected autopsied human hearts (25.0% females, 46.6±19.1 years old). Three (3) types of LAAs were distinguished: the cauliflower type (no bend, limited overall length, compact structure [36.5%]); the chicken wing type (substantial bend in the dominant lobe [37.5%]), and the arrowhead type (no bend, one dominant lobe of substantial length [26.0%]). Additional accessory lobes were present in 55.5% of all LAAs. Significant variations between category types were noted in LAA length (chicken wing: 35.7±9.8 mm, arrowhead: 30.8±10.1 mm, cauliflower: 22.3±9.6 mm [p0.001]) and in the thickness of pectinate muscles located within the LAA apex (arrowhead: 1.2±0.7 mm; cauliflower: 1.1±0.6 mm; chicken wing: 0.9±0.6 mm [p0.001]). Left atrial appendage volume and orifice size were not affected by the type of LAA shape. The age of the donor was positively correlated with LAA volume (r=0.29, p=0.005), body length (r=0.26, p=0.012), and area of the orifice (r=0.36, p0.001). Donors with an oval LAA orifice were significantly older than those with round orifices (50.2±16.6 vs 43.7±20.4 years [p=0.014]) and had significantly heavier hearts (458.2±104.8 vs 409.6±114.1g [p=0.002]).This study delivered a new simple classification system of the LAA based on its body shape. An increase in age and heart weight was associated with LAA enlargement and a more oval-shaped orifice. Results of current study may help to estimate the different thrombogenic properties associated with each LAA type and be an assistance during planning and performing interventions on LAA.

Aim. The study was aimed on the importance evaluation of the false chords (FC) diagnostics in the left ventricle (LV) of the heart at early age to predict connective tissue dysplasia (CTD) development. Material and methods. The study performed at cardiorheumatological department of MAI “CCCH №11” of Yekaterinburg city. Case histories of 200 patients analyzed, of those had undergone treatment in the department last 6 months. Group consisted of children aged 1 month to 17 year old, mean age 9,7±4,6 y. o. Phenotype of CTD was evaluated according to theGent score criteria (2010) and the Score by Kadurina T. I. et al. Heart structure and functioning were assessed with bi-dimensional transthoracic echocardiography. Statistics was done with SPSS Statistics 17.0 and Microsoft Office Excel 2013. Results. All children had phenotype markers of CTD syndrome. Significance assessment of CTD by Kadurina score was 8,1±3,8 (2-33) points, that is grade 1 severity of CTD. In 17% (n=34) of children there was moderate CTD grade, and in 10% (n=20) there were dysplastic changes in ≥3 organ systems. Most of patients (95,5%) had FC (2,0±0,5 U) localized in various areas of the LV. Chords always correlated with phenotypic CTD markers in other physiological systems. And the number of concomitant markers significantly increased with the children’s age. Conclusion. In most cases CTD syndrome is associated with the changes in the heart, and FC inLV can be regarded as easy approachable and most early and reliable phenotypical marker of this systemic disorder.

BackgroundEmpagliflozin (empa), a selective sodium–glucose cotransporter (SGLT)2 inhibitor, reduced cardiovascular mortality and hospitalization for heart failure in patients with type 2 diabetes at high cardiovascular risk independent of glycemic control. The cardiovascular protective effect of empa was evaluated in an experimental model of metabolic syndrome, the obese ZSF1 rat, and its’ lean control.MethodsLean and obese ZSF1 rats were either non-treated or treated with empa (30 mg/kg/day) for 6 weeks. Vascular reactivity was assessed using mesenteric artery rings, systolic blood pressure by tail-cuff sphygmomanometry, heart function and structural changes by echocardiography, and protein expression levels by Western blot analysis.ResultsEmpa treatment reduced blood glucose levels from 275 to 196 mg/dl in obese ZSF1 rats whereas normoglycemia (134 mg/dl) was present in control lean ZSF1 rats and was unaffected by empa. Obese ZSF1 rats showed increased systolic blood pressure, and blunted endothelium-dependent relaxations associated with the appearance of endothelium-dependent contractile responses (EDCFs) compared to control lean rats. These effects were prevented by the empa treatment. Obese ZSF1 rats showed increased weight of the heart and of the left ventricle volume without the presence of diastolic or systolic dysfunction, which were improved by the empa treatment. An increased expression level of senescence markers (p53, p21, p16), tissue factor, VCAM-1, SGLT1 and SGLT2 and a down-regulation of eNOS were observed in the aortic inner curvature compared to the outer one in the control lean rats, which were prevented by the empa treatment. In the obese ZSF1 rats, no such effects were observed. The empa treatment reduced the increased body weight and weight of lungs, spleen, liver and perirenal fat, hyperglycemia and the increased levels of total cholesterol and triglycerides in obese ZSF1 rats, and increased blood ketone levels and urinary glucose excretion in control lean and obese ZSF1 rats.ConclusionEmpa reduced glucose levels by 28% and improved both endothelial function and cardiac remodeling in the obese ZSF1 rat. Empa also reduced the increased expression level of senescence, and atherothrombotic markers at arterial sites at risk in the control lean, but not obese, ZSF1 rat.

Congenital heart disease (CHD) is the most common type of birth defects, which occurs 1 in every 110 births in the United States. CHD usually comes with severe variations in heart structure and great artery connections that can be classified into many types. Thus highly specialized domain knowledge and time-consuming human process is needed to analyze the associated medical images. On the other hand, due to the complexity of CHD and the lack of dataset, little has been explored on the automatic diagnosis (classification) of CHDs. In this paper, we present ImageCHD, the first medical image dataset for CHD classification. ImageCHD contains 110 3D Computed Tomography (CT) images covering most types of CHD, which is of decent size compared with existing medical imaging datasets. Classification of CHDs requires the identification of large structural changes without any local tissue changes, with limited data. It is an example of a larger class of problems that are quite difficult for current machine-learning based vision methods to solve. To demonstrate this, we further present a baseline framework for automatic classification of CHD, based on a state-of-the-art CHD segmentation method. Experimental results show that the baseline framework can only achieve a classification accuracy of 82.0% under selective prediction scheme with 88.4% coverage, leaving big room for further improvement. We hope that ImageCHD can stimulate further research and lead to innovative and generic solutions that would have an impact in multiple domains. Our dataset is released to the public [1].

Purpose: Diffusion MRI requires acquisition of multiple diffusion‐weighted images, resulting in long scan times. Here, we investigate combining compressed sensing and a fast imaging sequence to dramatically reduce acquisition times in cardiac diffusion MRI. Methods: Fully sampled and prospectively undersampled diffusion tensor imaging data were acquired in five rat hearts at acceleration factors of between two and six using a fast spin echo (FSE) sequence. Images were reconstructed using a compressed sensing framework, enforcing sparsity by means of decomposition by adaptive dictionaries. A tensor was fit to the reconstructed images and fiber tractography was performed. Results: Acceleration factors of up to six were achieved, with a modest increase in root mean square error of mean apparent diffusion coefficient (ADC), fractional anisotropy (FA), and helix angle. At an acceleration factor of six, mean values of ADC and FA were within 2.5% and 5% of the ground truth, respectively. Marginal differences were observed in the fiber tracts. Conclusion: We developed a new k‐space sampling strategy for acquiring prospectively undersampled diffusion‐weighted data, and validated a novel compressed sensing reconstruction algorithm based on adaptive dictionaries. The k‐space undersampling and FSE acquisition each reduced acquisition times by up to 6× and 8×, respectively, as compared to fully sampled spin echo imaging. Magn Reson Med 76:248–258, 2016.

This paper is the outcome of the fourth UC Davis Systems Approach to Understanding Cardiac Excitation-Contraction Coupling and Arrhythmias Symposium, a biannual event that aims to bring together leading experts in subfields of cardiovascular biomedicine to focus on topics of importance to the field. The theme of the 2016 symposium was 'K+ Channels and Regulation'. Experts in the field contributed their experimental and mathematical modelling perspectives and discussed emerging questions, controversies and challenges on the topic of cardiac K+ channels. This paper summarizes the topics of formal presentations and informal discussions from the symposium on the structural basis of voltage-gated K+ channel function, as well as the mechanisms involved in regulation of K+ channel gating, expression and membrane localization. Given the critical role for K+ channels in determining the rate of cardiac repolarization, it is hardly surprising that essentially every aspect of K+ channel function is exquisitely regulated in cardiac myocytes. This regulation is complex and highly interrelated to other aspects of myocardial function. K+ channel regulatory mechanisms alter, and are altered by, physiological challenges, pathophysiological conditions, and pharmacological agents. An accompanying paper focuses on the integrative role of K+ channels in cardiac electrophysiology, i.e. how K+ currents shape the cardiac action potential, and how their dysfunction can lead to arrhythmias, and discusses K+ channel-based therapeutics. A fundamental understanding of K+ channel regulatory mechanisms and disease processes is fundamental to reveal new targets for human therapy.

Primary cardiac angiosarcomas are frequently found at a large size with infiltration into the adjacent heart structure owing to their asymptomatic characteristics until an advanced stage. Therefore, extensive resection is often required to achieve a good prognosis. We herein report a case of entire circumferential resection of the right atrium surrounded by angiosarcoma and excellent three-dimensional reconstruction of the right atrium.

Background: Hypertensive condition can lead to abnormalities in heart structure and electrical activity. The electrocardiogram (ECG) is a recording of the electrical activity of the heart and widely used to diagnose and detect heart problem. Objective: We conducted a comparative ECG analysis between two hypertension models (L-NAME and SHR) and their controls (Wistar and Wistar-Kyoto) at six and 15 th week of age. Methods: Blood pressure was measured at the end of the 15 th week, and electrocardiography was performed [...]

Background Chronic inflammation is linked to age-associated declines in heart structure and function that contribute to increased risks for cardiovascular mortality and frailty, a state of high vul...

Rationale: The ER stress response is activated by the accumulation of misfolded, toxic proteins in the endoplasmic reticulum (ER), and upregulates proteins that restore ER protein-folding capacity. The ER-transmembrane protein, activating transcription factor 6 (ATF6) senses ER stress and responds by transcriptionally inducing many of these genes and is thus a key component of the adaptive ER stress response. We previously showed that in the heart, ischemia activates ATF6. Furthermore, transgenic mouse hearts expressing a conditionally activated form of ATF6, and subjected to ex vivo ischemia/reperfusion, exhibited preserved heart function and smaller infarcts. Our lab also showed that by serving as a novel inducer of a global anti-oxidant gene program, endogenous ATF6 limits cardiac damage caused by reactive oxygen species during reperfusion. However, the effect of endogenous ATF6 in the failing heart is not known. Given that acute ischemia caused by occlusion of the coronary arteries is the cause of myocardial infarction (MI), we hypothesized that endogenous ATF6 limits infarct size and preserves heart function during MI. Additionally, since deleterious cardiac remodeling and heart failure can be long-term consequences of MI, we hypothesized that ATF6 can mitigate these effects. Objective/Methods: To examine the role of endogenous ATF6 in heart failure, in vivo, we used a mouse model of MI-induced heart failure in mice with a global deletion of the ATF6 gene (ATF6 KO). Infarct size was measured by TTC staining and heart function was observed via longitudinal echocardiogram. Results: We found that following infarction, ATF6 KO mouse hearts had larger infarcts compared to control. Thus, ischemic cardiac tissue in the peri-infarct region requires ATF6 to limit cardiac myocyte death. Interestingly, ejection fraction following MI decreased more over 13 weeks in ATF6 KO mice relative to control. While control and ATF6 KO mouse hearts hypertrophied to a similar degree, KO mice showed greater cardiac dilation. Conclusions: Together these findings show for the first time that endogenous ATF6 acts to preserve heart structure and function in an MI model of heart failure, suggesting that ATF6 may be a viable therapeutic target for treatment of this disease.

Feature tracking in cine cardiac magnetic resonance (CMR) is a quantitative technique to assess heart structure and function. We investigated 4-dimensional (4D) dynamics and morphology of the mitral annulus (MA) using a novel tracking system based on radially rotational long-axis cine CMR series. A total of 30 normal controls and patients with mitral regurgitation were enrolled. The spatiotemporal changes of the MA were characterized by an in-house developed program. Dynamic and morphological parameters extracted from all 18 radial slices were used as references and were compared with those from subsequently generated sub-datasets with different degrees of sparsity. An excellent agreement was found among all datasets including routine 2-, 3- and 4-chamber views for MA dynamics such as peak systolic velocity (Sm) and mitral annular plane systolic excursion (MAPSE). MA morphology for size and shape was addressed adequately by as few as 6 radial slices, but poorly by only three routine views. Patients with regurgitation showed significantly reduced mitral dynamics and mild annular deformation, which was consistent between three routine views and 18 reference slices. In conclusion, feature tracking cine CMR provided a comprehensive and distinctive profile for 4D MA dynamics and morphology, which may help in studying different cardiac diseases.

Introduction. Atrial fibrillation (AF) occurs in 8.0-22.0% of patients with acute myocardial infarction (MI). It is associated with a significant increase in both hospital mortality and mortality over a 5-year observation period. AF can be the result of a number of pathological processes – hemodynamic disorders, ischemia or AF (especially in patients with early AF), right ventricular infarction, pericarditis, excessive release of catecholamines, chronic lung diseases, acute hypoxia, use of sympathomimetics, hypokalemia, etc. Aim. To find out the incidence of AF, its association with structural changes in the heart, heart failure, and other factors in patients in the remote period after MI. Materials and methods. To assess the AF prevalence and its association with the changes in heart structure and heart failure 169 patients with previous MI (135 men, 34 women; mean age 57,3 ± 11,4 years) were included into the study. Mean time after the first MI was 4,96 ± 4,64 years. AF was found in 33 patients (19,5 %): in 23 patients (13,6 %) AF was considered as permanent, in 10 (5,9 %) as paroxysmal. Results. As result of a multiple logistic regression analysis, only the age and the volume of a right atrium were found as the independent predictors of AF. Every 10 years of life of the patients the probability of the permanent AF risk increases more then two-fold (110,0 %), and increase of the volume of right atrium for every 50,0 ml – three-fold (200,0 %). Prevalence of permanent AF increases with the growth of heart failure functional class whereas paroxysmal AF does not depend on heart failure severity. It was found that AF occurs in 19.5% of the patients in the remote period after MI, paroxysmal form – in 5.9%, permanent – in 13.6%. The frequency of continuous permanent AF in patients after MI increases with an increase of the severity of heart failure. At the same time, the functional class of heart failure was not an independent predictor of AF. Patients with permanent AF were older, had larger atrium, more severe heart failure, and greater degree of regurgitation through the mitral and tricuspid valves. Patients with paroxysmal form of arrhythmia occupied an intermediate position among the patients with a permanent form and without arrhythmia for most of the indices. Independent predictors of AF were only the age and volume of the right atrium. Conclusions. When assessing the risk of AF special attention should be paid to the parameters like the size of the right atrium and the degree of regurgitation through the tricuspid valve.

У статті наведені результати вивчення впливу підвищеної тиреоїдної функції на тлі інсулінорезистентності на показники структури і функції серця. Встановлено, що при підвищенні функції щитоподібної залози основною нозологічною формою ураження міокарда у пацієнтів без супутньої серцево-судинної патології є розвиток метаболічної ендокринної кардіоміопатії. Особливістю ураження серця при синдромі тиреотоксикозу є відсутність кардіосклеротичних, міокардитичних та ішемічних процесів. Особливостями клінічних, інструментальних і лабораторних змін у пацієнтів з підвищеною функцією щитоподібної залози є суб’єктивна маніфестація, тенденція до розвитку систолічної артеріальної гіпертензії, виражена гіполіпідемія, тенденція до гіперглікемії. Проявами електричної дисфункції міокарда при гіпертиреозі є збільшення частоти серцевих скорочень, виражена тенденція до підвищення аритмогенезу (здебільшого шлуночкового типу), порушення процесів реполяризації шлуночків і переважання електричної негомогенності міокарда як передсердь, так і шлуночків. Морфофункціональні зміни серця при синдромі тиреотоксикозу проявляються збільшенням розмірів його порожнин, маси міокарда лівого шлуночка, пришвидшеним розслабленням останнього. Ураження серця при тиреотоксикозі характеризується збільшенням тривалості і дисперсії інтервалу QTc, що свідчить про порушення процесів реполяризації міокарда, і збільшенням його електричної негомогенності, що може бути предиктором ризику розвитку шлуночкових порушень ритму. Зміни серцевої діяльності при тиреотоксикозі у пацієнтів чоловічої статі характеризуються більшою вираженістю електрофізіологічних і морфофункціональних змін міокарда порівняно з пацієнтами жіночої статі.

The aim of this study was to determine the impact of multi-slice computed tomography (MSCT) evaluation of coronary artery stenosis on left heart structure and systolic function. Coronary artery CT angiography was performed in 200 patients diagnosed with coronary heart disease, and then according to the AHA coronary artery 17-segment fractionation method, the Gensini score (GS) was determined for every narrow segment, and one-stop assessment of the correlation between left heart structure and function was performed. After the grouping of GS quartiles from low to high, there were differences between different patients with regard to LVDD, LADD, LVEDV, LVESV, MM, LVEF, and FS, while no difference in SV and CO. GS showed linear negative correlation with LVEF and FS, and linear positive correlation with LVDD, LADD, LVEDV, LVESV, and MM, while no correlation with SV and CO. That is, GS of coronary artery stenosis was negatively correlated with left ventricular systolic function and positively correlated with myocardial mass. The narrower the coronary artery, the worse the cardiac function and the higher the myocardial hypertrophy. Coronary artery stenosis was one of the important causes of the decrease in left ventricular systolic function and cardiac remodeling.

Cardiomyocytes grow during heart maturation or disease-related cardiac remodeling. We present evidence that the intercalated disc (ID) is integral to both longitudinal and lateral growth: increases in width are accommodated by lateral extension of the plicate tread regions and increases in length by sarcomere insertion within the ID. At the margin between myofibril and the folded membrane of the ID lies a transitional junction through which the thin filaments from the last sarcomere run to the ID membrane and it has been suggested that this junction acts as a proto Z-disc for sarcomere addition. In support of this hypothesis, we have investigated the ultrastructure of the ID in mouse hearts from control and dilated cardiomyopathy (DCM) models, the MLP-null and a cardiac-specific β-catenin mutant, cΔex3, as well as in human left ventricle from normal and DCM samples. We find that the ID amplitude can vary tenfold from 0.2 μm up to a maximum of ~2 μm allowing gradual expansion during heart growth. At the greatest amplitude, equivalent to a sarcomere length, A-bands and thick filaments are found within the ID membrane loops together with a Z-disc, which develops at the transitional junction position. Here, also, the tops of the membrane folds, which are rich in αII spectrin, become enlarged and associated with junctional sarcoplasmic reticulum. Systematically larger ID amplitudes are found in DCM samples. Other morphological differences between mouse DCM and normal hearts suggest that sarcomere inclusion is compromised in the diseased hearts., Cellular and Molecular Life Sciences, 71 (1), ISSN:1420-682X, ISSN:1420-9071

Objective: Despite a well-documented association between stress and depression with cardiac morbidity and mortality, there is no satisfactory explanation for the mechanisms linking affective and cardiac disorders. This study investigated cardiac electrophysiological properties in an animal model of depression. Methods: Depression-relevant physiological and behavioral parameters were measured in adult male wild-type rats during and after a period of intermittent social defeat stress (n = 12) or empty cage exposure (control, n = 11). Nine days after the last defeat/empty cage exposure, high-definition epicardial mapping was performed under anesthesia. Results: Stressed animals versus controls displayed a larger reduction in the circadian amplitude of heart rate (-32% [3%] versus 13 [2%]; p = .001) and body temperature (-33% [4%] versus -5% [2%]; p = .001) rhythms, had smaller body weight gain (+11% [1%] versus +17% [1%]; p

Menopausal hormone therapy does not seem to have any adverse effect on the structure and function of the heart, and may have a positive effect, according to new research published in PLOS One .1 The effect of menopausal hormone therapy, previously known as hormone replacement therapy (HRT), on cardiovascular health in post-menopausal women remains controversial and unclear. Extensive observational data had suggested menopausal hormone therapy was cardioprotective, leading to it being routinely prescribed for primary and secondary prevention of coronary heart disease. However, subsequent data from the Women’s Health Initiative and elsewhere have cast …

Most studies relating blood pressure (BP) to target organ damage measure BP at the brachial artery, but pulse pressure (PP) and systolic BP (SBP) in the aorta are lower than the corresponding peripheral measures. In adults, aortic (central) PP and SBP have been shown to be more closely related to target organ damage and cardiovascular events than peripheral pressures. We compared central and peripheral PP and their associations with concurrent measures of cardiac structure and function in a large, population-based cohort of adolescents.

Undernutrition during development increases the risk for adult cardiovascular disease. To determine if PUN alters heart structure function, and maximal exercise capacity in adulthood, newborn control mouse pups were fostered to dams fed a control (CON; 20% protein) or a protein-restricted diet (PUN; 8% protein; n=7-10 litters/treatment). At 21 d (PN21) pups were fed the CON diet ad lib. At PN70 a maximal treadmill test was performed to determine VO2peak; maximal vertical work was calculated for the final 30 sec. At PN80 cardiac function was evaluated by echocardiography. VO2peak was the same in CON and PUN mice and higher in males than females (249 + 9 and 169 + 6 ml/hr, respectively, P