Visual recognition of cardiac pathology based on 3D parametric model reconstruction

Visual recognition of cardiac images is important for cardiac pathology diagnosis and treatment.Due to the limited availability of annotated datasets,traditional methods usually extract features directly from twodimensional slices of three-dimensional(3D)heart images,followed by pathological classification.This process may not ensure the overall anatomical consistency in 3D heart.A new method for classification of cardiac pathology is therefore proposed based on 3D parametric model reconstruction.First,3D heart models are reconstructed based on multiple 3D volumes of cardiac imaging data at the end-systole(ES)and end-diastole(ED)phases.Next,based on these reconstructed 3D hearts,3D parametric models are constructed through the statistical shape model(SSM),and then the heart data are augmented via the variation in shape parameters of one 3D parametric model with visual knowledge constraints.Finally,shape and motion features of 3D heart models across two phases are extracted to classify cardiac pathology.Comprehensive experiments on the automated cardiac diagnosis challenge(ACDC)dataset of the Statistical Atlases and Computational Modelling of the Heart(STACOM)workshop confirm the superior performance and efficiency of this proposed approach.

Application and Prospect of Postmortem Imaging Technology in Forensic Cardiac Pathology:A Systemic Review

Postmortem imaging(PMI)technology known as virtual autopsy or virtopsy is regarded as a useful method of noninvasive or minimally invasive autopsy in forensic practice.Postmortem computed tomography is applicable to traumatic investigation,acute hemorrhage,pulmonary parenchyma disease,calcification(calculus,atherosclerosis),and gas accumulation.Postmortem magnetic resonance(PMMR)has been proven to have advantages in soft tissue identification.Cardiac death is one of the keys and difficult points in forensic practice.With the introduction and development of PMCT angiography and PMMR,it was proved to be a very promising tool in the investigation of cardiac death,including vascular cavities and ischemic myocardium.This article reviewed the applications of the latest PMI and its related technologies in forensic cardiac pathology,including advantages,limitations,and development prospects.

Aerobic interval training preconditioning protocols inhibit isoproterenol-induced pathological cardiac remodeling in rats:Implications on oxidative balance,autophagy,and apoptosis

This study aimed to investigate the potential cardioprotective effects of moderate and high-intensity aerobic interval training(MIIT and HIIT)preconditioning.The focus was on histological changes,pro-oxidant-antioxidant balance,autophagy initiation,and apoptosis in myocardial tissue incited by isoproterenol-induced pathological cardiac remodeling(ISO-induced PCR).Male Wistar rats were randomly divided into control(n=6),ISO(n=8),MIIT(n=4),HIIT(n=4),MIIT+ISO(n=8),and HIIT+ISO(n=8)groups.The MIIT and HIIT protocols were administered for 10 weeks,followed by the induction of cardiac remodeling using subcutaneous injection of ISO(100 mg/kg for two consecutive days).Alterations in heart rate(HR),mean arterial pressure(MAP),rate pressure product(RPP),myocardial oxygen consumption(MVO_(2)),cardiac hypertrophy,histopathological changes,prooxidant-antioxidant balance,autophagy biomarkers(Beclin-1,Atg7,p62,LC3Ⅰ/Ⅱ),and apoptotic cell distribution were measured.The findings revealed that the MIIT+ISO and HIIT+ISO groups demonstrated diminished myocardial damage,hemorrhage,immune cell infiltration,edema,necrosis,and apoptosis compared to ISO induced rats.MIIT and HIIT preconditioning mitigated HR,enhanced MAP,and preserved MVO_(2)and RPP.The pro-oxidant-antioxidant balance was sustained in both MIIT+ISO and HIIT+ISO groups,with MIIT primarily inhibiting pro-apoptotic autophagy progression through maintaining pro-oxidant-antioxidant balance,and HIIT promoting pro-survival autophagy.The results demonstrated the beneficial effects of both MIIT and HIIT as AITs preconditioning in ameliorating ISO-induced PCR by improving exercise capacity,hemodynamic parameters,and histopathological changes.Some of these protective effects can be attributed to the modulation of cardiac apoptosis,autophagy,and oxidative stress.

Vaspin alleviates pathological cardiac hypertrophy by regulating autophagy-dependent myocardial senescence

Background:Visceral adipose tissue-derived serine protease inhibitor(vaspin),a secretory adipokine,protects against insulin resistance.Recent studies have demonstrated that serum vaspin levels are decreased in patients with coronary artery disease and that vaspin protects against myocardial ischemia-reperfusion injury and atherosclerosis.However,it remains unclear whether vaspin exerts specific effects on pathological cardiac hypertrophy.Methods:An in vivo study was conducted using a cardiac hypertrophy model established by subcutaneous injection of isoproterenol(ISO)in C57BL/6 and vaspin-ko mice.Rapamycin was administered intraperitoneally to mice,for further study.H9c2 cells and neonatal rat ventricular myocytes(NRVMs)were treated with ISO to induce hypertrophy.Human vaspin fusion protein,the proteasome inhibitor MG132,and chloroquine diphosphate were used for further mechanistic studies.Results:Here,we provide the first evidence that vaspin knockdown results in markedly exaggerated cardiac hypertrophy,fibrosis,and cardiomyocyte senescence in mice treated with ISO.Conversely,the administration of exogenous recombinant human vaspin protected NRVMs in vitro against ISO-induced hypertrophy and senescence.Furthermore,vaspin significantly potentiated the ISO-induced decrease in autophagy.Both rapamycin and chloroquine diphosphate regulated autophagy in vivo and in vitro,respectively,and participated in vaspin-mediated cardioprotection.Moreover,the PI3K-AKT-mTOR pathway plays a critical role in vaspin-mediated autophagy in cardiac tissues and NRVMs.Our data showed that vaspin downregulated the p85 and p110 subunits of PI3K by linking p85 and p110 to NEDD4L-mediated ubiquitination degradation.Conclusion:Our results show,for the first time,that vaspin functions as a critical regulator that alleviates pathological cardiac hypertrophy by regulating autophagy-dependent myocardial senescence,providing potential preventive and therapeutic targets for pathological cardiac hypertrophy.

Sudden cardiac death and valvular pathology

Sudden death due to valvular heart disease is reported to range from 1% to 5% in native valves and around 0.2%-0.9%/year in prosthesis.The nature of the diseases is varied,from heritable,congenital to acquired.It may affect both genders in multiple age groups.The authors show and comment examples of the major nosologic aetiologies underlying unexpected exitus letalis of valvular nature.

The Structural Impact of Aortic Valve Replacement on Mitral Regurgitation

Background: Structural changes to the mitral annulus occur following aortic valve replacement (AVR) for severe aortic stenosis which may influence functional mitral regurgitation (MR). Methods: A retrospective review of 44 patients who underwent open AVR for aortic stenosis at a single center from 2010-2013 was performed. Patients undergoing concomitant aortic root surgery or with severe MR were excluded. MR was evaluated with preoperative and postoperative transthoracic echocardiograms. Univariate and multivariable analyses were performed to assess for factors associated with postoperative MR improvement and worsening. Results: Prior to AVR, none had severe MR, 5% (2 patients) had moderate, 9% (4 patients) mild-to-moderate, 46% (20 patients) mild, and 23% (9 patients) trace MR. Of patients with pre-operative MR, 44% (16 patients) experienced improvement of MR. Six patients had worsening of MR and the remaining 22 patients had no change. Cases of more severe MR were more likely to improve compared with mild or trace MR (P = 0.04). MR worsening was significantly more likely in patients with bicuspid aortic valves (83% vs. 24%;P = 0.004), and with larger aortic annulus diameters (P = 0.03). MR worsening was less frequent in cases of mitral annular calcification (0% vs 42%;P = 0.04) and left atrial enlargement (17% vs 65%;P = 0.03). Logistic regression analysis revealed negative predictors for MR improvement were mitral annular calcification (P = 0.04) and larger aortic annulus diastolic diameter (P = 0.05). Conclusion: Structural factors such as aortic annular size, mitral annular calcification and valve morphology may impact MR following AVR and should be investigated further as potential targets of surgical therapy.

Sudden cardiac death in anabolic androgenic steroids abuse: case report and literature review

Anabolic androgenic steroids (AAS) have several adverse effects on the cardiovascular system that may lead to a sudden cardiac death (SCD).We herein report a case involving a 24-year-old male,AAS abuser with intramuscular delivery in the 6 months before,who suffered a cardiorespiratory arrest at home's bathtub when returning from New Year's party.A forensic autopsy was performed according to the guidelines of the Association for European Cardiovascular Pathology (AECVP).The body showed hypertrophy of skeletal musculature,with low amount of subcutaneous fat and no signs of injury (body mass index,BMh 26.8 kg/m^(2)).On internal examination,there were multiorgan congestion,acute pulmonary edema,and cardiomegaly (420 g) with severe coronary atherosclerosis and superimposed acute occlusive thrombosis at the left main trunk and left anterior descendant.Areas of scarring were located at the intersection between the posterior wall and the posterior third of the septum (postero-septal).At histology,acute myocardial infarction at the anterior third of the septum and the anterior wall,and subacute myocardial infarction at apical septum and apical posterior wall were detected.Other findings were small intramyocardial vessel disease and myocytes hypertrophy.Chemicotoxicological analysis in blood showed ethanol ((0.90 ±0.05) g/L),stanazolol (11.31 μg/L),nandrolone (2.05μg/L) and testosterone (<1.00μg/L).When confronted with a sudden death in a young athlete we must pay attention to the physical phenotype that may suggest AAS abuse and perform a detailed examination of the heart.Chemicotoxicological analysis is a key to establish the relationship between SCD and AAS abuse.

MicroRNA-34c-5p provokes isoprenaline-induced cardiac hypertrophy by modulating autophagy via targeting ATG4B

Pathological cardiac hypertrophy serves as a significant foundation for cardiac dysfunction and heart failure. Recently, growing evidence has revealed that microRNAs(miRNAs) play multiple roles in biological processes and participate in cardiovascular diseases. In the present research, we investigate the impact of miRNA-34 c-5 p on cardiac hypertrophy and the mechanism involved. The expression of miR-34 c-5 p was proved to be elevated in heart tissues from isoprenaline(ISO)-infused mice. ISO also promoted miR-34 c-5 p level in primary cultures of neonatal rat cardiomyocytes(NRCMs). Transfection with miR-34 c-5 p mimic enhanced cell surface area and expression levels of foetal-type genes atrial natriuretic factor(Anf) and β-myosin heavy chain(β-Mhc) in NRCMs. In contrast, treatment with miR-34 c-5 p inhibitor attenuated ISO-induced hypertrophic responses. Enforced expression of miR-34 c-5 p by tail intravenous injection of its agomir led to cardiac dysfunction and hypertrophy in mice, whereas inhibiting miR-34 c-5 p by specific antagomir could protect the animals against ISO-triggered hypertrophic abnormalities. Mechanistically, miR-34 c-5 p suppressed autophagic flux in cardiomyocytes, which contributed to the development of hypertrophy. Furthermore, the autophagy-related gene 4 B(ATG4 B) was identified as a direct target of miR-34 c-5 p, and miR-34 c-5 p was certified to interact with 3’untranslated region of Atg4 b mRNA by dual-luciferase reporter assay. miR-34 c-5 p reduced the expression of ATG4 B, thereby resulting in decreased autophagy activity and induction of hypertrophy. Inhibition of miR-34 c-5 p abolished the detrimental effects of ISO by restoring ATG4 B and increasing autophagy. In conclusion, our findings illuminate that miR-34 c-5 p participates in ISO-induced cardiac hypertrophy, at least partly through suppressing ATG4 B and autophagy. It suggests that regulation of miR-34 c-5 p may offer a new way for handling hypertrophy-related cardiac dysfunction.