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Article ; Online: Myocardial

Liga, Riccardo / Gimelli, Alessia / Marzullo, Paolo / Ambrosio, Giuseppe / Cameli, Matteo / Cerbai, Elisabetta / Coiro, Stefano / Emdin, Michele / Marcucci, Rossella / Morrone, Doralisa / Palazzuoli, Alberto / Petronio, Anna Sonia / Savino, Ketty / Padeletti, Luigi / Pedrinelli, Roberto

Journal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology

2017 Volume 25, Issue 2, Page(s) 461–470

Abstract: ... ischemic heart disease to which hypertension predisposes as a risk factor. However, despite its fundamental role ...

Abstract	Sympathetic nervous system plays a pivotal role in essential hypertension and in the development of left ventricular hypertrophy. Moreover, cardiac sympathetic dys-regulation has been demonstrated as a key con-causal factor in the genesis and progression of pathologic conditions such as congestive heart failure and ischemic heart disease to which hypertension predisposes as a risk factor. However, despite its fundamental role in cardiac pathophysiology, the evaluation of cardiac sympathetic nervous system has never gained a wide clinical application, remaining mostly a research tool. In this context, nuclear imaging techniques are the only modalities to allow the direct evaluation of cardiac sympathetic nervous integrity, giving the chance to obtain objective measures of the sympathetic tone. This review, while summarizing the general profile of currently available tests for autonomic evaluation, focuses on
MeSH term(s)	3-Iodobenzylguanidine ; Animals ; Baroreflex ; Disease Models, Animal ; Echocardiography ; Heart/diagnostic imaging ; Heart/physiopathology ; Heart Failure/diagnostic imaging ; Humans ; Hypertension/complications ; Hypertrophy, Left Ventricular/diagnostic imaging ; Myocardial Ischemia/diagnostic imaging ; Myocardium/pathology ; Prognosis ; Risk Factors ; Sympathetic Nervous System/physiopathology ; Synaptic Transmission ; Tomography, Emission-Computed, Single-Photon
Chemical Substances	3-Iodobenzylguanidine (35MRW7B4AD)
Language	English
Publishing date	2017-08-10
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1212505-2
ISSN	1532-6551 ; 1071-3581
ISSN (online)	1532-6551
ISSN	1071-3581
DOI	10.1007/s12350-017-1029-2
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Article ; Online: Infliximab Limits Injury in Myocardial Infarction.

Journal of the American Heart Association

2024 Volume 13, Issue 9, Page(s) e032172

Abstract: ... the inflammatory response and consequent remodeling from ischemic myocardial injury.: Methods and results ... myocardial infarction and subjected to array-based proteome analysis. Clinically indistinguishable ... at myocardial infarction (MI), patients were stratified into vulnerable and resilient on the basis of 1-year ...

Abstract	Background: The purpose of this study was to investigate a therapeutic approach targeting the inflammatory response and consequent remodeling from ischemic myocardial injury. Methods and results: Coronary thrombus aspirates were collected from patients at the time of ST-segment-elevation myocardial infarction and subjected to array-based proteome analysis. Clinically indistinguishable at myocardial infarction (MI), patients were stratified into vulnerable and resilient on the basis of 1-year left ventricular ejection fraction and death. Network analysis from coronary aspirates revealed prioritization of tumor necrosis factor-α signaling in patients with worse clinical outcomes. Infliximab, a tumor necrosis factor-α inhibitor, was infused intravenously at reperfusion in a porcine MI model to assess whether infliximab-mediated immune modulation impacts post-MI injury. At 3 days after MI (n=7), infliximab infusion increased proregenerative M2 macrophages in the myocardial border zone as quantified by immunofluorescence (24.1%±23.3% in infliximab versus 9.29%±8.7% in sham; Conclusions: Profiling of coronary thrombus aspirates in patients with ST-segment-elevation MI revealed highest association for tumor necrosis factor-α in injury risk. Infliximab-mediated immune modulation offers an actionable pathway to alter MI-induced inflammatory response, preserving contractility and limiting adverse structural remodeling.
MeSH term(s)	Infliximab/therapeutic use ; Infliximab/pharmacology ; Animals ; Humans ; Male ; Middle Aged ; Ventricular Remodeling/drug effects ; Female ; Disease Models, Animal ; ST Elevation Myocardial Infarction/drug therapy ; ST Elevation Myocardial Infarction/immunology ; Ventricular Function, Left/drug effects ; Swine ; Aged ; Tumor Necrosis Factor-alpha/metabolism ; Stroke Volume/drug effects ; Coronary Thrombosis/prevention & control ; Coronary Thrombosis/drug therapy ; Myocardium/pathology ; Myocardium/metabolism ; Myocardium/immunology ; Troponin I/blood ; Troponin I/metabolism ; Macrophages/drug effects ; Macrophages/immunology ; Macrophages/metabolism
Chemical Substances	Infliximab (B72HH48FLU) ; Tumor Necrosis Factor-alpha ; Troponin I
Language	English
Publishing date	2024-05-03
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2653953-6
ISSN	2047-9980 ; 2047-9980
ISSN (online)	2047-9980
ISSN	2047-9980
DOI	10.1161/JAHA.123.032172
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Article ; Online: Myocardial blood flow quantification with SPECT.

Wells, R Glenn / Small, Gary R / Ruddy, Terrence D

Journal of medical imaging and radiation sciences

2024 Volume 55, Issue 2S, Page(s) S51–S58

Abstract: Introduction: The addition of absolute myocardial blood flow (MBF) data improves the diagnostic ... the use of SPECT to measure myocardial blood flow (MBF). Studies have evaluated SPECT MBF in large ... the sensitivity and specificity of the detection of multi-vessel disease over relative perfusion imaging and provides incremental ...

Abstract	Introduction: The addition of absolute myocardial blood flow (MBF) data improves the diagnostic and prognostic accuracy of relative perfusion imaging with nuclear medicine. Cardiac-specific gamma cameras allow measurement of MBF with SPECT. Methods: This paper reviews the evidence supporting the use of SPECT to measure myocardial blood flow (MBF). Studies have evaluated SPECT MBF in large animal models and compared it in humans with invasive angiographic measurements and against the clinical standard of PET MBF. The repeatability of SPECT MBF has been determined in both single-site and multi-center trials. Results: SPECT MBF has excellent correlation with microspheres in an animal model, with the number of stenoses and fractional flow reserve, and with PET-derived MBF. The inter-user coefficient of variability is ∼20% while the COV of test-retest MBF is ∼30%. SPECT MBF improves the sensitivity and specificity of the detection of multi-vessel disease over relative perfusion imaging and provides incremental value in predicting adverse cardiac events. Conclusion: SPECT MBF is a promising technique for providing clinically valuable information in the assessment of coronary artery disease.
MeSH term(s)	Tomography, Emission-Computed, Single-Photon/methods ; Humans ; Coronary Circulation/physiology ; Animals ; Coronary Artery Disease/diagnostic imaging ; Coronary Artery Disease/physiopathology ; Myocardial Perfusion Imaging/methods ; Sensitivity and Specificity ; Reproducibility of Results
Language	English
Publishing date	2024-03-28
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2426513-5
ISSN	1876-7982 ; 1939-8654
ISSN (online)	1876-7982
ISSN	1939-8654
DOI	10.1016/j.jmir.2024.02.016
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Article ; Online: Pop-Out Myocardial Infarction Induction in Mice.

Wang, Bingyan J / Chaudhry, Hina W

Methods in molecular biology (Clifton, N.J.)

2024 Volume 2803, Page(s) 137–144

Abstract: Myocardial infarction (MI) in mice is a widely used surgical model in preclinical cardiac repair ... studies to recapitulate human cardiovascular ischemic disease. Induction of reproducible infarct size is ...

Abstract	Myocardial infarction (MI) in mice is a widely used surgical model in preclinical cardiac repair studies to recapitulate human cardiovascular ischemic disease. Induction of reproducible infarct size is crucial for quantitative and analytical purpose. Here we describe a quick and reliable method to induce consistent infarct size in mice in less than a minute.
MeSH term(s)	Animals ; Myocardial Infarction/pathology ; Mice ; Disease Models, Animal ; Humans ; Myocardium/pathology ; Myocardium/metabolism
Language	English
Publishing date	2024-04-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-3846-0_10
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Article ; Online: Rat Model of Isoproterenol-Induced Myocardial Injury.

Gupta, Kirti / Bagang, Newly / Singh, Gaaminepreet / Laddi, Loveinder

Methods in molecular biology (Clifton, N.J.)

2024 Volume 2803, Page(s) 123–136

Abstract: ... to aggravation of myocardial injury. Subcutaneous or intraperitoneal ISO injection into rats can replicate ... several features of human heart disease, making it a useful tool for comprehending the underlying mechanisms and ... to induce myocardial injury. ...

Abstract	Isoproterenol (ISO) administration produces significant biochemical and histological changes including oxidative stress, reactive oxygen species (ROS) overproduction, and inflammation that leads to aggravation of myocardial injury. Subcutaneous or intraperitoneal ISO injection into rats can replicate several features of human heart disease, making it a useful tool for comprehending the underlying mechanisms and evaluating potential therapeutic strategies. In the present chapter, we elaborate on how depending on the precise experimental goals and the intended level of severity, different dosages and regimens are employed to induce myocardial injury.
MeSH term(s)	Isoproterenol/toxicity ; Animals ; Rats ; Disease Models, Animal ; Oxidative Stress/drug effects ; Reactive Oxygen Species/metabolism ; Myocardium/pathology ; Myocardium/metabolism ; Humans ; Male ; Heart Injuries/chemically induced ; Heart Injuries/pathology ; Heart Injuries/metabolism
Chemical Substances	Isoproterenol (L628TT009W) ; Reactive Oxygen Species
Language	English
Publishing date	2024-04-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-3846-0_9
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Article ; Online: Characterizing the immune response to myocardial infarction in pigs.

Schnitter, Florian / Stangl, Franziska / Noeske, Elisabeth / Bille, Maya / Stadtmüller, Anja / Vogt, Niklas / Sicklinger, Florian / Leuschner, Florian / Frey, Anna / Schreiber, Laura / Frantz, Stefan / Beyersdorf, Niklas / Ramos, Gustavo / Gladow, Nadine / Hofmann, Ulrich

Basic research in cardiology

2024 Volume 119, Issue 3, Page(s) 453–479

Abstract: Though myocardial infarction (MI) in pigs is a well-established translational large animal ... vivo by (immuno)histology, flow cytometry, and RNA sequencing of myocardial tissue on days 3, 7, and 14 ...

Abstract	Though myocardial infarction (MI) in pigs is a well-established translational large animal model, it has not yet been widely used for immunotherapy studies, and a comprehensive description of the immune response to MI in this species is lacking. We induced MI in Landrace pigs by balloon occlusion of the left anterior descending artery over 90 min. Within 14 days, the necrotic myocardium was progressively replaced by scar tissue with involvement of myofibroblasts. We characterized the immune response in the heart ex vivo by (immuno)histology, flow cytometry, and RNA sequencing of myocardial tissue on days 3, 7, and 14 after MI. Besides a clear predominance of myeloid cells among heart-infiltrating leukocytes, we detected activated T cells and an increasing proportion of CD4
MeSH term(s)	Animals ; Myocardial Infarction/immunology ; Myocardial Infarction/pathology ; Disease Models, Animal ; T-Lymphocytes, Regulatory/immunology ; Myocardium/pathology ; Myocardium/immunology ; Sus scrofa ; Swine ; Lymphocyte Activation ; Male ; Transcriptome ; Female ; Time Factors
Language	English
Publishing date	2024-03-15
Publishing country	Germany
Document type	Journal Article
ZDB-ID	189755-x
ISSN	1435-1803 ; 0300-8428 ; 0175-9418
ISSN (online)	1435-1803
ISSN	0300-8428 ; 0175-9418
DOI	10.1007/s00395-024-01036-2
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Article ; Online: Arterial thromboembolism in a cat with transient myocardial thickening.

Vollmar, C / Mitropoulou, A / Hassdenteufel, E / Hildebrandt, N / Schneider, M

Journal of veterinary cardiology : the official journal of the European Society of Veterinary Cardiology

2024 Volume 52, Page(s) 14–18

Abstract: ... cardiomyopathies; however, it has not been described in cats with transient myocardial thickening. A previously ... with transient myocardial thickening, with favorable long-term survival. ...

Abstract	Feline arterial thromboembolism has been reported to be secondary to various feline cardiomyopathies; however, it has not been described in cats with transient myocardial thickening. A previously healthy, one-year-old, castrated male cat presented with acute paraparesis and congestive heart failure. Echocardiography revealed asymmetric left ventricular free wall thickening and left atrial enlargement. Antithrombotic treatment and cardiac medication resulted in reperfusion and mobility on day seven in one limb and on day 10 in the other. Different complications were managed successfully, including worsening acute kidney injury, inflammation, pleural effusion, and anemia. After three weeks, the cat was discharged and prescribed oral antithrombotic drugs (clopidogrel and rivaroxaban) and cardiac medication. Within five months, echocardiographic findings normalized, and medical treatment was gradually discontinued. To date, the cat remains healthy at 1735 days after the initial diagnosis and 1494 days after the last antithrombotic medication. To the best of our knowledge, this is the first case report on feline arterial thromboembolism combined with transient myocardial thickening, with favorable long-term survival.
MeSH term(s)	Cats ; Animals ; Male ; Cat Diseases/drug therapy ; Cat Diseases/pathology ; Cat Diseases/diagnostic imaging ; Cat Diseases/diagnosis ; Thromboembolism/veterinary ; Thromboembolism/drug therapy ; Echocardiography/veterinary ; Cardiomyopathies/veterinary ; Cardiomyopathies/complications
Language	English
Publishing date	2024-01-20
Publishing country	Netherlands
Document type	Case Reports ; Journal Article
ZDB-ID	2198278-8
ISSN	1875-0834 ; 1760-2734
ISSN (online)	1875-0834
ISSN	1760-2734
DOI	10.1016/j.jvc.2024.01.002
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Article ; Online: Influence of trimetazidine on myocardial injury in mice with diabetic cardiomyopathy.

Zhao, Dongming / Ma, Jingming / Sun, Yuman / Huang, Wei / Fan, Jinyang / Ye, Mingzhe / Hu, Bo / Sun, Xinyi

Journal of diabetes and its complications

2024 Volume 38, Issue 5, Page(s) 108744

Abstract: ... the prognosis of patients. Trimetazidine (TMZ), as a drug affecting myocardial energy metabolism, mainly reduces ... mechanism is still unclear.: Objective: This study aims to investigate the impact of TMZ on myocardial ... administered physiological saline. Periodic measurements of blood glucose, blood lipids, and myocardial enzymes ...

Abstract	Introduction: The prevalence of diabetes mellitus is increasing year by year globally, and diabetic cardiomyopathy (DCM), as the most common complication of type 2 diabetes mellitus, seriously affects the prognosis of patients. Trimetazidine (TMZ), as a drug affecting myocardial energy metabolism, mainly reduces the oxidation rate of β-oxidation by inhibiting 3-ketoacyl-CoA thiolase (3-KAT), a key enzyme in β-oxidation of free fatty acid (FFA), so that the energy metabolism substrate of cardiomyocytes preferentially selects glucose rather than fatty acids, increases the content of intracellular adenosine triphosphate (ATP), enhances the contractile function of cardiomyocytes, and improves the state of cellular ischemia and hypoxia. Previous studies have shown that TMZ is closely related to the activation and induction of apoptosis of the MAPK pathway and AMPK pathway, and plays a role in the treatment of diabetic cardiomyopathy, but the specific mechanism is still unclear. Objective: This study aims to investigate the impact of TMZ on myocardial damage in mice exhibiting diabetic cardiomyopathy (DCM), and to furnish a laboratory foundation for the clinical treatment of diabetic cardiomyopathy. Method: Male db/db mice (6 weeks old, n = 21) and male wild-type (wt) (6 weeks old, n = 20) mice were selected for the study. The wt mice were randomly assigned to the wt group (n = 10) and wt + TMZ group (n = 10), while the remaining db/db mice were randomly allocated to the db/db group (n = 11) and db/db + TMZ group (n = 10). Following 8 weeks of feeding, the wt + TMZ group and db/db + TMZ group received TMZ via gavage, whereas the remaining groups were administered physiological saline. Periodic measurements of blood glucose, blood lipids, and myocardial enzymes were conducted in mice, with samples obtained after the 12th week for subsequent biochemical analysis, myocardial pathology assessment, immunohistochemistry, western blot analysis, and TUNEL staining (TdT-mediated dUTP Nick-End Labeling). Result: GLU, TC, TG, LDL-C, and CK-MB levels were significantly higher in db/db mice compared to wt mice (GLU: M ± SD wt 5.94 ± 0.37, db/db 17.63 ± 0.89, p < 0.05, ES = 0.991; TC: M ± SD wt 3.01 ± 0.32, db/db 6.97 ± 0.36, p < 0.05, ES = 0.972; TG: M ± SD wt 0.58 ± 0.2, db/db 1.75 ± 0.14, p < 0.05, ES = 0.920; LDL-C: M ± SD wt 1.59 ± 0.12, db/db 3.87 ± 0.14, p < 0.05, ES = 0.989; CK-MB: M ± SD wt 0.12 ± 0.01, db/db 0.31 ± 0.04, p < 0.05, ES = 0.928). HDL-C levels were significantly lower in db/db mice (M ± SD wt 1.89 ± 0.08, db/db 0.64 ± 0.09, p < 0.05, ES = 0.963). Histopathological analysis confirmed myocardial damage in db/db mice. Treatment with TMZ reduced GLU, TC, TG, LDL-C, and CK-MB levels (p < 0.05, ES > 0.9) and increased HDL-C levels compared to untreated db/db mice. Additionally, TMZ treatment significantly decreased myocardial cell apoptosis (p < 0.05, ES = 0.980). These results demonstrate the efficacy of TMZ in reversing myocardial injury in DCM mice. Conclusion: TMZ can mitigate myocardial damage in db/db mice by downregulating the expression of caspase-12, a protein associated with the endoplasmic reticulum stress (ERS) cell apoptosis pathway, consequently diminishing cell apoptosis. This underscores the protective efficacy of TMZ against myocardial damage in mice afflicted with DCM.
MeSH term(s)	Animals ; Trimetazidine/pharmacology ; Trimetazidine/therapeutic use ; Diabetic Cardiomyopathies/metabolism ; Diabetic Cardiomyopathies/drug therapy ; Mice ; Male ; Myocardium/pathology ; Myocardium/metabolism ; Mice, Inbred C57BL ; Apoptosis/drug effects ; Vasodilator Agents/therapeutic use ; Vasodilator Agents/pharmacology ; Disease Models, Animal ; Myocytes, Cardiac/drug effects ; Myocytes, Cardiac/metabolism ; Myocytes, Cardiac/pathology ; Diabetes Mellitus, Type 2/complications ; Diabetes Mellitus, Type 2/drug therapy ; Diabetes Mellitus, Type 2/metabolism
Chemical Substances	Trimetazidine (N9A0A0R9S8) ; Vasodilator Agents
Language	English
Publishing date	2024-04-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1105840-7
ISSN	1873-460X ; 1056-8727
ISSN (online)	1873-460X
ISSN	1056-8727
DOI	10.1016/j.jdiacomp.2024.108744
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Article ; Online: Endocardial HDAC3 is required for myocardial trabeculation.

Jang, Jihyun / Bentsen, Mette / Kim, Ye Jun / Kim, Erick / Garg, Vidu / Cai, Chen-Leng / Looso, Mario / Li, Deqiang

Nature communications

2024 Volume 15, Issue 1, Page(s) 4166

Abstract: ... into the pathogenesis of congenital heart disease and conceptual strategies to promote myocardial regeneration. ... Failure of proper ventricular trabeculation is often associated with congenital heart disease ...

Abstract	Failure of proper ventricular trabeculation is often associated with congenital heart disease. Support from endocardial cells, including the secretion of extracellular matrix and growth factors is critical for trabeculation. However, it is poorly understood how the secretion of extracellular matrix and growth factors is initiated and regulated by endocardial cells. We find that genetic knockout of histone deacetylase 3 in the endocardium in mice results in early embryo lethality and ventricular hypotrabeculation. Single cell RNA sequencing identifies significant downregulation of extracellular matrix components in histone deacetylase 3 knockout endocardial cells. Secretome from cultured histone deacetylase 3 knockout mouse cardiac endothelial cells lacks transforming growth factor ß3 and shows significantly reduced capacity in stimulating cultured cardiomyocyte proliferation, which is remarkably rescued by transforming growth factor ß3 supplementation. Mechanistically, we identify that histone deacetylase 3 knockout induces transforming growth factor ß3 expression through repressing microRNA-129-5p. Our findings provide insights into the pathogenesis of congenital heart disease and conceptual strategies to promote myocardial regeneration.
MeSH term(s)	Animals ; Mice, Knockout ; Endocardium/metabolism ; Mice ; MicroRNAs/metabolism ; MicroRNAs/genetics ; Histone Deacetylases/metabolism ; Histone Deacetylases/genetics ; Myocytes, Cardiac/metabolism ; Transforming Growth Factor beta3/metabolism ; Transforming Growth Factor beta3/genetics ; Cell Proliferation ; Myocardium/metabolism ; Endothelial Cells/metabolism ; Heart Defects, Congenital/genetics ; Heart Defects, Congenital/metabolism ; Heart Defects, Congenital/pathology ; Extracellular Matrix/metabolism ; Female
Chemical Substances	histone deacetylase 3
Language	English
Publishing date	2024-05-16
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-024-48362-6
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Article: Exploring Cardiac Exosomal RNAs of Acute Myocardial Infarction.

Jung, Seung Eun / Kim, Sang Woo / Choi, Jung-Won

Biomedicines

2024 Volume 12, Issue 2

Abstract: Background: Myocardial infarction (MI), often a frequent symptom of coronary artery disease (CAD ... is a leading cause of death and disability worldwide. Acute myocardial infarction (AMI), a major form ... of cardiovascular disease, necessitates a deep understanding of its complex pathophysiology to develop ...

Abstract	Background: Myocardial infarction (MI), often a frequent symptom of coronary artery disease (CAD), is a leading cause of death and disability worldwide. Acute myocardial infarction (AMI), a major form of cardiovascular disease, necessitates a deep understanding of its complex pathophysiology to develop innovative therapeutic strategies. Exosomal RNAs (exoRNA), particularly microRNAs (miRNAs) within cardiac tissues, play a critical role in intercellular communication and pathophysiological processes of AMI. Methods: This study aimed to delineate the exoRNA landscape, focusing especially on miRNAs in animal models using high-throughput sequencing. The approach included sequencing analysis to identify significant miRNAs in AMI, followed by validation of the functions of selected miRNAs through in vitro studies involving primary cardiomyocytes and fibroblasts. Results: Numerous differentially expressed miRNAs in AMI were identified using five mice per group. The functions of 20 selected miRNAs were validated through in vitro studies with primary cardiomyocytes and fibroblasts. Conclusions: This research enhances understanding of post-AMI molecular changes in cardiac tissues and investigates the potential of exoRNAs as biomarkers or therapeutic targets. These findings offer new insights into the molecular mechanisms of AMIs, paving the way for RNA-based diagnostics and therapeutics and therapies and contributing to the advancement of cardiovascular medicine.
Language	English
Publishing date	2024-02-14
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines12020430
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