Review of ultrasound contrast agents in current clinical practice with special focus on DEFINITY® in cardiac imaging

2020 ◽  
Author(s):  
Mohammed Salih ◽  
Syed Musadiq Ali ◽  
Nihar Jena ◽  
Karthik Ananthasubramaniam
Keyword(s):  
Daily Practice ◽  
Left Ventricular ◽  
Ultrasound Contrast Agents ◽  
Special Focus ◽  
Clinical Role ◽  
Case Examples ◽  
Us Fda ◽  
And Function ◽  
Ultrasound Microbubbles

Echocardiography is the most widely used noninvasive modality to evaluate the structure and function of the cardiac muscle in daily practice. However, up to 15–20% of echocardiograms are considered suboptimal. To enable accurate assessment of cardiac function and wall motion abnormality, the use of ultrasound microbubble contrast has shown substantial benefits in cases of salvaging nondiagnostic studies and enhancing the diagnostic accuracy in daily practice. DEFINITY® is a perflutren based, lipid shelled microbubble contrast agent, which is US FDA approved for left ventricular opacification. The basis of ultrasound microbubbles, its development, and the clinical role of DEFINITY (characteristics, indications and case examples, side effect profile and existing evidence) is the subject of discussion in this review.

scholarly journals Gremlin2 Regulates the Differentiation and Function of Cardiac Progenitor Cells via the Notch Signaling Pathway

2018 ◽  
Vol 47 (2) ◽  
pp. 579-589 ◽  
Author(s):  
Wei Li ◽  
Yaojun Lu ◽  
Ruijuan Han ◽  
Qiang Yue ◽  
Xiurong Song ◽  
...  
Keyword(s):  
Mouse Model ◽  
Progenitor Cells ◽  
Left Ventricular ◽  
Cardiac Repair ◽  
Cardiac Progenitor Cells ◽  
Cardiomyocyte Differentiation ◽  
Rt Pcr ◽  
And Function

Background/Aims: The transplantation of cardiac progenitor cells (CPCs) improves neovascularization and left ventricular function after myocardial infarction (MI). The bone morphogenetic protein antagonist Gremlin 2 (Grem2) is required for early cardiac development and cardiomyocyte differentiation. The present study examined the role of Grem2 in CPC differentiation and cardiac repair. Methods: To determine the role of Grem 2 during CPC differentiation, c-Kit+ CPCs were cultured in differentiation medium for different times, and Grem2, Notch1 and Jagged1 expression was determined by RT-PCR and western blotting. Short hairpin RNA was used to silence Grem2 expression, and the expression of cardiomyocyte surface markers was assessed by RT-PCR and immunofluorescence staining. In vivo experiments were performed in a mouse model of left anterior descending coronary artery ligation-induced MI. Results: CPC differentiation upregulated Grem2 expression and activated the Notch1 pathway. Grem2 knockdown inhibited cardiomyocyte differentiation, and this effect was similar to that of Notch1 pathway inhibition in vitro. Jagged1 overexpression rescued the effects of Grem2 silencing. In vivo, Grem2 silencing abolished the protective effects of CPC injection on cardiac fibrosis and function. Conclusions: Grem2 regulates CPC cardiac differentiation by modulating Notch1 signaling. Grem2 enhances the protective effect of CPCs on heart function in a mouse model of MI, suggesting its potential as the rapeutic protein for cardiac repair.

scholarly journals The Role of Glycocalyx and Caveolae in Vascular Homeostasis and Diseases

2021 ◽  
Vol 11 ◽  
Author(s):  
Simone Regina Potje ◽  
Tiago Dal-Cin Paula ◽  
Michele Paulo ◽  
Lusiane Maria Bendhack
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Cardiovascular Diseases ◽  
Endothelial Glycocalyx ◽  
Special Focus ◽  
Oxygen Species ◽  
Vascular Homeostasis ◽  
Structure Synthesis ◽  
And Function

This review highlights recent findings about the role that endothelial glycocalyx and caveolae play in vascular homeostasis. We describe the structure, synthesis, and function of glycocalyx and caveolae in vascular cells under physiological and pathophysiological conditions. Special focus will be given in glycocalyx and caveolae that are associated with impaired production of nitric oxide (NO) and generation of reactive oxygen species (ROS). Such alterations could contribute to the development of cardiovascular diseases, such as atherosclerosis, and hypertension.

scholarly journals Loss of Endothelial HIF-Prolyl hydroxylase 2 (PHD2) Induces Cardiac Hypertrophy and Fibrosis

2021 ◽  
Author(s):  
Zhiyu Dai ◽  
Jianding Cheng ◽  
Bin Liu ◽  
Dan Yi ◽  
Anlin Feng ◽  
...  
Keyword(s):  
Heart Failure ◽  
Cardiac Hypertrophy ◽  
Cardiac Fibrosis ◽  
Left Ventricular ◽  
Dependent Manner ◽  
Adaptive Responses ◽  
Genetic Ablation ◽  
Pathological Cardiac Hypertrophy ◽  
And Function

Cardiac hypertrophy and fibrosis are common adaptive responses to injury and stress, eventually leading to heart failure. Hypoxia signaling is important to the (patho)physiological process of cardiac remodeling. However, the role of endothelial Prolyl-4 hydroxylase 2 (PHD2)/hypoxia inducible factors (HIFs) signaling in the pathogenesis of heart failure remains elusive. We observed a marked decrease of PHD2 expression in heart tissues and cardiovascular endothelial cells from patients with cardiomyopathy. Mice with Tie2-Cre-mediated deletion of Egln1 (encoding PHD2) or tamoxifen-induced endothelial Egln1 deletion exhibited left ventricular hypertrophy and cardiac fibrosis. Genetic ablation and pharmacological inhibition of Hif2a but not Hif1a in endothelial Egln1 deficient mice normalized cardiac size and function. The present studies define for the first time an unexpected role of endothelial PHD2 deficiency in inducing cardiac hypertrophy and fibrosis in a HIF-2α dependent manner. Targeting PHD2/HIF-2α signaling may represent a novel therapeutic approach for the treatment of pathological cardiac hypertrophy and failure.

scholarly journals Role of Cardiac Magnetic Resonance Imaging in the Evaluation of Athletes with Premature Ventricular Beats

2022 ◽  
Vol 11 (2) ◽  
pp. 426
Author(s):  
Giulia Brunetti ◽  
Alberto Cipriani ◽  
Martina Perazzolo Marra ◽  
Manuel De Lazzari ◽  
Barbara Bauce ◽  
...  
Keyword(s):  
Cardiac Magnetic Resonance ◽  
Magnetic Resonance ◽  
Training Session ◽  
Left Ventricular ◽  
Special Focus ◽  
Premature Ventricular Beats ◽  
Myocardial Substrate ◽  
Diagnostic Work ◽  
Cmr Imaging

Premature ventricular beats (PVBs) in athletes are not rare. The risk of PVBs depends on the presence of an underlying pathological myocardial substrate predisposing the subject to sudden cardiac death. The standard diagnostic work-up of athletes with PVBs includes an examination of family and personal history, resting electrocardiogram (ECG), 24 h ambulatory ECG (possibly with a 12-lead configuration and including a training session), maximal exercise testing and echocardiography. Despite its fundamental role in the diagnostic assessment of athletes with PVBs, echocardiography has very limited sensitivity in detecting the presence of non-ischemic left ventricular scars, which can be revealed only through more in-depth studies, particularly with the use of contrast-enhanced cardiac magnetic resonance (CMR) imaging. The morphology, complexity and exercise inducibility of PVBs can help estimate the probability of an underlying heart disease. Based on these features, CMR imaging may be indicated even when echocardiography is normal. This review focuses on interpreting PVBs, and on the indication and role of CMR imaging in the diagnostic evaluation of athletes, with a special focus on non-ischemic left ventricular scars that are an emerging substrate of cardiac arrest during sport.

Heart rate reduction improves myocardial ischemia in swine: role of interventricular blood flow redistribution

1991 ◽  
Vol 261 (3) ◽  
pp. H910-H917 ◽  
Author(s):  
C. Indolfi ◽  
B. D. Guth ◽  
S. Miyazaki ◽  
T. Miura ◽  
R. Schulz ◽  
...  
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Left Ventricular ◽  
Regional Myocardial Blood Flow ◽  
Lv Function ◽  
Wall Thickening ◽  
Regional Dysfunction ◽  
Electrical Pacing ◽  
And Function

Regional myocardial blood flow (MBF) distribution and function upon slowing the heart rate (HR) during ischemia were studied in anesthetized swine, a species without coronary collaterals. Perfusion of the left anterior descending artery by a pump allowed controlled production of regional ischemia. Slowing tachycardia by electrical pacing (127 to 87 beats/min) caused marked improvement of regional dysfunction [% wall thickening (WTh) from 9 to 27%] and increased subendocardial MBF [from 0.31 to 0.55 ml.min-1.g-1 (P less than 0.001)] without change of subepicardial MBF. Total left ventricular (LV) MBF increased, whereas right ventricular (RV) MBF fell by 18% (P less than 0.02). The mechanism of MBF changes during slowed HR was assessed by surgically excluding the RV and comparing findings with previous experiments with RV intact when HR was slowed from 96 to 60 beats/min. A similar improvement of regional LV function occurred (8% vs. 30% WTh) with the RV excluded, but without a change in total flow to the LV bed, whereas subendocardial MBF increased and subepicardial MBF fell, indicating transmural redistribution only. These findings show that the RV vascular bed can contribute to LV perfusion in swine during ischemia, and they document the potential for “reverse RV steal” during slowed heart rate in this setting.

scholarly journals Functional Role of Class III Myosins in Hair Cells

2021 ◽  
Vol 9 ◽  
Author(s):  
Joseph A. Cirilo ◽  
Laura K. Gunther ◽  
Christopher M. Yengo
Keyword(s):  
Hearing Loss ◽  
Hair Cells ◽  
Atp Hydrolysis ◽  
Point Mutations ◽  
Special Focus ◽  
Myosin Isoforms ◽  
Class Iii ◽  
Myosin Motors ◽  
And Function

Cytoskeletal motors produce force and motion using the energy from ATP hydrolysis and function in a variety of mechanical roles in cells including muscle contraction, cargo transport, and cell division. Actin-based myosin motors have been shown to play crucial roles in the development and function of the stereocilia of auditory and vestibular inner ear hair cells. Hair cells can contain hundreds of stereocilia, which rely on myosin motors to elongate, organize, and stabilize their structure. Mutations in many stereocilia-associated myosins have been shown to cause hearing loss in both humans and animal models suggesting that each myosin isoform has a specific function in these unique parallel actin bundle-based protrusions. Here we review what is known about the classes of myosins that function in the stereocilia, with a special focus on class III myosins that harbor point mutations associated with delayed onset hearing loss. Much has been learned about the role of the two class III myosin isoforms, MYO3A and MYO3B, in maintaining the precise stereocilia lengths required for normal hearing. We propose a model for how class III myosins play a key role in regulating stereocilia lengths and demonstrate how their motor and regulatory properties are particularly well suited for this function. We conclude that ongoing studies on class III myosins and other stereocilia-associated myosins are extremely important and may lead to novel therapeutic strategies for the treatment of hearing loss due to stereocilia degeneration.

scholarly journals Emerging roles of epigenetics in the control of reproductive function: Focus on central neuroendocrine mechanisms

2021 ◽  
Author(s):  
Maria Jesus Vazquez ◽  
Silvia Daza-Dueñas ◽  
Manuel Tena-Sempere
Keyword(s):  
Perfect Match ◽  
Reproductive Function ◽  
Reproductive Capacity ◽  
Special Focus ◽  
Epigenetic Mechanisms ◽  
Reproductive Axis ◽  
Neuroendocrine Mechanisms ◽  
Essential Function ◽  
And Function

Abstract Reproduction is an essential function for perpetuation of the species. As such, it is controlled by sophisticated regulatory mechanisms, which allow a perfect match between environmental conditions and internal cues, to ensure adequate pubertal maturation and achievement of reproductive capacity. Besides classical genetic regulatory events, mounting evidence has documented that different epigenetic mechanisms operate at different levels of the reproductive axis to finely tune the development and function of this complex neuroendocrine system along the lifespan. In this mini-review, we will summarize recent evidence on the role of epigenetics in the control of reproduction, with special focus on the modulation of the central components of this axis. Particular attention will be paid to the epigenetic control of puberty and Kiss1 neurons, as major developments have taken place in this domain recently. In addition, the putative role of central epigenetic mechanisms in mediating the influence of nutritional and environmental cues on reproductive function will be also discussed.

scholarly journals Symbiosis and the Anthropocene

Symbiosis ◽  
2021 ◽  
Vol 84 (3) ◽  
pp. 239-270 ◽  
Author(s):  
Erik F. Y. Hom ◽  
Alexandra S. Penn
Keyword(s):  
Conceptual Framework ◽  
Ecosystem Processes ◽  
Structure And Function ◽  
Ecosystem Change ◽  
Anthropogenic Change ◽  
Case Examples ◽  
Evolutionary Innovation ◽  
The Earth ◽  
And Function

AbstractRecent human activity has profoundly transformed Earth biomes on a scale and at rates that are unprecedented. Given the central role of symbioses in ecosystem processes, functions, and services throughout the Earth biosphere, the impacts of human-driven change on symbioses are critical to understand. Symbioses are not merely collections of organisms, but co-evolved partners that arise from the synergistic combination and action of different genetic programs. They function with varying degrees of permanence and selection as emergent units with substantial potential for combinatorial and evolutionary innovation in both structure and function. Following an articulation of operational definitions of symbiosis and related concepts and characteristics of the Anthropocene, we outline a basic typology of anthropogenic change (AC) and a conceptual framework for how AC might mechanistically impact symbioses with select case examples to highlight our perspective. We discuss surprising connections between symbiosis and the Anthropocene, suggesting ways in which new symbioses could arise due to AC, how symbioses could be agents of ecosystem change, and how symbioses, broadly defined, of humans and “farmed” organisms may have launched the Anthropocene. We conclude with reflections on the robustness of symbioses to AC and our perspective on the importance of symbioses as ecosystem keystones and the need to tackle anthropogenic challenges as wise and humble stewards embedded within the system.

Clinical role of post-angioplasty hyperemic microvascular resistances in chronic ischemic left ventricular dysfunction

2017 ◽  
Vol 18 (5) ◽  
pp. 332-340 ◽  
Author(s):  
Riccardo Gorla ◽  
Edoardo Verna ◽  
Simone Scotti ◽  
Sergio Ghiringhelli ◽  
Laura Zoli ◽  
...  
Keyword(s):  
Left Ventricular Dysfunction ◽  
Ventricular Dysfunction ◽  
Left Ventricular ◽  
Clinical Role

PATHOGENETIC ROLE OF MYOCARDIAL FIBROSIS: FOCUS ON EXTRACELLULAR MATRIX

2020 ◽  
pp. 21-24
Author(s):  
T. M. Ambrosova ◽  
T. V. Ashcheulova
Keyword(s):  
Extracellular Matrix ◽  
Left Ventricular Hypertrophy ◽  
Myocardial Fibrosis ◽  
Cardiac Remodeling ◽  
Heart Muscle ◽  
Ventricular Hypertrophy ◽  
Collagen Type ◽  
Left Ventricular ◽  
And Function

The main cardiovascular diseases affect the processes of myocardial remodeling, which further contributes to the formation of systolic or diastolic heart dysfunction. The formation of myocardial dysfunction is primarily associated with left ventricular hypertrophy when under hemodynamic loading, firstly, wall rigidity increases, secondly, myocardial fibrosis is formed. The latter is one of the key factors of the hypertrophic process caused by the accumulation of collagen, which leads to a aggravation of the left ventricle relaxation processes. Cardiac remodeling is defined as a group of molecular, cellular, and interstitial changes that are clinically manifested by alterations in the size, shape, and function of heart as a result of the heart muscle injury. It has been determined that fibrosis is an early morphological sign of injury in patients with left ventricular overload, as well as a factor in the development of diastolic and systolic dysfunctions. Compensatory left ventricular hypertrophy transforms into heart failure due to the fibrosis development. In hypertrophy the content of elastic collagen type III decreases and rigid collagen type I increases. The essential role of the extracellular matrix in myocardial fibrosis formation is emphasized. Cardiac fibrosis is a process of pathological remodeling of the extracellular matrix, which leads to abnormalities in its composition and dysfunction of the heart muscle. The extracellular matrix plays a key role in organogenesis and post−traumatic healing in tissue injuries. The study of intercellular interactions of the extracellular matrix will provide a better understanding of the mechanisms of changes in geometry and function of the heart, and investigation of the activity of matrix components will open new opportunities for targeted therapeutic effects on molecular mechanisms of cardiac remodeling. Key words: diastolic dysfunction, extracellular matrix, myocardial fibrosis, cardiomyocytes, fibroblasts.

Sign in / Sign up

Export Citation Format

Share Document