The development of coronary vascularization

2018 ◽  
Author(s):  
Robert J. Tomanek ◽  
Adriana A. Silva Pires-Gomes ◽  
José Maria Pérez-Pomares
Keyword(s):  
Myocardial Infarction ◽  
Vascular System ◽  
Current Knowledge ◽  
Evolutionary Constraints ◽  
Myocardial Performance ◽  
Evolutionary Innovation ◽  
Cell Sources ◽  
Multiple Cell ◽  
Coronary Blood Vessels ◽  
Molecular Components

The coronary vascular system is a complex network of arteries, veins, and capillaries that supports myocardial performance, a topic previously reviewed by other authors. Disruption of coronary blood vessel form and/or function can underlie severe congenital and acquired cardiovascular conditions, from myocardial infarction to sudden death. Coronary blood vessels are an evolutionary innovation of vertebrates and form from multiple cell sources. Accordingly, the developmental complexity of coronary vessel morphogenesis is likely to reflect evolutionary constraints, as well as to explain the origins of coronary congenital anomalies (CCAs). In this chapter we summarize the current knowledge on coronary vascular development and identify the essential mechanistic cellular and molecular components of coronary morphogenesis. We will also provide plausible developmental explanations for some relevant CCAs.

scholarly journals A review of current knowledge of myeloproliferative disorders in the horse

2021 ◽  
Vol 63 (1) ◽  
Author(s):  
Katy Satué ◽  
Juan Carlos Gardon ◽  
Ana Muñoz
Keyword(s):  
Bone Marrow ◽  
Myeloid Leukemia ◽  
Current Knowledge ◽  
Myeloproliferative Neoplasms ◽  
Myeloproliferative Disorders ◽  
World Health ◽  
Chronic Granulocytic Leukemia ◽  
Current State ◽  
Multiple Cell ◽  
Health Organization

AbstractMyeloid disorders are conditions being characterized by abnormal proliferation and development of myeloid lineage including granulocytes (neutrophils, eosinophils and basophils), monocytes, erythroids, and megakaryocytes precursor cells. Myeloid leukemia, based on clinical presentation and proliferative rate of neoplastic cells, is divided into acute (AML) and myeloproliferative neoplasms (MPN). The most commonly myeloid leukemia reported in horses are AML-M4 (myelomonocytic) and AML-M5 (monocytic). Isolated cases of AML-M6B (acute erythroid leukemia), and chronic granulocytic leukemia have also been reported. Additionally, bone marrow disorders with dysplastic alterations and ineffective hematopoiesis affecting single or multiple cell lineages or myelodysplastic diseases (MDS), have also been reported in horses. MDSs have increased myeloblasts numbers in blood or bone marrow, although less than 20%, which is the minimum level required for diagnosis of AML. This review performed a detailed description of the current state of knowlegde of the myeloproliferative disorders in horses following the criteria established by the World Health Organization.

scholarly journals Evolutionary assembly patterns of prokaryotic genomes

2015 ◽  
Author(s):  
Maximilian O. Press ◽  
Christine Queitsch ◽  
Elhanan Borenstein
Keyword(s):  
Evolutionary Constraints ◽  
Historical Contingency ◽  
Phenotypic Characters ◽  
Functional Relationships ◽  
Evolutionary Innovation ◽  
Gene Level ◽  
Prokaryotic Genomes ◽  
Evolutionary Paths ◽  
Evolution Of Proteins ◽  
Sequence Substitution

AbstractEvolutionary innovation must occur in the context of some genomic background, which limits available evolutionary paths. For example, protein evolution by sequence substitution is constrained by epistasis between residues. In prokaryotes, evolutionary innovation frequently happens by macrogenomic events such as horizontal gene transfer (HGT). Previous work has suggested that HGT can be influenced by ancestral genomic content, yet the extent of such gene-level constraints has not yet been systematically characterized. Here, we evaluated the evolutionary impact of such constraints in prokaryotes, using probabilistic ancestral reconstructions from 634 extant prokaryotic genomes and a novel framework for detecting evolutionary constraints on HGT events. We identified 8,228 directional dependencies between genes, and demonstrated that many such dependencies reflect known functional relationships, including, for example, evolutionary dependencies of the photosynthetic enzyme RuBisCO. Modeling all dependencies as a network, we adapted an approach from graph theory to establish chronological precedence in the acquisition of different genomic functions. Specifically, we demonstrated that specific functions tend to be gained sequentially, suggesting that evolution in prokaryotes is governed by functional assembly patterns. Finally, we showed that these dependencies are universal rather than clade-specific and are often sufficient for predicting whether or not a given ancestral genome will acquire specific genes. Combined, our results indicate that evolutionary innovation via HGT is profoundly constrained by epistasis and historical contingency, similar to the evolution of proteins and phenotypic characters, and suggest that the emergence of specific metabolic and pathological phenotypes in prokaryotes can be predictable from current genomes.

The Effect of Smoking on Myocardial Performance Index in Middle-Aged Males after First Acute Myocardial Infarction

2012 ◽  
Vol 30 (2) ◽  
pp. 155-163 ◽  
Author(s):  
Ahmet Bacaksiz ◽  
Mehmet Kayrak ◽  
Mehmet Akif Vatankulu ◽  
Selim S. Ayhan ◽  
Osman Sonmez ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Performance Index ◽  
Myocardial Performance Index ◽  
Myocardial Performance ◽  
Middle Aged

Validation of the wall motion score and myocardial performance indexes as novel techniques to assess cardiac function in mice after myocardial infarction

2007 ◽  
Vol 292 (2) ◽  
pp. H1187-H1192 ◽  
Author(s):  
Yan Zhang ◽  
Junya Takagawa ◽  
Richard E. Sievers ◽  
Muhammad F. Khan ◽  
Mohan N. Viswanathan ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Wall Motion ◽  
Left Ventricular ◽  
Lv Function ◽  
Myocardial Performance ◽  
Ejection Time ◽  
Inflow Velocity ◽  
Mitral Inflow ◽  
Mitral Inflow Velocity ◽  
Deceleration Time

The aim of this study was to determine the feasibility and accuracy of wall motion score index (WMSI) and myocardial performance index (MPI) for measuring regional and global left ventricular (LV) function with use of high-resolution echocardiography after myocardial infarction (MI) in mice. In 48 mice, myocardial infarction was induced by ligation in the middle of the left anterior descending coronary artery. Echocardiography was performed under anesthesia at baseline and 1 mo after MI. WMSI was analyzed by a 16-segment model on short-axis views, and wall motion was scored as 1 for normal, 2 for hypokinetic, 3 for akinetic, 4 for dyskinetic, and 5 for aneurysmal. WMSI was calculated as the sum of scores divided by the total number of segments. MPI was calculated on the basis of isovolumetric contraction time (IVCT), isovolumetric relaxation time (IVRT), and ejection time (ET): MPI = (IVCT + IVRT)/ET. We measured LV ejection fraction (LVEF), end-systolic and end-diastolic volumes (ESV and EDV), fractional shortening (FS), and infarct size (IS). LVEF at 4 wk after MI was reduced at 32.8 ± 9.0%. Linear correlation analyses showed that WMSI (1.6 ± 0.3) correlated with LVEF ( r = −0.84, P < 0.0005), FS ( r = −0.43, P = 0.003), and IS (34.3 ± 15.3%, r = 0.86, P < 0.0005). MPI (0.67 ± 0.09) correlated with LVEF ( r = −0.67, P < 0.0005) and IS ( r = 0.72, P < 0.0005). MPI also correlated with mitral inflow velocity ( r = −0.68, P < 0.0005) and deceleration time ( r = −0.42, P = 0.003). Stepwise regression analysis revealed that WMSI was independently associated with IS. IS, FS, mitral inflow velocity, and deceleration time were independent determinants of MPI. In conclusion, echocardiographic assessments of WMSI and MPI in mice are feasible and correlate strongly with two-dimensional measurement of LV function and IS. These novel parameters provide additional noninvasive assessment of regional and global LV function in mice after MI.

scholarly journals Myocardial infarction remodeling that progresses to heart failure: a signaling misunderstanding

2018 ◽  
Vol 315 (1) ◽  
pp. H71-H79 ◽  
Author(s):  
Alan J. Mouton ◽  
Osvaldo J. Rivera ◽  
Merry L. Lindsey
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Wound Healing ◽  
Current Knowledge ◽  
Healing Process ◽  
Cell Types ◽  
Left Ventricular ◽  
Wound Healing Process ◽  
The Status ◽  
The Right

After myocardial infarction, remodeling of the left ventricle involves a wound-healing orchestra involving a variety of cell types. In order for wound healing to be optimal, appropriate communication must occur; these cells all need to come in at the right time, be activated at the right time in the right amount, and know when to exit at the right time. When this occurs, a new homeostasis is obtained within the infarct, such that infarct scar size and quality are sufficient to maintain left ventricular size and shape. The ideal scenario does not always occur in reality. Often, miscommunication can occur between infarct and remote spaces, across the temporal wound-healing spectrum, and across organs. When miscommunication occurs, adverse remodeling can progress to heart failure. This review discusses current knowledge gaps and recent development of the roles of inflammation and the extracellular matrix in myocardial infarction remodeling. In particular, the macrophage is one cell type that provides direct and indirect regulation of both the inflammatory and scar-forming responses. We summarize current research efforts focused on identifying biomarker indicators that reflect the status of each component of the wound-healing process to better predict outcomes.

Preoperative assessment and optimization

2017 ◽  
Author(s):  
Felix van Lier ◽  
Robert Jan Stolker
Keyword(s):  
Myocardial Infarction ◽  
Cardiovascular Risk ◽  
Risk Reduction ◽  
Myocardial Ischaemia ◽  
Current Knowledge ◽  
Thrombus Formation ◽  
Cardiac Risk ◽  
Risk Identification ◽  
Coronary Lesion

Perioperative cardiovascular complications (including myocardial ischaemia and myocardial infarction) are the predominant cause of morbidity and mortality in patients undergoing non-cardiac surgery. The pathophysiology of perioperative myocardial infarction is complex. Prolonged myocardial ischaemia due to the stress of surgery in the presence of a haemodynamically significant coronary lesion, leading to subendocardial ischaemia, and acute coronary artery occlusion after plaque rupture and thrombus formation contribute equally to these devastating events. Perioperative management aims at optimizing the patient’s condition by identification and modification of underlying cardiac risk factors and diseases. The first part of this chapter covers current knowledge on preoperative risk assessment. Current risk indices, the value of additional testing, and new preoperative cardiac risk makers are investigated. During recent decades there has been a shift from the assessment and treatment of the underlying culprit coronary lesion towards a systemic medical therapy aiming at prevention of myocardial oxygen supply–demand mismatch and coronary plaque stabilization. In the second part of this chapter, risk-reduction strategies are discussed, including β‎-blocker therapy, statins, and aspirins. A central theme in this chapter will focus on long-term cardiovascular risk reduction. Patients who undergo non-cardiac (vascular) surgery are particularly prone to long-term adverse cardiac outcomes. The goal of perioperative cardiovascular risk identification and modification should not be limited to the perioperative period, but should extend well into the postoperative period.

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