Production of Swine Myocardial Infarction and Ischemic Heart Failure Models Using a Three-Dimensional Bioprinted Occluder

2020 ◽  
Author(s):  
Han Byul Kim ◽  
Seungman Jung ◽  
Hyukjin Park ◽  
Doo sun Sim ◽  
Moon Ki Kim ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Three Dimensional ◽  
Ischemic Heart ◽  
Ischemic Heart Failure ◽  
Failure Models

scholarly journals ACE Inhibition Modulates Myeloid Hematopoiesis after Acute Myocardial Infarction and Reduces Cardiac and Vascular Inflammation in Ischemic Heart Failure

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 396
Author(s):  
Wolf-Stephan Rudi ◽  
Michael Molitor ◽  
Venkata Garlapati ◽  
Stefanie Finger ◽  
Johannes Wild ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Bone Marrow ◽  
Left Ventricular Function ◽  
Ventricular Function ◽  
Vascular Inflammation ◽  
Ace Inhibition ◽  
Left Ventricular ◽  
Ischemic Heart ◽  
Ischemic Heart Failure

Aims: Angiotensin-converting-enzyme inhibitors (ACE inhibitors) are a cornerstone of drug therapy after myocardial infarction (MI) and improve left ventricular function and survival. We aimed to elucidate the impact of early treatment with the ACE inhibitor ramipril on the hematopoietic response after MI, as well as on the chronic systemic and vascular inflammation. Methods and Results: In a mouse model of MI, induced by permanent ligation of the left anterior descending artery, immediate initiation of treatment with ramipril (10 mg/k/d via drinking water) reduced cardiac inflammation and the number of circulating inflammatory monocytes, whereas left ventricular function was not altered significantly, respectively. This effect was accompanied by enhanced retention of hematopoietic stem cells, Lin−Sca1−c-Kit+CD34+CD16/32+ granulocyte–macrophage progenitors (GMP) and Lin−Sca1−c-Kit+CD150−CD48− multipotent progenitors (MPP) in the bone marrow, with an upregulation of the niche factors Angiopoetin 1 and Kitl at 7 d post MI. Long-term ACE inhibition for 28 d limited vascular inflammation, particularly the infiltration of Ly6Chigh monocytes/macrophages, and reduced superoxide formation, resulting in improved endothelial function in mice with ischemic heart failure. Conclusion: ACE inhibition modulates the myeloid inflammatory response after MI due to the retention of myeloid precursor cells in their bone marrow reservoir. This results in a reduction in cardiac and vascular inflammation with improvement in survival after MI.

scholarly journals Role of P2X purinergic receptors in the rescue of ischemic heart failure

2008 ◽  
Vol 295 (3) ◽  
pp. H1191-H1197 ◽  
Author(s):  
Dmitry Sonin ◽  
Si-Yuan Zhou ◽  
Chunxia Cronin ◽  
Tatiana Sonina ◽  
Jeffrey Wu ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Infarct Size ◽  
Purinergic Receptors ◽  
P2x Receptors ◽  
Left Ventricular ◽  
Ischemic Heart ◽  
Post Myocardial Infarction ◽  
Ischemic Heart Failure

Evidence is accumulating to support the presence of P2X purinergic receptors in the heart. However, the biological role of this receptor remains to be defined. The objectives here were to determine the role of cardiac P2X receptors in modulating the progression of post-myocardial infarction ischemic heart failure and to investigate the underlying mechanism. The P2X4 receptor (P2X4R) is an important subunit of native cardiac P2X receptors, and the cardiac-specific transgenic overexpression of P2X4R (Tg) was developed as a model. Left anterior descending artery ligation resulted in similar infarct size between Tg and wild-type (WT) mice ( P > 0.1). However, Tg mice showed an enhanced cardiac contractile performance at 7 days, 1 mo, and 2 mo after infarction and an increased survival at 1 and 2 mo after infarction ( P < 0.01). The enhanced intact heart function was manifested by a greater global left ventricular developed pressure and rate of contraction of left ventricular pressure in vitro and by a significantly increased fractional shortening and systolic thickening in the noninfarcted region in vivo ( P < 0.05). The salutary effects on the ischemic heart failure phenotype were seen in both sexes and were not the result of any difference in infarct size in Tg versus WT hearts. An enhanced contractile function of the noninfarcted area in the Tg heart was likely an important rescuing mechanism. The cardiac P2X receptor is a novel target to treat post-myocardial infarction ischemic heart failure.

Importance of EuroSCORE-II in the Development of Acute Ischemic Heart Failure After Acute Anterior ST Elevation Myocardial Infarction

2016 ◽  
Vol 19 (2) ◽  
pp. 65-71
Author(s):  
İlker Gül ◽  
Mustafa Zungur ◽  
Ahmet Çağrı Aykan ◽  
Aysel İslamlı ◽  
Bekir Serhat Yıldız ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Ischemic Heart ◽  
St Elevation Myocardial Infarction ◽  
Ischemic Heart Failure ◽  
St Elevation

scholarly journals Comparison of Troponin Elevation, Prior Myocardial Infarction, and Chest Pain in Acute Ischemic Heart Failure

CJC Open ◽  
2020 ◽  
Vol 2 (3) ◽  
pp. 135-144
Author(s):  
Cassandra Freitas ◽  
Xuesong Wang ◽  
Yin Ge ◽  
Heather J. Ross ◽  
Peter C. Austin ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Chest Pain ◽  
Ischemic Heart ◽  
Ischemic Heart Failure ◽  
Troponin Elevation ◽  
Prior Myocardial Infarction

scholarly journals Quality of life in patients with coronary heart disease after myocardial infarction and with ischemic heart failure

2016 ◽  
Vol 2 ◽  
pp. 326-333 ◽  
Author(s):  
Joanna M. Moryś ◽  
Jerzy Bellwon ◽  
Stefan Höfer ◽  
Andrzej Rynkiewicz ◽  
Marcin Gruchała
Keyword(s):  
Quality Of Life ◽  
Myocardial Infarction ◽  
Heart Failure ◽  
Coronary Heart Disease ◽  
Heart Disease ◽  
Ischemic Heart ◽  
Ischemic Heart Failure

scholarly journals Post-myocardial infarction heart failure dysregulates the bone vascular niche

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Jedrzej Hoffmann ◽  
Guillermo Luxán ◽  
Wesley Tyler Abplanalp ◽  
Simone-Franziska Glaser ◽  
Tina Rasper ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Vascular Function ◽  
Ischemic Heart ◽  
Post Myocardial Infarction ◽  
Ischemic Heart Failure ◽  
Single Cell Rna Sequencing ◽  
Bone Vasculature ◽  
Infarction Heart ◽  
Age Independent

AbstractThe regulation of bone vasculature by chronic diseases, such as heart failure is unknown. Here, we describe the effects of myocardial infarction and post-infarction heart failure on the bone vascular cell composition. We demonstrate an age-independent loss of type H endothelium in heart failure after myocardial infarction in both mice and humans. Using single-cell RNA sequencing, we delineate the transcriptional heterogeneity of human bone marrow endothelium, showing increased expression of inflammatory genes, including IL1B and MYC, in ischemic heart failure. Endothelial-specific overexpression of MYC was sufficient to induce type H bone endothelial cells, whereas inhibition of NLRP3-dependent IL-1β production partially prevented the post-myocardial infarction loss of type H vasculature in mice. These results provide a rationale for using anti-inflammatory therapies to prevent or reverse the deterioration of bone vascular function in ischemic heart disease.

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