Spatial relationship of coronary sinus–great cardiac vein to mitral valve annulus and left circumflex coronary artery: implications for cardiovascular interventional procedures
The spatial relationship of the coronary sinus–great cardiac vein (CS–GCV) to free posterior portion of the mitral valve annulus (MVA) and left circumflex coronary artery (LCx) has gained importance with the advent of cardiovascular interventional procedures such as percutaneous transvenous mitral annuloplasty (PTMA) and mitral isthmus (MI) ablation. (Source: Cardiovascular Pathology)
Source: Cardiovascular Pathology - June 2, 2016 Category: Cardiology Authors: Arpandeep Randhawa, Abhimanyu Saini, Anjali Aggarwal, Uma Nahar Saikia, R. Shane Tubbs, Tulika Gupta, Manoj Kumar Rohit, Gurdeep Singh Kalyan, Daisy Sahni Tags: Original Article Source Type: research
Spatial relationship of coronary sinus- great cardiac vein to mitral valve annulus and left circumflex coronary artery: Implications for cardiovascular intervational procedures
The spatial relationship of the coronary sinus-great cardiac vein (CS-GCV) to free posterior portion of the mitral valve annulus (MVA) and left circumflex coronary artery (LCx) has gained importance with the advent of cardiovascular interventional procedures such as percutaneous transvenous mitral annuloplasty (PTMA) and mitral isthmus (MI) ablation. (Source: Cardiovascular Pathology)
Source: Cardiovascular Pathology - June 2, 2016 Category: Cardiology Authors: Arpandeep Randhawa, Abhimanyu Saini, Anjali Aggarwal, Uma Nahar Saikia, R. Shane Tubbs, Tulika Gupta, Manoj Kumar Rohit, Gurdeep Singh Kalyan, Daisy Sahni Source Type: research
Long noncoding RNA H19 controls DUSP5/ERK1/2 axis in cardiac fibroblast proliferation and fibrosis
Down-regulation of DUSP5 has been shown to increase cell proliferation. DUSP5 expression is regulated through epigenetic events involving LncRNA H19 human choriocarcinoma cell line. However, the molecular mechanisms of H19 modulating the DUSP5 expression in cardiac fibrosis remain largely unknown. Here, we identify H19 negatively regulation of DUSP5 gene expression in cardiac fibroblast and fibrosis tissues. In vivo, the expression levels of H19, DUSP5, α-SMA, p-ERK1/2, and ERK1/2 in cardiac fibrosis tissue were estimated by Western blotting, quantitative reverse transcription-polymerase chain reaction and immunohistochem...
Source: Cardiovascular Pathology - May 31, 2016 Category: Cardiology Authors: Hui Tao, Wei Cao, Jing-Jing Yang, Kai-Hu Shi, Xiao Zhou, Li-Ping Liu, Jun Li Source Type: research
Long non-coding RNA H19 controls DUSP5/ERK1/2 axis in cardiac fibroblast proliferation and fibrosis
Down-regulation of DUSP5 has been shown to increase cell proliferation. DUSP5 expression is regulated through epigenetic events involving LncRNA H19 human choriocarcinoma cell line. However, the molecular mechanisms of H19 modulating the DUSP5 expression in cardiac fibrosis remain largely unknown. Here, we identify H19 negatively regulation of DUSP5 gene expression in cardiac fibroblast and fibrosis tissues. In vivo, the expression levels of H19, DUSP5, α-SMA, p-ERK1/2 and ERK1/2 in cardiac fibrosis tissue were estimated by Western blotting, qRT-PCR and Immunohistochemistry. (Source: Cardiovascular Pathology)
Source: Cardiovascular Pathology - May 31, 2016 Category: Cardiology Authors: Hui Tao, Wei Cao, Jing-Jing Yang, Kai-Hu Shi, Xiao Zhou, Li-Ping Liu, Jun Li Source Type: research
Implications for the role of macrophages in a model of myocardial fibrosis: CCR2 −/− mice exhibit an M2 phenotypic shift in resident cardiac macrophages
Macrophages (M Φ) are functionally diverse and dynamic. Until recently, cardiac MΦ were assumed to be monocyte derived; however, resident cardiac MΦ (rCMΦ), present at baseline, were identified in myocardia and have been implicated in cardiac healing. Previously, we demonstrated that CCR2−/− mice are prote cted from myocardial fibrosis — an observation initially attributed to changes in infiltrating monocytes. Here, we reexplored this observation in the context of our new understanding of rCMΦ. (Source: Cardiovascular Pathology)
Source: Cardiovascular Pathology - May 30, 2016 Category: Cardiology Authors: Alec Falkenham, Tanya Myers, Chloe Wong, Jean Francois Legare Tags: Original Article Source Type: research
Case report and literature review: cardiac tamponade as a complication of pericardial extramedullary hematopoiesis
Pericardial effusion can cause cardiac tamponade physiology with resultant cardiogenic shock and death. Myelofibrosis, the replacement of marrow cavity by fibrous connective tissue, is a secondary complication of a group of disorders known as myeloproliferative neoplasms, which are clonal processes characterized by abnormal proliferative growth of one or more hematopoietic lineages. One consequence of myelofibrosis is the development of hematopoiesis at other anatomic sites, most commonly the spleen and liver, a phenomenon known as extramedullary hematopoiesis (EMH). (Source: Cardiovascular Pathology)
Source: Cardiovascular Pathology - May 30, 2016 Category: Cardiology Authors: Navin R. Mahadevan, Elizabeth A. Morgan, Richard N. Mitchell Tags: Case Report Source Type: research
Implications for the role of macrophages in a model of myocardial fibrosis: CCR2 −/− mice exhibit an M2 phenotypic shift in resident cardiac macrophages
Macrophages (M Φ) are functionally diverse and dynamic. Until recently, cardiac MΦ were assumed to be monocyte derived; however, resident cardiac MΦ (rCMΦ), present at baseline, were identified in myocardia and have been implicated in cardiac healing. Previously, we demonstrated that CCR2−/− mice are prote cted from myocardial fibrosis — an observation initially attributed to changes in infiltrating monocytes. Here, we reexplored this observation in the context of our new understanding of rCMΦ. (Source: Cardiovascular Pathology)
Source: Cardiovascular Pathology - May 30, 2016 Category: Cardiology Authors: Alec Falkenham, Tanya Myers, Chloe Wong, Jean Francois Legare Tags: Original Article Source Type: research
Implications for the Role of Macrophages in a Model of Myocardial Fibrosis: CCR2−/− Mice Exhibit An M2 Phenotypic Shift In Resident Cardiac Macrophages
Macrophages (MΦ) are functionally diverse and dynamic. Until recently, cardiac MΦ were assumed to be monocyte-derived; however, resident cardiac MΦ (rCMΦ), present at baseline, were identified in myocardia and have been implicated in cardiac healing. Previously, we demonstrated that CCR2−/− mice are protected from myocardial fibrosis – an observation initially attributed to changes in infiltrating monocytes. Here, we re-explored this observation in the context of our new understanding of rCMΦ. (Source: Cardiovascular Pathology)
Source: Cardiovascular Pathology - May 30, 2016 Category: Cardiology Authors: A. Falkenham, T. Myers, C. Wong, J.F. Legare Tags: Original Article Source Type: research
Case Report and Literature Review: Cardiac Tamponade as a Complication of Pericardial Extramedullary Hematopoiesis
Pericardial effusion can cause cardiac tamponade physiology with resultant cardiogenic shock and death. Myelofibrosis, the replacement of marrow cavity by fibrous connective tissue, is a secondary complication of a group of disorders known as myeloproliferative neoplasms, which are clonal processes characterized by abnormal proliferative growth of one or more hematopoietic lineages. One consequence of myelofibrosis is the development of hematopoiesis at other anatomic sites, most commonly the spleen and liver, a phenomenon known as extramedullary hematopoiesis (EMH). (Source: Cardiovascular Pathology)
Source: Cardiovascular Pathology - May 30, 2016 Category: Cardiology Authors: Navin R. Mahadevan, Elizabeth A. Morgan, Richard N. Mitchell Tags: Case Report Source Type: research
Associations of rs3918242 and rs2285053 MMP-9 and MMP-2 polymorphisms with the risk, severity, and short- and long-term complications of degenerative mitral valve diseases: a 4.8-year prospective cohort study
Degenerative forms of mitral valve diseases (MVDs) are very complex pathologies. Thus, it is difficult to make generalizations about the disease pathways or genetic risk factors contributing to these diseases. However, a key role of metalloproteinases (MMPs) in their pathophysiology is emerging. Thus, we performed for the first time a perspective study to assess eventual associations of some functional single nucleotide polymorphisms (SNPs) in MMP-2 and MMP-9 genes with the MVD risk, symptom severity, and short- and long-term (4.8 years) complications. (Source: Cardiovascular Pathology)
Source: Cardiovascular Pathology - May 19, 2016 Category: Cardiology Authors: Carmela Rita Balistreri, Alberto Allegra, Floriana Crapanzano, Calogera Pisano, Oreste Fabio Triolo, Vincenzo Argano, Giuseppina Candore, Domenico Lio, Giovanni Ruvolo Tags: Original Article Source Type: research
Associations of rs3918242 and rs2285053 MMP-9 and MMP-2 polymorphisms with the risk, severity, short and long-term complications of degenerative mitral valve diseases: a 4.8 years prospective cohort study
Degenerative forms of mitral valve diseases (MVDs) are very complex pathologies. Thus, it is difficult to make generalizations about the disease pathways or genetic risk factors contributing to these diseases. However, it is emerging a key role of metalloproteinases (MMPs) in their pathophysiology. Thus, we performed for the first time a perspective study to assess eventual associations of some functional SNPs in MMP-2 and MMP-9 genes with the MVD risk, symptom severity and short and long-term (4.8 years) complications. (Source: Cardiovascular Pathology)
Source: Cardiovascular Pathology - May 19, 2016 Category: Cardiology Authors: Carmela Rita Balistreri, Alberto Allegra, Floriana Crapanzano, Calogera Pisano, Oreste Fabio Triolo, Vincenzo Argano, Giuseppina Candore, Domenico Lio, Giovanni Ruvolo Tags: Original Article Source Type: research
FTY720 (Gilenya) treatment prevents spontaneous autoimmune myocarditis and dilated cardiomyopathy in transgenic HLA-DQ8-BALB/c mice
Although dilated cardiomyopathy (DCM) is often caused by viral infections, it frequently involves autoimmune mechanisms associated with particular HLA-DR and DQ alleles. Our homozygous HLA-DQ8Ab0 transgenic mice in the BALB/c background (HLA-DQ8BALB/c-Tg) developed early and progressive fatal heart failure from 4 to 5 weeks of age. Clinical signs of the disease included cyanotic eyes, tachycardia with dyspnea (from pale to cyanotic limbs), and terminal whole body edema. Sick mice had extremely dilated hearts, enlarged liver and spleen, and pleural/peritoneal effusion. (Source: Cardiovascular Pathology)
Source: Cardiovascular Pathology - May 16, 2016 Category: Cardiology Authors: Ferenc Boldizsar, Oktavia Tarjanyi, Katalin Olasz, Akos Hegyi, Katalin Mikecz, Tibor T. Glant, Tibor A. Rauch Tags: Original Article Source Type: research
