Posts Tagged: heart failure

Induced Pluripotent Stem Cells 10 Years Later For Cardiac Applications

Induced Pluripotent Stem Cells 10 Years Later: For Cardiac Applications

Yoshinori Yoshida, Shinya Yamanaka

Factors which possibly cause clonal differences of induced pluripotent stem cells (iPSCs). [Powerpoint File]

Induced Pluripotent Stem Cells 10 Years Later: For Cardiac Applications

Induced Pluripotent Stem Cells 10 Years Later: For Cardiac Applications

Yoshinori Yoshida, Shinya Yamanaka

Patient stratification based on drug responsiveness using induced pluripotent stem cells–derived cardiac myocytes. [Powerpoint File]

Contemporary Approaches to Modulating the Nitric Oxide–cGMP Pathway in Cardiovascular Disease

Contemporary Approaches to Modulating the Nitric Oxide–cGMP Pathway in Cardiovascular Disease

Jan R. Kraehling, William C. Sessa

Proteins and enzymes involved in the nitric oxide (NO)-nitric oxide–sensitive guanylate cyclase (NOsGC)–cGMP pathway and its modulators. Key players of the pathway are shown in blue, the positive modulators are shown in yellow, and the negative modulators in purple. Endothelial cells (EC) are shown in green (top), whereas the vascular smooth muscle cell (VSMC) is shown in red (bottom). The space between the 2 cells is called myoendothelial junction (MEJ). cGMP mediates its cellular functions through cGMP-modulated (cyclic nucleotide-gated [CNG]) cation channels, cGMP-dependent protein kinases (cGKs) and cGMP-regulated phosphodiesterases (PDEs). BH4 indicates tetrahydrobiopterin; CAV1, caveolin-1; CYB5R3, NADH-cytochrome b5 reductase 3; eNOS, endothelial nitric oxide synthase (NOS3); Hb2+/Hb3+, hemoglobin α (reduced/oxidized); and PDE, phosphodiesterase. [Powerpoint File]

Contemporary Approaches to Modulating the Nitric Oxide–cGMP Pathway in Cardiovascular Disease

Contemporary Approaches to Modulating the Nitric Oxide–cGMP Pathway in Cardiovascular Disease

Jan R. Kraehling, William C. Sessa

Mechanism of action of nitric oxide–sensitive guanylate cyclase (NOsGC) stimulators and activators. NOsGC stimulators bind to the enzyme and act in an allosteric manner. NO and NOsGC stimulators enhance the NOsGC activity synergistically. NOsGC activators occupy the heme binding site and work therefore only additively with NO. The oxidation of the heme-Fe2+ to heme-Fe3+ results in a weaker binding of heme to NOsGC, hence allowing the NOsGC activators to occupy the heme binding site easier. The schematic is derived from Zorn and Wells.111 [Powerpoint File]

Noninvasive Imaging in Adult Congenital Heart Disease

Noninvasive Imaging in Adult Congenital Heart Disease

Luke J. Burchill, Jennifer Huang, Justin T. Tretter, Abigail M. Khan, Andrew M. Crean, Gruschen R. Veldtman, Sanjiv Kaul, Craig S. Broberg

Three-dimensional (3D) echocardiographic quantification. In this example, left atrial and left ventricular volumes are measured using semiautomated border detection in a 3D echocardiogram. Ejection fraction can be derived without the geometric assumptions that limited 2D-derived measures, such as Simpson biplane and the area–length method. [Powerpoint File]

Noninvasive Imaging in Adult Congenital Heart Disease

Noninvasive Imaging in Adult Congenital Heart Disease

Luke J. Burchill, Jennifer Huang, Justin T. Tretter, Abigail M. Khan, Andrew M. Crean, Gruschen R. Veldtman, Sanjiv Kaul, Craig S. Broberg

Liver imaging in Fontan-associated liver disease. A, Contrast computed tomographic scan of upper abdomen in a patient with heterotaxy and a Fontan circulation demonstrating a well-circumscribed tumor measuring 5 cm in diameter in the right lobe of a midline liver (yellow asterix). B, Fluorodeoxyglucose-positron emission tomographic scan in the same patient demonstrating abnormal uptake in the right lobe of the liver in the region of the tumor. [Powerpoint File]

Current Interventional and Surgical Management of Congenital Heart Disease: Specific Focus on Valvular Disease and Cardiac Arrhythmias

Current Interventional and Surgical Management of Congenital Heart Disease: Specific Focus on Valvular Disease and Cardiac Arrhythmias

Kimberly A. Holst, Sameh M. Said, Timothy J. Nelson, Bryan C. Cannon, Joseph A. Dearani

Schematic representation of the possible lines of ablation to treat macro reentrant atrial tachycardia in the presence of various atrial anomalies associated with complex congenital heart disease. avn indicates atrioventricular node; CS, coronary sinus; FO, foramen ovale; HV, hepatic vein; IVC, inferior vena cava; LAA, left atrial appendage; LSVC, left superior vena cava; MV, mitral valve; PV, pulmonary valve; RAA, right atrial appendage; RSVC, right superior vena cava; TAPVR, total anomalous pulmonary venous return; and TV, tricuspid valve. Reproduced from Mavroudis et al53 with permission of the publisher. Copyright ©2008, The Society of Thoracic Surgeons. [Powerpoint File]

Cardioembolic Stroke

Cardioembolic Stroke

Hooman Kamel, Jeff S. Healey

Overlap among cryptogenic stroke, embolic stroke of undetermined source, and cardioembolic stroke. [Powerpiont File]

Novel Risk Markers and Risk Assessments for Cardiovascular Disease

Novel Risk Markers and Risk Assessments for Cardiovascular Disease

Mark R. Thomas, Gregory Y.H. Lip

Acute coronary syndromes. A, Foam cells (derived from macrophages [Ma]) and lymphocytes have a central role in the development of a lipid-rich atherosclerotic plaque with a necrotic core (NC). Rupture or erosion of an atherosclerotic plaque triggers platelet (P) adhesion to subendothelial components, resulting in the formation of an occlusive thrombus, which also recruits monocytes (M) and neutrophils (N). Platelet–leukocyte interactions cause the release of proinflammatory cytokines and recruited neutrophils also release neutrophil extracellular traps. B, Myocardial ischemia, caused by coronary artery obstruction, leads to the recruitment of neutrophils and monocytes toward chemokines. Leukocyte adhesion molecules then mediate transmigration of leukocytes. Monocytes may then differentiate into Ma, alongside Ma that are already resident within myocardial tissue. Fibroblasts (F) proliferate and differentiate into myofibroblasts (MF). C, Impaired myocardial contractility and hemodynamics results in myocardial stretch, leading to consequent renal disturbances. [Powerpoint File]

Novel Risk Markers and Risk Assessments for Cardiovascular Disease

Novel Risk Markers and Risk Assessments for Cardiovascular Disease

Mark R. Thomas, Gregory Y.H. Lip

Heart failure. A, Myocardial injury, which may be triggered by a variety of insults, can lead to (B) myocardial necrosis, systemic inflammation, and infiltration of leukocytes, predominantly neutrophils (N), driven by chemokines and cytokines. N release their granule contents, thereby exerting oxidative stress and phagocytose necrotic cells and dead cardiomyocytes (DC) in conjunction with activated macrophages (Ma). C, A subsequent transition toward a reparative phase involves downregulation of the inflammatory response, release of anti-inflammatory cytokines, such as interleukin-10, and proliferation of monocytes (Mo) and lymphocytes (L). Fibroblasts (F) proliferate and differentiate in to myofibroblasts (MF), which promote collagen production and fibrosis, mediated in particular by transforming growth factor-β. D, The subsequent formation of a collagen (C)-rich scar maintains structural integrity of the myocardium at the expense of contractility and electric conductivity. [Powerpoint File]

Novel Risk Markers and Risk Assessments for Cardiovascular Disease

Novel Risk Markers and Risk Assessments for Cardiovascular Disease

Mark R. Thomas, Gregory Y.H. Lip

Atrial fibrillation (AF). The pathophysiology of AF is complex. Atrial fibrosis and electric abnormalities, including abnormal calcium homeostasis and ion-channel dysfunction, play a particularly prominent role in precipitating AF, whereas inflammation and oxidative stress reinforce pathological changes in myocardial structure. After the onset of AF, reduced blood flow through the atria predisposes toward thrombosis. The formation of an atrial thrombus, with subsequent embolization to the brain, is one of the most important causes of stroke, which may have devastating consequences. It is well-recognized that thrombosis may not purely be related to stasis of blood within the atria, but likely also reflects multiple clinical risk factors for stroke, which are particularly common in patients with AF. [Powerpoint File]

Purinergic Signaling in the Cardiovascular System

Purinergic Signaling in the Cardiovascular System

Geoffrey Burnstock

Central vagal cardiocardiac reflex triggered by ATP.230 Illustration Credit: Ben Smith. [Powerpoint File]

Purinergic Signaling in the Cardiovascular System

Purinergic Signaling in the Cardiovascular System

Geoffrey Burnstock

Three P2 receptor subtypes, P2X1, P2Y1, and P2Y12, are involved in ADP-induced platelet activation. Clopidogrel is a P2Y12 receptor blocker that inhibits platelet aggregation and is in highly successful use for the treatment of thrombosis and stroke. A P2Y1 receptor antagonist, MRS 2500, inhibits shape change.234 Illustration Credit: Ben Smith. [Powerpoint FIle]

Advances in Echocardiographic Imaging in Heart Failure With Reduced and Preserved Ejection Fraction

Advances in Echocardiographic Imaging in Heart Failure With Reduced and Preserved Ejection Fraction

Alaa Mabrouk Salem Omar, Manish Bansal, Partho P. Sengupta

Myocardial mechanical dysfunction in heart failure. Subendocardial dysfunction attenuates left ventricular (LV) longitudinal function; this may be compensated by hypernormal or relatively preserved mechanical function in other directions. Progressive insult with transmural affection causes exhaustion of the compensatory mechanisms and development of dilated myocardial chambers and reduction of ejection fraction (EF). In the rare occasion of subepicardial dysfunction, for example in pericardial disease, longitudinal function may remain relatively preserved, whereas myocardial functions in circumferential direction are more affected (reduced circumferential shortening and torsion). [Powerpoint File]

Chronic Heart Failure and Inflammation: What Do We Really Know?

Chronic Heart Failure and Inflammation: What Do We Really Know?

Sarah A. Dick, Slava Epelman

Suppression of ongoing inflammation in heart failure (HF). The resolution of inflammation in chronic HF has been proposed to be an active process. Clinical trials and animal models of chronic HF have shown some success from stem cell transplants involving mesenchymal stem cells, cardiac progenitor cells, and cardiosphere-derived cells. The beneficial effect is autocrine in nature and likely involved cardiac macrophages; however, the mechanism is still not know. There is some evidence to suggest a role for colony-stimulating factor 1 (CSF-1) in mediating the survival of cardiac macrophages and perhaps other, as of yet identified, cytokines that promote an anti-inflammatory phenotype. This phenotype is also known to be induced by phagocytosis of dying cells, contributing to the expression of anti-inflammatory cytokines, such as interleukin (IL)-10. [Powerpoint File]