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Current Heart Failure Reports
Published in: Current Heart Failure Reports 4/2014

Open Access 01-12-2014 | Epidemiology of Heart Failure (CSP Lam, Section Editor)

New Insights in (Inter)Cellular Mechanisms by Heart Failure with Preserved Ejection Fraction

Authors: Carsten Tschöpe, Sophie Van Linthout

Published in: Current Heart Failure Reports | Issue 4/2014

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Abstract

Recently, a new paradigm for the development of heart failure with preserved ejection fraction (HFpEF) has been proposed, which identifies a systemic pro-inflammatory state induced by comorbidities as the origin of microvascular endothelial cell inflammation and subsequent concentric cardiac remodeling and dysfunction. This review further discusses the pivotal role of the inflamed endothelium in the pathogenesis of HFpEF-specific cardiac remodeling. The potential importance of reciprocal interactions of the endothelium with cardiac fibroblasts and cardiomyocytes and with the cardiac neurohumoral response in this cardiac remodeling process is outlined.
Literature
1.
Owan TE, Hodge DO, Herges RM, et al. Trends in prevalence and outcome of heart failure with preserved ejection fraction. N Engl J Med. 2006;355:251–9.PubMedCrossRef
2.
3.
King H, Aubert RE, Herman WH. Global burden of diabetes, 1995–2025: prevalence, numerical estimates, and projections. Diabetes Care. 1998;21:1414–31.PubMedCrossRef
4.
Flegal KM, Carroll MD, Kit BK, Ogden CL. Prevalence of obesity and trends in the distribution of body mass index among US adults, 1999–2010. JAMA. 2012;307:491–7.PubMedCrossRef
5.
Hamdani N, Paulus WJ. Myocardial titin and collagen in cardiac diastolic dysfunction: partners in crime. Circulation. 2013;128:5–8.PubMedCrossRef
6.•
Chung CS, Hutchinson KR, Methawasin M, et al. Shortening of the elastic tandem immunoglobulin segment of titin leads to diastolic dysfunction. Circulation. 2013;128:19–28. This article provides first evidence that titin stiffness, in the absence of any involvement of the extracellular matrix, is sufficient to induce HFpEF. PubMedCrossRef
7.••
Paulus WJ, Tschope C. A novel paradigm for heart failure with preserved ejection fraction: comorbidities drive myocardial dysfunction and remodeling through coronary microvascular endothelial inflammation. J Am Coll Cardiol. 2013;62:263–71. This review postulates a new paradigm for the development of HFpEF, which identifies a systemic proinflammatory state induced by comorbidities as the origin of microvascular endothelial cell inflammation and subsequent concentric cardiac remodeling and dysfunction.PubMedCrossRef
8.
Brutsaert DL. Cardiac endothelial-myocardial signaling: its role in cardiac growth, contractile performance, and rhythmicity. Physiol Rev. 2003;83:59–115.PubMed
9.
Zeiher AM, Fisslthaler B, Schray-Utz B, Busse R. Nitric oxide modulates the expression of monocyte chemoattractant protein 1 in cultured human endothelial cells. Circ Res. 1995;76:980–6.PubMedCrossRef
10.
Khan BV, Harrison DG, Olbrych MT, et al. Nitric oxide regulates vascular cell adhesion molecule 1 gene expression and redox-sensitive transcriptional events in human vascular endothelial cells. Proc Natl Acad Sci U S A. 1996;93:9114–9.PubMedCentralPubMedCrossRef
11.
Niu XF, Smith CW, Kubes P. Intracellular oxidative stress induced by nitric oxide synthesis inhibition increases endothelial cell adhesion to neutrophils. Circ Res. 1994;74:1133–40.PubMedCrossRef
12.
Riad A, Westermann D, Van Linthout S, et al. Enhancement of endothelial nitric oxide synthase production reverses vascular dysfunction and inflammation in the hindlimbs of a rat model of diabetes. Diabetologia. 2008;51:2325–32.PubMedCrossRef
13.
Dimmeler S, Haendeler J, Nehls M, Zeiher AM. Suppression of apoptosis by nitric oxide via inhibition of interleukin-1beta-converting enzyme (ICE)-like and cysteine protease protein (CPP)-32-like proteases. J Exp Med. 1997;185:601–7.PubMedCentralPubMedCrossRef
14.
Emanueli C, Van Linthout S, Salis MB, et al. Nitric oxide-releasing aspirin derivative, NCX 4016, promotes reparative angiogenesis and prevents apoptosis and oxidative stress in a mouse model of peripheral ischemia. Arterioscler Thromb Vasc Biol. 2004;24:2082–7.PubMedCrossRef
15.
Brunner H, Cockcroft JR, Deanfield J, et al. Endothelial function and dysfunction. Part II: association with cardiovascular risk factors and diseases. A statement by the Working Group on Endothelins and Endothelial Factors of the European Society of Hypertension. J Hypertens. 2005;23:233–46.PubMedCrossRef
16.
Goodwin BL, Pendleton LC, Levy MM, et al. Tumor necrosis factor-alpha reduces argininosuccinate synthase expression and nitric oxide production in aortic endothelial cells. Am J Physiol Heart Circ Physiol. 2007;293:H1115–21.PubMedCrossRef
17.
Gao X, Xu X, Belmadani S, et al. TNF-alpha contributes to endothelial dysfunction by upregulating arginase in ischemia/reperfusion injury. Arterioscler Thromb Vasc Biol. 2007;27:1269–75.PubMedCrossRef
18.
Spillmann F, Van Linthout S, Miteva K, et al. LXR agonism improves TNF-alpha-induced endothelial dysfunction in the absence of its cholesterol-modulating effects. Atherosclerosis. 2014;232:1–9.PubMedCrossRef
19.
Van Linthout S, Spillmann F, Lorenz M, et al. Vascular-protective effects of high-density lipoprotein include the downregulation of the angiotensin II type 1 receptor. Hypertension. 2009;53:682–7.PubMedCrossRef
20.
Almudever P, Milara J, De Diego A, et al. Role of tetrahydrobiopterin in pulmonary vascular remodelling associated with pulmonary fibrosis. Thorax. 2013;68:938–48.PubMedCrossRef
21.
Cai S, Khoo J, Mussa S, et al. Endothelial nitric oxide synthase dysfunction in diabetic mice: importance of tetrahydrobiopterin in eNOS dimerisation. Diabetologia. 2005;48:1933–40.PubMedCrossRef
22.
Gao X, Zhang H, Belmadani S, et al. Role of TNF-alpha-induced reactive oxygen species in endothelial dysfunction during reperfusion injury. Am J Physiol Heart Circ Physiol. 2008;295:H2242–9.PubMedCentralPubMedCrossRef
23.
24.
25.
Shah AM. Paracrine modulation of heart cell function by endothelial cells. Cardiovasc Res. 1996;31:847–67.PubMedCrossRef
26.
Zhang M, Shah AM. ROS signalling between endothelial cells and cardiac cells. Cardiovasc Res. 2014;102:249–57.PubMedCrossRef
27.
Brutsaert DL, Meulemans AL, Sipido KR, Sys SU. Effects of damaging the endocardial surface on the mechanical performance of isolated cardiac muscle. Circ Res. 1988;62:358–66.PubMedCrossRef
28.
Paulus WJ, Vantrimpont PJ, Shah AM. Paracrine coronary endothelial control of left ventricular function in humans. Circulation. 1995;92:2119–26.PubMedCrossRef
29.
Tschope C, Bock CT, Kasner M, et al. High prevalence of cardiac parvovirus B19 infection in patients with isolated left ventricular diastolic dysfunction. Circulation. 2005;111:879–86.PubMedCrossRef
30.
Lam CS, Brutsaert DL. Endothelial dysfunction: a pathophysiologic factor in heart failure with preserved ejection fraction. J Am Coll Cardiol. 2012;60:1787–9.PubMedCrossRef
31.
Murdoch CE, Chaubey S, Zeng L, et al. Endothelial NADPH oxidase-2 promotes interstitial cardiac fibrosis and diastolic dysfunction through pro-inflammatory effects and endothelial-mesenchymal transition. J Am Coll Cardiol. 2014;63:2734–41.
32.••
Van Linthout S, Miteva K, Tschope C. Crosstalk between fibroblasts and inflammatory cells. Cardiovasc Res. 2014;102:258–69. This review gives an extensive overview about how inflammatory cells contribute to (cardiac) fibroblast activation and how in turn fibroblasts contribute to the inflammatory process leading to chronic inflammation.PubMedCrossRef
33.
Ismahil MA, Hamid T, Bansal SS, et al. Remodeling of the mononuclear phagocyte network underlies chronic inflammation and disease progression in heart failure: critical importance of the cardiosplenic axis. Circ Res. 2014;114:266–82.PubMedCrossRef
34.
Savvatis K, van Linthout S, Miteva K, et al. Mesenchymal stromal cells but not cardiac fibroblasts exert beneficial systemic immunomodulatory effects in experimental myocarditis. PLoS One. 2012;7:e41047.PubMedCentralPubMedCrossRef
35.
van der Laan AM, Ter Horst EN, Delewi R, et al. Monocyte subset accumulation in the human heart following acute myocardial infarction and the role of the spleen as monocyte reservoir. Eur Heart J. 2014;35:376–85.PubMedCrossRef
36.
Westermann D, Lindner D, Kasner M, et al. Cardiac inflammation contributes to changes in the extracellular matrix in patients with heart failure and normal ejection fraction. Circ Heart Fail. 2011;4:44–52.PubMedCrossRef
37.
Kapur NK. Transforming growth factor-beta: governing the transition from inflammation to fibrosis in heart failure with preserved left ventricular function. Circ Heart Fail. 2011;4:5–7.PubMedCrossRef
38.
Kuwahara F, Kai H, Tokuda K, et al. Transforming growth factor-beta function blocking prevents myocardial fibrosis and diastolic dysfunction in pressure-overloaded rats. Circulation. 2002;106:130–5.PubMedCrossRef
39.
40.
Williams SM, Golden-Mason L, Ferguson BS, et al. Class I HDACs regulate angiotensin II-dependent cardiac fibrosis via fibroblasts and circulating fibrocytes. J Mol Cell Cardiol. 2014;67:112–25.PubMedCentralPubMedCrossRef
41.
Li P, Wang D, Lucas J, et al. Atrial natriuretic peptide inhibits transforming growth factor beta-induced Smad signaling and myofibroblast transformation in mouse cardiac fibroblasts. Circ Res. 2008;102:185–92.PubMedCrossRef
42.
Vettel C, Lammle S, Ewens S, et al. PDE2-mediated cAMP hydrolysis accelerates cardiac fibroblast to myofibroblast conversion and is antagonized by exogenous activation of cGMP signaling pathways. Am J Physiol Heart Circ Physiol. 2014;306:H1246–52.PubMedCrossRef
43.
Mehel H, Emons J, Vettel C, et al. Phosphodiesterase-2 is up-regulated in human failing hearts and blunts beta-adrenergic responses in cardiomyocytes. J Am Coll Cardiol. 2013;62:1596–606.PubMedCrossRef
44.
Westermann D, Becher PM, Lindner D, et al. Selective PDE5A inhibition with sildenafil rescues left ventricular dysfunction, inflammatory immune response and cardiac remodeling in angiotensin II-induced heart failure in vivo. Basic Res Cardiol. 2012;107:308.PubMedCrossRef
45.
Rizzo NO, Maloney E, Pham M, et al. Reduced NO-cGMP signaling contributes to vascular inflammation and insulin resistance induced by high-fat feeding. Arterioscler Thromb Vasc Biol. 2010;30:758–65.PubMedCentralPubMedCrossRef
46.
Dunkern TR, Feurstein D, Rossi GA, et al. Inhibition of TGF-beta induced lung fibroblast to myofibroblast conversion by phosphodiesterase inhibiting drugs and activators of soluble guanylyl cyclase. Eur J Pharmacol. 2007;572:12–22.PubMedCrossRef
47.
Redfield MM, Chen HH, Borlaug BA, et al. Effect of phosphodiesterase-5 inhibition on exercise capacity and clinical status in heart failure with preserved ejection fraction: a randomized clinical trial. JAMA. 2013;309:1268–77.PubMedCrossRef
48.
O’Riordan E, Mendelev N, Patschan S, et al. Chronic NOS inhibition actuates endothelial-mesenchymal transformation. Am J Physiol Heart Circ Physiol. 2007;292:H285–94.PubMedCrossRef
49.
Zeisberg EM, Tarnavski O, Zeisberg M, et al. Endothelial-to-mesenchymal transition contributes to cardiac fibrosis. Nat Med. 2007;13:952–61.PubMedCrossRef
50.
Fleenor BS, Marshall KD, Rippe C, Seals DR. Replicative aging induces endothelial to mesenchymal transition in human aortic endothelial cells: potential role of inflammation. J Vasc Res. 2012;49:59–64.PubMedCrossRef
51.
Kim M, Choi SH, Jin YB, et al. The effect of oxidized low-density lipoprotein (ox-LDL) on radiation-induced endothelial-to-mesenchymal transition. Int J Radiat Biol. 2013;89:356–63.PubMedCrossRef
52.
Widyantoro B, Emoto N, Nakayama K, et al. Endothelial cell-derived endothelin-1 promotes cardiac fibrosis in diabetic hearts through stimulation of endothelial-to-mesenchymal transition. Circulation. 2010;121:2407–18.PubMedCrossRef
53.
Lindner D, Zietsch C, Tank J, et al. Cardiac fibroblasts support cardiac inflammation in heart failure. Basic Res Cardiol. 2014;109:428.PubMedCrossRef
54.
Javed Q, Murtaza I. Therapeutic potential of tumour necrosis factor-alpha antagonists in patients with chronic heart failure. Heart Lung Circ. 2013;22:323–7.PubMedCrossRef
55.
Kuramochi Y, Cote GM, Guo X, et al. Cardiac endothelial cells regulate reactive oxygen species-induced cardiomyocyte apoptosis through neuregulin-1beta/erbB4 signaling. J Biol Chem. 2004;279:51141–7.PubMedCrossRef
56.
Narmoneva DA, Vukmirovic R, Davis ME, et al. Endothelial cells promote cardiac myocyte survival and spatial reorganization: implications for cardiac regeneration. Circulation. 2004;110:962–8.PubMedCentralPubMedCrossRef
57.
Scalera F. Intracellular glutathione and lipid peroxide availability and the secretion of vasoactive substances by human umbilical vein endothelial cells after incubation with TNF-alpha. Eur J Clin Investig. 2003;33:176–82.CrossRef
58.
van Wamel AJ, Ruwhof C, van der Valk-Kokshoorn LJ, et al. Stretch-induced paracrine hypertrophic stimuli increase TGF-beta1 expression in cardiomyocytes. Mol Cell Biochem. 2002;236:147–53.PubMedCrossRef
59.
van Wamel AJ, Ruwhof C, van der Valk-Kokshoom LE, et al. The role of angiotensin II, endothelin-1 and transforming growth factor-beta as autocrine/paracrine mediators of stretch-induced cardiomyocyte hypertrophy. Mol Cell Biochem. 2001;218:113–24.PubMedCrossRef
60.
61.
62.
Giordano FJ, Gerber HP, Williams SP, et al. A cardiac myocyte vascular endothelial growth factor paracrine pathway is required to maintain cardiac function. Proc Natl Acad Sci U S A. 2001;98:5780–5.PubMedCentralPubMedCrossRef
63.
Linke WA. Sense and stretchability: the role of titin and titin-associated proteins in myocardial stress-sensing and mechanical dysfunction. Cardiovasc Res. 2008;77:637–48.PubMed
64.
65.
Hamdani N, Franssen C, Lourenco A, et al. Myocardial titin hypophosphorylation importantly contributes to heart failure with preserved ejection fraction in a rat metabolic risk model. Circ Heart Fail. 2013;6:1239–49.PubMedCrossRef
66.
Grutzner A, Garcia-Manyes S, Kotter S, et al. Modulation of titin-based stiffness by disulfide bonding in the cardiac titin N2-B unique sequence. Biophys J. 2009;97:825–34.PubMedCentralPubMedCrossRef
67.
Hidalgo C, Hudson B, Bogomolovas J, et al. PKC phosphorylation of titin’s PEVK element: a novel and conserved pathway for modulating myocardial stiffness. Circ Res. 2009;105:631–8. 17 p following 638.PubMedCentralPubMedCrossRef
68.
Hamdani N, Bishu KG, von Frieling-Salewsky M, et al. Deranged myofilament phosphorylation and function in experimental heart failure with preserved ejection fraction. Cardiovasc Res. 2013;97:464–71.PubMedCrossRef
69.
Raskin A, Lange S, Banares K, et al. A novel mechanism involving four-and-a-half LIM domain protein-1 and extracellular signal-regulated kinase-2 regulates titin phosphorylation and mechanics. J Biol Chem. 2012;287:29273–84.PubMedCentralPubMedCrossRef
70.
Hamdani N, Krysiak J, Kreusser MM, et al. Crucial role for Ca2(+)/calmodulin-dependent protein kinase-II in regulating diastolic stress of normal and failing hearts via titin phosphorylation. Circ Res. 2013;112:664–74.PubMedCrossRef
71.
Borbely A, Falcao-Pires I, van Heerebeek L, et al. Hypophosphorylation of the Stiff N2B titin isoform raises cardiomyocyte resting tension in failing human myocardium. Circ Res. 2009;104:780–6.PubMedCrossRef
72.
Fukuda N, Wu Y, Nair P, Granzier HL. Phosphorylation of titin modulates passive stiffness of cardiac muscle in a titin isoform-dependent manner. J Gen Physiol. 2005;125:257–71.PubMedCentralPubMedCrossRef
73.
Kruger M, Kotter S, Grutzner A, et al. Protein kinase G modulates human myocardial passive stiffness by phosphorylation of the titin springs. Circ Res. 2009;104:87–94.PubMedCrossRef
74.••
van Heerebeek L, Hamdani N, Falcao-Pires I, et al. Low myocardial protein kinase G activity in heart failure with preserved ejection fraction. Circulation. 2012;126:830–9. This article demonstrated reduced myocardial cGMP concentration and protein kinase G activity in HFpEF compared to HFREF patients.PubMedCrossRef
75.
Schneider JC, El Kebir D, Chereau C, et al. Involvement of Ca2+/calmodulin-dependent protein kinase II in endothelial NO production and endothelium-dependent relaxation. Am J Physiol Heart Circ Physiol. 2003;284:H2311–9.PubMed
76.
Das SR, Drazner MH, Dries DL, et al. Impact of body mass and body composition on circulating levels of natriuretic peptides: results from the Dallas Heart Study. Circulation. 2005;112:2163–8.PubMedCrossRef
77.
Kondepudi A, Johnson A. Cytokines increase neutral endopeptidase activity in lung fibroblasts. Am J Respir Cell Mol Biol. 1993;8:43–9.PubMedCrossRef
78.
Carbone S, Shah KB, Van Tassell BW, et al. Obesity and diastolic heart failure: is inflammation the link? Transl Med. 2013;3:e124.
79.
van Heerebeek L, Hamdani N, Handoko ML, et al. Diastolic stiffness of the failing diabetic heart: importance of fibrosis, advanced glycation end products, and myocyte resting tension. Circulation. 2008;117:43–51.PubMedCrossRef
80.
Ramasamy R, Vannucci SJ, Yan SS, et al. Advanced glycation end products and RAGE: a common thread in aging, diabetes, neurodegeneration, and inflammation. Glycobiology. 2005;15:16R–28R.PubMedCrossRef
81.
Ziegler D, Buchholz S, Sohr C, et al. Oxidative stress predicts progression of peripheral and cardiac autonomic nerve dysfunction over 6 years in diabetic patients. Acta Diabetol. 2014. doi:10.​1007/​s00592-014-0601-3.
82.
Leinninger GM, Edwards JL, Lipshaw MJ, Feldman EL. Mechanisms of disease: mitochondria as new therapeutic targets in diabetic neuropathy. Nat Clin Pract Neurol. 2006;2:620–8.PubMedCrossRef
83.
Kunt T, Forst T, Schmidt S, et al. Serum levels of substance P are decreased in patients with type 1 diabetes. Exp Clin Endocrinol Diabetes. 2000;108:164–7.PubMedCrossRef
84.
McKenna K, Smith D, Tormey W, Thompson CJ. Acute hyperglycaemia causes elevation in plasma atrial natriuretic peptide concentrations in type 1 diabetes mellitus. Diabet Med. 2000;17:512–7.PubMedCrossRef
85.
Chottova Dvorakova M, Wiegand S, Pesta M, et al. Expression of neuropeptide Y and its receptors Y1 and Y2 in the rat heart and its supplying autonomic and spinal sensory ganglia in experimentally induced diabetes. Neuroscience. 2008;151:1016–28.PubMedCrossRef
86.
Borlaug BA, Olson TP, Lam CS, et al. Global cardiovascular reserve dysfunction in heart failure with preserved ejection fraction. J Am Coll Cardiol. 2010;56:845–54.PubMedCentralPubMedCrossRef
87.
Kapoun AM, Liang F, O’Young G, et al. B-type natriuretic peptide exerts broad functional opposition to transforming growth factor-beta in primary human cardiac fibroblasts: fibrosis, myofibroblast conversion, proliferation, and inflammation. Circ Res. 2004;94:453–61.PubMedCrossRef
88.
89.
Mehra MR, Uber PA, Park MH, et al. Obesity and suppressed B-type natriuretic peptide levels in heart failure. J Am Coll Cardiol. 2004;43:1590–5.PubMedCrossRef
90.
Taskiran M, Rasmussen V, Rasmussen B, et al. Left ventricular dysfunction in normotensive type 1 diabetic patients: the impact of autonomic neuropathy. Diabet Med. 2004;21:524–30.PubMedCrossRef
91.
92.••
Akiyama E, Sugiyama S, Matsuzawa Y, et al. Incremental prognostic significance of peripheral endothelial dysfunction in patients with heart failure with normal left ventricular ejection fraction. J Am Coll Cardiol. 2012;60:1778–86. This article outlines the prognostic significance of peripheral endothelial dysfunction in patients with HFpEF.PubMedCrossRef
93.
Schocken DD, Benjamin EJ, Fonarow GC, et al. Prevention of heart failure: a scientific statement from the American Heart Association Councils on Epidemiology and Prevention, Clinical Cardiology, Cardiovascular Nursing, and High Blood Pressure Research; Quality of Care and Outcomes Research Interdisciplinary Working Group; and Functional Genomics and Translational Biology Interdisciplinary Working Group. Circulation. 2008;117:2544–65.PubMedCrossRef
94.
Haag M, Van Linthout S, Schroder SE, et al. Endomyocardial biopsy derived adherent proliferating cells—a potential cell source for cardiac tissue engineering. J Cell Biochem. 2010;109:564–75.PubMed
95.
Ren G, Zhang L, Zhao X, et al. Mesenchymal stem cell-mediated immunosuppression occurs via concerted action of chemokines and nitric oxide. Cell Stem Cell. 2008;2:141–50.PubMedCrossRef
96.
Van Linthout S, Savvatis K, Miteva K, et al. Mesenchymal stem cells improve murine acute coxsackievirus B3-induced myocarditis. Eur Heart J. 2011;32:2168–78.PubMedCentralPubMedCrossRef
97.
Haag M, Stolk M, Ringe J, et al. Immune attributes of cardiac-derived adherent proliferating (CAP) cells in cardiac therapy. J Tissue Eng Regen Med. 2013;7:362–70.PubMedCrossRef
98.
Prather WR, Toren A, Meiron M, et al. The role of placental-derived adherent stromal cell (PLX-PAD) in the treatment of critical limb ischemia. Cytotherapy. 2009;11:427–34.PubMedCrossRef
99.
Mias C, Lairez O, Trouche E, et al. Mesenchymal stem cells promote matrix metalloproteinase secretion by cardiac fibroblasts and reduce cardiac ventricular fibrosis after myocardial infarction. Stem Cells. 2009;27:2734–43.PubMedCrossRef
100.
Miteva K, Haag M, Peng J, et al. Human cardiac-derived adherent proliferating cells reduce murine acute coxsackievirus B3-induced myocarditis. PLoS One. 2011;6:e28513.PubMedCentralPubMedCrossRef
Metadata
Title
New Insights in (Inter)Cellular Mechanisms by Heart Failure with Preserved Ejection Fraction
Authors
Carsten Tschöpe
Sophie Van Linthout
Publication date
01-12-2014
Publisher
Springer US
Published in
Current Heart Failure Reports / Issue 4/2014
Print ISSN: 1546-9530
Electronic ISSN: 1546-9549
DOI
https://doi.org/10.1007/s11897-014-0219-3

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