Journal
BASIC RESEARCH IN CARDIOLOGY
Volume 115, Issue 4, Pages -Publisher
SPRINGER HEIDELBERG
DOI: 10.1007/s00395-020-0798-y
Keywords
Heart failure with preserved ejection fraction; Coronary microvascular dysfunction; Cardiac lymphatic dysfunction; Inflammation; Myocardial fibrosis; Cardiac metabolism
Categories
Funding
- European Research Area Network Cardiovascular disease [LYMIT-DIS 2016]
- Fonds Wetenschappelijk Onderzoek [GOH7716N, 1160718N, G091018N]
- Agence National de la Recherche [16-ECVD-0004]
- Nederlandse organisatie voor Wetenschappelijk Onderzoek [ZonMw 2016T091, Vidi 91796338]
- Instituto de Salud Carlos III [AC16/00020, CB16/11/00483 and, PI18/01469]
- National Centre for Research and Development [ERA-CVD/LyMitDis/1/2017]
- European Research Area Network Cardiovascular disease [Macro ERA 2016]
- Dutch Heart Foundation
- FHU REMOD-VHF
- INSERM
- European Regional Development Fund [CPER/FEDER 2015 (DO-IT)]
- European Regional Development Fund [CPER/FEDER 2016 (PACT-CBS)]
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Heart failure with preserved ejection fraction (HFpEF) is a complex heterogeneous disease for which our pathophysiological understanding is still limited and specific prevention and treatment strategies are lacking. HFpEF is characterised by diastolic dysfunction and cardiac remodelling (fibrosis, inflammation, and hypertrophy). Recently, microvascular dysfunction and chronic low-grade inflammation have been proposed to participate in HFpEF development. Furthermore, several recent studies demonstrated the occurrence of generalized lymphatic dysfunction in experimental models of risk factors for HFpEF, including obesity, hypercholesterolaemia, type 2 diabetes mellitus (T2DM), hypertension, and aging. Here, we review the evidence for a combined role of coronary (micro)vascular dysfunction and lymphatic vessel alterations in mediating key pathological steps in HFpEF, including reduced cardiac perfusion, chronic low-grade inflammation, and myocardial oedema, and their impact on cardiac metabolic alterations (oxygen and nutrient supply/demand imbalance), fibrosis, and cardiomyocyte stiffness. We focus primarily on HFpEF caused by metabolic risk factors, such as obesity, T2DM, hypertension, and aging.
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