Ventricular–arterial coupling (VAC) plays a major role in the physiology of cardiac and aortic mechanics, as well as in the pathophysiology of cardiac disease. VAC assessment possesses independent ...diagnostic and prognostic value and may be used to refine riskstratification and monitor therapeutic interventions. Traditionally, VAC is assessed by the non‐invasive measurement of the ratio of arterial (Ea) to ventricular end‐systolic elastance (Ees). With disease progression, both Ea and Ees may become abnormal and the Ea/Ees ratio may approximate its normal values. Therefore, the measurement of each component of this ratio or of novel more sensitive markers of myocardial (e.g. global longitudinal strain) and arterial function (e.g. pulse wave velocity) may better characterize VAC. In valvular heart disease, systemic arterial compliance and valvulo–arterial impedance have an established diagnostic and prognostic value and may monitor the effects of valve replacement on vascular and cardiac function. Treatment guided to improve VAC through improvement of both or each one of its components may delay incidence of heart failure and possibly improve prognosis in heart failure. In this consensus document, we describe the pathophysiology, the methods of assessment as well as the clinical implications of VAC in cardiac diseases and heart failure. Finally, we focus on interventions that may improve VAC and thus modify prognosis.
University of Antwerp, Antwerp,
Belgium
Brutsaert, Dirk L.
Cardiac Endothelial-Myocardial Signaling: Its Role in
Cardiac Growth, Contractile Performance, and Rhythmicity. Physiol. Rev. 83: 59-115, ...2003. Experimental work during the past 15 years
has demonstrated that endothelial cells in the heart play an obligatory
role in regulating and maintaining cardiac function, in particular, at the endocardium and in the myocardial capillaries where endothelial cells directly interact with adjacent cardiomyocytes. The emerging field of targeted gene manipulation has led to the contention that
cardiac endothelial-cardiomyocytal interaction is a prerequisite for normal cardiac development and growth. Some of the
molecular mechanisms and cellular signals governing this interaction,
such as neuregulin, vascular endothelial growth factor, and
angiopoietin, continue to maintain phenotype and survival of
cardiomyocytes in the adult heart. Cardiac endothelial cells, like
vascular endothelial cells, also express and release a variety of auto-
and paracrine agents, such as nitric oxide, endothelin, prostaglandin
I 2 , and angiotensin II, which directly influence cardiac
metabolism, growth, contractile performance, and rhythmicity of the
adult heart. The synthesis, secretion, and, most importantly, the
activities of these endothelium-derived substances in the heart are
closely linked, interrelated, and interactive. It may therefore be
simplistic to try and define their properties independently from one
another. Moreover, in relation specifically to the endocardial
endothelium, an active transendothelial physicochemical gradient for
various ions, or blood-heart barrier, has been demonstrated.
Linkage of this blood-heart barrier to the various other
endothelium-mediated signaling pathways or to the putative vascular
endothelium-derived hyperpolarizing factors remains to be
determined. At the early stages of cardiac failure, all major
cardiovascular risk factors may cause cardiac endothelial activation as
an adaptive response often followed by cardiac endothelial dysfunction.
Because of the interdependency of all endothelial signaling pathways,
activation or disturbance of any will necessarily affect the others
leading to a disturbance of their normal balance, leading to further
progression of cardiac failure.
The heart is a highly structured organ consisting of different cell types, including myocytes, endothelial cells, fibroblasts, stem cells, and inflammatory cells. This pluricellularity provides the ...opportunity of intercellular communication within the organ, with subsequent optimization of its function. Intercellular cross-talk is indispensable during cardiac development, but also plays a substantial modulatory role in the normal and failing heart of adults. More specifically, factors secreted by cardiac microvascular endothelial cells modulate cardiac performance and either positively or negatively affect cardiac remodeling. The role of endothelium-derived small molecules and peptides-for instance NO or endothelin-1-has been extensively studied and is relatively well defined. However, endothelial cells also secrete numerous larger proteins. Information on the role of these proteins in the heart is scattered throughout the literature. In this review, we will link specific proteins that modulate cardiac contractility or cardiac remodeling to their expression by cardiac microvascular endothelial cells. The following proteins will be discussed: IL-6, periostin, tenascin-C, thrombospondin, follistatin-like 1, frizzled-related protein 3, IGF-1, CTGF, dickkopf-3, BMP-2 and-4, apelin, IL-1β, placental growth factor, LIF, WISP-1, midkine, and adrenomedullin. In the future, it is likely that some of these proteins can serve as markers of cardiac remodeling and that the concept of endothelial function and dysfunction might have to be redefined as we learn more about other factors secreted by ECs besides NO.
Abstract
Randomized clinical trials initially used heart failure (HF) patients with low left ventricular ejection fraction (LVEF) to select study populations with high risk to enhance statistical ...power. However, this use of LVEF in clinical trials has led to oversimplification of the scientific view of a complex syndrome. Descriptive terms such as ‘HFrEF’ (HF with reduced LVEF), ‘HFpEF’ (HF with preserved LVEF), and more recently ‘HFmrEF’ (HF with mid-range LVEF), assigned on arbitrary LVEF cut-off points, have gradually arisen as separate diseases, implying distinct pathophysiologies. In this article, based on pathophysiological reasoning, we challenge the paradigm of classifying HF according to LVEF. Instead, we propose that HF is a heterogeneous syndrome in which disease progression is associated with a dynamic evolution of functional and structural changes leading to unique disease trajectories creating a spectrum of phenotypes with overlapping and distinct characteristics. Moreover, we argue that by recognizing the spectral nature of the disease a novel stratification will arise from new technologies and scientific insights that will shape the design of future trials based on deeper understanding beyond the LVEF construct alone.
Heart failure (HF) is an important global health problem with great socioeconomic burden. Outcomes remain sub-optimal. Endothelium-cardiomyocyte interactions play essential roles in cardiovascular ...homeostasis, and deranged endothelium-related signalling pathways have been implicated in the pathophysiology of HF. In particular, disturbances in nitric oxide (NO)-mediated pathway and neuregulin-mediated pathway have been shown to contribute to the development of HF. These signalling pathways hold the potential as pathophysiological targets for new HF therapies, and may aid in patient selection for future HF trials.
Global left atrial failure in heart failure Triposkiadis, Filippos; Pieske, Burkert; Butler, Javed ...
European journal of heart failure,
11/2016, Letnik:
18, Številka:
11
Journal Article
Recenzirano
Odprti dostop
The left atrium plays an important role in the maintenance of cardiovascular and neurohumoral homeostasis in heart failure. However, with progressive left ventricular dysfunction, left atrial (LA) ...dilation and mechanical failure develop, which frequently culminate in atrial fibrillation. Moreover, LA mechanical failure is accompanied by LA endocrine failure deficient atrial natriuretic peptide (ANP) processing‐synthesis/development of ANP resistance) and LA regulatory failure (dominance of sympathetic nervous system excitatory mechanisms, excessive vasopressin release) contributing to neurohumoral overactivity, vasoconstriction, and volume overload (global LA failure). The purpose of the present review is to describe the characteristics and emphasize the clinical significance of global LA failure in patients with heart failure.
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