2017
DOI: 10.1161/jaha.117.006817
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Role of Volume Redistribution in the Congestion of Heart Failure

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Cited by 133 publications
(132 citation statements)
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References 112 publications
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“…94,95 Decreased arterial, and equally if not more importantly venous compliance, are conceptually driven by (i) obesity-mediated neurohormonal and inflammatory activation, and (ii) possibly by pure mechanical properties of the adipose tissue. 96 The splanchnic vascular compartment is the largest reservoir of intravascular blood volume, with the majority of the blood located in the venous system. It has been proposed that inter-compartmental volume redistribution from the abdominal/splanchnic compartment into the central compartment (chest and central vasculature) could be a key determinant of cardiovascular congestion and cause of cardiac decompensation.…”
Section: Vascular Compliance and Splanchnic Couplingmentioning
confidence: 99%
“…94,95 Decreased arterial, and equally if not more importantly venous compliance, are conceptually driven by (i) obesity-mediated neurohormonal and inflammatory activation, and (ii) possibly by pure mechanical properties of the adipose tissue. 96 The splanchnic vascular compartment is the largest reservoir of intravascular blood volume, with the majority of the blood located in the venous system. It has been proposed that inter-compartmental volume redistribution from the abdominal/splanchnic compartment into the central compartment (chest and central vasculature) could be a key determinant of cardiovascular congestion and cause of cardiac decompensation.…”
Section: Vascular Compliance and Splanchnic Couplingmentioning
confidence: 99%
“…Возможным объяснением неблагоприятного влияния повышения плотности печени на риск повторных госпитализаций с СН может быть концепция нарушенного внутрисосудистого распределения жидкости, подразумевающая важную роль емкостных сосудов печени в регуляции водного баланса при СН [22]. В условиях ХСН вследствие длительного венозного застоя и стойкой адренергической стимуляции развивается дезадаптация реакции емкостных сосудов, спазм и последующее перераспределение депонирующейся в них жидкости в системный кровоток, что резко увеличива-ОРИГИНАЛЬНЫЕ СТАТЬИ § ет эффективный объем циркулирующей крови и преднагрузку на сердце, тем самым приводя к появлению симптомов декомпенсации [22]. Соответственно, пациенты с высокими значениями плотности печени и, следовательно, с более выраженным застоем органа, характеризуются потенциально большим риском быстрого ухудшения СН.…”
Section: Discussionunclassified
“…Kardiologiia. 2018;58(S10): [20][21][22][23][24][25][26][27][28][29][30][31][32] Summary Objective: There is growing evidence that liver stiffness (LS) in decompensated heart failure (DHF) is related to congestion, however data about its impact on outcomes are limited. The aim of the study was to evaluate associations and long-term prognostic significance of LS measured by transient elastography (TE) in DHF.…”
mentioning
confidence: 99%
“…When the cardiac burden persists even under adequate diuretic therapy for unloading the heart, strategies to further reduce the cardiac burden or enhance cardiac power are required in parallel, such as by using inotropes, controlling blood pressure and heart rate, modulating cardiac re-synchronization, and ultrafiltration [ 47 , 80 ]. Appropriate use of vasodilators or blockade of the RAAS to increase venous capacitance may be an important therapeutic option for reducing the cardiac burden [ 13 , 14 ].…”
Section: Proposal For New Diuretic Classification and Achievement Of mentioning
confidence: 99%