Abstract
The contribution of the vasculature in the development and progression of heart failure (HF) syndromes is poorly understood and often neglected. Incorporating both arterial and venous systems, the vasculature plays a significant role in the regulation of blood flow throughout the body in meeting its metabolic requirements. A deterioration or imbalance between the cardiac and vascular interaction can precipitate acute decompensated HF in both preserved and reduced ejection fraction phenotypes. This is characterised by the increasingly recognised concept of ventricular-arterial coupling: a well-balanced relationship between ventricular and vascular stiffness, which has major implications in HF. Often, the cause of decompensation is unknown, with international guidelines mainly centred on arrhythmia, infection, acute coronary syndrome and its mechanical complications as common causes of decompensation; the vascular component is often underrecognised. A better understanding of the vascular contribution in cardiovascular failure can improve risk stratification, earlier diagnosis and facilitate earlier optimal treatment. This review focuses on the role of the vasculature by integrating the concepts of ventricular-arterial coupling, arterial stiffness and venous return in a failing heart.
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Take Home Messages
1. Functional causes of heart failure can be driven by a mismatch in ventricular-arterial stiffness, resulting in increased myocardial wall stress, oxygen demand and energetic inefficiency.
2. Prompt reversal of this ventricular-arterial mismatch may lead to an improvement in left ventricular contractility and relaxation, regardless of ejection fraction.
3. Heart failure with preserved ejection fraction is usually associated with increased arterial stiffness as reflected by a higher amplitude of early systolic wave reflections and increased pulse wave velocity, imposing a greater afterload on the stressed ventricle.
4. In a load-sensitive left ventricle with reduced compliance, modest increases in preload (e.g. from venoconstriction) and afterload (e.g. during exercise or stress) can lead to marked increases in left ventricular end-diastolic pressure and, in turn, fluid congestion.
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Joshi, M., Tran, P., Barber, T.M. et al. The Role of the Vasculature in Heart Failure. Curr Heart Fail Rep 20, 179–190 (2023). https://doi.org/10.1007/s11897-023-00602-4
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DOI: https://doi.org/10.1007/s11897-023-00602-4