Key result
Arterial stiffness and vascular load play a significant pathophysiologic role in heart failure, and reducing aortic stiffness may form an important future therapeutic target.
This review emphasizes the importance of arterial stiffness and ventricular-vascular coupling in heart failure pathophysiology, identifying aortic stiffness as a potential therapeutic target.
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Load sensitivity in HF warrants cautious afterload management; leaves open optimal vascular targets for trials.
“Men are born soft and supple; dead, they are stiff and hard. Plants are born tender and pliant; dead, they are brittle and dry. Thus whoever is stiff and inflexible is a disciple of death. Whoever is soft and yielding is a disciple of life. The hard and stiff will be broken. The soft and supple will prevail.” —Lao Tzu, 6th century BC Vascular load is an important determinant of ventricular function. This is particularly true of the failing heart, which is exquisitely load‐sensitive. Vascular load comprises 2 major components: resistive load, which arises primarily at the arteriolar resistance vessels, and pulsatile load, which is primarily determined by aortic stiffness and early return of reflected waves from the periphery to the heart. Assessment of pulsatile load is gaining increasing prominence as evidence grows of a significant pathophysiologic role for arterial stiffness in cardiovascular disease, including heart failure. Assessment of arterial stiffness and vascular load is reviewed here. The importance of optimal ventricular‐vascular coupling to maximize the efficiency of cardiac ejection is discussed. Current knowledge of arterial stiffness, vascular load, and ventricular‐vascular coupling in systolic heart failure and in heart failure with a normal ejection fraction (“diastolic failure”) is described. Reducing aortic stiffness may form an important future therapeutic target in patients with heart failure.
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Ooi et al. (2008) conducted a review in Heart failure. Arterial stiffness and vascular load was evaluated. Arterial stiffness and vascular load play a significant pathophysiologic role in heart failure, and reducing aortic stiffness may form an important future therapeutic target.
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