TY - JOUR
T1 - Ventricular-Vascular Interaction in Heart Failure
AU - Borlaug, Barry A.
AU - Kass, David A.
N1 - Funding Information:
Many of the changes in ventricular–arterial stiffness in HFpEF are chronic, because of alterations in the material properties of the cardiovascular system [25,61] . In the largest randomized trial of HF with near-normal EF, there was a borderline-significant treatment effect driven by a reduction in hospitalizations for HF [62] . This trial enrolled subjects who had HF and EF greater than 40%, however, and many would consider those who have EF less than 50% to 55% to have some element of systolic dysfunction [26,27] . ACE inhibitors, which also reduce vascular stiffness, may be useful in HFpEF [63] . Other treatments under evaluation include aldosterone [64,65] , TGF-β [66] , and chymase antagonists [67] . A large-scale randomized trial funded by the National Institutes of Health (NIH) is currently underway testing the efficacy of the aldosterone antagonist spironolactone in HFpEF.
PY - 2008/1
Y1 - 2008/1
N2 - Nearly half of all patients who have heart failure have preserved ejection fraction (HFpEF). Patients who have HFpEF tend to be older, female, and hypertensive, and characteristically display increased ventricular and arterial stiffening. In this article, we discuss the pathophysiology of abnormal ventriculoarterial stiffening and how it affects ventricular function, cardiovascular hemodynamics, reserve capacity, and symptoms. We conclude by exploring how novel treatment strategies targeting abnormal ventricular-arterial interaction might prove useful in the treatment of patients who have HFpEF.
AB - Nearly half of all patients who have heart failure have preserved ejection fraction (HFpEF). Patients who have HFpEF tend to be older, female, and hypertensive, and characteristically display increased ventricular and arterial stiffening. In this article, we discuss the pathophysiology of abnormal ventriculoarterial stiffening and how it affects ventricular function, cardiovascular hemodynamics, reserve capacity, and symptoms. We conclude by exploring how novel treatment strategies targeting abnormal ventricular-arterial interaction might prove useful in the treatment of patients who have HFpEF.
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U2 - 10.1016/j.hfc.2007.10.001
DO - 10.1016/j.hfc.2007.10.001
M3 - Review article
C2 - 18313622
AN - SCOPUS:39649106311
VL - 4
SP - 23
EP - 36
JO - Heart Failure Clinics
JF - Heart Failure Clinics
SN - 1551-7136
IS - 1
ER -