Author + information
- Barry Borlaug,
- Margaret Redfield,
- Vojtech Melenovsky,
- Garvan Kane,
- Barry Karon and
- Richard Rodeheffer
In cross sectional studies, left ventricular (LV) and arterial elastance (stiffness) increase with age and are correlated with one another. LV stiffening is a key mechanism causing heart failure with preserved ejection fraction (HFpEF) that is widely felt to be the consequence of arterial stiffening, but longitudinal data in support of this hypothesis are unavailable.
In a prospective, community-based study, echocardiography was performed in 788 subjects (age 60±9 years, 48% men) at entry and four years later to determine LV end systolic elastance (Ees), end diastolic elastance (Eed) and effective arterial elastance (Ea).
Over 4 years, blood pressure, Ea and LV mass decreased, in concert with 35% greater use of antihypertensive medicines (Figure). Despite reduced arterial afterload, Ees and Eed increased by 14% and 8% (each p<0.0001, Figure). Changes in Ees were correlated with changes in Eed (r=0.5, p<0.0001), but not with other measures of contractility, suggesting that the increase in Ees was reflective of passive LV stiffening rather than enhanced systolic function.
Despite reductions in systemic arterial afterload with medical therapy, LV systolic and diastolic stiffness increase over time in humans, indicating that arterial and ventricular stiffening with age are not always causally linked. Pathways involved in load-independent ventricular stiffening may be novel targets to prevent and treat age-associated cardiovascular diseases such as HFpEF.
Oral Contributions South, Room 104
Sunday, March 10, 2013, 11:15 a.m.-11:30 a.m.
Session Title: Joint Session of the Heart Failure Society of America and American College of Cardiology
Abstract Category: 17. Heart Failure: Therapy
Presentation Number: 925-5
- 2013 American College of Cardiology Foundation