Send to

Choose Destination
See comment in PubMed Commons below
Prog Cardiovasc Dis. 2007 Jan-Feb;49(4):252-62.

Ventricular-arterial and ventricular-ventricular interactions and their relevance to diastolic filling.

Author information

Department of Cardiovascular Medicine, University of Birmingham, Birmingham, United Kingdom.


Chronic heart failure is a common clinical problem, and, until recently, attention has focused predominantly on those patients with reduced left ventricular (LV) systolic function, as evidenced by a reduced LV ejection fraction. However, nearly half of all patients thought clinically to have heart failure have a "preserved" LV ejection fraction, variously defined as greater than 40% to 45% ("heart failure with normal ejection fraction" syndrome). The interaction of the heart with the systemic vasculature, termed ventricular-arterial coupling, is a key determinant of cardiovascular performance. The capacity of the body to augment cardiac output, regulate systemic blood pressure, and respond appropriately to elevations in heart rate and preload depends on both the properties of the heart and the properties of the vasculature into which the heart ejects blood. Although the marked increase of arterial and cardiac stiffness with aging can maintain ventricular-vascular coupling within a normal range, it does have detrimental effects on hemodynamic stability and cardiac reserve. Patients with heart failure with normal ejection fraction have been shown to have both arterial and ventricular stiffening, resulting in enhanced pressure-load dependence and sensitivity of blood pressure to circulating volume and diuretics. There is also indirect evidence to suggest that on exercise, increased external constraint to LV filling (as a result of diastolic ventricular interaction and pericardial constraint) may contribute to impaired use of the Starling mechanism in this group of patients.

[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons


    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center