Elsevier

Progress in Cardiovascular Diseases

Volume 49, Issue 4, January–February 2007, Pages 252-262
Progress in Cardiovascular Diseases

Ventricular-Arterial and Ventricular-Ventricular Interactions and Their Relevance to Diastolic Filling

https://doi.org/10.1016/j.pcad.2006.08.004Get rights and content

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.

Section snippets

Ventricular-Arterial Coupling

The interaction of the heart with the systemic vasculature, termed ventricular-arterial (V-A) 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. Normal physiologic V-A coupling matches these properties so that maximal

Dynamic Changes in Diastolic Function and the Effects of Loading Conditions

Diastolic abnormalities may involve active ventricular relaxation and/or passive ventricular filling. During dynamic exercise in health (and during moderate acute increases in cardiac afterload such as during handgrip exercise) there is an increase in the rate of LV active relaxation via sympathetically mediated activation of sarcoendoplasmic reticulum adenosine triphosphatase and via protein kinase A (PKA)–mediated phosphorylation of troponin I and of phospholamban and titin.38, 39, 40 This

Relevance of V-A Coupling to Diastolic Heart Failure

Many patients with HFpEF are hypertensive, typically with isolated “systolic” hypertension. Systolic hypertension is predominantly due to increased large artery stiffness and results in an increased pulsatile LV afterload (impedance) often leading to LV hypertrophy. A recent study showed that in older patients with “diastolic” heart failure, impaired exercise tolerance correlated with aortic stiffness, which was significantly increased compared with age-matched controls.49 Another study showed

Ventricular Interaction

The term “series ventricular interaction” refers to the phenomenon whereby each ventricle ejects all of the blood that it receives from the other ventricle, and is a consequence of the Frank-Starling mechanism. There are also important direct interactions between the ventricles during diastole and systole. Because the ventricles share a common interventricular septum, the compliance of one ventricle is influenced by changes in the volume, pressure, and/or compliance of the other. This

DVI and HFnEF?

At present, the relevance of ventricular-ventricular interactions is unknown in HFnEF. However, there is some indirect evidence to suggest that on exercise, increased external constraint to LV filling may contribute to impaired use of the Starling mechanism. Kitzman et al64 performed invasive cardiopulmonary exercise testing in 7 patients with CHF and a normal LVEF and no significant coronary artery disease or valvular heart disease, and compared them with 10 age- and sex-matched healthy

References (67)

  • C.H. Chen et al.

    Coupled systolic-ventricular and vascular stiffening with age: Implications for pressure regulation and cardiac reserve in the elderly

    J. Am. Coll. Cardiol.

    (1998)
  • H.L. Granzier et al.

    Passive tension in cardiac muscle: contribution of collagen, titin, microtubules, and intermediate filaments

    Biophys. J.

    (1995)
  • S.P. Robertson et al.

    The effect of troponin I phosphorylation on the Ca2+-binding properties of the Ca2+-regulatory site of bovine cardiac troponin

    J. Biol. Chem.

    (1982)
  • T. Sasaki et al.

    Molecular mechanism of regulation of Ca2+ pump ATPase by phospholamban in cardiac sarcoplasmic reticulum. Effects of synthetic phospholamban peptides on Ca2+ pump ATPase

    J. Biol. Chem.

    (1992)
  • J. Ross

    Afterload mismatch and preload reserve: A conceptual framework for the analysis of ventricular function

    Prog. Cardiovasc. Dis.

    (1976)
  • W.G. Hundley et al.

    Cardiac cycle-dependent changes in aortic area and distensibility are reduced in older patients with isolated diastolic heart failure and correlate with exercise intolerance

    J. Am. Coll. Cardiol.

    (2001)
  • C.H. Chen et al.

    Verapamil acutely reduces ventricular-vascular stiffening and improves aerobic exercise performance in elderly individuals

    J. Am. Coll. Cardiol.

    (1999)
  • D.J. Magorien et al.

    Hemodynamic correlates for timing intervals, ejection rate and filling rate derived from the radionuclide angiographic volume curve

    Am. J. Cardiol.

    (1984)
  • J.J. Atherton et al.

    Diastolic ventricular interaction in chronic heart failure

    Lancet

    (1997)
  • W.F. Kerwin et al.

    Ventricular contraction abnormalities in dilated cardiomyopathy: Effect of biventricular pacing to correct interventricular dyssynchrony

    J. Am. Coll. Cardiol.

    (2000)
  • C. Le Rest et al.

    Use of left ventricular pacing in heart failure: Evaluation by gated blood pool imaging

    J. Nucl. Cardiol.

    (1999)
  • D.W. Kitzman et al.

    Exercise intolerance in patients with heart failure and preserved left ventricular systolic function: failure of the Frank-Starling mechanism

    J. Am. Coll. Cardiol.

    (1991)
  • M. Klapholz et al.

    Clinical characteristics and co-morbid conditions of patients hospitalized for heart failure with normal systolic function; results of the New York heart failure consortium registry on diastolic dysfunction

    Circulation

    (2004)
  • J.S. Gottdiener et al.

    Outcome of congestive heart failure in elderly persons: Influence of left ventricular systolic function. The Cardiovascular Health Study

    Ann. Intern. Med.

    (2002)
  • Q. Malki et al.

    Clinical presentation, hospital length of stay, and readmission rate in patients with heart failure with preserved and decreased left ventricular systolic function

    Clin. Cardiol.

    (2002)
  • S.K. Gandhi et al.

    The pathogenesis of acute pulmonary edema associated with hypertension

    N. Engl. J. Med.

    (2001)
  • S.S. Lele et al.

    Determinants of exercise capacity in patients with coronary artery disease and mild to moderate systolic dysfunction. Role of heart rate and diastolic filling abnormalities

    Eur. Heart J.

    (1996)
  • L.R. Peterson et al.

    Peak exercise stroke volume: associations with cardiac structure and diastolic function

    J. Appl. Physiol.

    (2003)
  • W.C. Little et al.

    Left ventricular-arterial coupling in conscious dogs

    Am. J. Physiol.

    (1991)
  • W.C. Little et al.

    Effect of exercise on left ventricular-arterial coupling assessed in the pressure-volume plane

    Am. J. Physiol.

    (1993)
  • P.P. De Tombe et al.

    Ventricular stroke work and efficiency both remain nearly optimal despite altered vascular loading

    Am. J. Physiol.

    (1993)
  • H. Asanoi et al.

    Ventriculoarterial coupling in normal and failing heart in humans

    Circ. Res.

    (1989)
  • M.D. Feldman et al.

    Acute cardiovascular effects of OPC-18790 in patients with congestive heart failure. Time- and dose-dependence analysis based on pressure-volume relations

    Circulation

    (1996)
  • Cited by (68)

    • Double-outlet right ventricle

      2018, Critical Heart Disease in Infants and Children
    • Association of Thoracic Aorta Calcium Score With Left Ventricular Hypertrophy and Clinical Outcomes in Patients With Severe Aortic Stenosis After Aortic Valve Replacement

      2017, Annals of Thoracic Surgery
      Citation Excerpt :

      Moreover, arterial stiffening adversely affects the LV through increased afterload. This mechanism, termed as ventricular-vascular coupling, has been proposed as one of the important factors in the development of LVH [13]. Arterial stiffening is associated with atherosclerosis, and increased arterial stiffness is a common finding in AS patients who are relatively older and who often present with traditional risk factors for atherosclerosis.

    • Causes of exercise intolerance in heart failure with preserved ejection fraction: Searching for consensus

      2014, Journal of Cardiac Failure
      Citation Excerpt :

      Tachycardia would be predicted to unmask these deficits leading to a reduction in exercise preload. Finally, elevated filling pressures due to diastolic dysfunction could compromise left ventricular SV by compromising right ventricular SV or by accentuating ventricular interdependence.54–56 Given the widespread belief that diastolic dysfunction is an important factor compromising exercise tolerance, it is surprising that the exercise studies reviewed here do not demonstrate a consistent deficit in peak exercise SV.

    • Causes and Pathophysiology of Heart Failure with Preserved Ejection Fraction

      2014, Heart Failure Clinics
      Citation Excerpt :

      Patients with HFPEF were reported to have decreased Ea/Ees ratios when compared with those of age-matched controls, but not when compared with hypertensive controls without HF (Fig. 1C).18,20 The main features of LV diastolic dysfunction are: slowed LV relaxation, enhanced LV stiffness,21 reduced ventricular restoring forces,10 impaired diastolic suction,22 and ventricular dyssynchrony.23 From the practical point of view, characterization of diastolic function is more difficult than that of systolic function, and this is also reflected by the many currently used quantitative indices of LV diastolic function obtained by invasive hemodynamic tests and noninvasive investigations.

    View all citing articles on Scopus
    View full text