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. 2021 Jul;23(7):1097-1105.
doi: 10.1002/ejhf.2121. Epub 2021 Feb 21.

Contributions of cardiac dysfunction and volume status to central haemodynamics in chronic heart failure

Wayne L Miller  1 , Hidemi Sorimachi  1 , Diane E Grill  2 , Karen Fischer  2 , Barry A Borlaug  1
Affiliations

Contributions of cardiac dysfunction and volume status to central haemodynamics in chronic heart failure

Wayne L Miller et al. Eur J Heart Fail. 2021 Jul.

Abstract

Aims: Elevated cardiac filling pressures producing clinical congestion in heart failure (HF) patients may be secondary to intravascular volume expansion or abnormalities in cardiac diastolic properties. The objective of this study was to assess the extent to which measures of myocardial function and intravascular volume correlate with haemodynamic abnormalities in chronic HF.

Methods and results: Subjects underwent invasive haemodynamic assessment, measurement of total blood volume (TBV) using radiolabel indicator-dilution methodology, and echocardiography to evaluate cardiac structure and function. Patients were divided into those with hypervolaemia (defined as TBV > +8% above referenced normal volume) and normal volume ('euvolaemia') (TBV ≤ + 8%). Of 66 patients, 39 (59%) were hypervolaemic and 27 (41%) normal TBV. Central venous pressure (CVP, P = 0.01) and pulmonary capillary wedge pressure (PCWP, P < 0.001) were higher in hypervolaemic compared with euvolaemic patients; however, 15% of hypervolaemic patients displayed normal pressures. Of euvolaemic patients, 70% displayed elevated CVP and 63% elevated PCWP. PCWP was moderately correlated with TBV (r = 0.42), left ventricular diastolic function (e' velocity, r = -0.44), and left atrial strain (r = -0.47). In multivariable regression TBV, left ventricular e', and left atrial strain were independently associated with PCWP (all P < 0.05).

Conclusions: While hypervolaemic patients displayed elevations in filling pressures, a substantial proportion (15%) had normal pressures, and of all subjects with elevated filling pressures nearly one third had normal TBVs. Importantly, of patients with normal volumes, a majority (>60%) display elevated filling pressures. Combined analysis of volume, pressure, and cardiac function may be helpful to guide comprehensive assessments of HF status.

Keywords: Cardiac filling pressures; Cardiac function; Heart failure; Intravascular volume.

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Conflict of interest statement

Conflict of Interest

None.

Figures

Figure 1.
Figure 1.
Compared to normal volume HF patients (euvolemic, black), patients with increased intravascular volume (hypervolemic, red) displayed more right ventricular dilatation (end diastolic area, RVEDA), greater left atrial enlargement (left atrial volume index, LAVI), and lower left atrial strain. *p<0.001 compared to normal volume.
Figure 2.
Figure 2.
While central venous pressure (CVP, left) and pulmonary capillary wedge pressure (PCWP, right) were higher on average in hypervolemic patients (red boxes), >60% of euvolemic patients (black circles) still displayed elevated CVP (>6 mmHg) and elevated PCWP (>15 mmHg, dotted lines).
Figure 3.
Figure 3.
Compared to euvolemic patients with normal PCWP (black), patients with euvolemia but high PCWP (gray) displayed more myocardial dysfunction, with lower left ventricular global longitudinal strain (GLS), lower early diastolic relaxation velocities (e’), and decreased left atrial strain. *p<0.05 compared to normal PCWP.
Figure 4.
Figure 4.
Correlations between pulmonary artery (PA) wedge pressures, left atrial function (strain), diastolic relaxation (e’), and intravascular blood volume.
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References

    1. Forrester JS, Water DD. Hospital treatment of congestive heart failure. Management according to hemodynamic profiles. Am J Med. 1978; 65(1):173–180. - PubMed
    1. Forrester JS, Diamond G, Chatterjee K, Swan HJ. Medical therapy of acute myocardial infarction by application of hemodynamic subsets (first of two parts). N Engl J Med. 1976; 295(24):1356–1362. - PubMed
    1. Stevenson LW. Are hemodynamic goals viable in tailoring heart failure therapy? Hemodynamic goals are relevant. Circulation. 2006; 113:1020–1027. - PubMed
    1. Binanay C, Califf RM, Hasselblad V, O’Connor CM, Shah MR, Sopko G, Stevenson LW, ESCAPE Investigators, ESCAPE study coordinators. Evaluation study of congestive heart failure and pulmonary artery catheterization effectiveness: The ESCAPE Trial. JAMA. 2005; 294(13):1625–1633. - PubMed
    1. Levey AS, Coresh J, Balk E, Kausz AT, Levin A, Steffes MW, Hogg RJ, Perrone RD, Lau J, Eknoyan G. National Kidney Foundation practice guidelines for chronic kidney disease: Evaluation, classification, and stratification. Ann Intern Med. 2003;139:137–147. - PubMed

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