The impact of extra cardiac comorbidities on pressure volume relations in heart failure and preserved ejection fraction

Abstract

Background: Extracardiac comorbidities are common in patients with heart failure and a preserved ejection fraction (HFPEF). We sought to evaluate the relationship between comorbidities and ventricular structure and function in patients with HFPEF through evaluation of pressure-volume analysis.

Methods and results: Two hundred twenty Chinese patients with a preserved ejection fraction who were either healthy (n = 75), hypertensive without heart failure (HTN; n = 89), or hypertensive with HFPEF (HFPEF; n = 56) were studied. Using echocardiographic measures, estimated end-systolic and end-diastolic pressure-volume relationships, and the area between them as a function of EDP, the isovolumic pressure-volume areas (PVA(iso)), were calculated. Ventricular capacitance, as measured by V(30), was larger in patients with HFPEF compared with normal control subjects and tended to be larger compared with hypertensive control subjects. The presence of diabetes and renal insufficiency was independently associated with greater ventricular capacitance in patients with HFPEF. The PVA(iso) was increased in patients with HFPEF compared with HTN and normal control subjects, and in particular, it was increased in HFPEF patients with multiple comorbidities.

Conclusions: The presence of comorbid conditions is associated with altered pressure-volume relations and enhanced pump function in subjects with HFPEF, supporting an important role for extracardiac comorbidities in the pathophysiology of patients with this condition.

Figure 1

(Upper Figures) Pressure-volume analyses demonstrating the normal PV loop and the determinants of ventricular function, including the ESPVR and the EDPVR (Panel A). Shifts in the ESPVR are often equated with changes in inotropic state (Panel B), while shifts in the EDPVR toward smaller volumes or reduced capacitance (diastolic dysfunction) or toward larger volumes or increased capacitance (remodeling). The ESPVR is characterized by the slope [E_es] and the volume axis intercept [V₀], which can be described collectively by the V₁₂₀, the volume of the left ventricle required to generate an end systolic pressure of 120 mm Hg (Panel C). Shifts in the EDPVR can be characterized by V₃₀, the ventricular volume at a pressure of 30 mm Hg, (Panel C). See Methods section for additional details. (Lower Figures) Demonstration of how PVA_iso is calculated from the PV diagram (Panels D and E). One value for PVA_iso (shaded area) can be obtained for each end-diastolic PV point shown by the black circles along the EDPVR. The points of a, b, and c in Panel D correspond to the solid line PVA_iso curve in Panel E. With shifts of the ESPVR and EDPVR (not shown), the PVA_iso curve can show increased or decreased cardiac function (dashed PVA_iso curves), Panel E.

Figure 2

Estimated graphical representation of the end-diastolic pressure-volume relationships among the studied populations. Hypertensive without heart failure (HTN), heart failure with preserved ejection fraction and 0,1, and 2+ comorbidities, HFPEF-0, HFPEF-1, HFPEF-2, respectively

Figure 3

PVA_iso relationships, demonstrating cardiac function, in patients with HTN, in normal controls, and in HFPEF with varied comorbidity burden (0,1, or 2+ comorbidities)