title: Combined ventricular systolic and arterial stiffening in patients with heart failure and preserved ejection fraction: implications for systolic and diastolic reserve limitations.
abstract: BACKGROUND
  Heart failure with preserved ejection fraction (HF-nlEF) is common in aged individuals with systolic hypertension and is frequently ascribed to diastolic dysfunction. We hypothesized that such patients also display combined ventricular-systolic and arterial stiffening that can exacerbate blood pressure lability and diastolic dysfunction under stress.
  
  
  RESULTS
  Left ventricular pressure-volume relations were measured in patients with HF-nlEF (n=10) and contrasted with asymptomatic age-matched (n=9) and young (n=14) normotensives and age- and blood pressure-matched controls (n=25). End-systolic elastance (stiffness) was higher in patients with HF-nlEF (4.7+/-1.5 mm Hg/mL) than in controls (2.1+/-0.9 mm Hg/mL for normotensives and 3.3+/-1.0 mm Hg/mL for hypertensives; P<0.001). Effective arterial elastance was also higher (2.6+/-0.5 versus 1.9+/-0.5 mm Hg/mL) due to reduced total arterial compliance; the latter inversely correlated with end-systolic elastance (P=0.0001). Body size and stroke volumes were similar and could not explain differences in ventricular-arterial stiffening. HF-nlEF patients also displayed diastolic abnormalities, including higher left ventricular end-diastolic pressures (24.3+/-4.6 versus 12.9+/-5.5 mm Hg), caused by an upward-shifted diastolic pressure-volume curve. However, isovolumic relaxation and the early-to-late filling ratio were similar in age- and blood pressure-matched controls. Ventricular-arterial stiffening amplified stress-induced hypertension, which worsened diastolic function, and predicted higher cardiac energy costs to provide reserve output.
  
  
  CONCLUSIONS
  Patients with HF-lnEF have systolic-ventricular and arterial stiffening beyond that associated with aging and/or hypertension. This may play an important pathophysiological role by exacerbating systemic load interaction with diastolic function, augmenting blood pressure lability, and elevating cardiac metabolic demand under stress.
authors.affiliation: Division of Cardiology, Department of Medicine, Johns Hopkins School of Medicine, Baltimore, MD, USA.
authors.forename: Miho
authors.initials: M
authors.lastname: Kawaguchi
authors.forename: Ilan
authors.initials: I
authors.lastname: Hay
authors.forename: Barry
authors.initials: B
authors.lastname: Fetics
authors.forename: David A
authors.initials: DA
authors.lastname: Kass
mesh_terms: D000328:Adult; D000368:Aged; D001158:Arteries / Q000503:physiopathology*; D003710:Demography; D003971:Diastole; D004548:Elasticity; D005260:Female; D006333:Heart Failure / Q000150:complications / Q000175:diagnosis* / Q000503:physiopathology; D006334:Heart Function Tests; D006439:Hemodynamics; D006801:Humans; D008297:Male; D008875:Middle Aged; D012016:Reference Values; D013318:Stroke Volume; D013599:Systole; D018754:Ventricular Dysfunction / Q000150:complications / Q000175:diagnosis* / Q000503:physiopathology