title: Exercise hemodynamics enhance diagnosis of early heart failure with preserved ejection fraction.
abstract: BACKGROUND
  When advanced, heart failure with preserved ejection fraction (HFpEF) is readily apparent. However, diagnosis of earlier disease may be challenging because exertional dyspnea is not specific for heart failure, and biomarkers and hemodynamic indicators of volume overload may be absent at rest.
  
  
  RESULTS
  Patients with exertional dyspnea and ejection fraction >50% were referred for hemodynamic catheterization. Those with no significant coronary disease, normal brain natriuretic peptide assay, and normal resting hemodynamics (mean pulmonary artery pressure <25 mm Hg and pulmonary capillary wedge pressure [PCWP] <15 mm Hg) (n=55) underwent exercise study. The exercise PCWP was used to classify patients as having HFpEF (PCWP ≥25 mm Hg) (n=32) or noncardiac dyspnea (PCWP <25 mm Hg) (n=23). At rest, patients with HFpEF had higher resting pulmonary artery pressure and PCWP, although all values fell within normal limits. Exercise-induced elevation in PCWP in HFpEF was confirmed by greater increases in left ventricular end-diastolic pressure and was associated with blunted increases in heart rate, systemic vasodilation, and cardiac output. Exercise-induced pulmonary hypertension was present in 88% of patients with HFpEF and was related principally to elevated PCWP, as pulmonary vascular resistances dropped similarly in both groups. Exercise PCWP and pulmonary artery systolic pressure were highly correlated. An exercise pulmonary artery systolic pressure ≥45 mm Hg identified HFpEF with 96% sensitivity and 95% specificity.
  
  
  CONCLUSIONS
  Euvolemic patients with exertional dyspnea, normal brain natriuretic peptide, and normal cardiac filling pressures at rest may have markedly abnormal hemodynamic responses during exercise, suggesting that chronic symptoms are related to heart failure. Earlier and more accurate diagnosis using exercise hemodynamics may allow better targeting of interventions to treat and prevent HFpEF progression.
authors.affiliation: Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Rochester, Minn 55905, USA. borlaug.barry@mayo.edu
authors.forename: Barry A
authors.initials: BA
authors.lastname: Borlaug
authors.forename: Rick A
authors.initials: RA
authors.lastname: Nishimura
authors.forename: Paul
authors.initials: P
authors.lastname: Sorajja
authors.forename: Carolyn S P
authors.initials: CS
authors.lastname: Lam
authors.forename: Margaret M
authors.initials: MM
authors.lastname: Redfield
mesh_terms: D000368:Aged; D000704:Analysis of Variance; D002302:Cardiac Output / Q000502:physiology; D016009:Chi-Square Distribution; D015897:Comorbidity; D003971:Diastole; D004417:Dyspnea / Q000175:diagnosis / Q000503:physiopathology; D005080:Exercise Test; D005260:Female; D006333:Heart Failure / Q000175:diagnosis* / Q000503:physiopathology*; D006439:Hemodynamics; D006801:Humans; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D011669:Pulmonary Wedge Pressure / Q000502:physiology; D012372:ROC Curve; D012189:Retrospective Studies; D012680:Sensitivity and Specificity; D013318:Stroke Volume / Q000502:physiology*