title: Pathophysiological rationale and diagnostic targets for diastolic stress testing.
abstract: Cardiopulmonary functional reserve measured as peak oxygen uptake is predicted better at rest by measures of cardiac diastolic function than by systolic function. Normal adaptations in the trained heart include resting bradycardia, increased LV end-diastolic volume and augmented early diastolic suction on exercise. In normal populations early diastolic relaxation declines with age and end-diastolic stiffness increases, but in healthy older subjects who have exercised throughout their lives diastolic function can be well preserved. The mechanisms by which LV diastolic filling and pressures can be impaired during exercise include reduced early diastolic recoil and suction (which can be exacerbated by increased late systolic loading), increased preload and reduced compliance. Abnormal ventricular-arterial coupling and enhanced ventricular interaction may contribute in particular circumstances. One common final pathway that causes breathlessness is an increase in LV filling pressure and left atrial pressure. Testing elderly subjects with breathlessness of unknown aetiology in order to detect worsening diastolic function during stress is proposed to diagnose heart failure with preserved EF. In invasive studies, the most prominent abnormality is an early and rapid rise in pulmonary capillary wedge pressure. A systematic non-invasive diagnostic strategy would use validated methods to assess different mechanisms of inducible diastolic dysfunction and not just single parameters that offer imprecise estimates of mean LV filling pressure. Protocols should assess early diastolic relaxation and filling as well as late diastolic filling and compliance, as these may be affected separately. Better refined diagnostic targets may translate to more focused treatment.
authors.affiliation: Wales Heart Research Institute, Cardiff University, Cardiff, UK.
authors.forename: Tamás
authors.initials: T
authors.lastname: Erdei
authors.affiliation: Department of Cardiology, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
authors.forename: Svend
authors.initials: S
authors.lastname: Aakhus
authors.affiliation: Cardiology Clinic, Universita Piemonte Orientale, Novara, Italy.
authors.forename: Paolo
authors.initials: P
authors.lastname: Marino
authors.affiliation: Department of Physiology, Institute for Cardiovascular Research, VU University Medical Center, Amsterdam, The Netherlands.
authors.forename: Walter J
authors.initials: WJ
authors.lastname: Paulus
authors.affiliation: Department of Cardiology, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
authors.forename: Otto A
authors.initials: OA
authors.lastname: Smiseth
authors.affiliation: Wales Heart Research Institute, Cardiff University, Cardiff, UK.
authors.forename: Alan G
authors.initials: AG
authors.lastname: Fraser
mesh_terms: D000222:Adaptation, Physiological; D000367:Age Factors; D000368:Aged; D002316:Cardiotonic Agents; D003971:Diastole; D004417:Dyspnea / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology; D018618:Echocardiography, Doppler, Color; D018619:Echocardiography, Doppler, Pulsed; D025401:Echocardiography, Stress / Q000379:methods*; D005080:Exercise Test; D017079:Exercise Tolerance; D005260:Female; D006333:Heart Failure / Q000150:complications / Q000175:diagnosis* / Q000503:physiopathology / Q000628:therapy; D006801:Humans; D008297:Male; D008875:Middle Aged; D011237:Predictive Value of Tests; D011379:Prognosis; D012307:Risk Factors; D013997:Time Factors; D016277:Ventricular Function, Left
chemical_list: D002316:Cardiotonic Agents