title: Improvement in left ventricular diastolic stiffness induced by physical training in patients with dilated cardiomyopathy.
abstract: BACKGROUND
  Diastolic dysfunction in long-term heart failure is accompanied by abnormal neurohormonal control and ventricular stiffness. The diastolic phase is determined by a balance between pressure gradients and intrinsic ventricular wall properties: according to a mathematical model, the latter (ie, left ventricular [LV] elastance, K(LV)) may be calculated by the formula: K(LV) = (70/[DT-20])(2) mm Hg/mL, where DT is the transmitral Doppler deceleration time.
  
  
  RESULTS
  In 54 patients with chronic systolic heart failure (39 men, 15 women; age 65 +/- 10 years; New York Heart Association [NYHA], 2.3 +/- 0.9; ejection fraction [EF], 32% +/- 5%), we analyzed the relationship between K(LV) and an index of neurohormonal derangement (levels of brain natriuretic peptide [BNP]), and investigated whether 3 months of physical training could modulate diastolic operating stiffness. Patients were randomized to physical training (n = 27) or to a control group (n = 27). Before and after training, patients underwent Doppler echocardiogram and cardiopulmonary stress test. At baseline, ventricular stiffness was related to BNP levels (P < .01). Training improved NYHA class, exercise performance, and estimated pulmonary pressure. BNP was reduced. Ventricular volumes, mean blood pressure, and EF remained unchanged. A 27% reduction of elastance was observed (K(LV), 0.111 +/- 0.044 from 0.195 +/- 0.089 mm Hg/mL; P < .01), whose magnitude was related to changes in BNP (P < .05) and to K(LV) at baseline (P < .01). No changes in K(LV) were observed in controls after 3 months (0.192 +/- 0.115 from 0.195 +/- 0.121 mm Hg/mL).
  
  
  CONCLUSIONS
  In heart failure, left ventricular diastolic stiffness is related to neurohormonal derangement and is modified by physical training. This improvement in LV compliance could result from a combination of hemodynamic improvement and regression of the fibrotic process.
authors.affiliation: Divisione di Cardiologia, Ospedale San Luca, Istituto Auxologico Italiano Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS), Milano, Italy.
authors.forename: Gabriella
authors.initials: G
authors.lastname: Malfatto
authors.forename: Giovanna
authors.initials: G
authors.lastname: Branzi
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Osculati
authors.forename: Paola
authors.initials: P
authors.lastname: Valli
authors.forename: Paola
authors.initials: P
authors.lastname: Cuoccio
authors.forename: Francesca
authors.initials: F
authors.lastname: Ciambellotti
authors.forename: Gianfranco
authors.initials: G
authors.lastname: Parati
authors.forename: Mario
authors.initials: M
authors.lastname: Facchini
mesh_terms: D000368:Aged; D002311:Cardiomyopathy, Dilated / Q000097:blood / Q000503:physiopathology* / Q000628:therapy*; D003971:Diastole / Q000502:physiology; D015444:Exercise / Q000502:physiology*; D005260:Female; D005500:Follow-Up Studies; D054143:Heart Failure, Systolic / Q000097:blood / Q000503:physiopathology / Q000628:therapy; D006801:Humans; D008297:Male; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain / Q000097:blood; D018487:Ventricular Dysfunction, Left / Q000097:blood / Q000503:physiopathology* / Q000628:therapy*
chemical_list: D020097:Natriuretic Peptide, Brain