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, KLV) may be calculated by the formula: KLV = (70/[DT-20])2 mm Hg/mL, where DT is the transmitral Doppler deceleration time. Methods and 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 KLV 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 (KLV, 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 KLV at baseline (P < .01). No changes in KLV 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. © 2009 Elsevier Inc. All rights reserved.
Malfatto, G., Branzi, G., Osculati, G., Valli, P., Cuoccio, P., Ciambellotti, F., et al. (2009). Improvement in left ventricular diastolic stiffness induced by physical training in patients with dilated cardiomyopathy. JOURNAL OF CARDIAC FAILURE, 15(4), 327-333 [10.1016/j.cardfail.2008.10.032].
Improvement in left ventricular diastolic stiffness induced by physical training in patients with dilated cardiomyopathy
PARATI, GIANFRANCO;
2009
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, KLV) may be calculated by the formula: KLV = (70/[DT-20])2 mm Hg/mL, where DT is the transmitral Doppler deceleration time. Methods and 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 KLV 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 (KLV, 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 KLV at baseline (P < .01). No changes in KLV 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. © 2009 Elsevier Inc. All rights reserved.
I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
