BACKGROUND Many secondary abnormalities in chronic heart failure (CHF) may reflect physical deconditioning. There has been no prospective, controlled study of the effects of physical training on hemodynamics and autonomic function in CHF. METHODS AND RESULTS In a controlled crossover trial of 8 weeks of exercise training, 17 men with stable moderate to severe CHF (age, 61.8 +/- 1.5 years; left ventricular ejection fraction, 19.6 +/- 2.3%), increased exercise tolerance (13.9 +/- 1.0 to 16.5 +/- 1.0 minutes, p less than 0.001), and peak oxygen uptake (13.2 +/- 0.9 to 15.6 +/- 1.0 ml/kg/min, p less than 0.01) significantly compared with controls. Training increased cardiac output at submaximal (5.9-6.7 l/min, p less than 0.05) and peak exercise (6.3-7.1 l/min, p less than 0.05), with a significant reduction in systemic vascular resistance. Training reduced minute ventilation and the slope relating minute ventilation to carbon dioxide production (-10.5%, p less than 0.05). Sympathovagal balance was altered by physical training when assessed by three methods: 1) RR variability (+19.2%, p less than 0.05); 2) autoregressive power spectral analysis of the resting ECG divided into low-frequency (-21.2%, p less than 0.01) and high-frequency (+51.3%, p less than 0.05) components; and 3) whole-body radiolabeled norepinephrine spillover (-16%, p less than 0.05). These measurements all showed a significant shift away from sympathetic toward enhanced vagal activity after training. CONCLUSIONS Carefully selected patients with moderate to severe CHF can achieve significant, worthwhile improvements with exercise training. Physical deconditioning may be partly responsible for some of the associated abnormalities and exercise limitation of CHF, including abnormalities in autonomic balance.

No abstract

No abstract

Background Changes in the myocardium in acute ischemia are dynamic and complex and the characteristics of myocardial tissue on cardiovascular magnetic resonance (CMR) in the acute setting are not fully defined. We investigated changes in edema and late gadolinium enhancement (LGE) with serial imaging early after acute MI, relating these to global and segmental myocardial function at 6 months. Methods and Results CMR scans were performed on 30 patients with ST elevation MI (STEMI) treated by primary PCI at each of 4 time points: 12-48 hours (24H); 5-7 days (1W); 14-17 days (2W); and 6 months (6M). All patients showed edema at 24H. The mean volume of edema (% LV) was 37 ± 16 at 24H and 39 ± 17 at 1W with a reduction to 24 ± 13 (P < 0.01) by 2W. Myocardial segments with edema also had increased signal on LGE at 24H (kappa = 0.77; P < 0.001). The volume of LGE decreased significantly between 24H and 6M (27 ± 15 % vs. 22 ± 12 %; P = 0.002). Of segments showing LGE at 24H, 50% showed resolution by six months. In segments with such a reduction in LGE, 65% also showed improved wall motion (P < 0.0001). The area of LGE measured at 6M correlated more strongly with troponin at 48h (r = 0.9; P < 0.01) than LGE at 24H (r = 0.7). The difference in LGE between 24H and 6M had profound effects on the calculation of salvage index (26 ± 21 % at 24H vs. 42 ± 23 % at 6M; P = 0.02). Conclusions Myocardial edema is maximal and constant over the first week post MI, providing a stable window for the retrospective evaluation of area at risk. By contrast, myocardial areas with high signal intensity in LGE images recede over time with corresponding recovery of function, indicating that acutely detected LGE does not necessarily equate with irreversible injury and may severely underestimate salvaged myocardium.