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Forty-four patients were tested 2, 6 and 12 months after an isolated aortic valve implantation in order to evaluate the influence of training and vocational assistance on physical work capacity and the rate of reemployment. They were randomly allocated to a training group (A) or a control group (B). Training was carried out from the eighth to the twelfth week after operation and the socio-occupational status was evaluated. Training increased physical work capacity, expressed as cumulated work (CW), by 58 per cent (P less than 0.001), decreased the rate-pressure product (RPP) by 13 per cent (P less than 0.001) and the rate of perceived exertion (RPE) by 13 per cent (P less than 0.001) at the highest comparable work load. The CW was 38 per cent higher in the training than the control group after 6 (P less than 0.02) and 37 per cent after 12 months (P less than 0.025). After one year 81 per cent in group A and 65 per cent in group B were working (NS). Reemployment correlated significantly with the CW and inversely with the duration of sick leave prior to operation. Thus, physical training shortly after aortic valve operation rapidly and persistently improves physical work capacity while return to work is less influenced by training and socio vocational assistance.

Exercise capacity, heart rate variability, and QOL improved after 2 months of exercise training in patients with chronic AF. Heart rates at rest and during exercise decreased.

This study examines the hypothesis that nifedipine may increase splanchnic vascular capacitance and thus change the distribution of blood between the splanchnic and pulmonary circulation in heart failure patients. Relative regional blood volumes were determined by equilibrium blood pool scintigraphy during a 10 min baseline period and for 30 min after nifedipine 20 mg sublingually, with simultaneous recordings of systemic and pulmonary arterial pressures, hepatic venous wedge pressure, and cardiac output. Eight patients with ischaemic heart failure received nifedipine. Four patients served as controls. Nifedipine reduced mean arterial pressure and systemic vascular resistance in every patient. There were no significant changes in the relative blood volumes of the intestinal, hepatic, or splenic regions or in hepatic venous wedge pressure (reflecting portal venous pressure), suggesting unchanged splanchnic vascular pressure-volume relationship. Nifedipine caused a 6.3 +/- 1.0% increase in relative pulmonary blood volume and a slight increase in pulmonary vascular distending pressure from 16.1 +/- 2.9 mmHg to 17.5 +/- 2.8 mmHg (P < 0.05), suggesting that the increase in pulmonary blood volume was passively mediated. In conclusion, nifedipine did not change splanchnic vascular capacitance, but caused a small increase in pulmonary blood volume, which probably was a passive response to increased distending pressure.

In this study we assessed the short- and long-term effects of 4-weeks of exercise training (MI) soon after myocardial infarction in patients on beta-blocker treatment. Thirty-seven male patients < or = 65 years of age were included in the study, 19 of them randomized to exercise training (ET) and 18 to a control group (Ctr). Cumulated work (CW), calculated in kiloJoules (kJ), was recorded before immediately after the intervention period and again six months after the MI. In the short term the mean (SD) CW increased by 22% (from 65(20) to 79(25) kJ) in the ET group, compared with no change in the Ctr patients (65(24) vs 65(21) kJ) (p = 0.009). At late follow-up CW was 14% above baseline in the ET patients (65(20) vs 74(20) kJ) p = 0.036, compared with only 6% in the 15 Ctr patients who were still available for follow-up (68(24) vs 72(29) kJ), but without a significant between-group difference. In post-MI patients on beta-blocker treatment, and with a high baseline exercise capacity, physical training improved exercise capacity in the short term, but there was no significant between-group difference at long-term follow-up.

Five simple clinical variables, including infarct size, can assist in the selection of patients for exercise training after myocardial infarction.

Nitroprusside reduced venous pressure in patients with congestive heart failure by active relaxation of intestinal and pulmonary capacitance vessels. Hepatic vascular volume was probably reduced by a passive mechanism.

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