Background-Thrombocytopenia in cirrhotic patients may be due to deficient production of thrombopoietin. Aims-To determine the relation between thrombopoietin and thrombocytopenia in cirrhotic patients before and after orthotopic liver transplantation. Methods-Thrombopoietinconcentrations and platelet counts were measured in 43 cirrhotic patients and 21 normal controls and serially for 14 days after transplantation in 23/43 patients. Results-27 of the 43 patients had thrombocytopenia (platelet count less than 120 × 10 9 /l; group 1) whereas 16 patients had normal platelet count (group 2). Thrombopoietin concentrations were lower in group 1 than in group 2 (92. Conclusions-Inadequate thrombopoietin production may contribute to cirrhotic thrombocytopenia. Thrombopoietin production is restored after liver transplantation leading to the resolution of thrombocytopenia. (Gut 1999;44:754-758)
Background-The inability to match lung perfusion to ventilation because of a reduced cardiac output on exercise contributes to reduced exercise capacity in chronic heart failure.Objective-To quantify ventilation to perfusion matching at rest and at peak exercise in patients with chronic heart failure and relate this to haemodynamic and ventilatory variables of exercise capacity. Design-Eight men in New York Heart Association class II underwent maximal bicycle ergometry with i gas anasis. Main outcome measures-On separate days, ventilation and perfusion gamma camera imaging was performed at rest, and at 80% of previous peak exercise heart rate during bicycle ergometry. The vertical distribution of mismatch between ventilation and perfusion (V/Q) was estimated from subtracted profiles of activity (ventilation and perfusion) to derive a numerical index of global mismatch. Results-Maximal mean (SD) oxygen consumption on bicycle ergometry was 16-0 (4.5) ml min-' kg-'. There was a reduction in the global V/Q mismatch index from 23-96 (5.90) to 14-88 (7.90) units (p < 0.01) at rest and at peak exercise. Global V/Q mismatch index at peak exercise correlated negatively with maximal minute ventilation (R = -0 90, p < 0-01) and with maximal mean arterial pressure (R = -0 79, p < 0.05), although no relation was seen with maximal oxygen consumption. The reduction in global V/Q mismatch index from rest to peak exercise correlated with maximal oxygen consumption (R = 0-88, p < 0.01), and with maximal minute ventilation (R = 0-87, p < 0.01). Conclusions-During exercise in patients with chronic heart failure, there is a reduction in the global V/Q mismatch index. A lower global V/Q mismatch index at peak exercise is associated with higher maximal ventilation. The reduction in global VIQ mismatch index on exercise correlates weli with maximal exercise capacity. This may imply that the inability to perfuse adequately all regions of lung on exercise and match this to ventilation is a factor determiniing exercise capacity in chronic heart failure.(Br Heart J 1993;70:241-246)
Abnormal patterns of diastolic ventricular filling are well recognized in chronic heart failure, but their relationship to the severity of heart failure is not known. The present study evaluates the relationship of diastolic filling indices to the severity of heart failure and to exercise capacity. In 40 patients with chronic heart failure secondary to ischaemic left ventricular impairment, exercise capacity was measured as peak oxygen consumption (VO2max) by progressive treadmill exercise. Left ventricular function was assessed by M-mode and Doppler echocardiographic indices. Peak aortic velocity correlated weakly with VO2max (R = +0.38, P less than 0.05). VO2max did not correlate with other systolic indices, including mean aortic acceleration, time to peak velocity, or isovolumic contraction time. VO2max correlated with the mitral inflow E/A ratio (R = -0.57, P less than 0.005) and with the Doppler estimate of isovolumic relaxation time (R = -0.48, P less than 0.01). Two distinct patterns of diastolic filling were observed: subjects with mild-to-moderate heart failure (NYHA grade II, VO2max 15-20 ml.kg-1.min-1) had abnormally low E/A ratios and long isovolumic relaxation times, whereas those with severe heart failure (NYHA grade III-IV, VO2max less than 12 ml.kg-1.min-1) had abnormally high E/A ratios and short isovolumic relaxation times. Different patterns of abnormal diastolic filling with different degrees of severity of heart failure may explain some of the previous controversy as to the prevalence of abnormal diastolic function in chronic heart failure. Exercise capacity in chronic heart failure appears more closely related to abnormalities of diastolic filling pattern than to indices of systolic function.
Bronchoconstriction is seen at rest in patients with chronic heart failure, and may contribute towards exercise limitation. To investigate the effect of bronchodilator agents on exercise capacity, 10 patients (mean age 60 years, range 39-72) in New York Heart Association class II and III heart failure, underwent symptom-limited maximal exercise testing after inhalation of nebulized salbutamol (5 mg), ipratropium bromide (500 micrograms) or placebo delivered on separate days in a randomized, double-blinded study. There was an increase in forced expiratory volume in one second from pre-treatment to after nebulizer, 2.28 +/- 0.20 to 2.38 +/- 0.19 l (P < 0.05) with salbutamol, and 2.27 +/- 0.21 to 2.37 +/- 0.21 l (P < 0.05) with ipratropium bromide. There was an increase in maximal oxygen consumption after salbutamol 17.9 +/- 1.3 ml.kg-1.min-1 (P < 0.05) and ipratropium bromide 17.0 +/- 1.4 ml.kg-1.min-1 (P < 0.05), compared with placebo 16.3 +/- 1.4 ml.kg-1.min +/- 1. Peak minute ventilation during exercise also increased after salbutamol 52.8 +/- 4.5 l.min-1 (P < 0.05), compared with placebo 46.1 +/- 3.1 l.min-1. The small but significant increase in exercise capacity in chronic heart failure following bronchodilator agents implies that a degree of bronchoconstriction is present in these patients and contributes to exercise limitation.
The length of stride is reduced in severe heart failure, and when healthy controls adopt this gait the oxygen cost of walking is increased. A short-stepping gait may contribute to the limitation of exercise capacity in heart failure.
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