Search

Objectives: The aim of this study was to characterize cardiac sympathetic nervous function in patients with severe heart failure and to investigate the influence of the cause of heart failure, hemodynamic variables and central nervous system catecholamine release on cardiac sympathetic tone., Background: Although heart failure is generally accompanied by sympathoexcitation, the integrity of cardiac sympathetic nerve function in heart failure remains controversial, particularly in relation to nerve firing activity and to the capacity of sympathetic nerves to recapture norepinephrine. Additionally, the location of the afferent and central neural pathways implicated in heart failure-induced sympathoexcitation remains unclear., Methods: Radiotracer techniques were applied in 41 patients with severe heart failure and 15 healthy control subjects to study the biochemical aspects of whole body and cardiac sympathetic activity. Hemodynamic indexes of cardiac performance were measured in the heart failure group, and their association with sympathetic activity was studied. Jugular venous catechol spillover was measured to study the central noradrenergic control of sympathetic outflow., Results: Sympathoexcitation was evident in the heart failure group, reflected by a 62% increase (p < 0.001) in total body and a 277% increase (p < 0.001) in cardiac norepinephrine spillover rates. These changes were accompanied by significant increases in the cardiac spillover of the norepinephrine precursor dihydroxyphenylalanine, the sympathetic cotransmitter neuropeptide Y and the extraneuronal metabolite 3-methoxy-4-hydroxyphenylglycol. The level of cardiac sympathetic activity was significantly correlated (r = 0.59, p < 0.001) with the mean pulmonary artery pressure. An increase in the spillover of dihydroxyphenylalanine and 3-methoxy-4-hydroxyphenylglycol from the brain was present, suggesting activation of central noradrenergic neurons., Conclusions: Cardiac sympathetic activation is present in severe heart failure, bearing a close relation with pulmonary artery pressures, independent of heart failure etiology. Activation of noradrenergic neurons in the brain is also present and may be the underlying central nervous mechanism of the sympathoexcitation observed in heart failure.

We studied 925 consecutive patients hospitalised with acute stroke to determine how stroke type, age, gender and risk factors influence acute, in-hospital outcome. Stroke types included carotid territory cortical or large subcortical infarction (52%), vertebrobasilar infarction (12%), lacunar infarction (11%), intracerebral haemorrhage (16%), and subarachnoid haemorrhage (9%). Mean age (mean +/- 1 SD) was 66 +/- 15 years, but patients with cerebral infarction were older than those with cerebral haemorrhage. The prevalence of hypertension, diabetes mellitus and cardiac disease increased with age across all stroke types, while the prevalence of smoking decreased with age. Mortality was 19% overall, but varied significantly between stroke types, highest in intracerebral haemorrhage (34%), and lowest in lacunar infarction (1%). Age had a marked adverse effect on mortality, independent of stroke type, the probability of death increasing by 3 +/- 0.5% per year from 20-92 years, whereas gender had no effect. Cardiac disease and diabetes were independent adverse prognostic factors (Odds Ratios 1.6 and 1.5 respectively). Cerebral haemorrhage, age, cardiac disease and diabetes all independently worsen acute stroke outcome.