Small cardiac noradrenaline stores predicted death from worsening heart failure (HR 4.18, P<0.05), whereas large stores were related to sudden death (HR 2.81, P<0.05).
Cohort (n=116)
Does the level of cardiac sympathetic activity and noradrenaline stores predict the mode of death in patients with congestive heart failure?
In heart failure, high sympathetic activity with intact innervation predicts sudden death, whereas sympathetic depletion predicts death from worsening heart failure.
Effect estimate: HR 4.18 (worsening HF); HR 2.81 (sudden death)
p-value: p=<0.05
Aims To investigate whether strong cardiac sympathetic activity contributes primarily to sudden death or to worsening heart failure, and to determine the relationship of the size of cardiac noradrenaline stores to the mode of death. Methods and Results The study population comprised 116 patients with congestive heart failure (ejection fraction 19±7%) and a mean follow-up of 18±19 months. Cardiac sympathetic nervous function was measured using coronary sinus blood sampling and noradrenaline isotope dilution methodology. Cardiac sympathetic activity was estimated from cardiac noradrenaline spillover, and noradrenaline stores from the overflow of the tritiated noradrenaline metabolite 3Hdihydroxyphenylglycol, which is produced by monoamine oxidase inside nerve endings. Small cardiac noradrenaline stores (below median) predicted death from worsening heart failure (hazard ratio=4·18, P<0·05), particularly if cardiac noradrenaline spillover was elevated (hazard ratio=2·36 per tertile, P<0·01), indicating progression of disease associated with defective sympathetic innervation. In contrast, large stores (hazard ratio=2·81, P<0·05), especially if coupled with increased noradrenaline spillover (hazard ratio=1·64 per tertile, P<0·05), were related to sudden death. Conclusion High cardiac sympathetic activity is a risk factor for sudden death, particularly in the presence of intact cardiac sympathetic innervation. Conversely, progression of myocardial disease and heart failure is closely associated with depletion of sympathetic nerves in the heart, especially if rates of noradrenaline release paradoxically remain high.
Hans‐Peter Brunner‐La Rocca (Sun,) conducted a cohort in Congestive heart failure (n=116). Cardiac sympathetic nervous activity (noradrenaline stores and spillover) vs. Small vs large cardiac noradrenaline stores was evaluated on Death from worsening heart failure or sudden death (HR 4.18 (worsening HF); HR 2.81 (sudden death), p=<0.05). Small cardiac noradrenaline stores predicted death from worsening heart failure (HR 4.18, P<0.05), whereas large stores were related to sudden death (HR 2.81, P<0.05).