Key result
Congestive failure was associated with a 64% reduction in myocardial noradrenaline, related to a 54% reduction in tyrosine hydroxylase activity and an 88% increase in mean wedge pulmonary pressure.
Observational
Cardiac noradrenaline depletion in congestive heart failure is driven by decreased biosynthesis (reduced tyrosine hydroxylase) and increased degradation (elevated COMT).
Tyrosine hydroxylase reduction may underlie noradrenaline depletion in HF; leaves open causal role and therapeutic relevance.
Biopsies of myocardium were obtained from patients with acquired and congenital heart disease at the time of cardiopulmonary bypass and assayed for content of noradrenaline and the activities of the rate limiting biosynthetic enzyme — tyrosine hydroxylase, and the degradative enzymes — monoamine oxidase and catechol-0-methyl transferase (COMT). The 64% reduction in myocardial noradrenaline in patients with congestive failure was related directly to a 54% reduction in tyrosine hydroxylase activity and inversely to an 88% increase in mean wedge pulmonary artery pressure. The activity of the extraneuronal enzyme, COMT, was increased 115% in hearts of those with congestive failure, due in part to fibrotic replacement of innervated contractile muscle.
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DeQuattro et al. (1973) conducted an observational in Congestive failure. Congestive failure was evaluated on Myocardial noradrenaline content and enzyme activities. Congestive failure was associated with a 64% reduction in myocardial noradrenaline, related to a 54% reduction in tyrosine hydroxylase activity and an 88% increase in mean wedge pulmonary pressure.
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