Myocardial catecholamine concentrations in dilated cardiomyopathy and heart failure of different origins

Abstract

Myocardial catecholamine concentrations were determined in endomyocardial biopsies from patients with heart failure to assess if tissue catecholamine levels relate to the severity of myocardial damage or the aetiology of the underlying disease. Methodological studies revealed a good reproducibility of catecholamine determinations in biopsies; the variance between paired biopsies was below 17% when myocardial catecholamines were related to non-collagen protein (NCP). Myocardial norepinephrine (in pg micrograms-1 NCP) levels were comparable in patients with dilated cardiomyopathy (DCM, 5.3 +/- 3.4, n = 22) and in patients with coronary or valvular heart disease (5.6 +/- 4.7, n = 14). In both groups, a significant reduction of myocardial norepinephrine was found (controls 12.0 +/- 3.4, P less than 0.0006). In a subgroup of patients with heart failure and a LVEF less than 30% (3.9 +/- 3.5, n = 17) myocardial norepinephrine content was lower than in patients with heart failure and LVEF of 31-55% (6.6 +/- 3.4, n = 19) (both P less than 0.05 against controls: 12.0 +/- 3.4, n = 16). A correlation between myocardial norepinephrine and LVEF was found in DCM (P less than 0.001, r = 0.70). The loss of myocardial norepinephrine is a characteristic feature of heart failure. It is independent of the origin of failure, but correlates with the impairment of LV function.

Angiotensin I-Converting Enzyme Inhibition Increases Cardiac Catecholamine Content and Reduces Monoamine Oxidase Activity via an Angiotensin Type 1 Receptor-Mediated Mechanism

“…In the past, many clinical trials evaluated the pronounced antihypertensive and cardioprotective effects of ACE inhibitors, and in this context, the contributions of diminished plasma noradrenaline levels to their antihypertensive and cardioprotective effects were discussed. The therapeutic significance of this action was revealed for the treatment of heart failure where a pathological sympathetic stimulation was associated with decreased cardiac noradrenaline levels (Regitz et al, 1991) due to an impairment of neuronal catecholamine uptake (Böhm et al, 1995). Kawai et al (1999) were the first to demonstrate that cardiac noradrenaline content in heart failure is increased by ACE inhibitors due to an enhanced cardiac neuronal uptake of noradrenaline; this should reflect one of the cardioprotective mechanisms of ACE inhibitors.…”

Ativação adrenérgica intramiocárdica na cardiomiopatia chagásica e doença arterial coronariana

“…It is very difficult to study a control group consisting of healthy individuals for comparison with diseased groups due to ethical problems. However, the literature has shown some control groups consisting of volunteer prisoners and patients previously suspected of having myocarditis, hemochromatosis, and endomyocardial fibrosis who underwent endomyocardial biopsy, but whose biopsies were diagnosed as normal 6,12,14,19 . In these cases, the levels of myocardial norepinephrine were similar to those found in patients with coronary artery disease with normal left ventricular function.…”

“…Subsequently, other studies showed the relation between left ventricular ejection fraction (LVEF) and the intramyocardial norepinephrine concentration in dilated valvular, ischemic and hypertrophic cardiomyopathy [12][13][14][15] . Chronic Chagas' cardiomyopathy is characterized by an intense reduction in the heart neuronal population, as documented in necroscopic studies of chagasic patients who died of heart failure 16 .…”

The structure of myocardial nerve plexus of human auricle of the right atrium and its relation to myocardial ischemia, functional status of the heart, and age

“…Šių pokyčių dydis priklauso nuo vainikinių kraujagyslių stenozės laipsnio, miokardo infarkto apimties ir stadijos (22,23). Tiriant dešiniosios ausytės miokardo nervinį rezginį, šio rezginio pokyčių priklausomumo nuo vainikinių kraujagyslių stenozės laipsnio įrodyti nepavyko.…”