title: Left ventricular mass is linked to cardiac noradrenaline in normotensive and hypertensive patients.
abstract: BACKGROUND
  Left ventricular hypertrophy constitutes a powerful independent risk factor for heart failure, sudden death and ventricular dysrhythmia. Experimental data suggest that, apart from increased cardiac work load, noradrenaline may be one of the factors triggering myocardial hypertrophy.
  
  
  OBJECTIVE
  To test the hypothesis that the extent of left ventricular hypertrophy is coupled to cardiac noradrenaline independently from the magnitude of arterial blood pressure.
  
  
  METHODS
  Following exclusion of coronary artery disease by cardiac catheterization, cardiac noradrenaline release was measured in relation to left ventricular mass in 25 patients with arterial hypertension (HT), of whom five had left ventricular hypertrophy (HT + LVH) and 20 had normal left ventricular mass (HT - LVH), seven normotensive patients with hypertrophic cardiomyopathy (HCM) and a normotensive control group (n = 7). Noradrenaline was measured in arterial and coronary venous plasma using high-performance liquid chromatography. Coronary blood flow was quantified using the gas chromatographic argon method. Indices of left ventricular mass were calculated from the end-diastolic thicknesses of the interventricular septum and the posterior wall determined by echocardiography.
  
  
  RESULTS
  The coronary venous plasma concentration of noradrenaline was significantly higher in HT - LVH, HT + LVH and HCM than it was in normotensives. Whereas in normotensives there was a net uptake of noradrenaline (17 +/- 10 pmol/min) across the coronary circulation, a net release of noradrenaline was observed in HT - LVH (69 +/- 26 pmol/min), in HT + LVH (121 +/- 55 pmol/min) and in HCM (341 +/- 96 pmol/min). In a multivariate linear regression analysis model, left ventricular mass correlated significantly with the net noradrenaline release rate (r = 0.64, P < 0.001), whereas arterial blood pressure as an additional independent variable did not correlate with left ventricular mass.
  
  
  CONCLUSIONS
  The present data demonstrate that an increased left ventricular mass in normotensive and in hypertensive patients is closely coupled to an increased cardiac sympathetic activity, supporting the need for additional studies to determine whether adjunctive sympatholytic therapy is beneficial in patients with left ventricular hypertrophy and increased cardiac noradrenaline release.
authors.affiliation: Department of Medicine, Heinrich Heine University, Düsseldorf, Germany.
authors.forename: M
authors.initials: M
authors.lastname: Kelm
authors.forename: S
authors.initials: S
authors.lastname: Schäfer
authors.forename: S
authors.initials: S
authors.lastname: Mingers
authors.forename: M
authors.initials: M
authors.lastname: Heydthausen
authors.forename: M
authors.initials: M
authors.lastname: Vogt
authors.forename: W
authors.initials: W
authors.lastname: Motz
authors.forename: B E
authors.initials: BE
authors.lastname: Strauer
mesh_terms: D006328:Cardiac Catheterization; D004837:Epinephrine / Q000097:blood; D005260:Female; D006801:Humans; D006973:Hypertension / Q000150:complications* / Q000378:metabolism; D017379:Hypertrophy, Left Ventricular / Q000150:complications* / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism*; D009638:Norepinephrine / Q000378:metabolism*
chemical_list: D009638:Norepinephrine; D004837:Epinephrine