title: The effects of long-term treatment on left ventricular hypertrophy in patients with essential hypertension: relation to changes in neurohumoral factors.
abstract: This study compared the effects of 1 year of monotherapy with a calcium-channel antagonist (nilvadipine; NIL), an angiotensin-converting enzyme (ACE) inhibitor (temocapril; TEM), or a new vasodilator (cadralazine; CAD) on left ventricular (LV) hypertrophy in essential hypertension. Furthermore, to elucidate the mechanism responsible for regression of LV hypertrophy after treatment, LV mass index (LVMI) by echocardiography, plasma renin activity (PRA), aldosterone (PAC), norepinephrine, and atrial natriuretic peptide (ANP) concentration were measured before and after treatment. Thirty-six patients were randomly assigned to the NIL, TEM, or CAD groups. Blood pressure (BP) before treatment was 174 +/- 10/104 +/- 7, 173 +/- 18/103 +/- 8, and 171 +/- 16/103 +/- 7 mm Hg (mean +/- SD) in NIL, TEM, and CAD groups, respectively. BP was lower after treatment with each of the three test drugs than after the placebo period, and there were no differences in BP reduction among three groups. LVMI, in NIL and TEM, was reduced from 129 +/- 48 to 115 +/- 39 g/m2 and from 117 +/- 39 to 88 +/- 20 g/m2 (p < 0.05 and p < 0.01, respectively), whereas, in the CAD group, it was increased (110 +/- 30 to 138 +/- 27 g/m2; p < 0.01). In the CAD group, PAC decreased and ANP increased significantly. The change in LVMI correlated with that in BP for TEM and with that in ANP in all patients. These data indicated that LV volume overload as well as LV pressure overload may contribute to LV hypertrophy and that monotherapy with CAD is not desirable from the point of view of LV mass reduction in essential hypertension.
authors.affiliation: Second Department of Internal Medicine, Toyama Medical and Pharmaceutical University, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Ueno
authors.forename: M
authors.initials: M
authors.lastname: Takata
authors.forename: S
authors.initials: S
authors.lastname: Tomita
authors.forename: S
authors.initials: S
authors.lastname: Oh-hashi
authors.forename: K
authors.initials: K
authors.lastname: Yasumoto
authors.forename: H
authors.initials: H
authors.lastname: Inoue
mesh_terms: D000328:Adult; D000368:Aged; D000450:Aldosterone / Q000097:blood; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D009320:Atrial Natriuretic Factor / Q000097:blood; D002121:Calcium Channel Blockers / Q000627:therapeutic use*; D004452:Echocardiography; D005260:Female; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000473:pathology; D017379:Hypertrophy, Left Ventricular / Q000188:drug therapy*; D008297:Male; D008875:Middle Aged; D009543:Nifedipine / Q000031:analogs & derivatives* / Q000627:therapeutic use; D009638:Norepinephrine / Q000097:blood; D011724:Pyridazines / Q000009:adverse effects / Q000627:therapeutic use; D012083:Renin / Q000097:blood; D013841:Thiazepines / Q000627:therapeutic use; D014665:Vasodilator Agents / Q000627:therapeutic use*
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D000959:Antihypertensive Agents; D002121:Calcium Channel Blockers; D011724:Pyridazines; D013841:Thiazepines; D014665:Vasodilator Agents; C035100:nilvadipine; D000450:Aldosterone; D009320:Atrial Natriuretic Factor; C055603:temocapril hydrochloride; C031877:cadralazine; D012083:Renin; D009543:Nifedipine; D009638:Norepinephrine