title: The effects on cardiac arrhythmias of antihypertensive therapy causing regression of left ventricular hypertrophy.
abstract: To examine the effects of antihypertensive therapy causing regression of left ventricular hypertrophy on cardiac arrhythmias, 26 hypertensive subjects were treated with ramipril with felodipine if required, and followed for 6 months after blood pressure control. Compared with baseline, left ventricular mass index (LVMI) was significantly reduced both at blood pressure control and after a further 6 months of treatment (baseline, blood pressure control, 6 months after blood pressure control; LVMI 142 +/- 3.6, 131 +/- 3.4, 123 +/- 3.8* g/m2, *P < .01 compared with baseline). There was a significant relationship between the decrease in systolic blood pressure and the decrease in LVMI after 6 months of blood pressure control compared with baseline (r = 0.41, P = .05). Compared with baseline, the average total number of ventricular ectopics decreased after blood pressure was controlled (88 +/- 59 and 21 +/- 12 respectively); however this reduction was not maintained after 6 months of further treatment, either before (78 +/- 50) or after drug washout (86 +/- 40). Compared with baseline (639 +/- 590) supraventricular ectopic total was not initially reduced after blood pressure control (650 +/- 604), but was reduced after a further 6 months of treatment (294 +/- 261). This reduction was maintained after drug washout (267 +/- 254), although this did not reach statistical significance. Radionuclide scanning at baseline was not a predictor of patients with the highest risk of arrhythmia and there was no correlation between improvement or worsening of a defect with changes in ventricular ectopic total. In conclusion, antihypertensive therapy with ramipril and felodipine, although causing regression of left ventricular hypertrophy did not lead to a sustained reduction in ventricular ectopic total.
authors.affiliation: The Peart-Rose Clinic, Department of Cardiology, St. Mary's Hospital, London, England.
authors.forename: J
authors.initials: J
authors.lastname: Mayet
authors.forename: N
authors.initials: N
authors.lastname: Chapman
authors.forename: M
authors.initials: M
authors.lastname: Shahi
authors.forename: N R
authors.initials: NR
authors.lastname: Poulter
authors.forename: D A
authors.initials: DA
authors.lastname: Cunningham
authors.forename: S
authors.initials: S
authors.lastname: Dave
authors.forename: J
authors.initials: J
authors.lastname: Kooner
authors.forename: P S
authors.initials: PS
authors.lastname: Sever
authors.forename: R A
authors.initials: RA
authors.lastname: Foale
authors.forename: S A
authors.initials: SA
authors.lastname: Thom
mesh_terms: D000328:Adult; D000368:Aged; D000959:Antihypertensive Agents / Q000627:therapeutic use*; D001145:Arrhythmias, Cardiac / Q000503:physiopathology*; D001794:Blood Pressure / Q000187:drug effects; D005260:Female; D006321:Heart / Q000503:physiopathology; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000188:drug therapy* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged
chemical_list: D000959:Antihypertensive Agents