title: QT-interval variability and autonomic control in hypertensive subjects with left ventricular hypertrophy.
abstract: Left ventricular hypertrophy is a risk factor for sudden death. Malignant ventricular arrhythmias originate from altered cardiac repolarization. Ample data have described spatial abnormalities in cardiac repolarization [QT interval (QT) dispersion] in subjects with hypertension; more data are needed on temporal changes. This study was designed to assess the QT variability index (QTVI), the slope between QT and the RR interval (QT-RR(slope)) and spectral QT variability in subjects with arterial hypertension. The results were compared with those from a population at high risk of sudden death, i.e. patients with hypertrophic cardiomyopathy (HCM) who had received an implantable cardioverter/defibrillator (ICD), and those from normotensive control subjects. A total of 44 hypertensive subjects, six patients with HCM and an ICD and 33 control subjects underwent simultaneous short-term recording (256 beats) of QT, RR and systolic blood pressure variability, in the supine position, during controlled breathing. QTVI and spectral components of QT variability in the hypertensive group were significantly higher than in normotensive control subjects (P<0.001), but significantly lower than in patients with HCM and an ICD (P<0.001). The severity of left ventricular hypertrophy correlated significantly with QTVI and the ratio of low-frequency (LF) to high-frequency (HF) power obtained from the RR variability spectra (RR(LF/HF), slope=0.24, P<0.05; QTVI, slope=4.06, P<0.0001; intercept, slope=2.40, P<0.05; chi(2)=38.8; P<0.0001). The QT--RR slope was significantly higher only in patients with HCM and an ICD (P<0.001). In conclusion, the increased QTVI and the correlation of this index with left ventricular hypertrophy indicates that hypertension increases temporal cardiac repolarization abnormalities. At the level of the cardiac sinus node, this alteration is associated with increased sympathetic and reduced vagal modulation. As already noted in patients with HCM, the increased QTVI could be a factor responsible for triggering malignant ventricular arrhythmias in subjects with hypertension.
authors.affiliation: Dipartimento di Scienze dell'Invecchiamento, I Clinica Medica, Policlinico Umberto I, 00161 Rome, Italy. gianfranco.pccirillo@uniroma1.it
authors.forename: Gianfranco
authors.initials: G
authors.lastname: Piccirillo
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Germanò
authors.forename: Raffaele
authors.initials: R
authors.lastname: Quaglione
authors.forename: Marialuce
authors.initials: M
authors.lastname: Nocco
authors.forename: Filippo
authors.initials: F
authors.lastname: Lintas
authors.forename: Marco
authors.initials: M
authors.lastname: Lionetti
authors.forename: Antonio
authors.initials: A
authors.lastname: Moisè
authors.forename: Maddalena
authors.initials: M
authors.lastname: Ragazzo
authors.forename: Vincenzo
authors.initials: V
authors.lastname: Marigliano
authors.forename: Mauro
authors.initials: M
authors.lastname: Cacciafesta
mesh_terms: D000328:Adult; D001341:Autonomic Nervous System / Q000503:physiopathology*; D001794:Blood Pressure; D016022:Case-Control Studies; D004562:Electrocardiography; D005260:Female; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D017379:Hypertrophy, Left Ventricular / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D012815:Signal Processing, Computer-Assisted