QT-interval variability and autonomic control in hypertensive subjects with left ventricular hypertrophy

2002 ◽  
Vol 102 (3) ◽  
pp. 363-371 ◽  
Author(s):  
Gianfranco PICCIRILLO ◽  
Giuseppe GERMANÒ ◽  
Raffaele QUAGLIONE ◽  
Marialuce NOCCO ◽  
Filippo LINTAS ◽  
...  
Keyword(s):  
Sudden Death ◽  
Left Ventricular Hypertrophy ◽  
Qt Interval ◽  
Ventricular Arrhythmias ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Cardiac Repolarization ◽  
Control Subjects ◽  
Qt Variability ◽  
Normotensive Control

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-RRslope) 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 (RRLF/HF, slope = 0.24, P < 0.05; QTVI, slope = 4.06, P < 0.0001; intercept, slope = 2.40, P < 0.05; χ2 = 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.

Left Ventricular Hypertrophy in Adolescents with Elevated Blood Pressure: Assessment by Chest Roentgenography, Electrocardiography, and Echocardiography

PEDIATRICS ◽  
1981 ◽  
Vol 67 (2) ◽  
pp. 255-259
Author(s):  
W. Pennock Laird ◽  
David E. Fixler
Keyword(s):  
Blood Pressure ◽  
Left Ventricular Hypertrophy ◽  
Surface Area ◽  
Body Surface Area ◽  
Body Surface ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Elevated Blood ◽  
Control Subjects ◽  
Normotensive Control

The purpose of this study was to assess the prevalence of left ventricular hypertrophy in adolescents with persistently elevated blood pressures. Chest roentgenograms, electrocardiograms, and echocardiograms were performed on 50 adolescents with elevated blood pressure and 50 matched normotensive control subjects. No subject in either group demonstrated cardiomegaly on x-ray. Interpretation of the electrocardiograms indicated that similar numbers of both hypertensive (7/50) and control subjects (8/50) had ECG evidence of left ventricular hypertrophy. The echocardiograms showed that the mean left ventricular wall thickness (LVWT) in the hypertensive adolescents was 7.8 mm ± 0.1 (SE), compared with 6.5 ± 0.1 in the control subjects (P &lt; .001). When the measurements were indexed to body surface area, the difference remained highly significant. Indexed left ventricular mass (LVM)/body surface area (BSA) was also significantly greater (P &lt; .001) in the hypertensive (84.2 gm/sq m ± 2.1) than in the control subjects (72.0 ± 2.1). Using data from the normotensive control subjects, we defined the 95th percentile for both LVWT/BSA and LVM/BSA. Among hypertensive adolescents, 9/50 had LVWT/BSA and 8/50 had LVM/BSA above this level. For control subjects, only 1/50 had elevated LVWT/BSA values and 2/50 elevated LVM/BSA values. This study demonstrates that hypertensive adolescents have an increased prevalence of left ventricular hypertrophy and that echocardiography is the most useful noninvasive method to detect these changes.

Influence of posture and handgrip on the QT interval in left ventricular hypertrophy and in chronic heart failure

1999 ◽  
Vol 96 (4) ◽  
pp. 403-407 ◽  
Author(s):  
Patrick DAVEY
Keyword(s):  
Heart Failure ◽  
Left Ventricular Hypertrophy ◽  
Qt Interval ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Qtc Interval ◽  
Dominant Hand ◽  
Control Subjects ◽  
Qt Intervals ◽  
And Control

In certain disease states prolongation of the QT interval has been shown to be arrhythmogenic. Whether QTc interval changes with position and thus whether certain positions are more arrhythmogenic than others is not known for different diseases that predispose to arrhythmias, and was therefore studied. Patients with left ventricular hypertrophy and heart failure, and the appropriate matched controls, were recruited. Subjects were studied in the lying, sitting, standing and squatting positions and had QT intervals determined by computer algorithm 2 min after each position change. After resting, QT interval was determined while the subjects performed maximum handgrip exercise with their dominant hand. QT intervals were rate-corrected using Bazett's method. QTc interval is prolonged in heart failure patients compared with either left ventricular hypertrophy or control subjects in the lying and sitting position, but not in the standing or squatting position. The QTc intervals for heart failure and control subjects were, respectively, 443±7 ms versus 421±6 ms when lying (P< 0.05), 451±10 ms versus 419±6 ms when sitting (P< 0.05), 429±10 versus 414±7 ms when standing (P not significant) and 437±10 versus 419±8 ms when squatting (P not significant). The values for patients with hypertrophy did not differ from control values. Maximum handgrip does not affect the QTc interval in heart failure, but prolongs it in both the hypertrophy and control groups. Position and static exercise are important modifiers of QTc interval and their effect depends on the condition of the left ventricle.

scholarly journals Is hypertensive left ventricular hypertrophy a cause of sustained ventricular arrhythmias in humans?

2021 ◽  
Author(s):  
R. Nadarajah ◽  
P. A. Patel ◽  
M. H. Tayebjee
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Ventricular Arrhythmias ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Systemic Hypertension ◽  
Electrolyte Disturbance ◽  
Electrocardiographic Monitoring ◽  
Homogenous Distribution ◽  
Artery Disease ◽  
Asymptomatic Coronary Artery Disease

AbstractSudden cardiac death (SCD) is most commonly secondary to sustained ventricular arrhythmias (VAs). This review aimed to evaluate if left ventricular hypertrophy (LVH) secondary to systemic hypertension in humans is an isolated risk factor for ventricular arrhythmogenesis. Animal models of hypertensive LVH have shown changes in ion channel function and distribution, gap junction re-distribution and fibrotic deposition. Clinical data has consistently exhibited an increase in prevalence and complexity of non-sustained VAs on electrocardiographic monitoring. However, there is a dearth of trials suggesting progression to sustained VAs and SCD, with extrapolations being confounded by presence of co-existent asymptomatic coronary artery disease (CAD). Putatively, this lack of data may be due to the presence of more homogenous distribution of pathophysiological changes seen in those with hypertensive LVH versus known pro-arrhythmic conditions such as HCM and myocardial infarction. The overall impression is that sustained VAs in the context of hypertensive LVH are most likely to be precipitated by other causes such as CAD or electrolyte disturbance.

Magnitude of Left Ventricular Hypertrophy and Risk of Sudden Death in Hypertrophic Cardiomyopathy

2000 ◽  
Vol 342 (24) ◽  
pp. 1778-1785 ◽  
Author(s):  
Paolo Spirito ◽  
Pietro Bellone ◽  
Kevin M. Harris ◽  
Paola Bernabò ◽  
Paolo Bruzzi ◽  
...  
Keyword(s):  
Hypertrophic Cardiomyopathy ◽  
Sudden Death ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Left Ventricular

Risk of ventricular arrhythmias in left ventricular hypertrophy: The Framingham Heart Study

1987 ◽  
Vol 60 (7) ◽  
pp. 560-565 ◽  
Author(s):  
Daniel Levy ◽  
Keaven M. Anderson ◽  
Daniel D. Savage ◽  
Susan A. Balkus ◽  
William B. Kannel ◽  
...  
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Framingham Heart Study ◽  
Ventricular Arrhythmias ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Heart Study

scholarly journals The cardiovascular system in patients with symptomatic and mild primary hyperparathyroidism

2009 ◽  
Vol 55 (3) ◽  
pp. 25-29 ◽  
Author(s):  
I V Voronenko ◽  
N G Mokrysheva ◽  
L Ya Rozhinskaya ◽  
A L Syrkin
Keyword(s):  
Parathyroid Hormone ◽  
Left Ventricular Hypertrophy ◽  
Primary Hyperparathyroidism ◽  
Cardiovascular System ◽  
Qt Interval ◽  
Ventricular Hypertrophy ◽  
Left Ventricular Diastolic Dysfunction ◽  
Left Ventricular ◽  
Ionized Calcium ◽  
Mild Primary Hyperparathyroidism

The cardiovascular system was analyzed in patients with symptomatic (n = 31) and mild primary hyperparathyroidism (n = 34) whose mean age was 54.6 years; 95% females). In the patients with symptomatic primary hyperparathyroidism, the PQ interval was longer and the QT interval was significantly shorter than those in patients with mild hyperparathyroidism. Left ventricular hypertrophy was noted in 45.2% of patients with symptomatic and in 15.2% of those with mild hyperparathyroidism (p = 0.013). Left ventricular diastolic dysfunction was also more common in the group of symptomatic hyperparathyroidism. There was a statistically significant correlation between the levels of parathyroid hormone, total and ionized calcium and the duration of QT interval and the determinants of diastolic function and left ventricular hypertrophy. The revealed cardiovascular disorders in patients with primary hyperparathyroidism are presumed to depend on the increase rate of parathyroid hormone and total and ionized calcium.

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