Ventricular arrhythmias in aortic valve disease: a further marker of impaired left ventricular function

Martínez-Useros, C; Tornos, Pilar; Montoyo, J; Miralda, Gaietà Permanyer; Alijarde, M; Castillo, Herminio García del; Soler‐Soler, Jordi

doi:10.1016/0167-5273(92)90081-d

Cited by 21 publications

(15 citation statements)

References 18 publications

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“…Some researchers think that ventricular tachycardia due to cardiac muscle hypertrophy can cause SCD (11)(12)(13). In severe AS an increase in mechanical stretch due to pressure overload can cause myocyte hypertrophy.…”

Section: Discussionmentioning

confidence: 99%

Short-term effect of transcatheter aortic valve implantation on QT dispersion

Kasapkara¹,

Ayhan²,

Durmaz³

et al. 2015

Turk J Med Sci

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Background/aim: Electrophysiological changes are observed following mechanical stretches due to pressure overload in patients with severe aortic stenosis (AS). The electrical instability occurs after depolarization and dispersion of repolarization. The aim of this study was to evaluate changes in ventricular repolarization following transcatheter aortic valve implantation (TAVI). Materials and methods:The study population included 100 consecutive patients with severe AS that underwent TAVI. Electrocardiography (ECG) was performed at baseline, immediately after TAVI, and 1 week after TAVI. Results:The mean age of the patients was 78.2 ± 7.2 years. Thirty-four (34%) of the patients were male and 66 (66%) were female. Compared to the baseline, mean QT dispersion (QTd) immediately after TAVI and 1 week after TAVI decreased significantly (

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Section: Discussionmentioning

confidence: 99%

Short-term effect of transcatheter aortic valve implantation on QT dispersion

Kasapkara¹,

Ayhan²,

Durmaz³

et al. 2015

Turk J Med Sci

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“…Sudden death, although relatively rare, has been reported in asymptomatic patients with normal LV ejection fraction. Ventricular arrhythmias have been reported in patients with AR and were correlated with the degree of ventric-ular enlargement (11,13,15,22). However, those studies were not designed to address the issue of mortality in patients displaying more ventricular arrhythmias.…”

Section: H1893mentioning

confidence: 99%

Benefits of long-term β-blockade in experimental chronic aortic regurgitation

Plante¹,

Lachance²,

Champetier³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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The objective of this study was to assess the long-term effects of beta-blockade on survival and left ventricular (LV) remodeling in rats with aortic valve regurgitation (AR). The pharmacological management of chronic AR remains controversial. No drug has been definitively proven to delay the need for valve replacement or to affect morbidity and/or mortality. Our group has reported that the adrenergic system is activated in an animal model of AR and that adrenergic blockade may help maintain normal LV function. The effects of prolonged treatment with a beta-blocker are unknown. Forty Wistar rats with severe AR were divided into 2 groups of 20 animals each and treated with metoprolol (Met, 25 mg.kg(-1).day(-1)) or left untreated for 1 yr. LV remodeling was evaluated by echocardiography. Survival was assessed by Kaplan-Meir curves. Hearts were harvested for tissue analysis. All Met-treated animals were alive after 6 mo vs. 70% of untreated animals. After 1 yr, 60% of Met-treated animals were alive vs. 35% of untreated animals (P = 0.028). All deaths, except one, were sudden. There were no differences in LV ejection fraction (all >50%) or LV dimensions. LV mass tended to be lower in the Met-treated group. There was less subendocardial fibrosis in this group, as well as lower LV filling pressures (LV end-diastolic pressure). beta-Adrenergic receptor ratio (beta(1)/beta(2)) was improved. One year of treatment with Met was well tolerated. Met improved 1-yr survival, minimized LV hypertrophy, improved LV filling pressures, decreased LV subendocardial fibrosis, and helped restore the beta-adrenergic receptor ratio.

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“…These results are consistent with several investigators' observations of ventricular arrhythmias in patients with aortic valvular disease, even in the absence of coronary artery disease.24 Some investigators indicated that the frequency and complexity of ventricular arrhythmias were closely related to myocardial function. 23 On the other hand, we showed that the severity of arrhythmias was more prominent in patients with AS, even though they have normal systolic left ventricular function. It has been determined that serious arrhythmias, in valvular heart disease, were most frequently noted in patients with AS who also had a higher incidence of sudden death.24 Likewise, we found a good correlation between QTd and the number of 24-h ventricular premature beats (r = 0.53, p = 0.009).…”

Section: Discussionmentioning

confidence: 82%

Is ventricular repolarization heterogeneity a cause of serious ventricular tachyarrhythmias in aortic valve stenosis?

Batur

Açıl

Özer

et al. 2000

Clinical Cardiology

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SummaryBackground: It is well known that there is a close relation between sudden cardiac death and serious ventricular tachyarrhythmias in patients with aortic valve stenosis (AS). QT dispersion (QTd) reflects the ventricular repolarization heterogeneity and has been proposed as an indicator for ventricular arrhythmias.Hypothesis: This study investigated the QTd and its relevance to the clinical and echocardiographic variables.Methods: In all, 5 1 patients (33 men, 18 women, mean age

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Ventricular arrhythmias in aortic valve disease: a further marker of impaired left ventricular function

Cited by 21 publications

References 18 publications

Short-term effect of transcatheter aortic valve implantation on QT dispersion

Short-term effect of transcatheter aortic valve implantation on QT dispersion

Benefits of long-term β-blockade in experimental chronic aortic regurgitation

Is ventricular repolarization heterogeneity a cause of serious ventricular tachyarrhythmias in aortic valve stenosis?

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