Ventricular Premature Beats In Patients Research Articles

Autonomic influences related to frequent ventricular premature beats in patients without structural heart disease.

To study the possible role of autonomic influences on the occurrence of frequent premature ventricular beats (VPBs) in subjects without structural heart disease.24-hour Holter ECG recordings (≥1500 VPBs/d, sinus rhythm) of 20 symptomatic patients (9 women, 11 men, mean age 58.9 years) without structural heart disease were used for the study. The circadian distribution pattern of VPBs was studied (paired t test) by dividing the day into 3 periods (16:00–22:00–06:00–16:00), and correlations were analyzed between the absolute (ln transformed) and relative (% of total beats) average hourly numbers of VPBs and the hourly mean values of global and vagal time domain parameters of heart rate variability (Pearson correlation).No significant (P > .3 for every comparison) tendency for circadian distribution of VPBs was found. However, VPBs showed a significant correlation with rMSSD (r = 0.51 and P = .02 for the relative number), which became even stronger if VPBs were > 8000/d (r = 0.65 and P = .04 for both numbers).The significant correlation between the number of VPBs and a vagally mediated parameter underlines the triggering/permitting effect of parasympathetic tone on ventricular ectopy. This fact suggests that initiation of beta-blocker therapy could not be recommended routinely in these patients.

Mitral valve prolapse: a source of arrhythmias?

Cardiac arrhythmias are frequently detected in patients with mitral valve prolapse (MVP) The proper mechanisms causing ventricular arrhythmias in patients with MVP have not been fully investigated. In the current issue of the International Journal of Cardiovascular Imaging, Turker et al. [1] evaluated the clinical, echocardiographic and heart rate variability (HRV) parameters, and plasma concentrations of electrolytes and inflammatory markers in predicting ventricular arrhythmias in 58 consecutive patients with MVP. Ventricular arrhythmias were defined as the occurrence of ventricular premature contractions (VPCs), VPC couplets, and ventricular tachycardias documented by Holter analysis, continuous monitoring or by electrocardiography. Twenty patients (34%) showed ventricular arrhythmias, and 38 (66%) patients did not have ventricular arrhythmias. Seventeen patients had VPC, 2 patients had VPC couplets and one patient had ventricular tachycardia. Univariable predictors of ventricular arrhythmias included echocardiography-determined isovolumetric relaxation time and the presence of moderate to severe mitral regurgitation. Interestingly, multivariable logistic regression analysis showed that occurrence of moderate to severe mitral regurgitation was the only independent predictor of ventricular arrhythmias. Several recent studies did already address the relation between cardiac arrhythmias and the presence of MVP. Chen et al. [2] showed that improper autonomic tone is to be considered the etiology of arrhythmias in conjunction with MVP. Heart rate turbulence (HRT) and HRV are methods assessed for autonomic dysfunction. The authors studied the relationship of HRT, HRV and the number of ventricular premature beats in patients with MVP and non-significant mitral regurgitation. No significant correlation was found between the number of VPCs and HRT/HRV parameters. Markiewicz-Łoskot et al. [3] studied electrocardiographic abnormalities in ten young athletes with MVP. Abnormal ECG repolarization was found in seven athletes. Young athletes with MVP are therefore often predisposed to electrocardiographic abnormalities of ventricular repolarization. Cetinkaya et al. [4] evaluated the risk of vasovagal syncope and cardiac arrhythmias in 37 children with MVP. Arrhythmias and the risk of vasovagal syncope, indicated by a positive tilt test, were found to be increased in children with MVP. Similar to echocardiography [5–13], cardiovascular magnetic resonance (CMR) imaging can identify MVP by similar anatomic and functional criteria [13–30]. In addition, CMR allows tissue characterization in various cardiac diseases using hyperenhancement techniques [31–38]. In this way, CMR can identify myocardial fibrosis involving the papillary muscle in MVP patients. Delayed contrast enhancement (DCE) of papillary muscles is often present in a subgroup of patients with complex ventricular arrhythmias [39]. This tissue hyperenhancement is indicative of fibrosis which may act as a focus for arrhythmias. Kwon et al. [40, 41] using delayed contrast enhancement CMR, showed a clear association of myocardial fibrosis, electrocardiography and ventricular tachyarrhythmia in hypertrophic cardiomyopathy (HCM). HCM subjects with ventricular tachycardias showed a higher percentage of myocardial scarring on DCE-CMR. As a consequence, the presence of fibrotic papillary muscles in patients with MVP might give rise to both cardiac arrhythmias and mitral regurgitation. In addition to echocardiography and CMR, multislice computed tomography (MSCT) has recently been shown to evaluate the functional status of the mitral valve in patients with MVP [42–45]. MSCT may therefore have a major role in preoperative assessment of the mitral valve apparatus before mitral valve surgery. To summarize, nowadays the diagnosis of MVP can be made by several imaging techniques. Apart from echocardiography, CMR and MSCT are capable of accurately delineating the structure and function of the mitral valve. Next, there is a clear association between the level of incompetence of the mitral valve and the presence of cardiac arrhythmias, in particular in case of MVP. These findings have been proven both by echocardiography and DCE-CMR. The study by Turker et al. [1], using echocardiography, add to these results by showing that the occurrence of moderate to severe mitral regurgitation was the only independent predictor of ventricular arrhythmias in patients with MVP.

Circadian variation of heart rate turbulence and the number of ventricular premature beats in patients with mitral valve prolapse

Circadian variation of heart rate turbulence and the number of ventricular premature beats in patients with mitral valve prolapse

Relationship of heart rate turbulence, heart rate variability and the number of ventricular premature beats in patients with mitral valve prolapse and non-significant regurgitation

Cardiac arrhythmia is frequently detected in patients with mitral valve prolapse (MVP) and improper autonomic tone is considered the etiology. Heart rate turbulence (HRT) and heart rate variability (HRV) are methods assessed for autonomic dysfunction. To evaluate whether the number of ventricular premature contractions (VPCs) is influenced by HRT or HRV in patients with MVP. Holter monitoring for the number of VPCs and correlation analysis with HRT and HRV was performed. There were 31% and 3% with abnormal turbulence onset (TO) and turbulence slope (TS) values in totally 68 patients. No significant correlation is found between the number of VPCs and HRT, HRV parameters. In analysis the relationship between HRT and HRV parameters, TS has higher correlation with HRV than TO values, particular in time-domain.

Modeling the Blood Pressure Response to a Ventricular Premature Complex with Special Reference to Heart Rate Turbulence

Ventricular premature beats have been used to characterize a risk factor for patients after myocardial infarction. This risk stratification has recently been improved by estimating the so-called heart rate turbulence, i.e., the acceleration and subsequent deceleration of the sinus beats following a ventricular premature beat. This response is triggered by oscillations in aortic blood pressure following a ventricular premature beat. In the following we report on a model to fit blood pressure oscillations due to ventricular premature beats in patients following myocardial infarction. The data on which this analysis is based were derived from 39 patients with varying degrees of left ventricular dysfunction following myocardial infarction. The recording included high-quality ECG and a noninvasive beat-to-beat recording of blood pressure from a finger artery. Records were chosen such that 5 to 30 ventricular premature beats occurred within a 30-min recording period. In a first step, we fed our data, i.e., a given series of coupling intervals, into two established cardiac models (Ten-Voorde and Mrovka et al.) and observed the blood pressure behavior. It turned out that both models were not able to reflect the full range of the observed blood pressure oscillations. For this reason we expanded the model of Mrovka et al. (Am J Physiol Regul Integr Comp Physiol 279: R1171–R1175, 2000), such that the desired pattern approximately appeared. This was achieved by introducing a more subtle left ventricular function curve and keeping track of the endsystolic volume in the left ventricle. After parameter fitting, a detailed picture of the hemodynamics appeared for each patient. It was found that left ventricular function and, in particular, post-extrasystolic potentiation was crucial for the prediction of the blood pressure response following a ventricular premature beat. Thus, in patients following myocardial infarction, not only impaired baroreceptor function but also altered left ventricular contraction behavior contributes to the phenomenon of heart rate turbulence.

Prognostic significance of heart rate turbulence following ventricular premature beats in patients with idiopathic dilated cardiomyopathy.

Heart Rate Turbulence in Dilated Cardiomyopathy. The aim of this study was to investigate the prognostic significance of heart rate turbulence (HRT) characterized by HRT onset and slope after ventricular premature beats in patients with idiopathic dilated cardiomyopathy (IDC). Blinded HRT analysis was performed in 242 patients with IDC who were enrolled in the Marburg Cardiomyopathy database between 1992 and 2000. During 41 +/- 23 months of follow-up, 54 patients (22%) died or underwent heart transplant. On Cox univariate regression analysis, abnormal HRT onset, HRT slope, HRT onset combined with HRT slope, left ventricular (LV) ejection fraction, LV size, and New York Heart Association (NYHA) functional class III showed a significant association with total mortality or the need for heart transplant. On multivariate analysis, abnormal HRT onset identified patients without transplant-free survival, as did LV size and NYHA class III heart failure. Major arrhythmic events were observed in 42 patients (17%) during follow-up. On univariate analysis, abnormal HRT onset, HRT onset combined with HRT slope, male sex, NYHA class III, LV ejection fraction, and LV size were associated with a higher incidence of major arrhythmic events. On multivariate analysis, only LV ejection fraction remained as a significant arrhythmia risk predictor, with a relative risk of 2.2 per 10% decrease in ejection fraction (95% confidence interval 1.5-3.2). In this selected patient population with IDC, HRT onset is a significant predictor of transplant-free survival, as are LV size and NYHA class. For arrhythmia risk stratification, however, only LV ejection fraction remained a significant risk predictor on multivariate analysis.

Relationship between redistribution on exercise thallium-201 scintigraphy and repetitive ventricular premature beats in patients with recent myocardial infarction

The relationship between myocardial ischemia detected by exercise thallium-201 scintigraphy and repetitive ventricular premature beats (VPBs) during ambulatory monitoring was evaluated in 57 patients with recent myocardial infarction. Multivariate analysis was performed to obtain the relatively important factor related to repetitive VPBs with the use of the following variables: age, redistribution, left ventricular ejection fraction, serum potassium and magnesium concentration, QRS score, left ventricular aneurysm, and the number of diseased vessels. Thirty-five patients had redistribution, but only three of them had repetitive VPBs during exercise testing. The average heart rate before 79% of 398 episodes of repetitive VPBs during ambulatory monitoring was in the range of 56 to 70/min. These data indicate that most of repetitive VPBs during ambulatory monitoring were not provoked by exercise-induced acute myocardial ischemia. However, redistribution was found to be an important factor associated with repetitive VPBs. The electrical abnormality relating to a substrate characterized by chronic reversible ischemia may explain the association between redistribution and repetitive VPBs.

Sites of origin of ventricular premature beats in patients with and without cardiovascular disease evaluated by body surface mapping

The site of origin of ventricular premature beats (VPBs) was estimated by QRS maps and its distribution in two patient groups was studied. VPB origin was determined by comparing the body surface map of VPBs with that during electrical stimuli applied at various sites of the ventricle. Subjects were 100 patients without obvious underlying cardiovascular disease (Group N) and 289 patients with various heart diseases (Group D). Nine sites of origin of VPB were identified. In group N, VPBs of right ventricular origin were noted in 69%, those of left ventricular origin in 6%. There was a relatively high incidence of VPBs with foci estimated to be the divisions of the left bundle branch, and the age of patients with these VPBs was young. In Group D, VPBs of left ventricular origin showed a higher incidence (34.6%) and those of right ventricular origin a lower incidence (41.2%) than those in group N. The data suggest that VPBs originating from the apex and base of the ventricle strongly indicate the presence of basic heart disease and that VPBs originating in or near the divisions of the left bundle branch in younger subjects do not necessarily indicate cardiac disease.

Site of origin of ventricular premature beats in patients with mitral valve prolapse

This study examines the site of origin and possible etiology of ventricular premature beats (VPB) in patients with mitral valve prolapse. Ten patients with mitral valve prolapse documented by echocardiogram form the study group. All patients had prolapse of the posterior leaflet and three additionally had anterior prolapse. There were eight females and two males, with a mean age of 29.1 ± 11.1 years. All patients were having unifocal VPBs at rest. A vectorcardiogram (VCG) was taken of the VPB by a technique which allowed all VCG loops to be written from the same beat. The VCG analysis indicated that the VPB forces were directed anteriorly, inferiorly, and to the left in six patients. In two patients the VPB was directed posteriorly, inferiorly, and to the left, consistent with right ventricular origin. One of these patients had episodes of ventricular tachycardia. One was anterior, superior, and to the left, and one was markedly anterior, superior, and to the right. In all patients the initial portion of the QRS was inscribed slowly. The three patients with additional anterior prolapse did not show a common difference from those with isolated posterior prolapse. It is concluded that: (1) The majority of these VPBs originate from the posteriorbasal portion of the left ventricle. (2) They originate in the myocardium and not in the Purkinje tissue. (3) There is no relationship between the location of prolapse and the VPB morphology.