Frequent Premature Ventricular Complexes Originating from the Right Ventricular Outflow Tract Are Associated with Left Ventricular Dysfunction

Kanei, Yumiko; Friedman, Meir; Ogawa, Naomi; Hanon, Sam; Lam, Patrick; Schweitzer, Paul

doi:10.1111/j.1542-474x.2007.00204.x

Cited by 133 publications

(104 citation statements)

References 14 publications

(20 reference statements)

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“…15) Some studies have reported that ablation of PVCs originating from the RV outflow tract resulted in reduction of the LV volume and improvement of the LV ejection fraction (LVEF). [16][17][18][19][20] The burden of PVCs has been reported to be correlated with the LVEF and known to be an independent predictive factor for worsening LV systolic function in patients with untreated frequent PVCs. 17,18,21) However, the burden of PVCs was not correlated with the volume of the cardiac chambers or the LVEF in this study.…”

Section: Discussionmentioning

confidence: 99%

“…[16][17][18][19][20] The burden of PVCs has been reported to be correlated with the LVEF and known to be an independent predictive factor for worsening LV systolic function in patients with untreated frequent PVCs. 17,18,21) However, the burden of PVCs was not correlated with the volume of the cardiac chambers or the LVEF in this study. The burden of PVCs can episodically increase or decrease without treatment, regardless of accompanying LV remodeling or LV systolic dysfunction, 7,21) which might explain the discrepant relationship between the burden of PVCs and LVEF in this study.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Chronic Frequent Premature Ventricular Complexes Originating From Right and Non-Right Ventricular Outflow Tracts Change in Left Ventricular Function After Radiofrequency Catheter Ablation

et al. 2010

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SummaryFrequent premature ventricular complexes (PVCs) from the right ventricular outflow tract (RVOT) have recently been reported to be a cause of dilated cardiomyopathy. We studied the clinical impact of the elimination of PVCs from RVOT and non-RVOT.Thirty-six patients with symptomatic PVCs that were treated with radiofrequency catheter ablation (RFCA) were studied. The patients were assigned to one of two groups according to the origin of the PVCs (group I, RVOT-origin, n = 24; group II, non-RVOT-origin, n = 12) and observed for 10.5 ± 7.1 months.The burden of PVCs at baseline was 19.7 ± 10.6% and 18.7 ± 8.7% in group I and group II, respectively (P = 0.779). In group II, hypertension was more common (16.7% versus 58.3%, P = 0.020) and LV diastolic function was worse (Em, 8.7 ± 3.0 versus 6.4 ± 1.8 cm/second, P = 0.018). The LV end diastolic volume index (LVEDVI) decreased in both groups (59.7 ± 14.6 to 50.9 ± 9.6 mL/m 2 , P = 0.004 in group I; 60.0 ± 19.9 to 51.6 ± 12.4 mL/m 2 , P = 0.044 in group II), while the left atrial volume index (LAVI) decreased only in group I (36.7 ± 11.7 to 31.7 ± 10.0 mL/m 2 , P = 0.002 in group I; 35.6 ± 11.9 to 33.8 ± 10.3 mL/m 2 , P = 0.317 in group II). The left ventricular ejection fraction (LVEF) significantly improved in both groups (51.1 ± 6.6 to 59.8 ± 7.2 %, P < 0.01 in group I; 49.9 ± 6.9 to 59.0 ± 5.9 %, P < 0.01 in group II).RFCA of PVCs leads to a reduction of LV volume and improvement of LV systolic function regardless of the origin of the PVCs. Conversely, a non-RVOT-origin as well as an RVOT-origin of the PVCs can cause DCM-like changes in the left ventricle. (Int Heart J 2010; 51: 388-393)

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Chronic Frequent Premature Ventricular Complexes Originating From Right and Non-Right Ventricular Outflow Tracts Change in Left Ventricular Function After Radiofrequency Catheter Ablation

et al. 2010

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“…119 It is clear that the likelihood of TIC development increases with increasing PVC burden. However, what is also clear is that PVC burden is not the only contributing factor to impaired LV function.…”

Section: Ventricular Tachycardiamentioning

confidence: 99%

What About Tachycardia-induced Cardiomyopathy?

Ellis¹,

Josephson²

2013

Arrhythmia &Amp; Electrophysiology Review

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Cardiomyopathies are heterogeneous heart muscle disorders with a wide range of aetiologies and clinical manifestations. They are often defined by their causes (i.e. hypertension, prior myocardial infarction, valvular heart disease), although current major society definitions describe cardiomyopathy as the presence of abnormal myocardial structure and/or function in the absence of underlying structural heart disease. Long-standing tachycardia is a well-recognised cause of heart failure and left ventricular dysfunction, and has led to the nomenclature, tachycardia-induced cardiomyopathy (TIC). TIC is generally a reversible cardiomyopathy if the tachycardia can be treated effectively, either with medications, surgery or catheter ablation. TIC can also manifest in patients with baseline left ventricular dysfunction from underlying structural heart disease that develop a worsening of their myocardial dysfunction in the setting of prolonged tachycardia, which can be reversed with control of the tachycardia. The diagnosis is usually made after demonstrating recovery of left ventricular function with normalisation of heart rate in the absence of other identifiable aetiologies.TIC was first described in 1913 in a young patient who presented with congestive heart failure (CHF) and atrial fibrillation (AF) with rapid ventricular response.1 In the subsequent decades, further reports were written documenting cases of complete resolution of CHF after cardioversion of AF to sinus rhythm.2-4 A century after the first reported case, we are still working to expand our understanding of the mechanisms underlying this disorder. A variety of chronic or incessant tachyarrhythmias have been implicated in the pathogenesis of TIC, the most classic being AF, 5-7 atrial flutter, 8 incessant supraventricular tachycardia, 9-12 ventricular tachycardia [13][14][15][16] and premature ventricular depolarizations 17 (see Table 1). The most common presentation is a dilated cardiomyopathy with or without the causative tachycardia.Given that this diagnosis represents a potentially reversible cause of heart failure, its recognition is critically important. In this review, we will discuss the proposed mechanisms of TIC, the causative tachycardias and their treatment, outcomes for patients diagnosed with TIC, and future directions for research and clinical care. Experimental Models BackgroundThe first experimental model of TIC was described by Whipple et al. in 1962 where he demonstrated that rapid, prolonged atrial pacing resulted in low output heart failure.18 This model has since become widely used as a model to study CHF. Animal studies, primarily in dogs and pigs, have shown that sustained rapid atrial or ventricular pacing results in systolic heart failure that is neurohormonally and haemodynamically similar to left ventricular systolic dysfunction in humans. [19][20][21][22][23] The majority of what is known about the pathophysiologic mechanisms underlying TIC is supported by pacing-induced heart failure in animal models (see Table 2). It is ...

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“…The abnormal pattern of electric activation and LV dyssynchrony may cause disruption and further progression of dyssynergic LV wall motion. [15][16][17] Here we introduce a novel method to develop a HF model, in which two ventricular leads were implanted in the right ventricle, connected to the pacemaker atrial and ventricular holes, excites the ventricle twice in one pacemaker beat and doubles the heart rate, using a proper coupling interval and basic heart rate, which is different from traditional rapid pacing. Extending the AV interval makes the ventricular rate as smooth as possible.…”

Section: Discussionmentioning

confidence: 99%

“Pacing Bigeminal”

Gong¹,

Qin²,

Huang³

et al. 2016

Int. Heart J.

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SummaryA rapid pacing-induced heart failure model is commonly used in developing dilated cardiomyopathy (DCM). Traditionally, the right ventricular lead was connected with a single chamber pacemaker specific for animals that had a high frequency. However, the pacemaker used in this model is commercially unavailable. We developed a "pacing bigeminal" method using a commercially available dual-chamber (DDD) pacemaker to achieve high-frequency pacing. Twenty beagles were assigned to group A (n = 10) (pacing bigeminal method) and group B (n = 10) (traditional method). Echocardiographic measurements and electrocardiograms were obtained at baseline, at two weeks of pacing, and at 4 weeks of end pacing. LV anterior wall cardiac samples were obtained at 2 weeks of pacing and 4 weeks of end pacing for myocardial microscopic evaluation. Clinical manifestation and exposure time were also observed. After pacing for 10.5 ± 2.3 (7-14) days, the beagles in group B experienced heart failure, whereas in group A, only 7.9 ± 2.5 (5-12) days (P < 0.05) were needed to reach heart failure. Both methods could induce wide QRS duration, heart rate elevation, and myocardial microscopic changes (P > 0.05). In conclusion, this pacing bigeminal-induced heart failure method is feasible and can induce heart failure faster than the traditional method, which makes it a promising alternative method. (Int Heart J 2016; 57: 747-752) Key words: Animal model, Cardiac resynchronization therapy, Dilated cardiomyopathy D ilated cardiomyopathy (DCM) is an important cause of heart failure that is characterized by unexplained left ventricular (LV) dilatation and impaired systolic function.1) Cardiac resynchronization therapy (CRT) is a device therapy for end-stage HF, especially that caused by idiopathic DCM. In the wide application of CRT, the establishment of a suitable big-animal heart failure model is essential in basic research on DCM and CRT, because the devices are not easily used in small-animal models.Current DCM heart failure models of large animals include myocardial infarction, coronary microembolization, pacing-induced tachycardia, and toxic injury, 2,3) described in detail in the AHA Scientific Statement. 4) Regional myocardial infarction models mimic human ischemic cardiomyopathy, which mainly uses pigs instead of dogs because dogs have a well-developed collateral circulation, 5) which can result in higher variability in infarct size and subsequent remodeling. Coronary microembolization also resembles human ischemic cardiomyopathy, but it is time consuming and requires repeated injection with polystyrene microspheres. The limitations of the toxic model include variability of the response to doxorubicin and the degree of LV dysfunction and animal mortality caused by arrhythmias. 4)Chronic tachycardia-mediated DCM is a recognized clinical condition. 6,7) This disease model closely replicates the mechanical, structural, neurohormonal, and myocyte functional alterations of DCM in humans. [8][9][10][11] The predictability and reproducibility...

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Frequent Premature Ventricular Complexes Originating from the Right Ventricular Outflow Tract Are Associated with Left Ventricular Dysfunction

Abstract: We demonstrated a significant association between frequent RVOT PVCs and LV dysfunction in patients without structural heart disease.

Cited by 133 publications

References 14 publications

Chronic Frequent Premature Ventricular Complexes Originating From Right and Non-Right Ventricular Outflow Tracts Change in Left Ventricular Function After Radiofrequency Catheter Ablation

Chronic Frequent Premature Ventricular Complexes Originating From Right and Non-Right Ventricular Outflow Tracts Change in Left Ventricular Function After Radiofrequency Catheter Ablation

What About Tachycardia-induced Cardiomyopathy?

“Pacing Bigeminal”

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