A Case of Cardiomyopathy Induced by Premature Ventricular Complexes.

Shiraishi, Hiroaki; Ishibashi, Keiichiro; Urao, Norifumi; Tsukamoto, Masaki; Hyogo, Masayuki; Keira, Natsuya; Hirasaki, Satoshi; Shirayama, Takeshi; Nakagawa, Masao

doi:10.1253/circj.66.1065

Cited by 64 publications

(53 citation statements)

References 7 publications

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“…Identifying this entity is difficult, but it may be suggested by the pro- Improvement or resolution of cardiomyopathy has been reported after elimination or suppression of premature ventricular contractions (PVCs), which raises the question of a possible PVC-induced cardiomyopathy. [454][455][456][457] The proposed mechanisms underlying PVC-induced cardiomyopathy include ventricular dyssynchrony and increased myocardial oxygen demand. 458 This is supported by evidence that LBBB creates dyssynchrony that can impair diastolic function and worsen mitral regurgitation.…”

Section: Lbbb-induced Cardiomyopathy Pathophysiology and Epidemiologymentioning

confidence: 99%

Current Diagnostic and Treatment Strategies for Specific Dilated Cardiomyopathies: A Scientific Statement From the American Heart Association

Bozkurt¹,

Colvin²,

Cook³

et al. 2016

Circulation

603

663

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CLINICAL STATEMENTS AND GUIDELINEST he intent of this American Heart Association (AHA) scientific statement is to summarize our current understanding of dilated cardiomyopathies. There is special emphasis on recent developments in diagnostic approaches and therapies for specific cardiomyopathies. Recommendations in this document are based on published studies, published practice guidelines from the American College of Cardiology (ACC)/AHA 1 and other organizations, 2,3 and the multidisciplinary expertise of the writing group. Existing evidence in epidemiology, classification, diagnosis, and management of specific cardiomyopathies is usually derived from nonrandomized observational studies, registries, case reports, or expert opinion based on clinical experience, not large-scale randomized clinical trials or systematic reviews. Therefore, in this document, rather than using the standard ACC/AHA classification schema of recommendations and level of evidence, 4 we have included key management strategies at the end of each section and categorized our recommendations according to the level of consensus. Although the format of our recommendations might resemble the ACC/AHA classification of recommendations used in the ACC/AHA practice guidelines, because of the preponderance of expert opinion or level of evidence C evidence in our document, we elected to use different terminology to provide a distinction from the practice guidelines, in which stronger levels and quality of evidence with randomized clinical trials or meta-analyses are usually present. 4 The levels of evidence follow the AHA and ACC methods of classifying the level of certainty of the treatment effect. 4 DEfINITIoN of DILATED CArDIoMyopAThyThe term dilated cardiomyopathy (DCM) refers to a spectrum of heterogeneous myocardial disorders that are characterized by ventricular dilation and depressed myocardial performance in the absence of hypertension, valvular, congenital, or ischemic heart disease. 5 In clinical practice, the pathogenesis of heart failure (HF) has often been placed into 2 categories: ischemic and nonischemic cardiomyopathy. The term nonischemic cardiomyopathy has been interchangeably used with DCM. Although this approach might be practical, it fails to recognize that nonischemic cardiomyopathy can include cardiomyopathies caused by volume or pressure overload (such as hypertension or valvular heart disease) that are not conventionally accepted under the definition of DCM. 1,5 Again, in general practice and clinical research trials, the term ischemic cardiomyopathy is defined as cardiomyopathy caused by ischemic heart disease. Current use of ischemic cardiomyopathy terminology implies ventricular dilation and depressed myocardial contractility caused by ischemia or infarction. CLASSIfICATIoN of CArDIoMyopAThIESThe first classification on this topic categorized cardiomyopathies as heart muscle diseases with dilated (DCM), hypertrophic, restrictive, arrhythmogenic right ventricular (ARVC), or nonclassifiable cardiomyopathy in 1980. 5 Subse...

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Section: Lbbb-induced Cardiomyopathy Pathophysiology and Epidemiologymentioning

confidence: 99%

Current Diagnostic and Treatment Strategies for Specific Dilated Cardiomyopathies: A Scientific Statement From the American Heart Association

Bozkurt¹,

Colvin²,

Cook³

et al. 2016

Circulation

603

663

View full text Add to dashboard Cite

show abstract

“…9,10) In regard to the mechanism of deterioration of cardiac function in frequent PVC patients, possible explanations include the morbid condition due to ineffective contraction during PVC, a condition resembling bradycardic heart failure, 23) and asynchrony at the time of PVC appearance. 24) Overall, the number of PVCs was decreased without catheter ablation, and cardiac function was preserved. Especially, the number of PVC was more significantly decreased in the patients with underlying disease who received pharmacological therapy for underlying disease.…”

Section: Discussionmentioning

confidence: 96%

Long‐term Prognosis for Non‐ischemic Heart Disease Patients with Premature Ventricular Contraction and Non‐sustained Ventricular Tachycardia

Komoriya

Imai

Aoyama

et al. 2008

Journal of Arrhythmia

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There are few long-term reports of patients with frequent PVCs in the absence of ischemic heart disease. In 86 patients without ischemic heart disease, who had 1000 or more PVCs in 24-hour Holter ECG, the number of PVCs during 24-hours Holter ECG and echocardiographic parameters were followed at least 1 year (66:5 AE 39:7 months). PVC was significantly reduced in the patients with or without underlying diseases (UD). The reduction rate in the number of PVCs was prominent in patients with UD. PVC was significantly reduced in patients under medication, but not in patients without medication. In the comparison between the initial and follow up observation using Wilcoxon's rank test, the number of PVC was significantly reduced (P < 0:05), and EF was also improved (P < 0:05) in angiotensin converting enzyme inhibitor (ACEI) or angiotensin receptor blocker (ARB) group, and inblocker group. In Ca-antagonist group and antiarrhythmic drug group, the number of PVCs was also significantly reduced (P < 0:05). Multivariate analysis revealed significantly higher incidence (60% or more with PVC reduction) in ACEI/ARB group.These results suggest that the administration of ACEI/ARB may contribute to the reduction of PVC in non-ischemic heart disease cases with multiple PVC. (J Arrhythmia 2008; 24: 18-25)

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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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A Case of Cardiomyopathy Induced by Premature Ventricular Complexes.

Cited by 64 publications

References 7 publications

Current Diagnostic and Treatment Strategies for Specific Dilated Cardiomyopathies: A Scientific Statement From the American Heart Association

Current Diagnostic and Treatment Strategies for Specific Dilated Cardiomyopathies: A Scientific Statement From the American Heart Association

Long‐term Prognosis for Non‐ischemic Heart Disease Patients with Premature Ventricular Contraction and Non‐sustained Ventricular Tachycardia

“Pacing Bigeminal”

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