scholarly journals Novel technique targeting left ventricular summit premature ventricular contractions using radiofrequency ablation through a guidewire

Author(s):  
Michael Efremidis ◽  
Konstantinos Vlachos ◽  
George Bazoukis ◽  
Antonio Frontera ◽  
Claire A. Martin ◽  
...  
2015 ◽  
Vol 26 (4) ◽  
pp. 711-717 ◽  
Author(s):  
Zebulon Z. Spector ◽  
Stephen P. Seslar

AbstractBackgroundAdults with high premature ventricular contraction burden can develop left ventricular dilation, dysfunction, and strain, consistent with a cardiomyopathy, which is reversible with radiofrequency ablation of the premature ventricular contractions. Evidence in children with similar ectopy burden is limited. We performed a single-centre retrospective review to examine the prevalence of premature ventricular contraction-induced cardiomyopathy, natural history of ventricular ectopy, and progression to ventricular tachycardia in children with frequent premature ventricular contractions.MethodsChildren aged between 6 months and 18 years, with premature ventricular contractions comprising at least 20% of rhythm on 24-hour Holter monitor, were included in our study. Those with significant structural heart disease, ventricular tachycardia greater than 1% of rhythm at the time of premature ventricular contraction diagnosis, or family history of cardiomyopathy – except tachycardia-induced – were excluded. Cardiomyopathy was defined by echocardiographic assessment.ResultsA total of 36 children met the study criteria; seven patients (19.4%, 95% CI 6.2–32.6%) met the criteria for cardiomyopathy, mostly at initial presentation. Ectopy decreased to <10% of beats without intervention in 16.7% (95% CI 4.3–29.1%) of the patients. No patient progressed to having ventricular tachycardia as more than 1% of beats on follow-up Holter. Radiofrequency ablation was performed in three patients without cardiomyopathy.ConclusionsOur study demonstrates a higher prevalence of cardiomyopathy among children with high premature ventricular contraction burden than that previously shown. Ectopy tended to persist throughout follow-up. These trends suggest the need for a multi-centre study on frequent premature ventricular contractions in children. In the interim, regular follow-up with imaging to evaluate for cardiomyopathy is warranted.


2011 ◽  
Vol 109 (suppl_1) ◽  
Author(s):  
Masamichi Hirose ◽  
Yasuchika Takeishi ◽  
Hisashi Shimojo ◽  
Toshihide Kashihara ◽  
Tsutomu Nakada ◽  
...  

Introduction: Beneficial effects of nicorandil on the treatment of hypertensive heart failure (HF) and ischemic heart disease have been suggested. However, whether nicorandil has inhibitory effects on HF and ventricular arrhythmias caused by the activation of G protein alpha q (Gαq) -coupled receptor (GPCR) signaling pathway still remains unknown. We examined effects of chronic and acute administration of nicorandil on the development of HF and ventricular action potential (VAP) in transgenic mice with transient cardiac expression of activated Gαq (Gαq-TG), respectively. Method and Results: Nicorandil (6 mg/kg/day) or vehicle was chronically administered in Gαq-TG mice for 24 weeks from 8 weeks of age, and then ventricular function, and electrical and structural changes were investigated in the hearts. Chronic nicorandil administration improved the reduction of left ventricular fractional shortening (p < 0.001) in Gαq-TG hearts. During 10 min of electrocardiogram recording, premature ventricular contractions (more than 20 beats/min) were observed in 7 of 10 vehicle-treated Gαq-TG but in none of 10 nicorandil-treated Gαq-TG hearts (p < 0.01). QT interval was significantly shorter in nicorandil-treated Gαq-TG than in vehicle-treated Gαq-TG hearts (p < 0.05). Chronic nicorandil administration improved the increased ventricular interstitial fibrosis (p < 0.05) but not cardiac hypertrophy in Gαq-TG left ventricles. Real time RT-PCR revealed that mRNA expression levels of s sulfonylurea receptor 2B (SUR-2B) were decreased in vehicle-treatd Gαq-TG but not in nicorandil-treated Gαq-TG. In addition, chronic nicorandil increased endotherial nitric oxide syntheses gene expression in Gαq-TG hearts (p < 0.05). Acute nicorandil administration (1 microM) significantly shortened the prolonged VAP duration and reduced the number of PVCs in vehicle treated Gαq-TG hearts. Conclusions: These findings suggest that nicorandil inhibits ventricular electrical and structural remodeling and arrhythmias through the shortening of VAP duration and the increased expression of SUR-2B and eNOS in a mouse model of HF.


2020 ◽  
Vol 1 (54) ◽  
pp. 30-32
Author(s):  
Przemysław Mitkowski ◽  
Maciej Grymuza

The up-date of ESC Guidelines on the management of patients with heart failure was published last year. The beneficial effect of a new group of drugs (flozins, sacubitril/valsartan - ARNI) in patients with heart failure was pointed out. These drugs not only prevent the onset of heart failure but also reduce HF hospitalization rate and in patients with reduced left ventricular ejection fraction decrease risk of cardiovascular death and in case of empagliflozin, dapagliflozin or sacubitril/valsartan also total mortality. These latter medicines reduce also the likelihood of sudden cardiac death. ARNI reduce the number of appropriate ICD shocks, the incidence of non-sustained VT, premature ventricular contractions, and increase percentage of biventricular pacing in car­diac resynchronization recipients.


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