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Management of ventricular arrhythmias in heart failure: Current perspectives.

ABSTRACT: Congestive heart failure (HF) is a progressive affliction defined as the inability of the heart to sufficiently maintain blood flow. Ventricular arrhythmias (VAs) are common in patients with HF, and conversely, advanced HF promotes the risk of VAs. Management of VA in HF requires a systematic, multimodality approach that comprises optimization of medical therapy and use of implantable cardioverter-defibrillator and/or device combined with cardiac resynchronization therapy. Catheter ablation is one of the most important strategies with the potential to abolish or decrease the number of recurrences of VA in this population. It can be a curative strategy in arrhythmia-induced cardiomyopathy and may even save lives in cases of an electrical storm. Additionally, modulation of the autonomic nervous system and stereotactic radiotherapy have been introduced as novel methods to control refractory VAs. In patients with end-stage HF and refractory VAs, an institution of the mechanical circulatory support device and cardiac transplant may be considered. This review aims to provide an overview of current evidence regarding management strategies of VAs in HF with an emphasis on interventional treatment.

SUBMITTER: Peichl P

PROVIDER: S-EPMC8710622 | biostudies-literature | 2021 Dec

REPOSITORIES: biostudies-literature

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Management of ventricular arrhythmias in heart failure: Current perspectives.

Peichl Petr P Rafaj Adam A Kautzner Josef J

Heart rhythm O2 20211217 6Part B

Congestive heart failure (HF) is a progressive affliction defined as the inability of the heart to sufficiently maintain blood flow. Ventricular arrhythmias (VAs) are common in patients with HF, and conversely, advanced HF promotes the risk of VAs. Management of VA in HF requires a systematic, multimodality approach that comprises optimization of medical therapy and use of implantable cardioverter-defibrillator and/or device combined with cardiac resynchronization therapy. Catheter ablation is o ...[more]

PMID: 34988531

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Project description:BackgroundOsimertinib is a third-generation epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor that has become the first-line treatment for non-small cell lung cancer harboring EGFR mutations, with the potential risk of QT prolongation and heart failure. However, few cases have reported malignant ventricular arrhythmias. Here, we report a case of recurrent ventricular fibrillation (VF) and Torsade de Pointes (TdP) secondary to QT prolongation and heart failure induced by osimertinib.Case summaryA 70-year-old woman presented with chest tightness and dyspnea for 1 week and ventricular fibrillation upon admission, with a medical history of lung adenocarcinoma harboring an EGFR exon 21 p.L858R mutation. She was under osimertinib for 3 months. Electrocardiography after defibrillation suggested QTc prolongation (655 ms) and T wave alternans. Ultrasound cardiography displayed left ventricular ejection fraction (LVEF) of 29% and severe mitral regurgitation. Laboratory tests indicated elevated N-terminal pro-B-type natriuretic peptide and hypokalemia. Genetic testing suggested no pathogenic mutations. We considered acquired long QT syndrome and heart failure with reduced ejection fraction induced by osimertinib as the chief causes of ventricular arrhythmia and hypokalemia as an important trigger. Despite intubation, sedation, and the administration intravenous magnesium and potassium and lidocaine, the patient presented with recurrent TdP, which was managed by a low dose of isoproterenol (ISO, 0.17 ug/min). An implantable cardioverter defibrillator was declined. The patient is surviving without any relapse, with QTc of 490 ms and LVEF of 42% after a 6-month follow up.ConclusionRegular monitoring is required during osimertinib administration, considering the risk of life-threatening cardiac events, such as malignant arrhythmias and heart failure. ISO, with an individual dose and target heart rate, may be beneficial for terminating TdP during poor response to other therapies.

Project description:BackgroundBeneficial 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 (Gα(q)) -coupled receptor (GPCR) signaling still remains unknown. We investigated these inhibitory effects of nicorandil in transgenic mice with transient cardiac expression of activated Gα(q) (Gα(q)-TG).Methodology/principal findingsNicorandil (6 mg/kg/day) or vehicle was chronically administered to Gα(q)-TG from 8 to 32 weeks of age, and all experiments were performed in mice at the age of 32 weeks. Chronic nicorandil administration prevented the severe reduction of left ventricular fractional shortening and inhibited ventricular interstitial fibrosis in Gα(q)-TG. SUR-2B and SERCA2 gene expression was decreased in vehicle-treated Gα(q)-TG but not in nicorandil-treated Gα(q)-TG. eNOS gene expression was also increased in nicorandil-treated Gα(q)-TG compared with vehicle-treated Gα(q)-TG. Electrocardiogram demonstrated that premature ventricular contraction (PVC) was frequently (more than 20 beats/min) observed in 7 of 10 vehicle-treated Gα(q)-TG but in none of 10 nicorandil-treated Gα(q)-TG. The QT interval was significantly shorter in nicorandil-treated Gα(q)-TG than vehicle-treated Gα(q)-TG. Acute nicorandil administration shortened ventricular monophasic action potential duration and reduced the number of PVCs in Langendorff-perfused Gα(q)-TG mouse hearts. Moreover, HMR1098, a blocker of cardiac sarcolemmal K(ATP) channels, significantly attenuated the shortening of MAP duration induced by nicorandil in the Gα(q)-TG heart.Conclusions/significanceThese findings suggest that nicorandil can prevent the development of HF and ventricular arrhythmia caused by the activation of GPCR signaling through the shortening of the QT interval, action potential duration, the normalization of SERCA2 gene expression. Nicorandil may also improve the impaired coronary circulation during HF.

Project description:BackgroundHeart failure with preserved ejection fraction (HFpEF) represents approximately half of heart failure, and its incidence continues to increase. The leading cause of mortality in HFpEF is sudden death, but little is known about the underlying mechanisms.MethodsDahl salt-sensitive rats were fed a high-salt diet (8% NaCl) from 7 weeks of age to induce HFpEF (n=38). Rats fed a normal-salt diet (0.3% NaCl) served as controls (n=13). Echocardiograms were performed to assess systolic and diastolic function from 14 weeks of age. HFpEF-verified and control rats underwent programmed electrical stimulation. Corrected QT interval was measured by surface ECG. The mechanisms of ventricular arrhythmias (VA) were probed by optical mapping, whole-cell patch clamp to measure action potential duration and ionic currents, and quantitative polymerase chain reaction and Western blotting to investigate changes in ion channel expression.ResultsAfter 7 weeks of a high-salt diet, 31 of 38 rats showed diastolic dysfunction and preserved ejection fraction along with signs of heart failure and hence were diagnosed with HFpEF. Programmed electric stimulation demonstrated increased susceptibility to VA in HFpEF rats (P<0.001 versus controls). The arrhythmogenicity index was increased (P<0.001) and the corrected QT interval on ECG was prolonged (P<0.001) in HFpEF rats. Optical mapping of HFpEF hearts demonstrated prolonged action potentials (P<0.05) and multiple reentry circuits during induced VA. Single-cell recordings of cardiomyocytes isolated from HFpEF rats confirmed a delay of repolarization (P=0.001) and revealed downregulation of transient outward potassium current (Ito; P<0.05). The rapid components of the delayed rectifier potassium current (IKr) and the inward rectifier potassium current (IK1) were also downregulated (P<0.05), but the current densities were much lower than for Ito. In accordance with the reduction of Ito, both Kcnd3 transcript and Kv4.3 protein levels were decreased in HFpEF rat hearts.ConclusionsSusceptibility to VA was markedly increased in rats with HFpEF. Underlying abnormalities include QT prolongation, delayed repolarization from downregulation of potassium currents, and multiple reentry circuits during VA. Our findings are consistent with the hypothesis that potassium current downregulation leads to abnormal repolarization in HFpEF, which in turn predisposes to VA and sudden cardiac death.

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Management of ventricular arrhythmias in heart failure: Current perspectives.

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Management of ventricular arrhythmias in heart failure: Current perspectives.

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