Incidence Of Ventricular Arrhythmias Research Articles

Ten-year follow-up of cardiac resynchronization therapy patients with non-ischemic dilated cardiomyopathy assessed by radionuclide angiography: a single-center cohort study.

Relatively few data are available on long-term survival and incidence of ventricular arrhythmias in cardiac resynchronization therapy (CRT) patients. We investigated long-term outcomes of CRT patients with non-ischemic dilated cardiomyopathy stratified as responders or non-responders according to radionuclide angiography. Fifty patients with non-ischemic dilated cardiomyopathy undergoing CRT were assessed by equilibrium Tc99 radionuclide angiography with bicycle exercise at baseline and after 3months. Intra- and interventricular dyssynchrony were derived by Fourier phase analysis. Patient clinical outcome was assessed after 10years. At 3months, 50% of patients were identified as CRT responders according to an increase in LV ejection fraction ≥ 5%. During a follow-up of 109 ± 48months, 30% of patients died and 6% underwent heart transplantation. Age and history of paroxysmal atrial fibrillation were found to be predictors of all-cause mortality. CRT responders showed lower risk of death from cardiac causes than non-responders. At follow-up, 38% of patients presented at least one episode of sustained ventricular tachycardia, with a similar percentage between responders and non-responders. At long-term follow-up, non-ischemic CRT recipients identified as responders by radionuclide angiography were found to be at lower risk of worsening heart failure death than non-responders. Long-term risk for sustained ventricular arrhythmia was similar between CRT responders and non-responders.

Arrhythmic Mitral Valve Prolapse and Mitral Annular Disjunction: Clinical Features, Pathophysiology, Risk Stratification, and Management

Mitral valve prolapse (MVP) is a common cause of valvular heart disease. Although many patients with MVP have a benign course, there is increasing recognition of an arrhythmic phenotype associated with ventricular arrhythmias and sudden cardiac death (SCD). Pathophysiologic mechanisms associated with arrhythmias include cardiac fibrosis, mechanical stress induced changes in ventricular refractory periods, as well as electrophysiologic changes in Purkinje fibers. Clinically, a variety of risk factors including demographic, electrocardiographic, and imaging characteristics help to identify patients with MVP at the highest at risk of SCD and arrhythmias. Once identified, recent advances in treatment including device therapy, catheter ablation, and surgical interventions show promising outcomes. In this review, we will summarize the incidence of ventricular arrhythmias and SCD in patients with MVP, the association with mitral annular disjunction, mechanisms of arrhythmogenesis, methods for arrhythmic and SCD risk stratification including findings with multimodality imaging, and treatments for the primary and secondary prevention of SCD.

A carvedilol analogue, VK-II-86, prevents hypokalaemia-induced ventricular arrhythmia through novel multi-channel effects.

QT prolongation and intracellular Ca2+ loading with diastolic Ca2+ release via ryanodine receptors (RyR2) are the predominant mechanisms underlying hypokalaemia-induced ventricular arrhythmia. We investigated the antiarrhythmic actions of two RyR2 inhibitors: dantrolene and VK-II-86, a carvedilol analogue lacking antagonist activity at β-adrenoceptors, in hypokalaemia. Surface ECG and ventricular action potentials (APs) were recorded from whole-heart murine Langendorff preparations. Ventricular arrhythmia incidence was compared in hearts perfused with low [K+ ], and those pretreated with dantrolene or VK-II-86. Whole-cell patch clamping was used in murine and canine ventricular cardiomyocytes to study effects of dantrolene and VK-II-86 on AP parameters in low [K+ ] and effects of VK-II-86 on the inward rectifier current (IK1 ), late sodium current (INa_L ) and the L-type Ca2+ current (ICa ). Effects of VK-II-86 on IKr were investigated in transfected HEK-293 cells. A fluorogenic probe quantified the effects of VK-II-86 on oxidative stress in hypokalaemia. Dantrolene reduced the incidence of ventricular arrhythmias induced by low [K+ ] in explanted murine hearts by 94%, whereas VK-II-86 prevented all arrhythmias. VK-II-86 prevented hypokalaemia-induced AP prolongation and depolarization but did not alter AP parameters in normokalaemia. Hypokalaemia was associated with decreased IK1 and IKr , and increased INa-L , and ICa . VK-II-86 prevented all hypokalaemia-induced changes in ion channel activity and oxidative stress. VK-II-86 prevents hypokalaemia-induced arrhythmogenesis by normalizing calcium homeostasis and repolarization reserve. VK-II-86 may provide an effective treatment in hypokalaemia and other arrhythmias caused by delayed repolarization or Ca2+ overload.

Score for risk assesment of life-treating ventricular arrhythmia incidence in patients with implantable cardioverter-defibrillator and history of myocardial infarction

Score for risk assesment of life-treating ventricular arrhythmia incidence in patients with implantable cardioverter-defibrillator and history of myocardial infarction

Abstract 9112: Dexmedetomidine Reduces Incidences of Ventricular Arrhythmias in Adults

Introduction: Ventricular arrhythmias, including ventricular tachycardia (VT) and ventricular fibrillation (VF), are associated with high mortality and morbidity. Sedation through agents like benzodiazepines, propofol, and opiates are mainstays of treatment but are limited by side effects. Dexmedetomidine is a α2-presynaptic receptor agonist with a safe and efficacious sedative profile. Furthermore, it has been recently proposed as a sedative agent in VT due its additional antiarrhythmic properties. Methods: A systemic literature review was conducted of MEDLINE, EMBASE, Cochrane, and Scopus. Randomized controlled trials comparing the incidence of ventricular arrhythmias of dexmedetomidine with placebo or an alternative sedative agent were included. Two researchers independently extracted the data and performed quality assessments. Results: We identified 6 studies that met the selection criteria. Our meta-analysis demonstrated significant reduction of the overall risk of ventricular arrhythmias in patients receiving dexmedetomidine (RR 0.35, 95% CI 0.16, 0.76). Furthermore, there was no significant difference in risk of mortality (RR 0.59 95% CI 0.12, 3.02). Dexmedetomidine also significantly increased the risk of bradycardia (RR 2.78 95% CI 2.00, 3.87). There was no significant difference in risk of tachycardia (RR 0.59 95% CI 0.12, 3.02) or hypotension (RR 1.07 95% CI 0.64, 1.81). Conclusions: Our study demonstrates that the dexmedetomidine reduces the risk of VA by 65% compared to control. Further prospective research is necessary to clarify the antiarrhythmic and sedative properties of dexmedetomidine and its potential effect on patient outcomes.

Transcription factor Meis1 act as a new regulator of ischemic arrhythmias in mice

IntroductionThe principal voltage-gated Na+ channel, NaV1.5 governs heart excitability and conduction. NaV1.5 dysregulation is responsible for ventricular arrhythmias and subsequent sudden cardiac death (SCD) in post-infarct hearts. The transcription factor Meis1 performs a significant role in determining differentiation fate and regenerative capability of cardiomyocytes. However, the functions of Meis1 in ischemic arrhythmias following myocardial infarction (MI) are still largely undefined. ObjectivesHere we aimed to study whether Meis1 could act as a key regulator to mediate cardiac Na+ channel and its underlying mechanisms. MethodsHeart-specific Meis1 overexpression was established by AAV9 virus injection in C57BL/6 mice. The QRS duration, the incidence of ventricular arrhythmias and cardiac conduction velocity were evaluated by ECG, programmed electrical stimulation and optical mapping techniques respectively. The conventional patch clamp technique was performed to explore the INa characteristics of isolated mouse ventricular myocytes. In vitro, Meis1 was also overexpressed in hypoxic-treated neonatal cardiomyocytes. The analysis of immunoblotting and immunofluorescence were used to detect the changes in the expression of NaV1.5 in each group. ResultsWe found that forced expression of Meis1 rescued the prolongation of QRS complex, produced anti-arrhythmic activity and improved epicardial conduction velocity in infarcted mouse hearts. In terms of mechanisms, cardiac electrophysiological changes of MI mice can be ameliorated by the recovery of Meis1, which is characterized by the restoration of INa current density and NaV1.5 expression level of cardiomyocytes in the marginal zone of MI mouse hearts. Furthermore, in vitro studies showed that Meis1 was also able to rescue hypoxia-induced decreased expression and dysfunction of NaV1.5 in ventricular myocytes. We further revealed that E3 ubiquitin ligase CDC20 led to the ubiquitination and degradation of Meis1, which blocked the transcriptional regulation of SCN5A by Meis1 and ultimately led to the electrophysiological remodeling in ischemic-hypoxic cardiomyocytes. ConclusionCDC20 mediates ubiquitination of Meis1 to govern the transcription of SCN5A and cardiac electrical conduction in mouse cardiomyocytes. This finding uncovers a new mechanism of NaV1.5 dysregulation in infarcted heart, and provides new therapeutic strategies for malignant arrhythmias and sudden cardiac death following MI.

EphrinB2-RhoA upregulation attenuates sympathetic hyperinnervation and decreases the incidence of ventricular arrhythmia after myocardial infarction

BackgroundCardiac sympathetic hyperinnervation after myocardial infarction (MI) is associated with a high incidence of lethal arrhythmia. Erythropoietin-producing hepatoma interactor B2 (EphrinB2), a diffusible axonal chemorepellent that can induce growth cone collapse and axon repulsion of several neuronal populations, is crucial in neurodevelopment during disease development and progression. However, whether EphrinB2 could inhibit cardiac sympathetic hyperinnervation after MI remains unclear. Methods and resultsA rat model of MI was developed by left anterior descending coronary artery ligation. EphrinB2 expression was markedly increased in the infarcted border at 3 days after MI. Downregulation of EphrinB2 by intramyocardial injection of lentivirus carrying EphrinB2-shRNA significantly increased sympathetic hyperinnervation along with downregulated RhoA expression. In contrast, injection of EphrinB2-overexpressing lentivirus markedly upregulated EphrinB2, concomitant with inhibition of sympathetic sprouting and upregulated RhoA expression, accompanied by decreased incidence of ventricular arrhythmias (VAs). However, co-administering EphrinB2-overexpressing lentivirus and Fasudil (Rho kinase inhibitor) nearly abolished the inhibition of nerve sprouting effect. Additionally, EphrinB2 expression did not affect nerve growth factor level in the infarcted heart. ConclusionsOverexpression of EphrinB2 may ameliorate MI-induced sympathetic hyperinnervation and further reduce the incidence of VAs, at least in part by activating RhoA-mediated axonal retraction.

Ventricular arrhythmias in mouse models of diabetic kidney disease

Chronic kidney disease (CKD) affects more than 20 million people in the US, and it is associated with a significantly increased risk of sudden cardiac death (SCD). Despite the significance, the mechanistic relationship between SCD and CKD is not clear and there are few effective therapies. Using optical mapping techniques, we tested the hypothesis that mouse models of progressive diabetic kidney disease (DKD) exhibit enhanced ventricular arrhythmia incidence and underlying arrhythmia substrates. Compared to wild-type mice, both Leprdb/db eNOS−/− (2KO) and high fat diet plus low dose streptozotocin (HFD + STZ) mouse models of DKD experienced sudden death and greater arrhythmia inducibility, which was more common with isoproterenol than programmed electrical stimulation. 2KO mice demonstrated slowed conduction velocity, prolonged action potential duration (APD), and myocardial fibrosis; both 2KO and HFD + STZ mice exhibited arrhythmias and calcium dysregulation with isoproterenol challenge. Finally, circulating concentrations of the uremic toxin asymmetric dimethylarginine (ADMA) were elevated in 2KO mice. Incubation of human cardiac myocytes with ADMA prolonged APD, as also observed in 2KO mice hearts ex vivo. The present study elucidates an arrhythmia-associated mechanism of sudden death associated with DKD, which may lead to more effective treatments in the vulnerable DKD patient population.

Impact of Maturation on Myocardial Response to Ischemia and the Effectiveness of Remote Preconditioning in Male Rats.

Aging attenuates cardiac tolerance to ischemia/reperfusion (I/R) associated with defects in protective cell signaling, however, the onset of this phenotype has not been completely investigated. This study aimed to compare changes in response to I/R and the effects of remote ischemic preconditioning (RIPC) in the hearts of younger adult (3 months) and mature adult (6 months) male Wistar rats, with changes in selected proteins of protective signaling. Langendorff-perfused hearts were exposed to 30 min I/120 min R without or with prior three cycles of RIPC (pressure cuff inflation/deflation on the hind limb). Infarct size (IS), incidence of ventricular arrhythmias and recovery of contractile function (LVDP) served as the end points. In both age groups, left ventricular tissue samples were collected prior to ischemia (baseline) and after I/R, in non-RIPC controls and in RIPC groups to detect selected pro-survival proteins (Western blot). Maturation did not affect post-ischemic recovery of heart function (Left Ventricular Developed Pressure, LVDP), however, it increased IS and arrhythmogenesis accompanied by decreased levels and activity of several pro-survival proteins and by higher levels of pro-apoptotic proteins in the hearts of elder animals. RIPC reduced the occurrence of reperfusion-induced ventricular arrhythmias, IS and contractile dysfunction in younger animals, and this was preserved in the mature adults. RIPC did not increase phosphorylated protein kinase B (p-Akt)/total Akt ratio, endothelial nitric oxide synthase (eNOS) and protein kinase Cε (PKCε) prior to ischemia but only after I/R, while phosphorylated glycogen synthase kinase-3β (GSK3β) was increased (inactivated) before and after ischemia in both age groups coupled with decreased levels of pro-apoptotic markers. We assume that resistance of rat heart to I/R injury starts to already decline during maturation, and that RIPC may represent a clinically relevant cardioprotective intervention in the elder population.

Рівень маркерів системного запалення і клінічний перебіг стабільної ішемічної хвороби серця в пацієнтів зі стенозувальним атеросклерозом коронарних артерій та без нього

The aim – to investigate the relation between levels of inflammatory factors and clinical course of the ischemic heart disease with and without coronary atherosclerosis. Materials and methods. We examined 105 patients with stable ischemic heart disease (IHD), age 36 to 84 years (mean age 58.5 ± 9.47 years). There were 48.6 % (n = 51) men and 51.4 % (n = 54) women. Based on angiography data, patients were divided into two groups: group I – 53 patients with IHD and non-obstructive coronary arteries (INOCA), group II – 52 patients diagnosed with stable IHD with more than 50 % stenosis. In addition to general clinical methods of examination, the levels of interleukin-6 (IL-6) and highly sensitive C-reactive protein (hsCRP) were determined in all patients. The control group consisted of 20 healthy individuals compared by age and sex. Results. According to the results, it was found that in patients with IHD the level of IL-6 was significantly higher compared to the control, in group I: 4.40 [2.12–9.56] pg/ml and 2.46 [2.29–3.47] pg/ml, respectively (p = 0.027), and in group II – 4.15 [2.80–6.68] pg/ml, which also differed from the control group (p = 0.006). There was no significant difference in the level of IL-6 between groups of patients with IHD depending on the lesion of the coronary arteries (p = 0.99). Among patients with IHD, the level of IL-6 was increased in 40.7 % (n = 22) of patients with INOCA and 34.6 % (n = 18) in patients with stenotic atherosclerosis (group II) (p = 0.22). However, the proportion of women with elevated levels of IL-6 was higher in the INOCA (66.7 %) compared to women with stenotic atherosclerosis (26.7 %) (p = 0.033). Positive correlations were found between the level of IL-6 and the incidence of ventricular arrhythmias in patients of group I (r = 0.44, p = 0.025), as well as between IL-6 and positive cycling stress-test (r = 0.39, p = 0.01), IL-6 and hsCRP (r = 0.43, p = 0.004). According to the results of multivariate regression logistic analysis, an association was established in patients with INOCA between elevated levels of IL-6 and age, hsCRP, history of myocardial infarction and the number of affected vessels (p = 0.04, p = 0.01, p = 0.04, p = 0.037 respectively). Conclusions. Significant differences in the level of IL-6 were found in patients with IHD compared to the control group. It was found that in patients with elevated levels of IL-6, there was higher proportion of women in the INOCA group, compared to the patients with stenotic atherosclerosis. An association was established in patients with INOCA between elevated levels of IL-6 and age, history of myocardial infarction and the number of affected vessels. Key words: ischemic heart disease, INOCA, іnterleukin-6, highly sensitive C-reactive protein.

Phenotypic Expression, Natural History, and Risk Stratification of Cardiomyopathy Caused by Filamin C Truncating Variants.

Filamin C truncating variants (FLNCtv) cause a form of arrhythmogenic cardiomyopathy: the mode of presentation, natural history, and risk stratification of FLNCtv remain incompletely explored. We aimed to develop a risk profile for refractory heart failure and life-threatening arrhythmias in a multicenter cohort of FLNCtv carriers. FLNCtv carriers were identified from 10 tertiary care centers for genetic cardiomyopathies. Clinical and outcome data were compiled. Composite outcomes were all-cause mortality/heart transplantation/left ventricle assist device (D/HT/LVAD), nonarrhythmic death/HT/LVAD, and sudden cardiac death/major ventricular arrhythmias. Previously established cohorts of 46 patients with LMNA and 60 with DSP-related arrhythmogenic cardiomyopathies were used for prognostic comparison. Eighty-five patients carrying FLNCtv were included (42±15 years, 53% men, 45% probands). Phenotypes were heterogeneous at presentation: 49% dilated cardiomyopathy, 25% arrhythmogenic left dominant cardiomyopathy, 3% arrhythmogenic right ventricular cardiomyopathy. Left ventricular ejection fraction was <50% in 64% of carriers and 34% had right ventricular fractional area changes (RVFAC=(right ventricular end-diastolic area - right ventricular end-systolic area)/right ventricular end-diastolic area) <35%. During follow-up (median time 61 months), 19 (22%) carriers experienced D/HT/LVAD, 13 (15%) experienced nonarrhythmic death/HT/LVAD, and 23 (27%) experienced sudden cardiac death/major ventricular arrhythmias. The sudden cardiac death/major ventricular arrhythmias incidence of FLNCtv carriers did not significantly differ from LMNA carriers and DSP carriers. In FLNCtv carriers, left ventricular ejection fraction was associated with the risk of D/HT/LVAD and nonarrhythmic death/HT/LVAD. Among patients referred to tertiary referral centers, FLNCtv arrhythmogenic cardiomyopathy is phenotypically heterogeneous and characterized by a high risk of life-threatening arrhythmias, which does not seem to be associated with the severity of left ventricular dysfunction.

Impact of exercise capacity on the long-term incidence of atrial arrhythmias in heart failure

We sought to demonstrate the impact of improved peak exercise oxygen consumption (V̇O2) during maximal exercise testing after cardiac rehabilitation (CR) on the incidence of arrhythmias in patients with heart failure (HF). The present study comprised of 220 patients with HF, and peak V̇O2 was examined at 2 and 5 months after CR. Of the 220 patients, 110 (50%) had a low peak V̇O2 of < 14 mL/min/kg at 2 months. The peak V̇O2 improved in 86 of these 110 (78%) patients at 5 months after CR. During a median follow-up of 6 years, the patients with improvement in peak V̇O2, compared to those without peak V̇O2 improvement, had a lower rate of mortality (4% vs. 29%, log-rank, P < 0.001) and HF hospitalization (6 vs. 17%, log-rank, P = 0.044) and a lower incidence of new-onset atrial arrhythmias (9 vs. 27%, log-rank, P = 0.013), with no difference in the incidence of ventricular arrhythmias between groups (1 vs. 4%, log-rank, P = 0.309). The majority of deaths in the patients without an improved peak V̇O2 were because of cardiovascular events (73%), particularly progressive HF (55%). Early detection and management of atrial arrhythmias may improve outcomes in patients without peak V̇O2 improvement after CR.

Effect of dapagliflozin on ventricular arrhythmias, resuscitated cardiac arrest, or sudden death in DAPA-HF.

AimsThe aim of this study was to examine the effect of dapagliflozin on the incidence of ventricular arrhythmias and sudden death in patients with heart failure and reduced ejection fraction (HFrEF).Methods and resultsIn a post hoc analysis of DAPA-HF, we examined serious adverse event reports related to ventricular arrhythmias or cardiac arrest, in addition to adjudicated sudden death. The effect of dapagliflozin, compared with placebo, on the composite of the first occurrence of any serious ventricular arrhythmia, resuscitated cardiac arrest, or sudden death was examined using Cox proportional hazards models. A serious ventricular arrhythmia was reported in 115 (2.4%) of the 4744 patients in DAPA-HF (ventricular fibrillation in 15 patients, ventricular tachycardia in 86, ‘other’ ventricular arrhythmia/tachyarrhythmia in 12, and torsade de pointes in 2 patients). A total of 206 (41%) of the 500 cardiovascular deaths occurred suddenly. Eight patients survived resuscitation from cardiac arrest. Independent predictors of the composite outcome (first occurrence of any serious ventricular arrhythmia, resuscitated cardiac arrest or sudden death), ranked by chi-square value, were log-transformed N-terminal pro-B-type natriuretic peptide, history of ventricular arrhythmia, left ventricular ejection fraction, systolic blood pressure, history of myocardial infarction, male sex, body mass index, serum sodium concentration, non-white race, treatment with dapagliflozin, and cardiac resynchronization therapy. Of participants assigned to dapagliflozin, 140/2373 patients (5.9%) experienced the composite outcome compared with 175/2371 patients (7.4%) in the placebo group [hazard ratio 0.79 (95% confidence interval 0.63–0.99), P = 0.037], and the effect was consistent across each of the components of the composite outcome.ConclusionsDapagliflozin reduced the risk of any serious ventricular arrhythmia, cardiac arrest, or sudden death when added to conventional therapy in patients with HFrEF.Clinical trial registration ClinicalTrials.gov unique identifier: NCT03036124 (DAPA-HF).

Effect of age and sex on the incidence of ventricular arrhythmia in a rat model of acute ischemia

BackgroundThe impact of sex and age on the arrhythmic susceptibility within the setting of acute ischemia is masked by the fact that acute coronary events result from coronary artery disease appearing with age much earlier among men than among women. Methods and resultsLAD ligation or sham operations were performed in rats of both sexes at the age 3 and 24 months. An ECG was recorded continuously for 6 h after the operation. The number of early and late premature ventricular beats (PVBs), episodes of ventricular tachycardia (VT) and fibrillation (VF), heart rate, QRS, QT and Tpeak-Tend duration were analysed. Epicardial action potentials were recorded in vivo, Ca2+ signaling was evaluated in isolated cardiomyocytes, fibrosis and connexin-43 expression and localization were measured in the septum. PVBs, VT and VF episodes are much more common in older males than in young males and females independently from their age. Fibrosis with varying intensity in different muscle layers, hypertrophy of cardiomyocytes, reduced number of gap junctions and their appearance on the lateral myocyte membrane, QT prolongation, increase transmural dispersion of repolarisation and a decreased function of SERCA2a may increase the propensity to arrhythmia within the setting of acute ischemia. ConclusionWe show that the male sex, especially in case of older individuals is a strong predictor of increased arrhythmic susceptibility within the acute ischemia setting regardless of its impact on the occurrence of cardiovascular diseases. A personalized sex-dependent prevention treatment is needed to reduce the mortality in acute phases of myocardial infarction.

Blockade of NaV1.8 Increases the Susceptibility to Ventricular Arrhythmias During Acute Myocardial Infarction.

SCN10A/NaV1.8 may be associated with a lower risk of ventricular fibrillation in the setting of acute myocardial infarction (AMI), but if and by which mechanism NaV1.8 impacts on ventricular electrophysiology is still a matter of debate. The purpose of this study was to elucidate the contribution of NaV1.8 in ganglionated plexi (GP) to ventricular arrhythmias in the AMI model. Twenty beagles were randomized to either the A-803467 group (n = 10) or the control group (n = 10). NaV1.8 blocker (A-803467, 1 μmol/0.5 mL per GP) or DMSO (0.5 mL per GP) was injected into four major GPs. Ventricular effective refractory period, APD90, ventricular fibrillation threshold, and the incidence of ventricular arrhythmias were measured 1 h after left anterior descending coronary artery occlusion. A-803467 significantly shortened ventricular effective refractory period, APD90, and ventricular fibrillation threshold compared to control. In the A-803467 group, the incidence of ventricular arrhythmias was significantly higher compared to control. A-803467 suppressed the slowing of heart rate response to high-frequency electrical stimulation of the anterior right GP, suggesting that A-803467 could inhibit GP activity. SCN10A/NaV1.8 was readily detected in GPs, but was not validated in ventricles by quantitative RT-PCR, western blot and immunohistochemistry. While SCN10A/NaV1.8 is detectible in canine GPs but not in ventricles, blockade of NaV1.8 in GP increases the incidence of ventricular arrhythmias in AMI hearts. Our study shows for the first time an influence of SCN10A/NaV1.8 on the regulation of ventricular arrhythmogenesis via modulating GP activity in the AMI model.

Heart Rate Variability as an Indicator of Autonomic Nervous System Disturbance in Behcet's Disease.

BackgroundBehçet’s disease (BD) is a multisystemic vasculiti where cardiac involvement is not common. Previous studies have shown that the incidence of ventricular arrhythmia and sudden cardiac death (SCD) is higher in patients with BD than in the healthy population. Among various possible explanations, autonomic nervous system (ANS) dysfunction has been suggested. Few studies have evaluated ANS function in patients with BD, and the results obtained are controversial.ObjectiveWe aimed to assess cardiac autonomic function by heart rate variability (HRV) in patients with BD; to evaluate circadian changes in HRV; and to study the relationship between HRV parameters and disease parameters.MethodsThirty-six patients with Behçet’s disease (median age 42 years, 28 men) and 36 age- and sex-matched healthy volunteers were included. HRV analyses were performed in the time and frequency domains for the entire 24-hour period and for the daytime and nighttime periods. BD activity was studied with Behcet’s disease current activity form (BDCAF).ResultsPatients with BD had significantly lower values of SDNN compared to controls. PNN50, RMSSD, and HF components mean values were significantly reduced in patients than in controls implying parasympathetic impairment. LF was comparable between the two groups, whereas LF/HF ratio was significantly higher in BD group. The circadian rhythm of HRV was preserved in patient group. There was no significant correlation of CRP or disease duration with HRV indices in Behçet’s subjects. BDCAF score was found to be negatively correlated with LF/HF.ConclusionPatients with BD, despite no cardiovascular involvement, have reduced parasympathetic activity compared with controls. However, circadian rhythms of autonomic function were preserved. As known, there is strong evidence for the role of the ANS in the pathogenesis of ventricular arrhythmias. Thus, being a practical tool, HRV can be an interesting approach for the rhythmic follow-up of BD patients.

Severity of spleep apnea syndrome and life-threatening tachyarrhythmias in patients with implantable cardioverter defibrillator.

Sleep apnea syndrome (SAS) has been reported to be associated with a higher incidence of ventricular arrhythmias. The aim of this study was twofold: (1) to investigate whether in SAS patients receiving an implantable cardioverter defibrillator (ICD) the severity of SAS was associated with the occurrence of ventricular arrhythmias; (2) to assess whether changes in nocturnal apnoic/hypopnoic episodes may favor the occurrence of life-threatening arrhythmias, that is, sustained ventricular tachycardia (VT)/fibrillation (VF), requiring ICD intervention. We enrolled 46 patients with documented SAS at polysomnography (apnea/hypopnea index [AHI]>5) who also had a left ventricle ejection fraction (LVEF)<35% and, according to primary prevention indications, implanted an ICD (Boston Scientific Incepta) able to daily monitor apnoic/hypopnoic episodes occurring during sleep. Patients were followed at 3-month intervals. At a mean follow-up of 18 months, 21 episodes of sustained VT/FV requiring ICD intervention were documented in eight patients (17.4%). Baseline AHI was significantly higher in patients with compared to those without ICD intervention. ICD interventions, however, were not preceded by any worsening of apnoic/hypopnoic episodes. The respiratory disturbance index (RDI) of the week during the event, indeed, was not different from that recorded during the previous 2weeks (25.4 ± 11, 25.6 ± 10 and 25.1 ± 10, respectively; p=.9). In patients with SAS who received an ICD for primary prevention of sudden death, those with ICD interventions showed a more severe form of the disease at baseline. ICD interventions, however, were not preceded by any significant changes in SAS severity.

Premature ventricular contraction increases the risk of heart failure and ventricular tachyarrhythmia

Premature ventricular contraction (PVC), a common arrhythmia affecting 1–2% of the general population, has been considered to have a benign clinical course. However, people with PVC often develop heart failure and ventricular arrhythmias such as ventricular tachycardia. We aimed to clarify the risk of heart failure and lethal ventricular arrhythmias in people with PVC. The Korean National Health Insurance Service database was used for this study. People who underwent nationwide health check-ups in 2009 were enrolled in this study and clinical follow-up data until December 2018 were analyzed. Newly diagnosed PVC in 2009 (≥ 1 inpatient or outpatient claim) were identified and cumulative incidence of heart failure (≥ 1 inpatient claim) and ventricular arrhythmias (≥ 1 inpatient or outpatient claim) were compared. A total of 4515 people were first diagnosed with PVC in 2009 among 9,743,582 people without prior history of PVC, heart failure, or ventricular arrhythmias. People with newly diagnosed PVC in 2009 had a significantly higher incidence of heart failure compared to those without PVC [adjusted hazard ratio (HR) 1.371; 95% confidence interval (CI) 1.177–1.598; p < 0.001]. Significant interaction was observed between age and PVC with young age people at greater risk of developing heart failure for having PVC. The incidence of ventricular arrhythmia was also significantly increased in people with PVC (HR 5.588; 95% CI 4.553–6.859; p < 0.001). Age and chronic kidney disease had significant interactions with PVC. In conclusion, the incidence of heart failure and ventricular arrhythmia was significantly increased in people with PVC. Outpatient follow-up of people with PVC can be helpful to detect early signs of heart failure or advanced forms of ventricular arrhythmia.

Long-Term Prognostic Significance of Ventricular Repolarization Dispersion in Patients with Cardiac Sarcoidosis

Cardiac sarcoidosis (CS) is frequently complicated by fatal ventricular arrhythmias. T-peak to T-end interval to QT interval ratio (TpTe/QT) on electrocardiograms (ECG) was proposed as a marker of ventricular repolarization dispersion. Although this ratio could be associated with the incidence of ventricular arrhythmias in cardiovascular diseases, its prognostic implication in patients with CS is unclear. We sought to investigate whether TpTe/QT was associated with long-term clinical outcomes in patients with CS. Ninety consecutive patients with CS in 2 tertiary hospitals who had ECG data before initiation of immunosuppressive therapy between November 1995 and March 2019 were examined. The primary outcome was a composite of advanced atrioventricular block, ventricular tachycardia or ventricular fibrillation (VT/VF), heart failure hospitalization, and all-cause death. During a median follow-up period of 4.70 (interquartile range 2.06-7.23) years, the primary outcome occurred in 21 patients (23.3%). Survival analyses revealed that the primary outcome (p < 0.001), especially VT/VF or sudden cardiac death (p=0.002), occurred more frequently in patients with higher TpTe/QT (≥ 0.242, the median) than in those with lower TpTe/QT. Multivariable Cox regression analysis showed that a higher TpTe/QT was independently associated with increased subsequent risk of adverse events (hazard ratio1.11, 95% confidence interval 1.03-1.20, p=0.008) even after adjustment for the significant covariates. In conclusion, a higher TpTe/QT was associated with worse long-term clinical outcomes, especially fatal ventricular arrhythmic events, in patients with cardiac sarcoidosis, suggesting the importance of assessing TpTe/QT as a surrogate for risk stratification in these patients.

Risk Factors Associated with the Incidence of Ventricular Arrhythmias Complicating Acute Myocardial Infarction and Prognosis Analysis

Ventricular arrhythmias (VTA) usually occur following acute myocardial infarction (AMI). However, risk factors for VTA attack after AMI have been not well-recognized. The purpose of the study is to identify risk factors associated with the incidence of VTA complicating AMI. A total of 200 patients with AMI who were admitted to our hospital from February 2018 to February 2020 were retrospectively analyzed. These 200 patients were classified into a non-VTA group ( n = 140 ) and a VTA group ( n = 60 ) based on the occurrence of VTA within 24 after AMI. Patients in the VTA group were older than those in the non-VTA group. The VTA group had more numbers of WBCs and neutrophils than the non-VTA group. The level of serum potassium was lower, but the levels of cTnT and CK-MB were higher in the VTA group than in the non-VTA group. The VTA group presented an increase in proportions of anterior MI, TpTe, and proportions of Killip classification ≥ class II but a decline in LVEF when comparable to the non-VTA group. The two groups were not significantly different concerning other variables including sex, tobacco use, alcohol consumption, diabetes mellitus, hypertension, heart rate, Scr, SUA, BUN, PTL counts, TC, TG, HDL-C, LDL-C, D-dimer, BNP, LVS, LVP, and LVEDd. The levels of hsCRP, endothelin-1, and TNF-α were remarkably higher in the VTA group than in the non-VTA group ( P &lt; 0.001 ). Multivariate logistic regression analysis was performed, with clinical variables including age, WBCs, neutrophils, serum potassium, cTnT, CK-MB, hsCRP, endothelin-1, TNF-α, anterior MI, TpTe, proportions of Killip classification ≥ class II, and LVEF as an independent variable and with the occurrence of VTA as a dependent variable. It was revealed that serum potassium, cTnT, CK-MB, hsCRP, endothelin-1, TpTe, proportions of Killip classification ≥ class II, and LVEF were independent risk factors of VTA complicating AMI. Compared with the non-VTA group, the incidence rate of simple left heart failure, total heart failure, stroke, and dyslipidemia in the VTA group was significantly higher than those in the non-VTA group ( P &lt; 0.05 ). It was found that the proportion of all-cause deaths within one year outside the hospital was higher in the VAT group than in the non-VAT group ( P &lt; 0.05 ). Collectively, the study demonstrates serum potassium, cTnT, CK-MB, hsCRP, endothelin-1, TpTe, proportions of Killip classification ≥ class II, and LVEF were independent risk factors of VTA complicating AMI.