Occurrence Of Ventricular Arrhythmias Research Articles

Characteristics and Prognostic Relevance of Ventricular Arrhythmia in Patients with Myocarditis.

Myocarditis is characterized by various clinical manifestations, with ventricular arrhythmia (VA) as a frequent symptom at initial presentation. Here, we investigated characteristics and prognostic relevance of VA in patients with myocarditis. The study population consisted of 76 patients with myocarditis, verified by biopsy and/or cardiac magnetic resonance (CMR) imaging, including 38 consecutive patients with VA (45 ± 3 years, 68% male) vs. 38 patients without VA (NVA) (38 ± 2 years, 84% male) serving as a control group. VA was monomorphic ventricular tachycardia in 55% of patients, premature ventricular complexes in 50% and ventricular fibrillation in 29%. The left ventricular ejection fraction at baseline was 47 ± 2% vs. 40 ± 3% in VA vs. NVA patients (p = 0.069). CMR showed late gadolinium enhancement more often in VA patients (94% vs. 69%; p = 0.016), incorporating 17.6 ± 1.8% vs. 8.2 ± 1.3% of myocardial mass (p < 0.001). Radiofrequency catheter ablation for VA was initially performed in nine (24%) patients, of whom five remained free from any recurrence over 24 ± 3 months. Taken together, in patients with myocarditis, reduced left ventricular ejection fraction does not predict VA occurrence but CMR shows late gadolinium enhancement more frequently and to a larger extent in VA than in NVA patients, potentially guiding catheter ablation as a reasonable treatment of VA in this population.

Usefulness of the MADIT-ICD Benefit Score in a Large Mixed Patient Cohort of Primary Prevention of Sudden Cardiac Death.

Background: Decision-making in primary prevention is not always trivial and many clinical scenarios are not reflected in current guidelines. To help evaluate a patient’s individual risk, a new score to predict the benefit of an implantable defibrillator (ICD) for primary prevention, the MADIT-ICD benefit score, has recently been proposed. The score tries to predict occurrence of ventricular arrhythmias and non-arrhythmic death based on data from four previous MADIT trials. We aimed at examining its usefulness in a large single-center register of S-ICD patients with various underlying cardiomyopathies. Methods and results: All S-ICD patients with a primary preventive indication for ICD implantation from our large single-center database were included in the analysis (n = 173). During a follow-up of 1227 ± 978 days, 27 patients developed sustained ventricular arrhythmias, while 6 patients died for non-arrhythmic reasons. There was a significant correlation for patients with ischemic cardiomyopathy (ICM) (n = 29, p = 0.04) to the occurrence of ventricular arrhythmia. However, the occurrence of ventricular arrhythmias could not sufficiently be predicted by the MADIT-ICD VT/VF score (p = 0.3) in patients with (n = 142, p = 0.19) as well as patients without structural heart disease (n = 31, p = 0.88) and patients with LV-EF < 35%. Of the risk factors included in the risk score calculation, only non-sustained ventricular tachycardias were significantly associated with sustained ventricular arrhythmias (p = 0.02). Of note, non-arrhythmic death could effectively be predicted by the proposed non-arrhythmic mortality score as part of the benefit score (p = 0.001, r = 0.3) also mainly driven by ICM patients. Age, diabetes mellitus, and a BMI < 23 kg/m2 were key predictors of non-arrhythmic death implemented in the score. Conclusion: The MADIT-ICD benefit score adds a new option to evaluate expected benefit of ICD implantation for primary prevention. In a large S-ICD cohort of primary prevention, the value of the score was limited to patients with ischemic cardiomyopathy. Future research should evaluate the performance of the score in different subgroups and compare it to other risk scores to assess its value for daily clinical practice.

Ventricular tachycardia and acute myocardial infarction induced by coronary artery spasm in patient without coronary artery disease

Coronary artery spasm, marked by coronary vasoconstriction, is one of the etiologies of myocardial ischemia, often presenting as vasospastic angina. Vasospastic angina is diagnosed when angina which predominantly occurs at rest, is accompanied by ST-segment changes in ECG, or in the setting of borderline ECG changes, a positive provocation test through coronary angiography is required. Although coronary artery spasms could manifest in wide clinical settings, the occurrence of ventricular arrhythmias and acute myocardial infarction solely caused by spasms without evidence of prior coronary artery disease is rare. This case report is about a 46-year-old man who presented with ventricular tachycardia and acute myocardial infarction that later was found to be secondary to coronary vasospasm observed directly through coronary angiography. We aim to emphasize the importance of coronary artery spasms as the etiology of malignant ventricular arrhythmias and acute myocardial infarction manifestation. Optimization in treatment and prevention shall reduce future life-threatening complications of coronary artery spasms.

A narrative review on sacubitril/valsartan and ventricular arrhythmias.

Sacubitril/valsartan, the first angiotensin receptor neprilysin inhibitor approved by the Food and Drug Administration for marketing, has been shown to reduce the risk of cardiovascular death or heart failure hospitalization and improve symptoms in patients with chronic heart failure with a reduced ejection fraction. However, some researchers have also found that sacubitril/valsartan has an antiarrhythmic effect. The mechanism by which sacubitril/valsartan reduces the mortality associated with malignant ventricular arrhythmias is not precise. Many studies have concluded that ventricular arrhythmia is associated with a reduction in myocardial fibrosis. This article reviews the current understanding of the effects of sacubitril/valsartan on the reduction of ventricular arrhythmia and explains its possible mechanisms. The results of this study suggest that sacubitril/valsartan reduces the occurrence of appropriate implantable cardioverter-defibrillator shocks. Meanwhile, sacubitril/valsartan may reduce the occurrence of ventricular arrhythmias by affecting 3 pathways of B-type natriuretic peptide, Angiotensin II, and Bradykinin. The conclusion of this study is that sacubitril/valsartan reduces the number of implantable cardioverter-defibrillator shocks and ventricular arrhythmias in heart failure with reduced ejection fraction patients.

Depolarization and repolarization dynamics after His-bundle pacing: Comparison with right ventricular pacing and native ventricular conduction.

BackgroundThe current study aimed to evaluate changes in electrical depolarization and repolarization parameters after His‐bundle pacing (HBP) compared with right ventricular pacing (RVP) and its association with ventricular arrhythmia (VA).MethodsForty‐one patients (13 with HBP, 14 with RVP, and 14 controls [AAI mode]) were evaluated. After continuous pacing algorithm, QRS duration, QT interval, QTc, JT interval, T‐peak to T‐end (Tpe), and Tpe/QT ratio were measured on electrocardiography at baseline and 1 week, 1 month, and 6 months postoperatively. We investigated VA occurrence and adverse events after implantation.ResultsAt 6 months, QRS duration was significantly shorter in the HBP (121.6 ± 15.6 ms) than in the RVP (150.1 ± 14.9 ms) group. The QT intervals were lower in the HBP (424.0 ± 40.9 ms) and control (405.9 ± 23.0 ms) groups than in the RVP (453.0 ± 40.2 ms) group. The Tpe and Tpe/QT ratios at 6 months differed significantly between the HBP and RVP groups (Tpe, 69.8 ± 19.7 ms vs 87.4 ± 11.9 ms and Tpe/QT, 0.16 ± 0.03 vs 0.19 ± 0.02, respectively). The Tpe and Tpe/QT ratios were similarly shortened in the HBP and control groups. VA occurred less frequently in the HBP (15%) and control (7.1%) groups than in the RVP (50%) group (p = 0.020). The non‐RVP group showed significantly lower rates of VA and major adverse events than the RVP group. Patients with VA demonstrated significantly longer QRS duration, QT interval, Tpe, and Tpe/QT at 6 months than those without VA.ConclusionHBP showed better depolarization and repolarization stability than RVP.

Serum uric acid and the risk of ventricular arrhythmias: a systematic review.

Uric acid (UA) is the end product of purine degradation in humans. It promotes inflammation via activation of pro-inflammatory cytokines and increases oxidative stress. The serum uric acid level has emerged as an independent risk factor of cardiovascular disease such as ventricular arrhythmias (VA). Here we had done a systematic review to assess the association between serum UA levels and the occurrence of VA. This systematic review included a total of four clinical studies with 99.383 patients for analysis. The scientific quality of all four studies was good. Three studies showed that serum uric acid levels were associated with VA in many populations. In contrast, one study with a large sample size evaluated that serum uric acid increases premature ventricle contraction prevalence. A significant association between serum uric acid level and VA was found in four studies (p&lt;0.01; p&lt;0.101; p=0.002; p=0.008). In conclusion, this systematic review shows an association between serum UA levels and VA.

Incessant Malignant Ventricular Arrhythmia in a Patient with Advanced Heart Failure: A Case Report

Introduction The occurrence of refractory ventricular arrhythmia in patients with heart failure (HF) is a therapeutic dilemma. These patients, especially in the presence of advanced disease, may experience multiple triggering factors for ventricular arrhythmia, such as myocardial fibrosis, ischemia, hydroelectrolytic disorders, ventricular distention, the arrhythmogenic potential of drugs, and the underlying disease itself.– Conversely, sustained ventricular arrhythmias cause hemodynamic compromise, resulting in further ischemia and ventricular distension. This can lead to a vicious cycle of hemodynamic worsening with an increasingly [...]

M6A methyltransferase METTL3 participated in sympathetic neural remodeling post-MI via the TRAF6/NF-κB pathway and ROS production

ObjectiveSudden cardiac death caused by ventricular arrhythmias (VAs) is the main cause of high mortality in patients with myocardial infarction (MI). Sympathetic neural remodeling caused by inflammation after MI is closely associated with the occurrence of VAs. METTL3, the earliest identified m6A methyltransferase, is critical in mediating inflammatory responses. Our aim was to investigate whether the m6A methyltransferase METTL3 was involved in sympathetic remodeling post-MI and its specific mechanism. Methods and resultsA rat MI model was established via left coronary artery ligation. The expression of METTL3, TRAF6, NOX2, and NF-κB increased at 3 days and remained elevated at 7 days after MI, as determined via Western blotting. METTL3 was primarily present in macrophages, as determined via immunofluorescence. Intramyocardial injection of lentivirus carrying METTL3-shRNA inhibited METTL3 expression in vivo. Methylated immunoprecipitation-qPCR determined the METTL3 knockdown inhibited the m6A level of TRAF6 mRNA 3′-UTR. The co-immunoprecipitation experiment proved that METTL3 combines with TRAF6. Western blotting showed that silencing METTL3 inhibited TRAF6 level, NF-κB activation, and ROS production; decreased cytokine release (TNF-α and IL-1β); and downregulated nerve growth factor expression. Finally, METTL3 knockdown reduced sympathetic remodeling after MI, as determined via immunofluorescence assays of tyrosine hydroxylase and growth-associated protein 43. Programmed electrical stimulation, renal sympathetic nerve activity recording, and haemodynamic measurements showed that METTL3 inhibition decreased sympathetic activity and improved cardiac function. ConclusionsDownregulation of METTL3 expression attenuated the excessive sympathetic neural remodeling induced by MI, further reducing the incidence of VAs and improving cardiac function. This was partly associated with the inhibition of the TRAF6/NF-κB pathway and ROS production.

The peri-infarct gray zone of myocardial fibrosis is a better predictor of ventricular arrhythmias than dense core fibrosis in patients with previous myocardial infarction

Abstract Funding Acknowledgements Type of funding sources: None. Background Current sudden cardiac death (SCD) risk stratification relies heavily on left ventricular ejection fraction (LVEF), but markers to refine risk assessment are needed. Dense core fibrosis (DCF) and peri-infarct "gray zone" of myocardial fibrosis (GZF) on late gadolinium enhancement (LGE) cardiac magnetic resonance (CMR) have been proposed as potential arrhythmogenic substrates. The aim of our study was to determine whether DCF and GZF could predict the occurrence of ventricular arrhythmias in patients with previous myocardial infarction. Methods We performed a single centre retrospective study enrolling consecutive patients with previous myocardial infarction undergoing CMR before implantable cardioverter-defibrillator (ICD) implantation. Areas of LGE were subdivided into "core" DCF and "peri-infarct" GZF zones based on signal intensity (&amp;gt;5 SD, and 2-5 SD above the mean of reference myocardium, respectively). The primary endpoint was a composite of sudden arrhythmic death, appropriate ICD shock, ventricular fibrillation (VF), or sustained ventricular tachycardia (VT) as detected by the device. Results A total of 88 patients (median age 61 years [IQR 54-73], 84% male, median LVEF 30% [IQR 23-36%], 14% secondary prevention) were included. During a median follow-up of 23 months [IQR 9-38], 13 patients reached the primary endpoint (10 appropriate ICD shock, 2 sustained VT or VF, and 1 sudden arrhythmic death). Patients who attained the primary endpoint had similar DCF (30.4g ± 14.7 vs. 28.0g ± 15.3; P = 0.601) but a greater amount of GZF (18.1g ± 9.6 vs. 11.9g ± 6.7; P = 0.005). On univariate analysis, GZF was associated with the composite endpoint (HR: 1.09 per gram; 95%CI: 1.02-1.15; P = 0.006), whereas DCF was not (HR: 1.01 per gram; 95%CI: 0.98-1.05; P = 0.571). After adjustment for LVEF, GZF remained independently associated with the primary endpoint (adjusted HR: 1.06 per gram; 95% CI: 1.01-1.12; P = 0.035). Decision tree analysis identified 11.9g of GZF as the best cut-off to predict life-threatening arrhythmic events. The primary endpoint occurred in 11 out of the 35 patients (31.4%) with GZF ≥11.9g, but in only 2 of the 53 patients (3.8%) with GZF &amp;lt;11.9g – Figure. Conclusions The extent of peri-infarct GZF seems to be a better predictor of ventricular arrhythmias than DCF. This parameter may be useful to identify a subgroup of patients with previous myocardial infarction at increased risk of life-threatening arrhythmic events.

P300 ACUTE MYOCARDITIS COMPLICATED BY VENTRICULAR ARRHYTHMIAS

Abstract Background Many kinds of arrhythmias may occur in patients with myocarditis at any stage of the disease. However, as compared to the other clinical presentations, arrhythmic myocarditis has been poorly described in literature. Case Report A 20–year–old girl, without CVRF or comorbidities, presented at the ED because of palpitations and epigastric pain irradiated to left arm. 12–lead ECG evinced elevated HR and aspecific repolarization abnormalities. Blood samples showed high cTn value and normal PCR value. Echocardiography showed a preserved LVEF, without abnormalities. Patient was hospitalized with a diagnosis of suspect acute myocarditis. Following hospital stay has been complicated by recurrent episodes of chest pain with concomitant increase of cTn that finally had presented a sinusoidal trend (peak 12830ng/L). At the same time, continuous ECG monitoring has been showing frequent but short term ventricular extrasystole activity, so B–blocker therapy was optimized. On ECG monitoring, appearance of short runs of asymptomatic mono– and polymorphic NSVT and after a few days appearance of polymorphic NSVT “torsade de pointes” like, symptomatic for presyncope. New changes in kinetics appear on the echocardiogram: hypokinesia of medio–apical segments of lateral, anterior wall septum. Therapy with metoprolol and lidocaine iv was started with subsequent stabilization of the rhythm. CMR presented data suggestive of myocarditis. Patient performed several BEM at different time and centers: diagnostic signs of myocarditis were not be found. Autoimmune and infectious disease screening, abdominal echography and a PET TC total body were been performed to research a potential etiology, without positive result. Patient has been discharged with wearable defibrillator and we waited for the ICD implantation in secondary prevention. Follow–up CMR showed a resolution of inflammation and no signs of fibrosis. Blood samples did not demonstrate a rise of cTn. After discharged, she has not had news onset of ventricular arrhythmias. Conclusion The mechanisms underlying the occurrence of ventricular arrhythmias during myocardial inflammation are less clear. Arrhythmias usually being self–limited with no recurrences that follow the acute phase. Management of acute life–threatening arrhythmias is generally supportive and there is a lack of evidence to support the use of specific antiarrhythmic agents. Wearable life vest has been presented as a possible therapeutic option.

Prevalence of exercise-induced arrhythmias in young athletes with fragmented QRS pattern in lead V1

Abstract Funding Acknowledgements Type of funding sources: None. Background Resting 12-lead electrocardiogram (ECG) in apparently health athletes has specific pattern, typically associate to heart remodelling in response to regular exercise. (1,2) Moreover, these adaptations were correlated to typical ventricular arrhythmias, not associated with underlying cardiac abnormalities.(3) Recently, also fragmented QRS complex in lead V1 (fQRSV1), representing right ventricular (RV) activation, seems related to training-induced RV remodelling in athletes, where its prevalence is greater.(4) Purpose Evaluate presence of fQRSV1pattern at resting ECG in a population of young athletes and its relationship with training-associated structural heart adaptations and exercise-induced ventricular arrhythmias. Methods This study retrospectively enrolled subjects who consecutively undergo to annual pre-participation screening and also to transthoracic echocardiography assessment, from January 2015 to September 2020. For each participant, medical history, physical examination, resting ECG, maximal standardized exercise test and echocardiographic evaluation were collected. All ECG were reviewed by two independent physicians to evaluate fQRSV1 pattern. Results 684 young athletes (mean age 14.87±1.96 years, 36% female) were included and the overall prevalence of fQRSV1was 27%. Figure 1 shows an example of fQRSV1 pattern. Principal subject characteristics and evaluations data are shown in Table 1. fQRSV1 subjects presented a significantly wider QRS interval (p=0.004) and lower heart rate at rest (p=0.001). Exercise workload expressed in METs and exercise duration were higher in subjects with fQRSV1 (p=0.002 and p=0.023, respectively). Echocardiographic data showed that subjects with fQRSV1differ in morphological and functional right ventricular (RV) characteristics, especially had a higher indexed RV end diastolic diameter (p=0.019) and higher TAPSE (p=0.013). Patients with fQRSV1did not show an increased occurrence of supraventricular or ventricular arrhythmias, regardless of morphology, neither for isolated nor for repetitive events. Conclusion Overall prevalence of fQRSV1 pattern in young athletes is comparable with the one studied in other population of adult athletes in previous studies. Adolescent athletes with fQRSV1 present structural heart characteristic that differ from subjects without this ECG pattern, especially in RV feature. No differences in prevalence of any type of exercise-induced arrhythmias was shown, especially in common ventricular arrhythmias consistent with origin from the right ventricular outflow tract, previously described in healthy athletes.

Clinical Applications of FDG-PET Scan in Arrhythmic Myocarditis

Background18F-fluorodeoxyglucose positron emission tomography (FDG-PET) scan has no recognized role in diagnosis, prognosis, and disease monitoring in patients with arrhythmic myocarditis. ObjectivesThe purpose of this study was to investigate the value of FDG-PET scan in arrhythmic myocarditis. MethodsThe authors enrolled 75 consecutive patients (age 47 ± 14 years, 65% men) undergoing FDG-PET scan for arrhythmic myocarditis. Myocarditis was diagnosed by endomyocardial biopsy (EMB) and, whenever applicable, cardiac magnetic resonance (CMR). ResultsIndications for FDG-PET scan included either contraindication to CMR (n = 50) or mismatch between CMR and EMB (n = 25). Overall, 50 patients (67%) had positive FDG-PET. Sensitivity was 75% referring to EMB, and 73% to CMR. Specificity was 67% referring to EMB, and 59% to CMR. FDG-PET accuracy was lower in the presence of borderline myocarditis, and either late (>30 days) or on-immunosuppression FDG-PET scanning. Anteroseptal distribution pattern, found in 12 of 50 (24%) patients including 7 of 7 cardiac sarcoidosis cases, was associated with greater occurrence of ventricular arrhythmias and atrioventricular blocks in 4.2 ± 1.7 years of follow-up (10 of 12 vs 7 of 38, and 7 of 12 vs 0 of 38, respectively; both P < 0.001). In 39 patients (52%), FDG-PET was repeated by 13 ± 2 months, allowing immunosuppression withdrawal after FDG uptake normalization either by first (76%) or second reassessment (24%). ConclusionsFDG-PET scan may be a clinically useful diagnostic technique in arrhythmic myocarditis, in particular when CMR is unsuitable because of irregular heartbeat or implantable cardioverter-defibrillator–related artifacts. Anteroseptal FDG distribution is associated with a worse arrhythmic outcome and should raise the suspicion of cardiac sarcoidosis. During follow-up, repeated FDG-PET allows myocarditis monitoring to guide immunosuppression withdrawal.

PO-626-04 THE PERI-INFARCT “GRAY ZONE” OF MYOCARDIAL FIBROSIS IS A BETTER PREDICTOR OF VENTRICULAR ARRHYTHMIAS THAN DENSE CORE FIBROSIS IN PATIENTS WITH PREVIOUS MYOCARDIAL INFARCTION

Current sudden cardiac death (SCD) risk stratification relies heavily on left ventricular ejection fraction (LVEF), but markers to refine risk assessment are needed. Dense core fibrosis (DCF) and peri-infarct “gray zone” of myocardial fibrosis (GZF) on late gadolinium enhancement (LGE) cardiac magnetic resonance (CMR) have been proposed as arrhythmogenic substrates. We aimed to determine whether DCF and GZF could predict the occurrence of ventricular arrhythmias in patients with previous myocardial infarction. We performed a single centre retrospective study enrolling consecutive patients with previous myocardial infarction undergoing CMR before implantable cardioverter-defibrillator (ICD) implantation. Areas of LGE were subdivided into “core” DCF and “peri-infarct” GZF zones based on signal intensity (>5 SD, and 2-5 SD above the mean of reference myocardium, respectively). The primary endpoint was a composite of sudden arrhythmic death, appropriate ICD shock, ventricular fibrillation (VF), or sustained ventricular tachycardia (VT) as detected by the device. A total of 88 patients (median age 61 years [IQR 54-73], 84% male, median LVEF 30% [IQR 23-36%]) were included. During a median follow-up of 23 months [IQR 9-38], 13 patients reached the primary endpoint. Patients who attained the primary endpoint had similar DCF (30.4g ± 14.7 vs. 28.0g ± 15.3; P = 0.601) but a greater amount of GZF (18.1g ± 9.6 vs. 11.9g ± 6.7; P = 0.005). On univariate analysis, GZF was associated with the composite endpoint (HR: 1.09 per gram; 95%CI: 1.02-1.15; P=0.006), whereas DCF was not (HR: 1.01 per gram; 95%CI: 0.98-1.05; P=0.571). After adjustment for LVEF, GZF remained independently associated with the primary endpoint (adjusted HR: 1.06 per gram; 95% CI: 1.01-1.12; P=0.035). Decision tree analysis identified 11.9g of GZF as the best cut-off to predict arrhythmic events. The primary endpoint occurred in 11 out of the 35 patients (31.4%) with GZF ≥11.9g, but in only 2 of the 53 patients (3.8%) with GZF <11.9g - Figure. The extent of peri-infarct GZF seems to be a better predictor of ventricular arrhythmias than DCF. This parameter may be useful to identify a subgroup of patients with previous myocardial infarction at increased risk of life-threatening arrhythmic events.

Effect of high-throughput screening of circRNA01724 on a rat model of myocardial ischemia ventricular arrhythmia.

BackgroundIt is considered that circRNA can participate in regulating the occurrence and effects of ventricular arrhythmia (VA) through competing endogenous RNA (ceRNA) mechanism, regulating pre-mRNA and regulating parental gene expression. Therefore, we used animal modeling and high-throughput differential screening to screen out circRNA related to VA and study its possible mechanism of action on VA.MethodsThe rat model of myocardial ischemia VA was established. High-throughput screening of the differentiated circRNA was conducted and verified by real-time quantitative polymerase chain reaction (qRT-PCR) and Western blot. Lv-circRNA01724 lentivirus was constructed using molecular biology. Primary isolation of the rat cardiomyocytes, hypoxia modeling, Lv-circRNA01724 transfection, mode of action verification, and dual luciferase detection of circRNA01724 and miR-323-5p was performed.ResultsThrough qRT-PCR verification of circRNA01724, circRNA02230, circRNA02088, miR-323-5p, miR-330-5p, and miR-324-3p expressions, circRNA01724 was selected as the research object. Detection by Western blot showed significantly lower Cx43, ZO-1, and α-catenin expressions in rat myocardial tissue in the model group compared with the control group at 1, 7, 14, and 28 days old. On identification of the isolated primary rat cardiomyocytes by immunofluorescence, the α-SMA characteristic protein expression indicated that the isolation was successful. Verification of rat cardiomyocytes transfected with Lv-circRNA01724 suggested overexpression in cells. The miR-323-5p was also highly expressed in the rat cardiomyocyte hypoxia model following Lv-circRNA01724 transfection. Detection by flow cytometry showed that modeling of the transfected Lv-circRNA01724 had a significant increased apoptotic rate. Detection by Western blot showed that modeling of the transfected Lv-circRNA01724 cells had significantly decreased Cx43, ZO-1, and α-catenin compared with the model group.ConclusionsHigh-throughput screening of circRNA01724 can promote the apoptosis of hypoxic cardiomyocytes, which is related to the rat model of myocardial ischemia VA and may be a potential target for the treatment of VA.

Predictors of Hospital Admissions for Ventricular Arrhythmia or Cardiac Arrest in Patients With Cardiomyopathy

Although ventricular dysfunction is associated with the occurrence of ventricular arrhythmia (VA), most patients with cardiomyopathy do not experience VA. We therefore investigated other predictors of VA in a large contemporary cohort of patients with cardiomyopathy. All patients at a large academic medical system with left ventricular ejection fraction (LVEF) ≤50% were enrolled at the time of first documented low LVEF. Predictors of hospital admission for VA were examined using multivariable Cox models. The incidence of implantable defibrillator (ICD) placement was also examined. A total of 18,003 patients were enrolled. Over a median follow-up of 3.35years, 389 patients (2.2%) were admitted for VA (304 of 12,037 [2.5%] among patients with LVEF ≤35% vs 85 of 5,966 [1.4%] among those with LVEF 36% to 50%). Predictors of VA hospitalization included lower LVEF (hazard ratio (HR)=1.43 per 10% decrease, p <0.001), the presence of an ICD at baseline (HR=1.63, p=0.010), higher blood glucose (HR=1.02 per 10mg/100ml increase, p=0.050), the presence of end-stage renal disease (HR=3.59, p <0.001), and the presence of liver cirrhosis (HR=1.93, p=0.013). During follow-up, 626 patients were implanted with a new ICD. In addition to being admitted with VA, a lower LVEF and a history of coronary artery disease or heart failure were the main predictors of ICD therapy in this population. In conclusion, in addition to more severe cardiomyopathy and the presence of an implanted ICD, metabolic derangements on initial contact are independent predictors of hospital admissions for VA in patients with cardiomyopathy. Noncardiac co-morbidities play an important role in stratifying patients with cardiomyopathy for their risk of VA or cardiac arrest.

Ventricular arrhythmias are associated with increased QT interval and QRS dispersion in patients with ST-elevation myocardial infarction

Introduction and ObjectivesThe electrocardiogram continues to be essential in the diagnosis of acute myocardial infarction, and a useful tool in arrhythmic risk stratification. We aimed to determine which electrocardiographic variables can successfully predict the occurrence of ventricular arrhythmias (VA) in patients following ST-segment elevation myocardial infarction (STEMI). MethodsWe performed an observational study including 667 patients with STEMI admitted to the University Hospital in Sancti Spíritus, Cuba. Demographic variables, cardiovascular risk factors, and clinical variables were recorded. Electrocardiographic variables included QT interval duration (measured and corrected) and QT dispersion, QRS duration and dispersion, JT interval duration and ST-segment elevation magnitude. We also determined left ventricular ejection fraction and glomerular filtration rate. A binary statistical regression model and a regression tree were used to determine the variables that successfully predicted VA. ResultsVA occurred in 92 (13.8%) patients, within the first 48 hours in 68 (73.9%) and after this period in 24 (26.1%) patients. The variables associated with VA were QT interval duration >529 ms and QT dispersion >66 ms, QRS dispersion >50 ms, and the presence of ST-segment elevation in six or more leads. ConclusionsThe main predictor of VA occurring during the initial 48 hours was QT interval duration, while, after this period, it was QRS dispersion.

Peculiarities of heart rhythm disorders in patients with myocardial infarction without elevation of ST segment depending on the degree of coronary artery lesions

Summary. The prevalence of myocardial infarction and its leading role in the structure of overall and cardiovascular mortality encourages the search for predictors of complicated course of disease and the search for optimal means to prevent adverse events. The aim of the study – to establish features of cardiac arrhythmias in patients with myocardial infarction without ST-segment elevation depending on the degree of coronary artery lesions. Materials and Methods. The study involved 156 patients with NSTEMI aged 38 to 80 years. All patients were examined according to the current treatment protocol for patients with acute coronary syndrome without ST segment elevation and daily Holter ECG monitoring was performed for 3-5 days after hospitalization. Results. It was found that the degree of coronary artery lesions is positively correlated with the likelihood of severe adverse ventricular arrhythmias and episodes of silent myocardial ischemia in the early period. Conclusions. By determining the total score of coronary artery disease, it is possible to stratify the adverse course of NSTEMI, in particular, the occurrence of fatal ventricular arrhythmias in the early period.

Association of Premature Ventricular Contraction Burden on Serial Holter Monitoring With Arrhythmic Risk in Patients With Arrhythmogenic Right Ventricular Cardiomyopathy

A high burden of premature ventricular contractions (PVCs) at disease diagnosis has been associated with an overall higher risk of ventricular arrhythmias in arrhythmogenic right ventricular cardiomyopathy (ARVC). Data regarding dynamic modification of PVC burden at follow-up with Holter monitoring and its impact on arrhythmic risk in ARVC are scarce. To describe changes in the PVC burden and to assess whether serial Holter monitoring is dynamically associated with sustained ventricular arrhythmias during follow-up in patients with ARVC. In this cohort study, patients with a definite ARVC diagnosis, available Holter monitoring results at disease diagnosis, and at least 2 additional results of Holter monitoring during follow-up were enrolled from 6 ARVC registries in North America and Europe. Data were collected from June 1 to September 15, 2021. The association between prespecified variables retrieved at each Holter monitoring follow-up (ie, overall PVC burden; presence of sudden PVC spikes, defined as absolute increase in PVC burden ≥5000 per 24 hours or a relative ≥75% increase, with an absolute increase of ≥1000 PVCs; presence of nonsustained ventricular tachycardia [NSVT]; and use of β-blockers and class III antiarrhythmic drugs) and sustained ventricular arrhythmias occurring within 12 months after that Holter examination was assessed using a mixed logistical model. In 169 enrolled patients with ARVC (mean [SD] age, 36.3 [15.0] years; 95 men [56.2%]), a total of 723 Holter examinations (median, 4 [IQR, 4-5] per patient) were performed during a median follow-up of 54 (IQR, 42-63) months and detected 75 PVC spikes and 67 sustained ventricular arrhythmias. The PVC burden decreased significantly from the first to the second Holter examination (mean, 2906 [95% CI, 1581-4231] PVCs per 24 hours; P < .001). A model including 24-hour PVC burden (odds ratio [OR] 1.50 [95% CI, 1.10-2.03]; P = .01), PVC spikes (OR, 6.20 [95 CI, 2.74-13.99]; P < .001), and NSVT (OR, 2.29 [95% CI, 1.10-4.51]; P = .03) at each follow-up Holter examination was associated with sustained ventricular arrhythmia occurrence in the following 12 months. These findings suggest that in patients with ARVC, changes in parameters derived from each Holter examination performed during follow-up are associated with the risk of sustained ventricular arrhythmias within 12 months of disease diagnosis.

Occurrence and morphology of ventricular arrhythmias in apparently normal hearts in relation to late gadolinium enhancement on cardiovascular magnetic resonance.

Cardiac magnetic resonance (CMR) is the gold standard for evaluating myocardial fibrosis. Few studies have explored the association between ventricular arrhythmias (VAs) and fibrosis in apparently normal hearts. We aimed to investigate the association between the occurrence and morphology of VAs and left ventricular late gadolinium enhancement (LV-LGE) in patients without known structural heart diseases. This study enrolled 78 patients with apparently normal hearts who underwent 24-h ambulatory Holter electrocardiogram (ECG) and CMR examinations simultaneously. The presence and extent of LGE was determined using CMR imaging and compared based on occurrence and morphology of VAs. The clinical characteristics were also recorded and calculated. LV-LGE was observed in 19 (37.3%) and 4 (14.8%) patients with and without VAs, respectively (P = 0.039). It was more frequently observed in patients with polymorphic VAs (P = 0.024). The polymorphic VAs had a higher tendency of LGE extent than monomorphic VAs, while the difference did not reach statistical significance (P = 0.055). In multivariable analyses, the presence of polymorphic VAs [hazard ratio (HR) 11.19, 95% CI 1.64-76.53, P = 0.014] and hypertension (HR 4.64, 95% CI 1.08-19.99, P = 0.039) were associated with greater prevalence of LV-LGE. In patients without structural heart diseases, besides hypertension, multiple VA morphologies on Holter ambulatory ECG measurements is another important marker of increased incidence of myocardial fibrosis.

Reduced myocardial septal function assessed by cardiac magnetic resonance feature tracking in patients with hypertrophic obstructive cardiomyopathy: associated with histological myocardial fibrosis and ventricular arrhythmias.

Echocardiographic studies suggest that strain is related to myocardial fibrosis (MF) and ventricular arrhythmias (VA) in hypertrophic cardiomyopathy (HCM) patients. Cardiac magnetic resonance feature tracking (CMR-FT) also allows strain analysis, but little is known whether it provides incremental value to late gadolinium enhancement imaging (LGE). This study aimed to explore the relationship between CMR-FT-derived strain parameters and histopathology MF and VA and its incremental value to LGE in obstructive HCM (HOCM) patients undergoing septal myectomy. One hundred and twenty-three symptomatic HOCM patients underwent CMR examination, followed by septal myectomy. The abnormally increased histological MF was defined as higher than the mean + 2 standard deviation (SD) of nine control autopsy subjects who had no history of cardiovascular disease. Septal strain parameters and septal LGE were evaluated at the site of surgical myectomy. Among HOCM patients without LGE, septal circumferential (P = 0.003), longitudinal (P = 0.001), and radial (P = 0.02) strains were significantly impaired in patients with increased histological MF than those without. Histological MF was significantly associated with septal circumferential strain (r = 0.32, P < 0.001), septal longitudinal strain (r = 0.42, P < 0.001), and septal radial strain (r = -0.27, P = 0.003). On multivariate analysis, septal longitudinal strain was independently associated with histological MF [β, 0.19 (0.05-0.34); P = 0.01], and VA [odds ratio, 1.10 (1.01-1.19); P = 0.02]. Moreover, septal longitudinal strain was incremental to septal %LGE in detecting increased MF (P = 0.001) and VA (P = 0.048). Septal longitudinal strain at CMR is independently related to histological MF and occurrence of VA in HOCM patients. Moreover, it provides incremental value over LGE in detecting increased MF and VA.