High Risk Of Ventricular Arrhythmias Research Articles

Correlation of signal averaged electrocardiography findings with fibrosis on cardiac magnetic resonance imaging

Abstract Background Signal averaged electrocardiogram (SAECG) is a non invasive test to record delayed depolarization of myocardium with slow conduction that can potentially be the substrate for monomorphic ventricular tachycardia in high risk patients. Cardiac magnetic resonance imaging (cMRI) techniques for fibrosis imaging using late gadolinium enhancement (LGE) and T1 mapping remain the gold standard for characterization of myocardial tissue and triaging patients for risk of ventricular arrhythmias. However, cMRI remains unavailable in some areas, is time consuming, expensive and impossible for some patients to obtain due to claustrophobia, renal impairment or implanted hardware. To date, data is lacking with regards to correlation of findings between these two modalities. Purpose To investigate whether late potentials identified by SAECG correlate with the presence of fibrosis seen with cMRI. If correlation is established, SAECG could potentially be used as a non-invasive, cheaper, more convenient and readily available tool for risk stratification in patients at high risk for ventricular arrhythmias. Methods SAECGs were obtained in 25 consecutive patients undergoing cMRI. Patients with wide QRS (>120 ms) on ECG were excluded. Positive SAECG was defined as at least 1/3 abnormal criteria. Standard criteria were used. Results of the 2 modalities were compared. Sensitivity and specificity of SAECG for diagnosing fibrosis on cMRI were calculated. Results The mean age of the patients was 50.3±5.8 years and the mean ejection fraction was 48.9±5.8% as determined by cMRI. Forty-eight percent of the patients had fibrosis on cMRI by either LGE, T1 mapping or both. The sensitivity and specificity of SAECG were 75% and 100%, respectively. Seven patients had history of ventricular tachycardia and 6 patients had dilated cardiomyopathy. Conclusion SAECG is extremely specific in identifying patients with myocardial fibrosis on cMRI. A positive test may confer a lesser indication to pursue cMRI solely for purposes of risk stratification, and may correlate with risk of ventricular arrhythmia. Funding Acknowledgement Type of funding sources: None.

MAGIC OF ADVANCED IMAGING AND IMMUNOTHERAPY IN CARDIAC SARCOIDOSIS

TOPIC: Cardiovascular Disease TYPE: Medical Student/Resident Case Reports INTRODUCTION: This case report emphasizes the role of advanced imaging and immunotherapy in the diagnosis and management of cardiac sarcoidosis (CS). CASE PRESENTATION: A 52-year-old healthy male presented with near-syncope for 5 days. He had a blood pressure of 164/67 mmHg and a heart rate of 43 bpm. Electrocardiogram revealed complete-heart-block (CHB) with a ventricular rate of 38/min. Troponin T and electrolytes were normal, and Lyme's serology was negative. Echocardiogram was normal. Cardiac magnetic resonance imaging (CMR) revealed late gadolinium enhancement (LGE) affecting the mid inferior segment at the right ventricle (RV) insertion site (Figure 1). A cardiac and whole-body 18F-fluorodeoxyglucose positron emission tomography (FDG-PET) scan showed focal areas of increased FDG uptake in the LV involving mid and basal anteroseptal segments, mid inferoseptal segment, basal inferolateral, and basal inferior segments with normal perfusion (Figure 2). The scan also revealed hypermetabolic bilateral hilar and mediastinal lymphadenopathy. A diagnosis of CS was made. An Implantable-Cardioverter-defibrillator (ICD) was placed and the patient was discharged on 40mg of prednisone and 20mg of leflunomide. Within 4 months, he went from 100% RV pacing to 0%. Eventually, the corticosteroid was tapered off. At follow-up after 1.5 years, RV pacing remained 0% on Leflunomide 20mg. DISCUSSION: One should always suspect CS in young patients with high-grade AV block. During the workup of CHB (Figure 3), the 2017 Japanese Circulation Society Working Group Criteria for diagnosing CS was followed (1). The patient had 2 characteristic findings strongly suggestive of sarcoidosis: (a) hilar lymphadenopathy and (b) significant tracer accumulation in the myocardium and hilar lymph nodes on FDG-PET scan. He also met 2 major criteria strongly suggestive of CS: (a) LGE on CMR and (b) abnormal myocardial FDG uptake. These findings, per the criteria, establish the clinical diagnosis of CS. The mainstay of treatment for CS is corticosteroids +/- steroid-sparing agents to decrease intra-cardiac inflammation (1). CHB patients with CS have a high risk of ventricular arrhythmias, hence should receive ICD (2). The addition of antimetabolite adjuvants is more effective than corticosteroids alone (3). They may reduce the total time of glucocorticoid therapy and keep patients in remission. CONCLUSIONS: Clinical diagnosis of CS can be established with FDG-PET imaging and CMR. CS patients with advanced heart block should receive ICD. Corticosteroids are the mainstay of treatment. Immunotherapy is an effective adjunct that can help taper the glucocorticoids and keep patients in remission. Early introduction of these agents should be considered in these patients. REFERENCE #1: 1. Trivieri MG et al. Challenges in Cardiac and Pulmonary Sarcoidosis: JACC State-of-the-Art Review. J Am Coll Cardiol 2020;76:1878-1901 REFERENCE #2: 2. Nordenswan H-K et al. Outcome of Cardiac Sarcoidosis Presenting With High-Grade Atrioventricular Block. Circulation: Arrhythmia and Electrophysiology 2018;11:e006145 REFERENCE #3: 3. Nagai S, Yokomatsu et al. Treatment with methotrexate and low-dose corticosteroids in sarcoidosis patients with cardiac lesions. Intern Med 2014;53:427-33. DISCLOSURES: No relevant relationships by Roy Chung, source=Web Response No relevant relationships by Sachin Kumar, source=Web Response No relevant relationships by Raunak Nair, source=Web Response

Long-term follow-up and sex differences in adults operated for tetralogy of Fallot

ObjectiveAdults operated for tetralogy of Fallot (TOF) have high risk of ventricular arrhythmias (VA). QRS duration >180 ms is an established risk factor for VA. We aimed to investigate heart...

Increased QT Dispersion and High Risk of Ventricular Arrhythmias is Associated with Hyperuricemia in Individuals with Normal Renal Function

Abstract Background and aim: Uric acid elevation has been shown to be an important risk factor for cardiovascular and cerebrobascular disease. QT dispersion (QTd) is a parameter that shows the heterogeneity of ventricular repolarization and can be calculated noninvasively from surface electrocardiography. Increased QTd has been associated with severe arrhythmia and risk of sudden death in many patients and disease groups. In this context, we aimed to investigate the effect of uric acid levels on QTd and the effects of decrease in uric acid levels on QTd. Methods: A total of 225 patients with normal renal function were included in the study; 133 of these patients were hyperuricemic (>7 mg/dL), and the remaining 72 patients were normouricemic (Group 1). The hyperuricemic patients were randomly divided into 2 groups, one group (n = 67) was given placebo (Group 2) for 4 months, and the remaining 66 patients were given allopurinol 300 mg/day (Group 3). Results: Hyperuricemic patients had higher hsCRP and QTd and lower eGFR values compared to the normouricemic control group. After 4 months of treatment, 66 patients treated with allopurinol showed a significant decrease in serum uric acid, systolic and diastolic blood pressure, and hsCRP levels, and a significant increase in eGFR. Although the QTd values in the treatment group did not decrease to the same levels as in the normouricemic control group, a statistically significant decrease was found compared to their baseline values. In hyperuricemic control and normouricemic control patients, there were no differences in the levels of uric acid, hsCRP, eGFR, systolic and diastolic blood pressure, and QTd values compared to baseline values. Conclusions: There was a significant association between elevated serum uric acid and QTd, as well as with inflammatory biomarkers. Also, patients who had received hypouricemic therapy during the follow-up period presented a significant decrease in inflammatory markers as well as QTd. This indicates the beneficial effects of decreasing uric acid levels in decreasing the risk for future major adverse events related to ventricular arrhythmias.

Safety and efficacy of flecainide associated with beta-blockers in arrhythmogenic right ventricular cardiomyopathy.

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an inherited cardiomyopathy associated with a high risk of ventricular arrhythmia (VA). Current guidelines recommend beta-blockers as first-line medical therapy and if ineffective, sotalol or amiodarone. We describe our experience, as a tertiary centre for ARVC, with the effectiveness and tolerance of flecainide in addition to beta-blockers to prevent VA in ARVC. We retrospectively included 100 consecutive ARVC patients who received flecainide with beta-blockers between May 1999 and November 2017. Treatment persistence and related side effects were assessed, as was VA-free survival on treatment, 24-h Holter monitoring and programmed ventricular stimulation (PVS) off- and on-treatment. Tolerance was good, with 10% flecainide discontinuations (lack of efficacy in six, atrial fibrillation in one, and side effects in three). No Brugada-induced electrocardiography pattern on flecainide or haemodynamic impairment was reported. Premature ventricular contraction burden at 24-h Holter monitoring was significantly decreased under treatment [median 415 (interquartile range, IQR 97-730) vs. 2370 (1572-3400) at baseline, P < 0.0001, n = 46]. Among the 33 patients with PVS under treatment, PVS was positive in 40% on-treatment vs. 94% off-treatment (P < 0.001). During a median follow-up of 47 months (IQR 23-73), 22 patients presented sustained VA on treatment, corresponding to an event rate of 5% [95% confidence interval (CI) (0.6-9)] at 1 year and 25% [95% CI (14-35)] at 5 years under treatment. No patient died. This study suggests that flecainide and beta-blockers association is complementary to implantable cardioverter-defibrillator and catheter ablation and is safe for treating persistent symptomatic VA in patients with ARVC.

Clinical characteristics and risk stratification of desmoplakin cardiomyopathy.

AimsDesmoplakin (DSP) cardiomyopathy is an increasingly recognized form of arrhythmogenic cardiomyopathy. With a genotype-specific approach, we characterized the diagnosis, natural history, and risk for ventricular arrhythmia and heart failure in DSP cardiomyopathy.Methods and resultsWe followed 91 individuals [45 probands, 34% male, median age 27.5 years (interquartile interval 20.0–43.9)] with pathogenic or likely pathogenic DSP variants for a median of 4.3 years. Regarding the ventricular involvement, left predominance was most common (n = 22, 28%) followed by bi-ventricular in 12 (15%) and right predominance in 5 (6%). Myocardial injury (chest pain, elevated troponin, normal coronary angiogram) occurred in 20 (22%) individuals. Incidence rates of sustained ventricular arrhythmia and heart failure (ventricular dysfunction ± symptoms) were 5.9 [95% confidence interval (CI): 3.9–9.1] and 6.7 (95% CI: 4.5–9.8) per 100 person-years, respectively. In univariate regression, myocardial injury was associated with sustained ventricular arrhythmia [hazard ratio (HR) 2.53, 95% CI: 1.05–6.11] and heart failure (HR 7.53, 95% CI: 3.10–18.26). After adjustment, left ventricular ejection fraction <35% and right ventricular dysfunction were prognostic for sustained ventricular arrhythmia while proband status and myocardial injury were prognostic for heart failure (all P < 0.05). The sensitivity of the arrhythmogenic right ventricular cardiomyopathy Task Force Criteria in diagnosing left dominant disease was 0.73; 5/22 (23%) of patients with sustained ventricular arrhythmias did not meet these criteria.Conclusion DSP cardiomyopathy affects both ventricles and carries high risk for ventricular arrhythmia and heart failure. Myocardial injury is associated with worse disease outcomes. Both diagnosis and risk stratification of DSP cardiomyopathy need refinement.

Strain echocardiography improves prediction of arrhythmic events in ischemic and non-ischemic dilated cardiomyopathy

BackgroundRecent evidence suggests that an implantable cardioverter defibrillator (ICD) in non-ischemic cardiomyopathy (NICM) may not offer mortality benefit. We aimed to investigate if etiology of heart failure and strain echocardiography can improve risk stratification of life threatening ventricular arrhythmia (VA) in heart failure patients. MethodsThis prospective multi-center follow-up study consecutively included NICM and ischemic cardiomyopathy (ICM) patients with left ventricular ejection fraction (LVEF) <40%. We assessed LVEF, global longitudinal strain (GLS) and mechanical dispersion (MD) by echocardiography. Ventricular arrhythmia was defined as sustained ventricular tachycardia, sudden cardiac death or appropriate shock from an ICD. ResultsWe included 290 patients (67 ± 13 years old, 74% males, 207(71%) ICM). During 22 ± 12 months follow up, VA occurred in 32(11%) patients. MD and GLS were both markers of VA in patients with ICM and NICM, whereas LVEF was not (p = 0.14). MD independently predicted VA (HR: 1.19; 95% CI 1.08–1.32, p = 0.001), with excellent arrhythmia free survival in patients with MD <70 ms (Log rank p < 0.001). Patients with NICM and MD <70 ms had the lowest VA incidence with an event rate of 3%/year, while patients with ICM and MD >70 ms had highest VA incidence with an event rate of 16%/year. ConclusionPatients with NICM and normal MD had low arrhythmic event rate, comparable to the general population. Patients with ICM and MD >70 ms had the highest risk of VA. Combining heart failure etiology and strain echocardiography may classify heart failure patients in low, intermediate and high risk of VA and thereby aid ICD decision strategies.

QT interval estimation in patients with right bundle branch block using validated formulas for left bundle branch block

Abstract Funding Acknowledgements Type of funding sources: None. BACKGROUND Adequate measurement of the QT interval is of paramount importance in order to identify patients at higher risk for ventricular arrhythmias. Previous studies have described different methods to estimate baseline QT in patients with left bundle branch block (LBBB). However, the evidence regarding the assessment of QT interval in the setting of right bundle branch block (RBBB) is scarce. PURPOSE We aimed to analyze the feasibility and accuracy of the different formulas described for LBBB in the estimation of the QT interval in RBBB. METHODS We enrolled patients who underwent left sided electrophysiologic procedures. All patients were in sinus rhythm and had narrow QRS. Pacing was performed from the left atrial appendage for baseline measurements, and from the left aspect of the interventricular septum (selective capture of the left bundle was attempted) to measure RBBB QT and QRS. Pacing cycle length was 800 ms or slightly below patients´ intrinsic rhythm at both locations. Measurements were performed manually (using digital calipers) according to current recommendations and corrected using Bazett. Validated formulas for LBBB QT considered are described in table 1. RESULTS 50 patients (42 cryoballoon pulmonary veins isolation (PVI), 4 radiofrequency PVI, 4 concealed left accessory pathways). 70% were male. Mean age was 62 ± 11 years old. Left ventricle ejection fraction was 58 ± 10%. 66% and 60% of the patients were taking betablockers and antiarrhythmic drugs, respectively. Mean pacing cycle length was 707 ± 99 ms. Baseline measurements: QRS 95 ± 10, QT 391 ± 36, QTc 467 ± 39 ms. RBBB measurements: QRS 165 ± 21, QT 448 ± 46, QTc 531 ± 52 ms. Correlations between baseline and estimated QTc were good for all the formulas (table 1). Reliability analysis showed that both Yankelson and Wang methods had the highest intraclass correlation coefficients (ICC) when trying to estimate baseline QTc. CONCLUSIONS Previously described formulas for LBBB exhibit marked differences regarding reliability in the estimation of QTc interval in the setting of RBBB. According to our results, Yankelson’s method shows the most consistent agreement when estimating baseline QTc interval in patients with RBBB. Table 1.LBBB METHODFormula to estimate baseline QTcPearson’s R correlation coefficientCI (95%)Intraclass correlation coefficientCI (95%)YankelsonQTc - QRS + 95 (m) or 88 (f)0.805(0.632-0.977)0.882(0.788-0.934)Bogossian**QT - (QRS/2)0.813(0.644-0.982)0.756(-0.127-0.919)Wang**QT - (0.86*QRS - 71)0.801(0.627-0.974)0.834(0.465-0.930)Tang-Rabkin0.945*QTcRabkin - 260.722(0.521-0.923)0.711(0.019-0.885)RautaharjuQT - 155*(60/heart rate - 1) - 0.93*(QRS - 139) - 22 (m) or - 34 (f)0.780(0.599-0.961)0.105(-0.017-0.381)**Bogossian and Wang required additional HR correction (Bazett). Abstract Figure 1. Bland-Altman

Safety and efficacy of flecainide associated with beta-blockers in arrhythmogenic right ventricular cardiomyopathy

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an inherited cardiomyopathy characterized by progressive fibro-fatty replacement of cardiomyocytes and associated with a high risk of ventricular arrhythmia (VA). Current guidelines recommend beta-blockers as first-line medical therapy and if ineffective, sotalol or amiodarone. To describe our experience, as a tertiary center for ARVC, with the effectiveness and tolerance of flecainide in addition to beta-blockers to prevent VA in ARVC. We retrospectively included 100 consecutive ARVC patients who received flecainide with beta-blockers between May 1999 and November 2017. Treatment persistence and related side effects were assessed, as was VA-free survival on treatment, 24-hr Holter monitoring and programmed ventricular stimulation (PVS) off- and on-treatment. Tolerance was good, with 10% flecainide discontinuations (lack of efficacy in 6, atrial fibrillation in one and side effects in 3). No Brugada-induced electrocardiography pattern on flecainide or hemodynamic impairment was reported. Premature ventricular contraction burden at 24-hr Holter monitoring was significantly decreased under treatment (median 415 [interquartile range 97–730] vs. 2370 [1572–3400] at baseline, P < 0.0001, n = 46). Among the 33 patients with PVS under treatment, PVS was positive in 40% on-treatment versus 94% off-treatment ( P < 0.001). During a median follow-up of 47 months (interquartile range 23–73), 22 patients presented sustained VA on treatment, corresponding to an event rate of 5% (95% confidence interval [0.6–9]) at 1 year and 25% (95% confidence interval [14–35]) at 5 years under treatment ( Fig. 1 ). No patient died. This study suggests that flecainide and beta-blockers association is complementary to ICD and catheter ablation and is safe for treating persistent symptomatic VA in patients with ARVC.

The mitral annulus disjunction of mitral valve prolapse: Presentation and outcome

To assess in MVP-patients, MAD prevalence, phenotypic characteristics and long-term outcome. A cohort of 595 (278 female, age 61 ± 16 years) consecutive patients with isolated MVP, comprehensive clinical, rhythmic, Doppler-echocardiographic and consistent MAD assessment, was examined. MAD prevalence, associated MVP-phenotype and outcome [survival, ventricular arrhythmias (VA)] were analyzed. To balance important baseline differences, we also propensity score matched patients with and without MAD (no-MAD). MAD presence was common (186 – 31%) in MVP, generally in younger patients and was not random but independently associated with severe myxomatous disease and larger left ventricle ( P ≤ 0.005). Age-matched-cohort survival after MVP diagnosis was not worse with MAD (10-year 93 ± 2% for no-MAD and 97 ± 1% for MAD, P = 0.4), even adjusted-comprehensively for MVP characteristics ( P = 0.8) and accounting for time-dependent mitral-surgery ( P = 0.6). During follow-up, 218 patients were diagnosed with VA post-30 days from MVP diagnosis (159 with ventricular tachycardia-VT). MAD was independently associated with higher risk of VA (adjusted-hazard-ratio 2.39[1.79–3.22]) and VT (2.79[1.98–3.94], both P < 0.0001). MAD link to VA persisted with time-dependent mitral-surgery (adjusted-hazard-ratio 2.25[1.65–3.01], P < 0.0001), strongly under medical-management (adjusted-hazard-ratio 2.91[1.95–4.35], P < 0.0001) but weakly post-mitral-surgery (adjusted-hazard-ratio 1.77[1.12–2.79], P = 0.01). This large cohort with MVP comprehensively characterized, shows that MAD is frequent at MVP diagnosis and strongly linked to advanced-myxomatous-degeneration. MAD presence is independently associated with long-term excess-incidence of VA and VT. However, within the first 10 years post-diagnosis MAD is not linked to excess-mortality and while reassurance should be provided from the survival point of view careful monitoring for arrhythmias is in order with MAD.

Estratificación del riesgo de arritmias ventriculares en pacientes con tetralogía de Fallot reparada

Introduction and objectivesRisk stratification of ventricular arrhythmias in patients with repaired tetralogy of Fallot (rTOF) remains unresolved. We aimed to identify right ventricular (RV) electrophysiological parameters potentially associated with a higher risk of ventricular arrhythmias in patients with rTOF. MethodsWe included all consecutive patients with rTOF who underwent RV electroanatomical mapping at a single tertiary center. We used logistic regression modeling to identify those variables associated with an increased risk of clinical or induced ventricular tachycardia (VT), or clinical VT exclusively. ResultsTwenty-one of the 56 patients included had clinical or induced VT. A high-frequency of premature ventricular contractions/nonsustained VT (OR, 11.34; 95%CI, 1.50-85.97; P=.019), an HV interval > 55 ms (OR, 21.20; 95%CI, 3.12-144.14; P=.002), and RV activation time (ms) (OR [per 10ms intervals], 1.34; 95%CI, 1.02-1.75; P=.035) proved to be associated with clinical or induced VT. The model including this information had good discrimination ability, with an area under the curve of 0.884 (95%CI, 0.79-0.97; P <.001). When considering only clinical VT as the outcome of interest, only an HV interval > 55ms (OR, 9.65; 95%CI, 1.41-66.14; P=.021) and high-frequency of premature ventricular contractions/nonsustained VT (OR, 13.14; 95%CI, 1.95-88.54; P=.008) were independently associated (area under the curve of 0.836 [95%CI, 0.663-1.000; P=.002]). ConclusionsHigh-frequency of premature ventricular contractions/nonsustained VT, an HV interval> 55ms and RV activation time are factors associated with an increased risk of ventricular arrhythmias in patients with rTOF.

Risk stratification of ventricular arrhythmias in repaired tetralogy of Fallot

Introduction and objectivesRisk stratification of ventricular arrhythmias in patients with repaired tetralogy of Fallot (rTOF) remains unresolved. We aimed to identify right ventricular (RV) electrophysiological parameters potentially associated with a higher risk of ventricular arrhythmias in patients with rTOF. MethodsWe included all consecutive patients with rTOF who underwent RV electroanatomical mapping at a single tertiary center. We used logistic regression modeling to identify those variables associated with an increased risk of clinical or induced ventricular tachycardia (VT), or clinical VT exclusively. ResultsTwenty-one of the 56 patients included had clinical or induced VT. A high-frequency of premature ventricular contractions/nonsustained VT (OR, 11.34; 95%CI, 1.50-85.97; P=.019), an HV interval > 55 ms (OR, 21.20; 95%CI, 3.12-144.14; P=.002), and RV activation time (ms) (OR [per 10ms intervals], 1.34; 95%CI, 1.02-1.75; P=.035) proved to be associated with clinical or induced VT. The model including this information had good discrimination ability, with an area under the curve of 0.884 (95%CI, 0.79-0.97; P <.001). When considering only clinical VT as the outcome of interest, only an HV interval > 55ms (OR, 9.65; 95%CI, 1.41-66.14; P=.021) and high-frequency of premature ventricular contractions/nonsustained VT (OR, 13.14; 95%CI, 1.95-88.54; P=.008) were independently associated (area under the curve of 0.836 [95%CI, 0.663-1.000; P=.002]). ConclusionsHigh-frequency of premature ventricular contractions/nonsustained VT, an HV interval> 55ms and RV activation time are factors associated with an increased risk of ventricular arrhythmias in patients with rTOF.

Safety and efficacy of flecainide in association with beta-blockers in arrhythmogenic right ventricular cardiomyopathy

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an inherited cardiomyopathy associated with a high risk of ventricular arrhythmia (VA). Current guidelines recommend beta-blockers as first line medical therapy and if ineffective, treatment by sotalol or amiodarone. To describe our experience as a tertiary centre for ARVC on flecainide effectiveness and tolerance in addition to beta-blockers to prevent ventricular arrhythmia in ARVC. We included one hundred ARVC patients treated with flecainide and beta-blocker diagnosed between May 1999 and November 2017. Ventricular events including sustained ventricular tachycardia (VT), ventricular fibrillation (VF) and ICD therapy were collected retrospectively in patient's medical records. Besides, a 24 hours Holter monitoring and a programmed ventricular stimulation (PVS) before and after introduction of flecainide were performed. Tolerance of flecainide was good with 9% discontinuation (6 for VA occurrence, 2 for side effect, 1 for atrial fibrillation). No Brugada-induced ECG pattern on flecainide was reported. PVC burden on 24 hours Holter monitoring ( n = 46 patients) was significantly decreased under treatment (2370; IQR1572–3400 versus 415; IQR97–730, P < 0.0001). Proportion of positive PVS was significantly decreased ( n = 32 patients) with 94% having positive PVS before treatment compared to 37.5% on flecainide ( P < 0.001) ( Fig. 1 ). During a median follow-up of 47 (IQR24–74) months, 23 patients had sustained VA (all monomorphic VT) on treatment (5% per patient–year). No sudden death occurred. This study suggests that flecainide and beta-blockers association is complementary to ICD and catheter ablation, and is safe to treat ARVC patients with persistent symptomatic VA.

Atenolol Reduces the Occurrence of Arrhythmias Induced by Isoproterenol in a Model of Hypertrophic Cardiomyopathy

Familial hypertrophic cardiomyopathy is caused by mutations in cardiac sarcomere proteins. Along with distinct histopathological features, it is also associated with a high risk of ventricular arrhythmias and sudden cardiac death during exercise. β1--adrenergic receptor blockers are administered as therapy in patients with hypertrophic cardiomyopathy because the drug improves diastolic function and reduces outflow-obstruction but its role as an antiarrhythmic during increased sympathetic stimulation has not been clarified.

Abstract 16173: Clinical Characteristics and Short-term Outcomes of Hospitalized Patients With Sars-cov-2 Infection and Reduced Left Ventricular Ejection Fraction

Introduction: Early studies of coronavirus disease 2019 (COVID-19) patients suggested that heart failure (HF) may lead to poorer prognosis. We evaluated demographics and short-term clinical outcomes of patients with evidence of left ventricular systolic dysfunction (LVSD) in comparison to those with preserved LV systolic function (PSF). Methods: In this retrospective study of patients hospitalized for COVID-19 between March and June 2, 2020 at Rush Health Systems in Metro Chicago, demographics, comorbidities and clinical outcomes of patients who demonstrated LVSD (ejection fraction [EF] &lt;50%) on transthoracic echocardiogram (TTE) were compared to that of controls with PSF. Results: Out of 1,312 hospitalized patients, 225 underwent TTE, and 44 patients showed LVSD. Demographics were similar between two groups, with exception of a higher prevalence of African American (AA) race (48 % vs. 29%; p=0.03) in the LVSD group. While 82% of patients in the LVSD cohort had history of chronic HF, only 26% of patients in the PSF had pre-existing HF (p&lt;0.001). Underlying comorbidities were similar between groups: obesity (39% vs. 36%; p=0.86), diabetes (57% vs. 57%; p=1.0), hypertension (70% vs. 66%; p=0.72) and end-stage renal disease (20% vs. 19%; p=0.83). Coronary artery disease trended toward a higher frequency (50% vs. 34%; p=0.058) in the LVSD group. Troponin elevation (18% vs. 12%; p=0.43), vasopressor use (57% vs. 56%; p=1.0), endotracheal intubation (59% vs. 57%; p=0.87), myocardial infarction (30% vs. 23%; p=0.43), ICU admission (75% vs. 75%; p=1.0), hospital length of stay (median 11 days vs. 15 days; p=0.4), and death (25% vs. 23%; p=0.84) were similar between groups. Patients with LVSD had higher incidence of sustained ventricular tachycardia or fibrillation than those with PSF (18% vs. 6%; p=0.016). Conclusions: In our COVID-19 admissions, LVSD was more common in AA patients. Patients with LVSD had a higher risk of ventricular arrhythmias. However, there were no differences between need for ICU admission or intubation, vasopressor requirements, length of stay or death between patients with LVSD and those without. Longitudinal follow-up studies are needed to identify differences in long-term sequelae of COVID-19 infection with evidence for LVSD.

Epicardial adipose tissue predicted prolonged QTc interval in patients with arterial hypertension

ABSTRACT Introduction: It is important to identify those at higher risk for ventricular arrhythmia among hypertensive patients. Epicardial adipose tissue (EAT) leads to electromechanical changes in the heart by endocrine and paracrine effects with cytokines and mediators. Higher amount of EAT carries the risk of QT prolongation. Therefore, we investigated the association between EAT thickness and QTc interval in patients with arterial hypertension. Methods: A total of 230 patients who previously diagnosed with arterial hypertension between February 2019 to March 2020 were included in the study. Patients with atrial fibrillation, U-wave, atrioventricular block, left anterior or posterior fascicular block, right bundle branch block, left bundle branch block, and taking QT-prolonging medication were excluded. The corrected QT (QTc) interval was calculated with Bazzet’s formula following the calculated QT interval in the semi-automatic application tool. EAT was measured at the point on the free wall of the right ventricle using transthoracic echocardiography. Results: The mean age was 62.1 ± 11.4 years and 95 (41.3%) of the patients were male. QTc was over 450 ms were considered as the prolonged interval. Both groups were similar in terms of age (p = .862), gender (p = .265) and other demographic characteristics. Left ventricle mass index (LVMI) (82.5 ± 29.5 vs 91.9 ± 32.6 g/1.7.m2, p = .051) and EAT thickness (5.3 ± 2.3 vs 6.6 ± 2.6 mm, p = .001) were higher in the prolonged QTc group. Serum potassium (K) level was lesser in the prolonged QTc group (4.2 ± 0.39 vs 4.1 ± 0.4 mmol/mL, p = .005). Multivariate Cox regression analysis revealed that EAT thickness [OR = 1.227, 95% CI: 1.081–1.393, p = .002] and serum K level [OR = 0.348, 95% CI: 0.157–0.772, p = .009] predicted the prolonged QTc interval, independently. Conclusion: EAT thickness predicted prolonged QTc interval in patients with arterial hypertension. Patients with higher amount of EAT should be followed by closely monitoring to prevent arrhythmic events that may develop in the future. In addition, medications that have a potential effect on QTc interval prolongation may be carefully used in patients with higher EAT thickness.

Circadian rhythm dynamics on multiscale entropy identifies autonomic dysfunction associated with risk of ventricular arrhythmias and near syncope in chronic kidney disease

BackgroundA discordant biological clock could potentially induce sudden cardiac death (SCD). We aimed to evaluate the circadian change of heart rate variability (HRV) and its relationship to the risks of ventricular arrhythmia (VA) and near syncope in patients with chronic kidney disease (CKD). MethodsIn this retrospective study, non-CKD and CKD patients were enrolled and underwent a 24-hour Holter examination for linear and nonlinear HRV analyses. The multiscale entropy (MSE) method was selected for nonlinear HRV analyses. The documented VAs or episodes of near syncope were classified as high-risk SCD group (n=8) and others as low-risk SCD group (n=21). ResultsIn linear analyses, time and frequency domains revealed no significant difference between groups. In nonlinear analyses with MSE, MSE5, MSE6–20, and MSEslope 5 were significantly lower (p=0.002, p<0.0001, and p=0.013) in the high-risk SCD group, compared to those in the low-risk SCD group, respectively. Comparing between daytime and nighttime within each group, the MSE5 revealed no difference in the high-risk SCD group (p=0.128), whereas the daytime was significantly higher in the low-risk SCD group (p=0.048). The area under the curve (AUC) analysis revealed MSE6–20 has the best predictive power associated with VAs and near syncope with a cut-off value of ≤24.64 (p<0.001). ConclusionsNonlinear analysis with MSE demonstrated the loss of circadian change in CKD patients and was associated with a higher risk for VAs and near syncope. The MSE method demonstrated the diurnal change of rhythm dynamics which identifies potential autonomic dysfunction leading to poor prognosis.

A preliminary report about the detection of ventricular repolarisation in patients with non-alcoholic fatty liver disease

ObjectivesNon-alcoholic fatty liver disease (NAFLD) is a multisystem disease which can affect the cardiovascular system as well. We conducted this study to determine the cardiac effects of NAFLD such as conduction of impulse and ventricular repolarisation on electrocardiography (ECG). MethodsIn this study, we recruited patients with risk factors for NAFLD (group I; n = 23) and NAFLD patients (group II; n = 74) from Shar Hospital in Sulaimani City, Iraq. We analysed anthropometric measurements, serum fasting lipid profile, glucose levels, liver enzymes, and ECG recordings. ResultsECG recordings showed significantly longer PR intervals, significantly shorter QTcB and JTc intervals, and a higher Tp-e/QTcB ratio in group II patients than in group I patients. These abnormalities were not associated with risk factors for diabetes. The TQ duration was significantly correlated with serum alanine aminotransferase (r = 0.411, p < 0.001) and aspartate aminotransferase (r = 0.272, p = 0.019) levels. ConclusionIn our study, the presence of significant abnormalities in ventricular repolarisation suggests that patients with newly diagnosed NAFLD have subclinical cardiac stress and a higher risk of ventricular arrhythmias.

Use of Chloroquine and Hydroxychloroquine in COVID-19 and Cardiovascular Implications: Understanding Safety Discrepancies to Improve Interpretation and Design of Clinical Trials.

Author(s): Oren, Ohad; Yang, Eric H; Gluckman, Ty J; Michos, Erin D; Blumenthal, Roger S; Gersh, Bernard J

Assessment of Arrhythmia Burden through the Use of an Implantable Cardiac Monitor in Patients with a Continuous Flow Left Ventricular Assist Device

The benefit of an ICD in patients with an LVAD remains unclear. There is a growing number of patients with LVADs who do not have concomitant ICDs and therefore implantable cardiac monitors (ICMs) are being used to monitor arrhythmia burden. We report our series of LVAD patients who underwent ICMs for long-term heart rhythm monitoring. We aim to (1) evaluate the burden of atrial and ventricular arrhythmias in patients with a LVAD following ICM implant and (2) to determine whether the ICM generated data results in interventions. Patients were recruited from the University of Rochester Advanced Heart Failure Service. All ICMs were implanted in the electrophysiology suite using standard sterile techniques. All patients were enrolled into remote ICM monitoring. Implantable cardiac monitors were implanted in 10 LVAD patients who did not already have an ICD. No ICM implant procedure related adverse events occurred. Adequate and interpretable signals were obtained from each ICM (9 Medtronic Reveal LINQs, 1 Biotronik BioMonitor) (Figure) with no appreciable artifact. Indications for ICM implant varied, and included documented tachyarrhythmia (VT and/or AF), syncope and presyncope (Table). During long-term monitoring (mean of 357.2 days), 4 patients (40%) had arrhythmia detected on ICM, with an average of 47.5 days to first arrhythmia detected. Decision was made to adjust medication therapy in all 4 of these patients and to implant an ICD in 2 patients (20%) due to ICM detected sustained VT resulting in compromised VAD function. In select LVAD patients, use of an ICM may be used to further risk stratify patients at high risk for ventricular arrhythmias and for whom an ICD implant may confer long term benefit. With observational data showing no survival benefit for ICD therapy in patients with continuous flow LVADs, ICMs may help guide therapy in patients without concomitant ICD. Future studies with larger sample size are warranted.