Premature Ventricular Complex Count Research Articles

DIAGNOSTIC RELIABILITY OF MEASUREMENT OF PREMATURE VENTRICULAR COMPLEX FREQUENCY RELATED TO DURATION OF AMBULATORY MONITORING

Background Premature ventricular complexes (PVCs) are generally quantified using a 24h ECG recording, but the diagnostic accuracy is unknown. We aimed to determine the day-to-day variability and optimal monitoring duration for PVC measurements among patients with frequent PVCs. Methods We included all patients who underwent a clinical ambulatory ECG recording lasting 25-30 days, using the PocketECG device (Medi-Lynx, USA) during 2017, who did not have atrial fibrillation, and in whom ≥1000 PVCs were registered during one of the monitored days. All arrhythmias were manually verified. PVC variability was calculated as the percentage of the mean daily PVC count after full recording. Results The study population consisted of 1,376 individuals (median age 76.0 years, 53% men). Figure 1a shows the population distribution of the mean daily PVC counts. The mean daily PVC count was 2780 (standard deviation: 1556, range 0 - 56,262). A single-day PVC count differed by 69% from the mean daily count. After 18 days the obtained mean PVC count differed (Less)

Sudden Cardiac Death Prediction in Arrhythmogenic Right Ventricular Cardiomyopathy: A Multinational Collaboration.

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is associated with ventricular arrhythmias (VA) and sudden cardiac death (SCD). A model was recently developed to predict incident sustained VA in patients with ARVC. However, since this outcome may overestimate the risk for SCD, we aimed to specifically predict life-threatening VA (LTVA) as a closer surrogate for SCD. We assembled a retrospective cohort of definite ARVC cases from 15 centers in North America and Europe. Association of 8 prespecified clinical predictors with LTVA (SCD, aborted SCD, sustained, or implantable cardioverter-defibrillator treated ventricular tachycardia >250 beats per minute) in follow-up was assessed by Cox regression with backward selection. Candidate variables included age, sex, prior sustained VA (≥30s, hemodynamically unstable, or implantable cardioverter-defibrillator treated ventricular tachycardia; or aborted SCD), syncope, 24-hour premature ventricular complexes count, the number of anterior and inferior leads with T-wave inversion, left and right ventricular ejection fraction. The resulting model was internally validated using bootstrapping. A total of 864 patients with definite ARVC (40±16 years; 53% male) were included. Over 5.75 years (interquartile range, 2.77-10.58) of follow-up, 93 (10.8%) patients experienced LTVA including 15 with SCD/aborted SCD (1.7%). Of the 8 prespecified clinical predictors, only 4 (younger age, male sex, premature ventricular complex count, and number of leads with T-wave inversion) were associated with LTVA. Notably, prior sustained VA did not predict subsequent LTVA (P=0.850). A model including only these 4 predictors had an optimism-corrected C-index of 0.74 (95% CI, 0.69-0.80) and calibration slope of 0.95 (95% CI, 0.94-0.98) indicating minimal over-optimism. LTVA events in patients with ARVC can be predicted by a novel simple prediction model using only 4 clinical predictors. Prior sustained VA and the extent of functional heart disease are not associated with subsequent LTVA events.

Early Mechanical Alterations in Phospholamban Mutation Carriers: Identifying Subclinical Disease Before Onset of Symptoms

ObjectivesThis study aimed to explore echocardiographic characteristics of phospholamban (PLN) p.Arg14del mutation carriers to investigate whether structural and/or functional abnormalities could be identified before onset of symptoms. BackgroundCarriers of the genetic PLN p.Arg14del mutation may develop arrhythmogenic and/or dilated cardiomyopathy. Overt disease is preceded by a pre-symptomatic phase of variable length in which disease expression seems to be absent. MethodsPLN p.Arg14del mutation carriers with an available echocardiogram were included. Mutation carriers were classified as pre-symptomatic if they had no history of ventricular arrhythmias (VAs), a premature ventricular complex count of <500/24 h, and a left ventricular (LV) ejection fraction of ≥45%. In addition, we included 70 control subjects with similar age and sex distribution as the pre-symptomatic mutation carriers. Comprehensive echocardiographic analysis (including deformation imaging) was performed. ResultsThe final study population consisted of 281 PLN p.Arg14del mutation carriers, 139 of whom were classified as pre-symptomatic. In comparison to control subjects, pre-symptomatic mutation carriers had lower global longitudinal strain and higher LV mechanical dispersion (both p < 0.001). In addition, post-systolic shortening (PSS) in the LV apex was observed in 43 pre-symptomatic mutation carriers (31%) and in none of the control subjects. During a median follow-up of 3.2 years (interquartile range: 2.1 to 5.6 years) in 104 pre-symptomatic mutation carriers, nonsustained VA occurred in 13 (13%). Presence of apical PSS was the strongest echocardiographic predictor of VA (multivariable hazards ratio: 5.11; 95% confidence interval [CI]: 1.37 to 19.08; p = 0.015), which resulted in a negative predictive value of 96% (95% CI: 89% to 98%) and a positive predictive value of 29% (95% CI: 21% to 40%). ConclusionsGlobal and regional LV mechanical alterations in PLN p.Arg14del mutation carriers precede arrhythmic symptoms and overt structural disease. Pre-symptomatic mutation carriers with normal deformation patterns in the apex are at low risk of developing VA within 3 years, whereas mutation carriers with apical PSS appear to be at higher risk.

Treatment with corticosteroids is associated with an increase in ventricular arrhythmia burden in patients with clinically manifest cardiac sarcoidosis: Insights from implantable cardioverter-defibrillator diagnostics.

We sought to explore the relationship between ventricular tachycardia (VT) and premature ventricular complex (PVC) burden (from implantable cardioverter-defibrillator diagnostics), before and during corticosteroid use in patients with newly diagnosed clinically manifest cardiac sarcoidosis (CS). A single-centre, prospective cohort study was performed in consecutive patients who met all of the following criteria: (1)presentation with clinically manifest CS, (2)abnormal myocardial fluoro-deoxyglucose (FDG) uptake on positron emission tomography scan, (3)plan for implantation with implantable cardioverter-defibrillatordevice that reports accurate PVC count, (4)plan to initiate corticosteroids after the device healing period. Data were collected during each device interrogation visit for all patients in the study. For each inter-visit period the total number of episodes of VT-sustained and nonsustained, and the number of PVCs was obtained. Each inter-visit period was classified into one of the following three periods: (1)New diagnosis of treatment-naive active disease without corticosteroids during the period. (2)Known treatment-naive active disease with corticosteroids initiated during the inter-visit period. (3)On corticosteroid therapy during the entire period. A total of 20 patients with a mean age of 59.7 ± 7.7 years were recruited and 82 inter-visit periods were analyzed. All patients were corticosteroid responders based on FDG uptake. The maximum left ventricular standardized uptake value was 11.14 ± 5.19 before corticosteroid initiation and 4.07 ± 0.88 after (p < .001). Patients with active untreated CS had an average of 496.4 ± 879.1 PVCs per day. After treatment with corticosteroids, the average PVC count increased to 1332.4 ± 1865.7/day during Period 2 (p = .036) and to 1590.1 ± 2362.2 per day during Period 3 (p = .008). There was also a statistically significant increase in episodes of nonsustained ventricular tachycardia (NSVT) before and after treatment with corticosteroids (p = .017). There were too few episodes of sustained ventricular arrhythmia to analyze. Overall, 18 out of 20 patients (90%) had an increase in PVC burden after corticosteroid initiation. This study demonstrated, on average, a threefold increase in daily PVC count in clinically manifest CS patients during treatment with corticosteroids compared to pretreatment. There was also a significant increase in episodes of NSVT. Clinicians and patients with active manifest CS should be aware that corticosteroids are unlikely to lead to a reduction in the burdens of PVC and NSVT.

1175Structural progression increases the risk of ventricular arrhythmias in patients with arrhythmogenic cardiomyopathy

Abstract Background Arrhythmogenic cardiomyopathy (AC) is an inheritable cardiomyopathy with incomplete penetrance, variable phenotype severity and poorly described disease progression. It is characterized by high risk of life-threatening ventricular arrhythmias and sudden cardiac death in young individuals. Risk stratification and selection of patients presenting without history of life-threatening arrhythmic events for cardioverter-defibrillator implantation in primary prevention remains challenging. Purpose We aimed to assess the impact of disease progression on arrhythmic outcomes in AC patients. Methods We included consecutive AC probands and mutation-positive family members with at least one complete follow-up evaluation. Echocardiographic and electrical parameters were defined according to the 2010 Revised Task Force criteria at inclusion and at last follow-up. Structural progression was defined as development of new echocardiographic diagnostic criteria. Electrical progression was defined as the development of new diagnostic depolarization, repolarization and/or premature ventricular complex count criteria during follow-up. Non-sustained ventricular tachycardia or ventricular tachycardia occurring during follow-up defined incident ventricular arrhythmic events. Results We included a total of 144 patients (48% female, 47% probands, 40±16 years old). At inclusion, 54 patients (37%) had a history of arrhythmic events, 30 patients (21%) had overt structural disease and 114 (79%) had no or minor structural disease. During 7.0 (IQR: 4.5 to 9.4) years of follow-up, 49 patients (43%) with no or minor structural disease at inclusion developed new structural criteria being defined as progressors. Among 80 participants with no or minor structural disease and no arrhythmic history at inclusion, a first arrhythmic event occurred in 14 (17%). The incidence of arrhythmic events was higher in progressors (11/27, 41%) than in non-progressors (3/53, 6%) (p&lt;0.001) (Figure). Structural progression was associated with higher risk of first arrhythmic events during follow-up when adjusted for sex, age at inclusion and follow-up duration, independent of electrical progression (7.6, 95% CI [1.5, 37.2], P=0.01). Incident arrhythmic events distribution Conclusion Almost half of patients without overt structural cardiac disease at genetic diagnosis develop new structural criteria during 7 years follow-up and 17% experienced their first ventricular arrhythmic event. Structural progression was independently associated with ventricular arrhythmic events during follow-up. These findings highlight the increased risk of arrhythmias when structural abnormalities are detected. Their finding may initiate the evaluation for primary prevention cardioverter-defibrillator implantation.

Circadian variability patterns predict and guide premature ventricular contraction ablation procedural inducibility and outcomes

Infrequent intraprocedural premature ventricular complexes (PVCs) may impede radiofrequency catheter ablation (RFA) outcome, and pharmacologic induction is unpredictable. The purpose of this study was to determine whether PVC circadian variation could help predict drug response. Consecutive patients referred for RFA with detailed Holter monitoring and frequent monomorphic PVCs were included. Patients were divided into 3 groups based on hourly PVC count relationship to corresponding mean heart rate (HR) during each of the 24 hours on Holter: fast-HR-dependent PVC (F-HR-PVC) type for a positive correlation (Pearson, P <.05), slow-HR-dependent PVC (S-HR-PVC) type for a negative correlation, and independent-HR-PVC (I-HR-PVC) when no correlation was found. Fifty-one of the 101 patients (50.5%) had F-HR-PVC, 39.6% I-HR-PVC, and 9.9% S-HR-PVC; 30.7% had infrequent intraprocedural PVC requiring drug infusion. The best predictor of infrequent PVC was number of hours with PVC count <120/h on Holter (area under the curve 0.80, sensitivity 83.9%, specificity 74.3%, for ≥2 h). Only F-HR-PVC patients responded to isoproterenol. Isoproterenol washout or phenylephrine infusion was successful for the 3 S-HR-PVC patients, and no drug could increase PVC frequency in the 12 I-HR-PVC patients. Long-term RFA success rate in patients with frequent PVCs at baseline (82.9%) was similar to those with infrequent PVC who responded to a drug (77.8%; P = .732) but significantly higher than for those who did not respond to any drug (15.4%; P <.0001). A simple analysis of Holter PVC circadian variability provides incremental value to guide pharmacologic induction of PVCs during RFA and predict outcome. Patients with infrequent I-HR-PVC had the least successful outcomes from RF ablation.

Risk Stratification in Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy–Associated Desmosomal Mutation Carriers

We investigated the role of phenotypic characteristics in stratifying the risk of sustained ventricular arrhythmias in patients harboring arrhythmogenic right ventricular dysplasia/cardiomyopathy-associated mutations. Clinical, electrocardiographic, and arrhythmic outcome (composite measure of first occurrence of sustained ventricular tachycardia/resuscitated sudden cardiac death/sudden cardiac death/appropriate implantable cardioverter-defibrillator therapy) data were obtained for 215 patients (104 families; 85% PKP-2). During a mean follow-up of 7 years, 86 (40%) patients experienced the arrhythmic outcome. Event-free survival was significantly lower among probands (P<0.001) and symptomatic (P<0.001) patients. Integration of ECG repolarization and depolarization abnormalities allowed for differential risk categorization. Event-free survival at 5 years for the low-risk ECG group (0-1 T inversions or minor depolarization changes) was 97% versus 81% for the intermediate-risk ECG group (2 T inversions+minor depolarization changes) versus 33% for the high-risk ECG group (≥3 T inversions±major or minor depolarization changes; P<0.001). Incremental arrhythmic risk was seen in patients with increasing premature ventricular complex count on a Holter (P<0.001). Proband status (hazard ratio, 7.7; 95% confidence interval, 2.8-22.5; P<0.001), ≥3 T-wave inversions (hazard ratio, 4.2; 95% confidence interval, 1.2-14.5; P=0.035), and male sex (hazard ratio, 1.8; 95% confidence interval, 1.2-2.8; P=0.004) were independent predictors of the first arrhythmic event on multivariable analysis. Pedigree evaluation, an ECG, and a Holter examination provide for comprehensive arrhythmic risk stratification in patients with arrhythmogenic right ventricular dysplasia/cardiomyopathy-associated mutations. We propose an approach to risk stratification based on these variables.

Incidence and Predictors of Implantable Cardioverter-Defibrillator Therapy in Patients With Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy Undergoing Implantable Cardioverter-Defibrillator Implantation for Primary Prevention

The purpose of this study was to define the incidence and predictors of implantable cardioverter-defibrillator (ICD) therapy in patients with arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) after placement of an ICD for primary prevention. Patients with a diagnosis of ARVD/C often receive an ICD for prevention of sudden cardiac death. Patients (n = 84) from the Johns Hopkins registry with definite or probable ARVD/C who underwent ICD implantation for primary prevention were studied. Detailed phenotypic, genotype, and ICD event information was obtained and appropriate ICD therapies were adjudicated based on intracardiac electrograms. Over a mean follow-up of 4.7 ± 3.4 years, appropriate ICD therapy was seen in 40 patients (48%), of whom 16 (19%) received interventions for potentially fatal ventricular fibrillation/flutter episodes. Proband status (p < 0.001), inducibility at electrophysiologic study (p = 0.005), presence of nonsustained ventricular tachycardia (p < 0 .001), and Holter premature ventricular complex count >1,000/24 h (p = 0.024) were identified as significant predictors of appropriate ICD therapy. The 5-year survival free of appropriate ICD therapy for patients with 1, 2, 3, and 4 risk factors was 100%, 83%, 21%, and 15%, respectively. Inducibility at electrophysiologic study (hazard ratio: 4.5, 95% confidence interval: 1.4 to 15, p = 0.013) and nonsustained ventricular tachycardia (hazard ratio: 10.5, 95% confidence interval: 2.4 to 46.2, p = 0.002) remained as significant predictors on multivariable analysis. Nearly one-half of the ARVD/C patients with primary prevention ICD implantation experience appropriate ICD interventions. Inducibility at electrophysiologic study and nonsustained ventricular tachycardia are independent strong predictors of appropriate ICD therapy. An increase in ventricular ectopy burden was associated with progressively lower event-free (appropriate ICD interventions) survival. Incremental risk of ventricular arrhythmias and ICD therapy was observed with the presence of multiple risk factors.

Effect of atenolol on symptomatic ventricular arrhythmia without structural heart disease: A randomized placebo-controlled study

Background Ventricular arrhythmia (VA) from the right ventricular outflow tract (RVOT) is a common problem. Symptomatic patients are usually treated with β-blockers. There is little data on the systematic evaluation of the efficacy of β-blocker. We determine the efficacy of atenolol in the treatment of symtomatic VA from RVOT compared with placebo. Methods and Results This was a randomized, double-blinded, placebo-controlled study. We prospectively studied 52 consecutive patients with symptomatic VA. Severity of symptoms, 24-hour ambulatory monitoring (AECG) and quality of life (QOL) were assessed at baseline and 1 month after atenolol. Exercise testing was performed at baseline. Average premature ventricular complex (PVC) count at baseline was 21,407 ± 1740 beats per 24 hours, and 19% had ventricular tachycardia as measured by AECG. Results of this study showed that atenolol significantly decreased symptom frequency (P =.03), PVC count (P =.001) and average heart rate (P <.001) measured by AECG, whereas placebo significantly decreased symptom frequency (P =.002) but had no effect on PVC count (P =.78) or average heart rate (P =.44). Neither atenolol nor placebo had an effect on QOL. Conclusions Atenolol improves symptoms and decreases PVC count from ambulatory monitoring. Placebo improved symptoms to the same extent as atenolol but had no effect on severity of VA. This might be the so-called placebo effect, which is a concern when treating patients or doing research on the effects of a drug. (Am Heart J 2002;144:e15.)

Spontaneous Variability of Ventricular Ectopic Activity in Patients with Sustained Ventricular Tachycardia and in Survivors of Cardiac Arrest

Background: Spontaneous variability of ventricular arrhythmia has been described in patients with chronic stable ventricular arrhythmias and in patients with chronic heart failure. However, no data are available on spontaneous variability in patients with sustained ventricular tachyarrhythmias. Thus, the present study was designed to prospectively determine the extent of spontaneous variability of ventricular arrhythmia in patients with sustained ventricular tachyarrhythmias and in survivors of cardiac arrest.Methods: Ventricular arrhythmia variability was determined in 470 patients (413 men, 57 women), age (mean ± SD) 64.6 ± 9.5 years with documented ventricular tachycardia (VT), cardiac arrest, or syncope who were prospectively enrolled in a randomized trial of the comparison of electrophysiological testing with Holter monitoring to predict antiarrhythmic drug efficacy. Coronary artery disease was present in 398 (85%) patients, and the mean left ventricular ejection fraction was 0.32 ± 0.13. They underwent two 24‐hour ambulatory recordings separated by 1 day. Spontaneous variability was determined for total premature ventricular complexes (PVCs), pairs, and VT events.Results: Arithmetic mean of hourly total PVCs on day 1 was 315 ± 425. The 95% confidence limit of spontaneous reduction in total PVC count was 71%. Corresponding values for pairs, VT events of 3–15 beats, &lt; 15 beats, or &lt; 15 seconds were 72%, 80%, 94%, and 95%, respectively. The percentage increases in total PVCs, pairs, and VT events 3–15 beats, &lt; 15 beats, and &lt; 15 seconds were 243%, 259%, 397%, 1553%, and 1756%, respectively. The percentage reduction required to show a true drug effect was 63% for patients with an ejection fraction &gt; 0.32 and 76% for those with an ejection fraction ltm 0.32 (P = 0.024). Patients who presented with unmonitored syncope showed less spontaneous variability than either patients with documented, sustained VT or cardiac arrest.Conclusions: Marked spontaneous variability of ventricular arrhythmias is observed in patients with sustained ventricular tachyarrhythmias. Variability is affected by the degree of left ventricular dysfunction. The lowest variability was observed in patients presenting with unmonitored syncope. Thus, large changes in arrhythmia frequency must be observed in this population, as in others, to be ascribed to drug effect.

Nitroglycerin and premature ventricular complexes in myocardial infarction.

Because of clinical observations suggesting that nitroglycerin may suppress premature ventricular complexes during acute ischaemia, a study was undertaken to assess the effect of nitroglycerin on the incidence of premature ventricular complexes in patients with acute myocardial infarction. Forty patients with acute myocardial infarction were studied. Twenty-six patients received 0.4 mg nitroglycerin sublingually every 4 hours for the first 24 hours after admission to the coronary care unit. The total premature ventricular complex count for the 26 patients for 15 minutes before nitroglycerin was 592, and 276 for the 15 minutes after the drug (P less than 0.005). In the remaining 14 patients on the same nitroglycerin schedule, a single electrocardiographic lead was continuously recorded on tape. During the first hour after nitroglycerin, the premature ventricular complex count decreased by 58 per cent, and the second and third hours showed a decrease from control count of 71 and 65 per cent respectively. By the end of 4 hours the ectopic count was back to control level. The data indicate that nitroglycerin may decrease the number of premature ventricular complexes for up to 3 hours in patients with acute myocardial infarction. The mechanism of action of nitroglycerin is not elucidated by this study, but the observation may be of value in further studies of specific antiarrhythmic therapy and prevention of arrhythmias in patients with coronary artery disease.