Premature ventricular contraction response-induced new-onset atrial fibrillation.
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ABSTRACT:
SUBMITTER: Friedman DJ
PROVIDER: S-EPMC6404101 | biostudies-literature | 2019 Mar
REPOSITORIES: biostudies-literature
Publications
Premature ventricular contraction response-induced new-onset atrial fibrillation.
Friedman Daniel J DJ Chasten Tiffany T Anderson Kenya K Mullenix Jessica J Rider Kimberly K Sun Albert Y AY
HeartRhythm case reports 20181130 3
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Project description:Background High burden of premature ventricular complex (PVC) leads to increased cardiovascular mortality. A recent nationwide population-based study demonstrated that PVC is associated with an increased risk of atrial fibrillation (AF). However, the relationship between PVC burden and new-onset AF has not been investigated. The purpose of the study is to elucidate whether PVC burden is associated with new-onset AF. Methods and Results We designed a single-center, retrospective, large population-based cohort study to evaluate the role of PVC burden and new-onset AF in Taiwan. Patients who were AF naïve with PVC were divided into the low burden group (<1000/day) and moderate-to-high burden group (≥1000/day) based on the 24-h Holter ECG report. New-onset AF was defined as a new or first detectable event of either a persistent or paroxysmal AF. A total of 16 030 patients who were AF naïve and underwent 24-h Holter ECG monitoring were enrolled in this study, with a mean follow-up time of 973 days. A propensity score-matched analysis demonstrated that the moderate-to-high burden PVC group had a higher risk of developing new-onset AF than that of the low burden PVC group (4.91% versus 2.73%, P<0.001). Multivariate Cox regression analysis showed that moderate-to-high burden of PVC is an independent risk factor for new-onset AF. The Kaplan-Meier analysis demonstrated that patients with moderate-to-high PVC burden were associated with higher risk of new-onset AF (log-rank P<0.001). Conclusions PVC burden is associated with new-onset AF. Patients with moderate-to-high PVC burden are at a higher risk of new-onset AF. Registration URL: https://www.clinicaltrials.gov; Unique identifier: NCT03877614.
| S-EPMC10111494 | biostudies-literature
Project description:Premature ventricular contraction (PVC) and atrial fibrillation (AF) are common arrhythmias affecting 1-2% of the general population. During PVC, retrograde ventriculo-atrial activation can occur and act like an atrial ectopy. However, the clinical significance of this phenomenon is not fully understood. We aimed to elucidate whether the clinical diagnosis of PVC can increase the risk of new-onset AF. We performed a nationwide population-based analysis using the Korean National Health Insurance Service database. A total of 9,537,713 people without prior history of PVC and AF were identified. Among these people, 4135 developed PVC in 2009, and people with and without PVC were followed until 2018. People who had PVC showed an increased risk of new-onset AF as compared with people without PVC (hazard ratio [HR] = 2.705; 95% confidence interval [CI] = 2.428-3.013; p < 0.001). The risk of ischemic stroke was also significantly increased in people with PVC (HR 1.160; 95% CI 1.048-1.284; p = 0.0041). New-onset AF developed in 72 people (19.3%) among 374 people with PVC who had ischemic stroke during their follow-up. A significant interaction was observed between PVC and age with people < 65 years at greater risk of new-onset AF for having PVC. In this observational analysis, the risk of new-onset AF and ischemic stroke was increased in people with PVC. Additional evaluation to identify AF in people with PVC can be helpful.
| S-EPMC7810887 | biostudies-literature
Project description:BackgroundFrequent premature ventricular contractions (PVCs) are associated with increased risk of sudden cardiac death and can cause secondary cardiomyopathy.ObjectiveWe sought to determine the mechanism(s) responsible for prolonged refractory period and left ventricular (LV) dysfunction demonstrated in our canine model of PVC-induced cardiomyopathy.MethodsSingle myocytes were isolated from LV free wall of PVC and control canines and used for patch-clamp recording, intracellular Ca(2+) measurements, and immunocytochemistry/confocal microscopy. LV tissues adjacent to the area of myocyte isolation were used for the immunoblot quantification of protein expression.ResultsIn the PVC group, LV ejection fraction decreased from 57.6% ± 1.5% to 30.4% ± 3.1% after ≥4 months of ventricular bigeminy. Compared to control myocytes, PVC myocytes had decreased densities of both outward (transient outward current [Ito] and inward rectifier current [IK1]) and inward (L-type Ca current [ICaL]) currents, but no consistent changes in rapid or slow delayed rectifier currents. The reduction in Ito, IK1, and ICaL was accompanied by decreased protein levels of their channel subunits. The extent of reduction in Ito, IK1, and ICaL varied among PVC myocytes, creating marked heterogeneity in action potential configurations and durations. PVC myocytes showed impaired Ca-induced Ca release from the sarcoplasmic reticulum (SR), without increase in SR Ca leak or decrease in SR Ca store. This was accompanied by a decrease in dyad scaffolding protein, junctophilin-2, and loss of Cav1.2 registry with Ca-releasing channels (ryanodine receptor 2).ConclusionPVCs increase dispersion of action potential configuration/duration, a risk factor for sudden cardiac death, because of the heterogeneous reduction in Ito, IK1, and ICaL. The excitation-contraction coupling is impaired because of the decrease in ICaL and Cav1.2 misalignment with respect to ryanodine receptor 2.
| S-EPMC4252777 | biostudies-literature
Project description:Arrhythmia can significantly alter the image quality of cardiovascular magnetic resonance (CMR); automatic detection and sorting of the most frequent types of arrhythmias during the CMR acquisition could potentially improve image quality. New CMR techniques, such as non-Cartesian CMR, can allow self-gating: from cardiac motion-related signal changes, we can detect cardiac cycles without an electrocardiogram. We can further use this data to obtain a surrogate for RR intervals (valley intervals: VV). Our purpose was to evaluate the feasibility of an automated method for classification of non-arrhythmic (NA) (regular cycles) and arrhythmic patients (A) (irregular cycles), and for sorting of common arrhythmia patterns between atrial fibrillation (AF) and premature ventricular contraction (PVC), using the cardiac motion-related signal obtained during self-gated free-breathing radial cardiac cine CMR with compressed sensing reconstruction (XD-GRASP).One hundred eleven patients underwent cardiac XD-GRASP CMR between October 2015 and February 2016; 33 were included for retrospective analysis with the proposed method (6 AF, 8 PVC, 19 NA; by recent ECG). We analyzed the VV, using pooled statistics (histograms) and sequential analysis (Poincaré plots), including the median (medVV), the weighted mean (meanVV), the total number of VV values (VVval), and the total range (VVTR) and half range (VVHR) of the cumulative frequency distribution of VV, including the median to half range (medVV/VVHR) and the half range to total range (VVHR/VVTR) ratios. We designed a simple algorithm for using the VV results to differentiate A from NA, and AF from PVC.Between NA and A, meanVV, VVval, VVTR, VVHR, medVV/VVHR and VVHR/VVTR ratios were significantly different (p values = 0.00014, 0.0027, 0.000028, 5×10-9, 0.002, respectively). Between AF and PVC, meanVV, VVval and medVV/VVHR ratio were significantly different (p values = 0.018, 0.007, 0.044, respectively). Using our algorithm, sensitivity, specificity, and accuracy were 93 %, 95 % and 94 % to discriminate between NA and A, and 83 %, 71 %, and 77 % to discriminate between AF and PVC, respectively; areas under the ROC curve were 0.93 and 0.89.Our study shows we can reliably detect arrhythmias and differentiate AF from PVC, using self-gated cardiac cine XD-GRASP CMR.
| S-EPMC5123392 | biostudies-other
Project description:BackgroundPremature ventricular complexes (PVCs) are ectopic heartbeats caused by early myocardial depolarizations, previously thought to be benign. Recent studies found high PVC burden above 24% can induce or contribute to cardiomyopathy and heart failure. We present a case of PVC-induced dilated cardiomyopathy (DCM).Case summaryA 68-year-old woman was admitted with pneumonia after an overseas trip with a preceding viral respiratory tract infection. An initial chest X-ray was suggestive of cardiomegaly. A transthoracic echocardiogram (TTE) revealed DCM with global systolic dysfunction (left ventricular ejection fraction <30%) without valvular lesions. Biochemistry and coronary angiography were normal. Clinical deterioration occurred despite medical therapy. A 24-h Holter monitoring detected 27% PVCs, which was thought to have caused DCM. As an alternative to cardiac resynchronization therapy and an implantable cardiac defibrillator for primary prevention, ablation of the PVC focus led to complete suppression of ectopy. Post-procedure TTEs and Holter monitoring showed normalized systolic function and low PVC burden.DiscussionBecause high PVC burden can lead to cardiomyopathy and heart failure, suppression of PVC should be considered to restore ventricular function for patients with structural heart disease and frequent symptomatic PVCs. This case highlights that PVCs may be a modifiable risk factor for heart failure that can be successfully treated with pharmacological therapies or catheter ablation.
| S-EPMC6458864 | biostudies-literature
Project description:Mechanisms behind development of premature ventricular contraction (PVC)-induced cardiomyopathy remain unclear. PVCs may adversely modulate the autonomic nervous system to promote development of heart failure. Afferent neurons in the inferior vagal (nodose) ganglia transduce cardiac activity and modulate parasympathetic output. Effects of PVCs on cardiac parasympathetic efferent and vagal afferent neurotransmission are unknown. The purpose of this study was to evaluate effects of PVCs on vagal afferent neurotransmission and compare these effects with a known powerful autonomic modulator, myocardial ischemia. In 16 pigs, effects of variably coupled PVCs on heart rate variability (HRV) and vagal afferent neurotransmission were evaluated. Direct nodose neuronal recordings were obtained in vivo, and cardiac-related afferent neurons were identified based on their response to cardiovascular interventions, including ventricular chemical and mechanical stimuli, left anterior descending (LAD) coronary artery occlusion, and variably coupled PVCs. On HRV analysis before versus after PVCs, parasympathetic tone decreased (normalized high frequency: 83.6?±?2.8 to 72.5?±?5.3; P < 0.05). PVCs had a powerful impact on activity of cardiac-related afferent neurons, altering activity of 51% of neurons versus 31% for LAD occlusion (P < 0.05 vs. LAD occlusion and all other cardiac interventions). Both chemosensitive and mechanosensitive neurons were activated by PVCs, and their activity remained elevated even after cessation of PVCs. Cardiac afferent neural responses to PVCs were greater than any other intervention, including ischemia of similar duration. These data suggest that even brief periods of PVCs powerfully modulate vagal afferent neurotransmission, reflexly decreasing parasympathetic efferent tone.NEW & NOTEWORTHY Premature ventricular contractions (PVCs) are common in many patients and, at an increased burden, are known to cause heart failure. This study determined that PVCs powerfully modulate cardiac vagal afferent neurotransmission (exerting even greater effects than ventricular ischemia) and reduce parasympathetic efferent outflow to the heart. PVCs activated both mechano- and chemosensory neurons in the nodose ganglia. These peripheral neurons demonstrated adaptation in response to PVCs. This study provides additional data on the potential role of the autonomic nervous system in PVC-induced cardiomyopathy.
| S-EPMC6766725 | biostudies-literature
Project description:Premature ventricular contractions (PVCs) commonly coexist with cardiomyopathy. Recently, PVCs have been identified as a possible cause of cardiomyopathy. We developed a PVC-induced cardiomyopathy animal model using a novel premature pacing algorithm to assess timeframe and reversibility of this cardiomyopathy and examine the associated histopathologic abnormalities.Thirteen mongrel dogs were implanted with a specially programmed pacemaker capable of simulating ventricular extrasystoles. Animals were randomly assigned to either 12 weeks of bigeminal PVCs (n = 7) or no PVCs (control, n = 6). Continuous 24-hour Holter monitoring corroborated ventricular bigeminy in the PVC group (PVC, 49.8% versus control, < 0.01%; P<0.0001). After 12 weeks, only the PVC group had cardiomyopathy, with a significant reduction in left ventricular ejection fraction (PVC, 39.7 ± 5.4% versus control, 60.7 ± 3.8%; P < 0.0001) and an increase in left ventricular end-systolic dimension (PVC, 33.3 ± 3.5 mm versus control, 23.7 ± 3.6 mm; P < 0.001). Ventricular effective refractory period showed a trend to prolong in the PVC group. PVC-induced cardiomyopathy was resolved within 2 to 4 weeks after discontinuation of PVCs. No inflammation, fibrosis, or changes in apoptosis and mitochondrial oxidative phosphorylation were observed with PVC-induced cardiomyopathy.This novel PVC animal model demonstrates that frequent PVCs alone can induce a reversible form of cardiomyopathy in otherwise structurally normal hearts. PVC-induced cardiomyopathy lacks gross histopathologic and mitochondrial abnormalities seen in other canine models of cardiomyopathy.
| S-EPMC3175603 | biostudies-literature
Project description:CONTEXT:Although the heritability of atrial fibrillation (AF) is established, the contribution of familial AF to predicting new-onset AF remains unknown. OBJECTIVE:To determine whether familial occurrence of AF is associated with new-onset AF beyond established risk factors. DESIGN, SETTING, AND PARTICIPANTS:The Framingham Heart Study, a prospective community-based cohort study started in 1948. Original and Offspring Cohort participants were aged at least 30 years, were free of AF at the baseline examination, and had at least 1 parent or sibling enrolled in the study. The 4421 participants in this analysis (mean age, 54 [SD, 13] years; 54% women) were followed up through December 31, 2007. MAIN OUTCOME MEASURES:Incremental predictive value of incorporating different features of familial AF (any familial AF, premature familial AF [onset ?65 years old], number of affected relatives, and youngest age of onset in a relative) into a risk model for new-onset AF. RESULTS:Across 11,971 examinations during the period 1968-2007, 440 participants developed AF. Familial AF occurred among 1185 participants (26.8%) and premature familial AF occurred among 351 participants (7.9%). Atrial fibrillation occurred more frequently among participants with familial AF than without familial AF (unadjusted absolute event rates of 5.8% and 3.1%, respectively). The association was not attenuated by adjustment for AF risk factors (multivariable-adjusted hazard ratio, 1.40; 95% confidence interval [CI], 1.13-1.74) or reported AF-related genetic variants. Among the different features of familial AF examined, premature familial AF was associated with improved discrimination beyond traditional risk factors to the greatest extent (traditional risk factors, C statistic, 0.842 [95% CI, 0.826-0.858]; premature familial AF, C statistic, 0.846 [95% CI, 0.831-0.862]; P = .004). Modest changes in integrated discrimination improvement were observed with premature familial AF (2.1%). Net reclassification improvement (assessed using 8-year risk thresholds of <5%, 5%-10%, and >10%) did not change significantly with premature familial AF (index statistic, 0.011; 95% CI, -0.021 to 0.042; P = .51), although categoryless net reclassification was improved (index statistic, 0.127; 95% CI, 0.064-0.189; P = .009). CONCLUSIONS:In this cohort, familial AF was associated with an increased risk of AF that was not attenuated by adjustment for AF risk factors including genetic variants. Assessment of premature familial AF was associated with a very slight increase in predictive accuracy compared with traditional risk factors.
| S-EPMC3073054 | biostudies-literature
Project description:BACKGROUND:Frequent premature ventricular contractions (PVCs) have been associated with PVC-induced cardiomyopathy (CM) in some patients. OBJECTIVE:The purpose of this study was to understand the cardiac consequences of different PVC burdens and the minimum burden required to induce left ventricular (LV) dysfunction. METHODS:Right ventricular apical PVCs at a coupling interval of 240 ms were introduced at different PVC burdens in 9 mongrel canines. A stepwise increase in PVC burden was implemented every 8 weeks from 0% (baseline), 7%, 14%, 25%, 33% to 50% using our premature pacing algorithm. Echocardiogram and 24-hour Holter were obtained at 4- and 8-week period for each PVC burden with a single blinded reader assessing all echocardiographic parameters including those assessed by speckle tracking imaging (EchoPAC workstation, General Electric). CM was defined as left ventricular ejection fraction (LVEF) <50% or LVEF drop >10% points. Interleukin-6 and pro-brain natriuretic peptide levels were obtained at the end of each PVC burden. RESULTS:The mean LVEF (mean heart rate) at 8 weeks for each PVC burden (0%, 7%, 14%, 33%, and 50%) were 57% ± 2.9% (85 ± 13 beats/min), 54.4% ± 3% (81 ± 10 beats/min), 53.3% ± 5% (77 ± 12 beats/min), 51.1% ± 4.2% (79 ± 14 beats/min), 47.7% ± 3.8% (80 ± 14 beats/min), and 44.7% ± 1.9% (157 ± 43 beats/min). PVC-induced CM was present in 11.1%, 44.4%, and 100% of animals with 25%, 33%, and 50% PVC burden, respectively. E/A ratio and radial strain decreased while left atrial size increased beyond 33% PVC burden. No changes in pro-brain natriuretic peptide and interleukin-6 levels were noted at any PVC burden. CONCLUSION:LV systolic function (LVEF and radial strain) declined linearly as PVC burden increased. PVC-induced CM developed in some canines with 25% and 33% PVC burden, but developed in all animals with 50% PVC burden.
| S-EPMC4762722 | biostudies-literature
Project description:BACKGROUND:The presence and significance of neural remodeling in premature ventricular contraction-induced cardiomyopathy (PVC-CM) remain unknown. OBJECTIVES:This study aimed to characterize cardiac sympathovagal balance and proarrhythmia in a canine model of PVC-CM. METHODS:In 12 canines, the investigators implanted epicardial pacemakers and radiotelemetry units to record cardiac rhythm and nerve activity (NA) from the left stellate ganglion (SNA), left cardiac vagus (VNA), and arterial blood pressure. Bigeminal PVCs (200 ms coupling) were applied for 12 weeks to induce PVC-CM in 7 animals then disabled for 4 weeks to allow complete recovery of left ventricular ejection fraction (LVEF), versus 5 sham controls. RESULTS:After 12 weeks of PVCs, LVEF (p = 0.006) and dP/dT (p = 0.007) decreased. Resting SNA (p = 0.002) and VNA (p = 0.04), exercise SNA (p = 0.01), SNA response to evoked PVCs (p = 0.005), heart rate (HR) at rest (p = 0.003), and exercise (p < 0.04) increased, whereas HR variability (HRV) decreased (p = 0.009). There was increased spontaneous atrial (p = 0.02) and ventricular arrhythmias (p = 0.03) in PVC-CM. Increased SNA preceded both atrial (p = 0.0003) and ventricular (p = 0.009) arrhythmia onset. Clonidine suppressed SNA and abolished all arrhythmias. After disabling PVC for 4 weeks, LVEF (p = 0.01), dP/dT (p = 0.047), and resting VNA (p = 0.03) recovered to baseline levels. However, SNA, resting HR, HRV, and atrial (p = 0.03) and ventricular (p = 0.03) proarrhythmia persisted. There was sympathetic hyperinnervation in stellate ganglia (p = 0.02) but not ventricles (p = 0.2) of PVC-CM and recovered animals versus sham controls. CONCLUSIONS:Neural remodeling in PVC-CM is characterized by extracardiac sympathetic hyperinnervation and sympathetic neural hyperactivity that persists despite normalization of LVEF. The altered cardiac sympathovagal balance is an important trigger and substrate for atrial and ventricular proarrhythmia.
| S-EPMC7006705 | biostudies-literature