RESUMEN
Frequent premature ventricular contractions (PVCs) promoted eccentric cardiac hypertrophy and reduced ejection fraction (EF) in a large animal model of PVC-induced cardiomyopathy (PVC-CM), but the molecular mechanisms and markers of this hypertrophic remodeling remain unexplored. Healthy mongrel canines were implanted with pacemakers to deliver bigeminal PVCs (50% burden with 200-220 ms coupling interval). After 12 weeks, left ventricular (LV) free wall samples were studied from PVC-CM and Sham groups. In addition to reduced LV ejection fraction (LVEF), the PVC-CM group showed larger cardiac myocytes without evident ultrastructural alterations compared to the Sham group. Biochemical markers of pathological hypertrophy, such as store-operated Ca2+ entry, calcineurin/NFAT pathway, ß-myosin heavy chain, and skeletal type α-actin were unaltered in the PVC-CM group. In contrast, pro-hypertrophic and antiapoptotic pathways including ERK1/2 and AKT/mTOR were activated and/or overexpressed in the PVC-CM group, which appeared counterbalanced by an overexpression of protein phosphatase 1 and a borderline elevation of the anti-hypertrophic factor atrial natriuretic peptide. Moreover, the potent angiogenic and pro-hypertrophic factor VEGF-A and its receptor VEGFR2 were significantly elevated in the PVC-CM group. In conclusion, a molecular program is in place to keep this structural remodeling associated with frequent PVCs as an adaptive pathological hypertrophy.
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Cardiomiopatías , Complejos Prematuros Ventriculares , Animales , Perros , Complejos Prematuros Ventriculares/complicaciones , Remodelación Ventricular , Modelos Animales de Enfermedad , Hipertrofia/complicacionesRESUMEN
Premature ventricular contractions (PVCs) are the most frequent ventricular arrhythmias in the overall population. PVCs are known to acutely enhance contractility by the post-extrasystolic potentiation phenomenon, but over time persistent PVCs promote PVC-induced cardiomyopathy (PVC-CM), characterized by a reduction of the left ventricular (LV) ejection fraction. Ca2+ cycling in myocytes commands muscle contraction and in this process, SERCA2 leads the Ca2+ reuptake into the sarcoplasmic reticulum (SR) shaping cytosolic Ca2+ signal decay and muscle relaxation. Altered Ca2+ reuptake can contribute to the contractile dysfunction observed in PVC-CM. To better understand Ca2+ handling using our PVC-CM model (canines with 50% PVC burden for 12 weeks), SR-Ca2+ reuptake was investigated by measuring Ca2+ dynamics and analyzing protein expression. Kinetic analysis of Ca2+ reuptake in electrically paced myocytes showed a ~ 21 ms delay in PVC-CM compared to Sham in intact isolated myocytes, along with a ~ 13% reduction in SERCA2 activity assessed in permeabilized myocytes. Although these trends were not statistically significant between groups using hierarchical statistics, relaxation of myocytes following contraction was significantly slower in PVC-CM vs Sham myocytes. Western blot analyses indicate a 22% reduction in SERCA2 expression, a 23% increase in phospholamban (PLN) expression, and a 50% reduction in PLN phosphorylation in PVC-CM samples vs Sham. Computational analysis simulating a 20% decrease in SR-Ca2+ reuptake resulted in a ~ 22 ms delay in Ca2+ signal decay, consistent with the experimental result described above. In conclusion, SERCA2 and PLB alterations described above have a modest contribution to functional adaptations observed in PVC-CM.
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Cardiomiopatías , Complejos Prematuros Ventriculares , Animales , Perros , Complejos Prematuros Ventriculares/metabolismo , Retículo Sarcoplasmático/metabolismo , Cinética , Cardiomiopatías/metabolismo , Células Musculares , ATPasas Transportadoras de Calcio del Retículo Sarcoplásmico , Calcio/metabolismo , Miocitos Cardíacos/metabolismoRESUMEN
Electrical disturbances, such as atrial fibrillation (AF), dyssynchrony, tachycardia, and premature ventricular contractions (PVCs), are present in most patients with heart failure (HF). While these disturbances may be the consequence of HF, increasing evidence suggests that they may also cause or aggravate HF. Animal studies show that longer-lasting left bundle branch block, tachycardia, AF, and PVCs lead to functional derangements at the organ, cellular, and molecular level. Conversely, electrical treatment may reverse or mitigate HF. Clinical studies have shown the superiority of atrial and pulmonary vein ablation for rhythm control and AV nodal ablation for rate control in AF patients when compared with medical treatment. Ablation of PVCs can also improve left ventricular function. Cardiac resynchronization therapy (CRT) is an established adjunct therapy currently undergoing several interesting innovations. The current guideline recommendations reflect the safety and efficacy of these ablation therapies and CRT, but currently, these therapies are heavily underutilized. This review focuses on the electrical treatment of HF with reduced ejection fraction (HFrEF). We believe that the team of specialists treating an HF patient should incorporate an electrophysiologist in order to achieve a more widespread use of electrical therapies in the management of HFrEF and should also include individual conditions of the patient, such as body size and gender in therapy fine-tuning.
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Fibrilación Atrial , Terapia de Resincronización Cardíaca , Ablación por Catéter , Insuficiencia Cardíaca , Fibrilación Atrial/cirugía , Humanos , Volumen Sistólico , Resultado del TratamientoRESUMEN
BACKGROUND: Operation of auto-threshold testing (ATT) algorithm in current dual chamber cardiac devices require temporary shortening of atrio-ventricular (AV) delay to accurately measure evoked potential (capture) after a pacing pulse. Near simultaneous AV pacing causes atrial pressure elevation and may be associated with atrial arrhythmias. OBJECTIVE: We evaluated the prevalence of atrial arrhythmias induced by ATT in Abbott devices. METHODS: Device clinic records were reviewed at a single center for patients with dual chamber Abbott pacemaker/ICD. ATT-induced atrial fibrillation (AF) cases were defined as new appropriate mode switch episodes while the ATT was operating. The auto-capture test trends were defined as unstable if there were deviations >1 V in capture threshold trend events that did not correlate with routine in-office testing. RESULTS: One hundred and seventy patients were programmed in dual chamber pacing mode. The ventricular ATT was active in 118 patients and of these 78 had true mode switch episodes. Six patients developed AF during ventricular ATT. Three patients had most recorded atrial arrhythmias in close association with ATT (63%, 66%, 100% vs 2%,9%, 33% in other patients with known prior AF). An unstable auto-capture trend curve was seen in 33 patients (6 showing ATT-induced AF) versus 85 patients with stable auto-capture curve and no ATT-induced AF (P = .0001, the χ2 test). CONCLUSION: Ventricular auto-capture algorithm use is associated with induction of AF in dual chamber Abbott devices with a prevalence of over 5%. AF occur more frequently (18%) in patients with erratic ventricular ATT trend results.
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Fibrilación Atrial , Desfibriladores Implantables , Marcapaso Artificial , Algoritmos , Fibrilación Atrial/diagnóstico , Fibrilación Atrial/epidemiología , Fibrilación Atrial/terapia , Estimulación Cardíaca Artificial/efectos adversos , Corazón , HumanosRESUMEN
AIMS: High premature ventricular contractions (PVCs) burden does not always predict the development of PVC-cardiomyopathy (CM). We sought to evaluate post-extrasystolic potentiation (PESP) of left ventricular ejection fraction (LVEF) to predict the severity of PVC-CM in an animal model. METHODS AND RESULTS: Right ventricular apical bigeminal PVCs were introduced for 12 weeks in 11 canines to induce PVC-CM. Echocardiograms were performed to obtain LVEF without ectopy (Echo-1) and during PVCs (200 and 350 ms coupling intervals, Echo-2, and Echo-3, respectively), and premature atrial contractions (PACs) (Echo-4) at baseline and after 12 weeks of bigeminal PVCs. PESP was calculated as delta-LVEF between the sinus beat post-ectopy LVEF (Echo-2, -3, and -4, respectively) and LVEF without PVC (Echo-1) at baseline and 12 weeks of high PVC burden. A hyperdynamic LV function (LVEF > 70%) was noted in all animals only with early-coupled PVCs (LVEF at 200 ms: 74.4 ± 6%) at baseline. While PVC PESP at 200 ms had a strong significant correlation with the final 12-week LVEF (R = 0.8, P = 0.003), PVC PESP at 350 ms and PAC PESP had a positive but non-significant correlation (R = 0.53, P = 0.09, and R = 0.29, P = 0.34, respectively). Premature ventricular contraction PESP at 350 ms was significantly higher after PVC-CM had developed (delta-LVEF baseline 2.7 ± 2.9% vs. 12 weeks 18.6 ± 12.3% P < 0.001). CONCLUSION: Bigeminal early-coupled PVCs cause hyperdynamic left ventricular function in the structurally normal canine heart due to PESP. The degree of PESP at baseline is inversely proportional to the PVC-CM severity at 12 weeks and maybe a predictor of PVC-CM as it may assess the myocardial adaptation reserve to PVCs.
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Cardiomiopatías , Complejos Prematuros Ventriculares , Animales , Perros , Ecocardiografía , Volumen Sistólico , Función Ventricular Izquierda , Complejos Prematuros Ventriculares/diagnósticoRESUMEN
BACKGROUND AND OBJECTIVES: The use of nonfluoroscopic three-dimensional electroanatomic mapping (3DM) systems reduces radiation exposure during ablation procedures. In this study, we sought to determine the value of 3DM during routine device implant procedures. METHODS: Seventy nonselected patients underwent implantation of a single chamber, dual chamber, or biventricular device guided by Ensite (Abbott Laboratories) to limit fluoroscopy use and compared with 70 consecutive patients, who underwent matching procedures with standard fluoroscopy use (FL) in the period immediately preceding the use of 3DM. The venous anatomy, right atrium, and ventricle and coronary sinus were mapped with 0.035 inch J-wire, quadripolar catheter, and/or angioplasty wire. The leads were advanced under real-time visualization in Ensite. RESULTS: 3DM reduced both fluoroscopy time and dose. Median fluoroscopy time for FL vs 3DM was 5.5 minutes (interquartile range [IQR]: 3.8-8.1) vs 0.9 minutes (IQR: 0.6-1.9) (P < .001) for single chamber devices, 6.3 minutes (IQR: 5.1-7.9) vs 3.3 minutes (IQR: 1.9-4) (P < .001) for dual-chamber devices, and 28.6 minutes (IQR: 19.6-36.2) to 14.7 minutes (IQR: 10.4-22.3) (P = .009) for biventricular devices, respectively. The median air kerma for FL vs 3DM was 15.4 mGy (IQR: 8.1-30.2) vs 4 mGy (IQR: 1.8-8) (P < .001) for single chamber devices, 16 mGy (IQR: 12-18.5) to 9.4 mGy (IQR: 7.5-11.3) (P = .001) for dual-chamber devices, and 324 mGy (IQR: 143-668.7) to 115 mGy (IQR:77-204) (P = .014) for biventricular devices, respectively. There were no procedural complications. At 3-month follow-up, there was no difference in voltage threshold measurements between the groups. CONCLUSION: The use of 3DM leads to significantly reduced fluoroscopy time and fluoroscopy dose during routine device implantation.
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Estimulación Cardíaca Artificial , Técnicas Electrofisiológicas Cardíacas , Imagenología Tridimensional , Marcapaso Artificial , Dosis de Radiación , Exposición a la Radiación/prevención & control , Radiografía Intervencional , Anciano , Terapia de Resincronización Cardíaca , Dispositivos de Terapia de Resincronización Cardíaca , Bases de Datos Factuales , Fluoroscopía , Humanos , Masculino , Seguridad del Paciente , Exposición a la Radiación/efectos adversos , Radiografía Intervencional/efectos adversos , Estudios Retrospectivos , Medición de Riesgo , Factores de Riesgo , Factores de Tiempo , Resultado del Tratamiento , VirginiaRESUMEN
INTRODUCTION: Frequent premature ventricular contractions (PVCs) can cause cardiomyopathy (CM). Postextrasystolic potentiation (PESP) and irregularity have been in implicated as triggers of PVC-CM. Because both phenomena can also be found in premature atrial contractions (PACs), it is speculated that frequent PACs have similar consequences. METHODS AND RESULTS: A single-center, retrospective study included all consecutive patients undergoing a 14-day Holter monitors (November 2014 to October 2016). Patients were divided into four groups by ectopy burden group 1 (<1%) and remaining by tertiles (group 2-4). Echocardiographic and arrhythmic data were compared between PAC and PVC burdens. In addition, a translational PAC animal model was used to assess the chronic effects of frequent PACs. A total 846 patients were reviewed. In contrast to PVCs, we found no difference in left ventricular ejection fraction (LVEF), end-systolic and end-diastolic dimensions and presence of CM (LVEF <50%) between different PAC groups. Multivariate regression analysis demonstrated that only PVC burden predicted low EF (odds ratio, 1.1; confidence interval, 1.03-1.13; P = .001). While there was a weak correlation between PAC burden and supraventricular tachycardia (SVT) episodes and atrial fibrillation (AF) burden (r = 0.19; P < .001), there was no correlation between PAC burden and LVEF or CM. Finally, atrial bigeminy in our animal model did not significantly decrease LVEF after 3 months. CONCLUSION: PAC burden is associated with increased AF and SVT episodes. In contrast to a high PVC burden, a high PAC burden is not associated with CM. Our findings suggest that heart rate irregularity and/or PESP may play a minimal role in the pathophysiology of PVC-CM.
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Fibrilación Atrial/etiología , Complejos Atriales Prematuros/complicaciones , Cardiomiopatías/etiología , Taquicardia Supraventricular/etiología , Complejos Prematuros Ventriculares/complicaciones , Potenciales de Acción , Animales , Fibrilación Atrial/diagnóstico , Fibrilación Atrial/fisiopatología , Complejos Atriales Prematuros/diagnóstico , Complejos Atriales Prematuros/fisiopatología , Cardiomiopatías/diagnóstico por imagen , Cardiomiopatías/fisiopatología , Enfermedad Crónica , Estudios Transversales , Modelos Animales de Enfermedad , Perros , Ecocardiografía , Electrocardiografía Ambulatoria , Femenino , Frecuencia Cardíaca , Humanos , Masculino , Estudios Retrospectivos , Medición de Riesgo , Volumen Sistólico , Taquicardia Supraventricular/diagnóstico , Taquicardia Supraventricular/fisiopatología , Factores de Tiempo , Función Ventricular Izquierda , Complejos Prematuros Ventriculares/diagnóstico , Complejos Prematuros Ventriculares/fisiopatologíaRESUMEN
BACKGROUND: Implantable cardioverter defibrillators (ICDs) must establish a balance between delivering appropriate shocks for ventricular tachyarrhythmias and withholding inappropriate shocks for lead-related oversensing ("noise"). To improve the specificity of ICD therapy, manufacturers have developed proprietary algorithms that detect lead noise. The SecureSenseTM RV Lead Noise discrimination (St. Jude Medical, St. Paul, MN, USA) algorithm is designed to differentiate oversensing due to lead failure from ventricular tachyarrhythmias and withhold therapies in the presence of sustained lead-related oversensing. METHODS AND RESULTS: We report 5 patients in whom appropriate ICD therapy was withheld due to the operation of the SecureSense algorithm and explain the mechanism for inhibition of therapy in each case. Limitations of algorithms designed to increase ICD therapy specificity, especially for the SecureSense algorithm, are analyzed. CONCLUSION: The SecureSense algorithm can withhold appropriate therapies for ventricular arrhythmias due to design and programming limitations. Electrophysiologists should have a thorough understanding of the SecureSense algorithm before routinely programming it and understand the implications for ventricular arrhythmia misclassification.
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Algoritmos , Arritmias Cardíacas/diagnóstico , Arritmias Cardíacas/terapia , Técnicas Electrofisiológicas Cardíacas/métodos , Procesamiento de Señales Asistido por Computador , Relación Señal-Ruido , Anciano , Arritmias Cardíacas/fisiopatología , Desfibriladores Implantables , Cardioversión Eléctrica , Falla de Equipo , Femenino , Humanos , Valor Predictivo de las Pruebas , Diseño de Prótesis , Reproducibilidad de los Resultados , Diseño de Software , Resultado del TratamientoRESUMEN
Arrhythmias frequently accompany heart failure and left ventricular dysfunction. Tachycardias, atrial fibrillation, and premature ventricular contractions can induce a reversible form of dilated cardiomyopathy (CM) known as arrhythmia-induced CM (AiCM). The intriguing question is why certain individuals are more susceptible to AiCM, despite similar arrhythmia burdens. The primary challenge is determining the extent of arrhythmias' contribution to left ventricular systolic dysfunction. AiCM should be considered in patients with a mean heart rate of >100 beats/min, atrial fibrillation, or a PVC burden of >10%. Confirmation of AiCM occurs when CM reverses upon eliminating the responsible arrhythmia. Therapy choice depends on the specific arrhythmia, patient comorbidities, and preferences. After left ventricular function is restored, ongoing follow-up is essential if an abnormal myocardial substrate persists. Accurate diagnosis and treatment of AiCM have the potential to enhance patients' quality of life, improve clinical outcomes, and reduce hospital admissions and overall health care costs.
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Arritmias Cardíacas , Humanos , Arritmias Cardíacas/etiología , Arritmias Cardíacas/terapia , Arritmias Cardíacas/fisiopatología , Cardiomiopatías/etiología , Cardiomiopatías/terapia , Cardiomiopatías/fisiopatología , Cardiomiopatías/diagnóstico , Cardiomiopatía Dilatada/terapia , Cardiomiopatía Dilatada/fisiopatología , Cardiomiopatía Dilatada/etiologíaRESUMEN
BACKGROUND: The prevalence of COVID-19 as the primary diagnosis among hospitalized patients with myocardial injury has increased during the pandemic and targeting elevated oxidant stress and inflammatory biomarkers may offer a potential role for novel therapies to improve outcomes. METHODS: At a single VA Medical Center from January 1 through December 31, 2021, troponin assays from patients being evaluated in the Emergency Room for consideration of admission were analyzed and peak levels from each patient were considered abnormal if exceeding the Upper Reference Limit (URL). Among admitted patients with an elevated troponin level, ICD-10 diagnoses were categorized, biomarker elevations were recorded, and independent predictors of death in patients with COVID-19 were determined at a median of 6-months following admission. RESULTS: Of 998 patients, 399 (40 %) had a negative troponin and were not included in the analysis. Additional patients with an elevated troponin were also excluded, either because they were not admitted (n = 68) or had a final diagnosis of Type 1 MI (n = 117). Of the remaining 414 patients with an elevated peak troponin, COVID-19 was the primary diagnosis in 43 patients (10 %) and was the 4th most common diagnosis of patients admitted with myocardial injury behind congestive heart failure, sepsis, and COPD or pneumonia. At a median of 6-months following admission, 18 (42 %) of the COVID-19 patients had died and independent predictors of death (Odd Ratio: Confidence Intervals) were age (1.18: 1.06â1.37), Troponin level (Log 10 transformed) (16.54: 2.30â266.65) and C-Reactive Protein (CRP) (1.30: 1.10â1.65). CONCLUSIONS: Newly diagnosed COVID-19 during the pandemic was a common cause of elevated troponin in hospitalized patients without a Type 1 MI. Age, peak troponin level and peak CRP level were independent predictors of poor outcomes and suggest a need to target these cardiac biomarkers, potentially with novel antioxidant or anti-inflammatory therapies.
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Biomarcadores , COVID-19 , Troponina , Humanos , COVID-19/sangre , COVID-19/mortalidad , Biomarcadores/sangre , Masculino , Femenino , Persona de Mediana Edad , Anciano , Troponina/sangre , SARS-CoV-2 , Infarto del Miocardio/sangre , Infarto del Miocardio/diagnósticoRESUMEN
BACKGROUND: The significance of autonomic dysfunction in premature ventricular contraction-induced cardiomyopathy (PVC-CM) remain unknown. OBJECTIVE: Utilizing a novel "dual stressor" provocative challenge combining exercise with premature ventricular contraction (PVCs), the authors characterized the functional and molecular mechanisms of cardiac autonomic (cardiac autonomic nervous system) remodeling in a PVC-CM animal model. METHODS: In 15 canines (8 experimental, 7 sham), we implanted pacemakers and neurotelemetry devices and subjected animals to 12 weeks of bigeminal PVCs to induce PVC-CM. Sympathetic nerve activity (SNA), vagal nerve activity (VNA), and heart rate were continuously recorded before, during, and after treadmill exercise challenge with and without PVCs, at baseline and after development of PVC-CM. Western blot and enzyme-linked immunosorbent assay were used to evaluate molecular markers of neural remodeling. RESULTS: Exercise triggered an increase in both SNA and VNA followed by late VNA withdrawal. With PVCs, the degree of exercise-induced SNA augmentation was magnified, whereas late VNA withdrawal became blunted. After PVC-CM development, SNA was increased at rest but failed to adequately augment during exercise, especially with PVCs, coupled with impaired VNA and heart rate recovery after exercise. In the remodeled cardiac autonomic nervous system, there was widespread sympathetic hyperinnervation and elevated transcardiac norepinephrine levels but unchanged parasympathetic innervation, indicating sympathetic overload. However, cardiac nerve growth factor was paradoxically downregulated, suggesting an antineurotrophic counteradaptive response to PVC-triggered sympathetic overload. CONCLUSIONS: Sympathetic overload, sympathetic dysfunction, and parasympathetic dysfunction in PVC-CM are unmasked by combined exercise and PVC challenge. Reduced cardiac neurotrophic factor might underlie the mechanisms of this dysfunction. Neuromodulation therapies to restore autonomic function could constitute a novel therapeutic approach for PVC-CM.
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INTRODUCTION: Phrenic nerve (PN) stimulation (PNS) frequently limits cardiac resynchronization therapy (CRT). Yet, pacing strategies to minimize PNS have not been systematically compared. We propose to: (1) compare different pacing strategies to minimize PNS in CRT and (2) evaluate differences between PN and left ventricular (LV) capture thresholds among LV pacing configurations. METHODS AND RESULTS: PN and LV thresholds were obtained using 6 LV configurations in 28 patients with any PNS during CRT implantation or replacement. Incidence of PNS was compared in all LV configurations by programming pacing output to (1) One Volt (V) above LV threshold, (2) triple pulse width (PW) at LV threshold, and (3) 1.5 times LV threshold for each patient. PN thresholds and PN strength-duration curves were statistically different between configurations (P < 0.05). RingâRVcoil and RingâCan had the largest difference between PN and LV thresholds. Pacing output programmed to 1.5 times LV threshold, 1 V above LV threshold, and triple PW at LV threshold had similar probability of PNS between LV configurations. However, 1 V above LV threshold and triple PW at LV threshold frequently resulted in poor (< 30%) LV capture safety margin (14-43% and 53-68%, respectively). Freedom from PNS (programmed output at twice LV threshold) was found in 88%, 84%, and 52% with 6, 3, or 2 available LV configurations, respectively. CONCLUSION: Multiple LV pacing configurations marginally increase the probability of avoiding PNS by electronic reprogramming. Pacing output programmed to 1.5 times LV threshold is an additional alternative to minimize PNS when electronic reprogramming options are limited.
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Estimulación Cardíaca Artificial/normas , Terapia de Resincronización Cardíaca/normas , Nervio Frénico/fisiología , Estimulación Cardíaca Artificial/métodos , Terapia de Resincronización Cardíaca/métodos , Estimulación Eléctrica/métodos , Humanos , Estudios ProspectivosRESUMEN
Nonischemic cardiomyopathies are a frequent occurrence. The understanding of the mechanism(s) and triggers of these cardiomyopathies have led to improvement and even recovery of left ventricular function. Although chronic right ventricular pacing-induced cardiomyopathy has been recognized for many years, left bundle branch block and pre-excitation have been recently identified as potential reversible causes of cardiomyopathy. These cardiomyopathies share a similar abnormal ventricular propagation that can be recognized by a wide QRS duration with left bundle branch block pattern; thus, we coined the term abnormal conduction-induced cardiomyopathies. Such abnormal propagation results in an abnormal contractility that can only be recognized by cardiac imaging as ventricular dyssynchrony. Appropriate diagnosis and treatment will not only lead to improved left ventricular ejection fraction and functional class, but may also reduce morbidity and mortality. This review presents an update of the mechanisms, prevalence, incidence, and risk factors, as well as their diagnosis and management, while highlighting current gaps of knowledge.
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Bloqueo de Rama , Cardiomiopatías , Humanos , Bloqueo de Rama/terapia , Volumen Sistólico , Función Ventricular Izquierda , Trastorno del Sistema de Conducción Cardíaco , Cardiomiopatías/diagnóstico , Cardiomiopatías/epidemiología , Cardiomiopatías/etiología , Arritmias Cardíacas/complicaciones , Resultado del TratamientoRESUMEN
Background: Left ventricular dyssynchrony (LVD) and postextrasystolic potentiation (PESP) associated with premature ventricular contractions (PVCs) may play a role in the development of premature ventricular contraction-induced cardiomyopathy (PVC-CM). Long-coupled (LC) PVCs have a greater LVD than short-coupled (SC) PVCs, whereas SC-PVCs have a stronger PESP than LC-PVCs. Objective: The purpose of this study was to compare SC-PVCs and LC-PVCs to evaluate the roles of LVD, PESP, and atrioventricular dissociation (AVD) in the development of PVC-CM. Methods: Thirty-six canines underwent pacemaker implantation to induce bigeminal right ventricular apical epicardial PVCs (50% burden) for 12 weeks. Telemetry assessed PVC burden and AVD. Animals were grouped as SC-PVC (coupling interval [CI] 200-220ms), LC-PVC (CI 330 ms), or sham (control). Echocardiographic changes, AVD, and hemodynamics were monitored for 12 weeks. Results: PVC burden was similar between SC-PVC and LC-PVC groups but was statistically higher in the SC-PVC group (50% vs 47.5%; P = .028). After 12 weeks, left ventricular ejection fraction (LVEF) significantly decreased in both SC-PVC and LC-PVC groups (47.1% ± 1.4% and 45.5% ± 2%, respectively) compared to sham group (61% ± 1.6%; P <.001). Overall AVD was similar between SC-PVC and LC-PVC groups, and there was no significant correlation between AVD and reduction in LVEF at 12 weeks (r = 0.09, P = .5; and r = 0.06, P = .8, respectively). Additionally, both SC-PVC and LC-PVC groups experienced substantial declines in max and min dP/dt after 12 weeks compared to baseline. Conclusion: Neither PVC CI nor AVD played an independent role in the development or severity of PVC-CM. LVD and PESP make equal relative contributions to the development of PVC-CM.
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Background: Strain imaging has been suggested as a tool to detect early left ventricular (LV) dysfunction due to frequent premature ventricular contractions (PVCs) in patients with preserved LV ejection fraction (EF). However, the progression of intraventricular dyssynchrony (IVD), radial, and circumferential strain (RS, CS) in PVC-cardiomyopathy (CM) are unknown. The aim of this study was to elucidate the progression patterns of CS, IVD, and electro-mechanical latency (EML) in PVC-CM. Methods and results: Pacemakers were implanted in 20 canines to reproduce ventricular bigeminy at 200ms (PVCs n = 11) for 12 weeks and compared to a sham group (n = 9). We obtained echocardiograms at baseline, 4-, 8- and 12-weeks. RS and CS were obtained at the LV mid-cavitary level. IVD was defined as the time between the earliest and latest peak RS. EML was defined as the time between the onset of QRS and the earliest peak RS. LVEF (62 ± 5 to 42 ± 7%, p < 0.01), CS (-18 ± 3 to -12 ± 3, p < 0.01), and EML (219 ± 37 to 283 ± 46ms, p = 0.02) changed significantly in the PVC group. Peak CS (-18 ± 3 to -14 ± 4, p = 0.02) and IVD (49 ± 31 to 122 ± 103, p = 0.05) had a significant change at 4-weeks despite preserved LVEF (51 ± 5%). IVD normalized while EML increased at weeks 8 and 12. Conclusion: Our findings consolidate the existing theory that changes in strain precede changes in LVEF in PVC-CM. While IVD becomes abnormal early in the development of PVC-CM, it pseudo-normalizes at advanced stages due to further increases in EML suggestive of cardiac contractility remodeling. These findings are consistent with recent published data where abnormal LV mechanics could be part of a substrate that can predispose to worse outcome in PVC-Cardiomyopathy.
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As a result of large, multicenter trials supporting ICDs for prevention of sudden cardiac arrest, there has been an exponential increase in ICD device therapy. Cardiologists and general practitioners are increasingly faced with the challenge to evaluate and troubleshoot device problems. In this review, we provide an overview of basic ICD function and malfunction and show examples of common ICD problems and troubleshooting.
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Desfibriladores Implantables , Taquicardia Ventricular/prevención & control , Falla de Equipo , HumanosRESUMEN
The medical community's understanding of the consequences of premature ventricular contractions (PVCs) and PVC-induced cardiomyopathy has been derived mostly from observational and large population-based studies. Due to the difficulty of predicting the development of PVC-cardiomyopathy, the acute and chronic cardiac effects of PVCs and the mechanism of PVC-cardiomyopathy have been derived from pre-clinical studies with large animal models. Recently, these studies have described myocardial substrates that could potentially increase morbidity and mortality in patients with frequent PVCs and PVC-cardiomyopathy. In this paper, we provide an up-to-date comprehensive review of these pre-clinical and clinical studies.
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Cardiomiopatías , Complejos Prematuros Ventriculares , Potenciales de Acción , Animales , Cardiomiopatías/diagnóstico , Cardiomiopatías/epidemiología , Cardiomiopatías/fisiopatología , Cardiomiopatías/terapia , Sistema de Conducción Cardíaco/fisiopatología , Frecuencia Cardíaca , Humanos , Prevalencia , Pronóstico , Factores de Riesgo , Investigación Biomédica Traslacional , Complejos Prematuros Ventriculares/diagnóstico , Complejos Prematuros Ventriculares/epidemiología , Complejos Prematuros Ventriculares/fisiopatología , Complejos Prematuros Ventriculares/terapiaRESUMEN
BACKGROUND: Tachycardia and heart rate irregularity are proposed triggers of premature ventricular contraction-induced cardiomyopathy (PVC-cardiomyopathy). Bigeminal premature atrial and ventricular contractions (PACs and PVCs) increase heart rate and result in rhythm irregularities but differ in their effects on ventricular synchrony. Comparing chronic bigeminal PACs with PVCs would provide insights into mechanisms of PVC-cardiomyopathy. OBJECTIVE: To compare the impact of chronic PACs and PVCs on ventricular hemodynamics, structure, and function. METHODS: Pacemakers were implanted in 27 canines to reproduce atrial (PACs, n = 7) or ventricular bigeminy (PVCs, n = 11) for 12 weeks, and compared to sham-operated animals (n = 9). Four additional animals were exposed to long-term bigeminal PVCs (48 weeks). Hemodynamic changes were assessed using a pressure-transducing catheter at baseline and 12 weeks. Cardiac remodeling was monitored by transthoracic echocardiography throughout the 12- and 48-week protocols in the respective groups. RESULTS: PVC group demonstrated a significant decrease in left ventricular (LV) ejection fraction and contractility (max dP/dt), impaired LV lusitropy (min dP/dt), and increase in LV dimensions and LV mass at 12 weeks without further deterioration beyond 16 weeks. Despite increased LV mass, relative wall thickness decreased, consistent with eccentric hypertrophy. No significant cardiac remodeling was noted in either sham or PAC groups at 12 weeks. CONCLUSION: In contrast to bigeminal PACs, PVCs result in a cardiomyopathy characterized by reduced LV ejection fraction, LV dilation, and eccentric hypertrophy that plateaus between 12 and 16 weeks. The lack of remodeling in chronic PACs suggests that tachycardia and heart rate irregularity do not play a significant role on the development of PVC-cardiomyopathy.