Ventricular bigeminy associated with myocardial ischemia in a dog with a colonic torsion: a case report.

BACKGROUND: Ventricular bigeminy due to myocardial ischemia has been reported in humans as well as in canine patients with obstructive gastrointestinal diseases. This is the first case report of ventricular bigeminy in a dog with a colonic torsion that resolved after fluid resuscitation and restoration of myocardial perfusion. CASE PRESENTATION: An 11-year-old, male neutered mixed breed dog presented with a one day history of vomiting, tenesmus, and lethargy. Physical examination identified an irregular heart rhythm and intermittent pulse deficits. A ventricular arrhythmia represented by ventricular premature complexes (VPCs) organized in bigeminy, was appreciated on a 3-lead electrocardiogram (ECG) with a single lead (II) view. Abdominal radiographs confirmed a colonic torsion. Prior to anesthetic induction, ventricular bigeminy was non responsive to fentanyl or lidocaine. The patient was anesthetized and intravascular volume deficit was identified by dampened plethysmographic wave amplitude (plethysomographic variability), audible softening of the Doppler sound, and more pronounced pulse deficits. Fluid resuscitation was achieved with a combination of intravenous crystalloid and colloid fluid therapy comprising 7.2% hypertonic saline and 6% hetastarch. The patient's cardiac rhythm converted to normal sinus after fluid resuscitation. The colonic torsion was surgically corrected. The patient recovered well from anesthesia and was ultimately discharged from the hospital 5 days later. CONCLUSIONS: The present case report highlights that myocardial ischemia can lead to ventricular arrythmias, such as ventricular bigeminy. This is the first documented case of ventricular bigeminy in the canine patient with a colonic torsion. Assessment of patient volume status and appropriate fluid resuscitation along with continuous electrocardiogram (ECG) monitoring are vital to patient stability under general anesthesia.

Contemporary clinical management of monomorphic idiopathic premature ventricular contractions: results of the European Heart Rhythm Association survey.

On behalf of the European Heart Rhythm Association, we designed a survey, whose aim was to understand the trend(s) in the clinical management of idiopathic monomorphic premature ventricular contractions (PVCs) among European cardiologists and cardiac electrophysiologists. A total of 202 participants in the survey answered 27 multiple-choice questions on the clinical presentation, diagnosis and treatment of idiopathic monomorphic PVCs. The most common symptom in patients with idiopathic monomorphic PVCs is palpitations, according to the majority of responders (87%), followed by fatigue (29%) and dizziness (18%). Complete blood cell count, renal function with electrolytes levels, and thyroid function are the blood tests requested by the majority of respondents (65%, 92%, and 93%, respectively). Coronary artery disease and structural heart disease needs to be ruled out, according to the vast majority of participants (99%). A 24-h Holter ECG is the preferred ECG modality to assess the burden of PVCs (86% of respondents). Among the different option treatments, beta-blockers and class I antiarrhythmic drugs are by far (81% of respondents) the preferred pharmacological option in comparison with calcium antagonists and class III antiarrhythmic drugs. Catheter ablation has also a good reputation: 99% of responders are keen to use it, especially in patients with high burden of PVCs and when signs of cardiomyopathy occur.

Effect of single ventricular premature contractions on response to cardiac resynchronization therapy.

BACKGROUND: We lack data on the effect of single premature ventricular contractions (PVCs) on the clinical and echocardiographic response after cardiac resynchronization therapy (CRT) device implantation. We aimed to assess the predictive value of PVCs at early, 1 month-follow up on echocardiographic response and all-cause mortality. METHODS: In our prospective, single-center study, 125 heart failure patients underwent CRT implantation based on the current guidelines. Echocardiographic reverse remodeling was defined as a ≥ 15% improvement in left ventricular ejection fraction (LVEF), end-systolic volume (LVESV), or left atrial volume (LAV) measured 6 months after CRT implantation. All-cause mortality was investigated by Wilcoxon analysis. RESULTS: The median number of PVCs was 11,401 in those 67 patients who attended the 1-month follow-up. Regarding echocardiographic endpoints, patients with less PVCs develop significantly larger LAV reverse remodeling compared to those with high number of PVCs. During the mean follow-up time of 2.1 years, 26 (21%) patients died. Patients with a higher number of PVCs than our median cut-off value showed a higher risk of early all-cause mortality (HR 0.97; 95% CI 0.38-2.48; P = 0.04). However, when patients were followed up to 9 years, its significance diminished (HR 0.78; 95% CI 0.42-1.46; P = 0.15). CONCLUSIONS: In patients undergoing CRT implantation, lower number of PVCs predicted atrial remodeling and showed a trend for a better mortality outcome. Our results suggest the importance of the early assessment of PVCs in cardiac resynchronization therapy and warrant further investigations.

Acute suppression of epicardial left ventricular summit premature ventricular ectopy by occlusive venogram.

We describe the unique phenomenon of occlusive venogram-induced suppression of premature ventricular complexes (PVC) arising from the epicardial left ventricular summit (LVS). Prior to ablation through the coronary sinus, routine occlusive venogram performed at the focus of PVC origin led to localized myocardial staining and simultaneous, sustained PVC suppression. Pace-mapping adjacent to the area of myocardial staining revealed near-identical PVC morphology match (98%). Routine occlusive venogram prior to ablation within the coronary venous system is safe and contributed to localization of the PVC focus.

Evaluation and Management of Premature Ventricular Complexes.

Premature ventricular complexes (PVCs) are extremely common, found in the majority of individuals undergoing long-term ambulatory monitoring. Increasing age, a taller height, a higher blood pressure, a history of heart disease, performance of less physical activity, and smoking each predict a greater PVC frequency. Although the fundamental causes of PVCs remain largely unknown, potential mechanisms for any given PVC include triggered activity, automaticity, and reentry. PVCs are commonly asymptomatic but can also result in palpitations, dyspnea, presyncope, and fatigue. The history, physical examination, and 12-lead ECG are each critical to the diagnosis and evaluation of a PVC. An echocardiogram is indicated in the presence of symptoms or particularly frequent PVCs, and cardiac magnetic resonance imaging is helpful when the evaluation suggests the presence of associated structural heart disease. Ambulatory monitoring is required to assess PVC frequency. The prognosis of those with PVCs is variable, with ongoing uncertainty regarding the most informative predictors of adverse outcomes. An increased PVC frequency may be a risk factor for heart failure and death, and the resolution of systolic dysfunction after successful catheter ablation of PVCs demonstrates that a causal relationship can be present. Patients with no or mild symptoms, a low PVC burden, and normal ventricular function may be best served with simple reassurance. Either medical treatment or catheter ablation are considered first-line therapies in most patients with PVCs associated with symptoms or a reduced left ventricular ejection fraction, and patient preference plays a role in determining which to try first. If medical treatment is selected, either ß-blockers or nondihydropyridine calcium channel blockers are reasonable drugs in patients with normal ventricular systolic function. Other antiarrhythmic drugs should be considered if those initial drugs fail and ablation has been declined, has been unsuccessful, or has been deemed inappropriate. Catheter ablation is the most efficacious approach to eradicate PVCs but may confer increased upfront risks. Original research remains necessary to identify individuals at risk for PVC-induced cardiomyopathy and to identify preventative and therapeutic approaches targeting the root causes of PVCs to maximize effectiveness while minimizing risk.

Catheter Ablation of Refractory Ventricular Fibrillation Storm After Myocardial Infarction.

BACKGROUND: Ventricular fibrillation (VF) storm after myocardial infarction (MI) is a life-threatening condition that necessitates multiple defibrillations. Catheter ablation is a potentially effective treatment strategy for VF storm refractory to optimal medical treatment. However, its impact on patient survival has not been verified in a large population. METHODS: We conducted a multicenter, retrospective observational study involving consecutive patients who underwent catheter ablation of post-MI refractory VF storm without preceding monomorphic ventricular tachycardia. The target of ablation was the Purkinje-related ventricular extrasystoles triggering VF. The primary outcome was in-hospital and long-term mortalities. Univariate logistic regression and Cox proportional-hazards analysis were used to evaluate clinical characteristics associated with in-hospital and long-term mortalities, respectively. RESULTS: One hundred ten patients were enrolled (age, 65±11years; 92 men; left ventricular ejection fraction, 31±10%). VF storm occurred at the acute phase of MI (4.5±2.5 days after the onset of MI during the index hospitalization for MI) in 43 patients (39%), the subacute phase (>1 week) in 48 (44%), and the remote phase (>6 months) in 19 (17%). The focal triggers were found to originate from the scar border zone in 88 patients (80%). During in-hospital stay after ablation, VF storm subsided in 92 patients (84%). Overall, 30 (27%) in-hospital deaths occurred. The duration from the VF occurrence to the ablation procedure was associated with in-hospital mortality (odds ratio for each 1-day increase, 1.11 [95% CI, 1.03-1.20]; P=0.008). During follow-up after discharge from hospital, only 1 patient developed recurrent VF storm. However, 29 patients (36%) died, with a median survival time of 2.2 years (interquartile range, 1.2-5.5 years). Long-term mortality was associated with left ventricular ejection fraction <30% (hazard ratio, 2.54 [95% CI, 1.21-5.32]; P=0.014), New York Heart Association class ≥III (hazard ratio, 2.68 [95% CI, 1.16-6.19]; P=0.021), a history of atrial fibrillation (hazard ratio, 3.89 [95% CI, 1.42-10.67]; P=0.008), and chronic kidney disease (hazard ratio, 2.74 [95% CI, 1.15-6.49]; P=0.023). CONCLUSIONS: In patients with MI presenting with focally triggered VF storm, catheter ablation of culprit triggers is lifesaving and appears to be associated with short- and long-term freedom from recurrent VF storm. Mortality over the long-term follow-up is associated with the severity of underlying cardiovascular disease and comorbidities in this specific patient population.

Systematic Review for the 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society.

BACKGROUND: Although large randomized clinical trials have found that primary prevention use of an implantable cardioverter-defibrillator (ICD) improves survival in patients with cardiomyopathy and heart failure symptoms, patients who receive ICDs in practice are often older and have more comorbidities than patients who were enrolled in the clinical trials. In addition, there is a debate among clinicians on the usefulness of electrophysiological study for risk stratification of asymptomatic patients with Brugada syndrome. AIM: Our analysis has 2 objectives. First, to evaluate whether ventricular arrhythmias (VAs) induced with programmed electrostimulation in asymptomatic patients with Brugada syndrome identify a higher risk group that may require additional testing or therapies. Second, to evaluate whether implantation of an ICD is associated with a clinical benefit in older patients and patients with comorbidities who would otherwise benefit on the basis of left ventricular ejection fraction and heart failure symptoms. METHODS: Traditional statistical approaches were used to address 1) whether programmed ventricular stimulation identifies a higher-risk group in asymptomatic patients with Brugada syndrome and 2) whether ICD implantation for primary prevention is associated with improved outcomes in older patients (>75 years of age) and patients with significant comorbidities who would otherwise meet criteria for ICD implantation on the basis of symptoms or left ventricular function. RESULTS: Evidence from 6 studies of 1138 asymptomatic patients were identified. Brugada syndrome with inducible VA on electrophysiological study was identified in 390 (34.3%) patients. To minimize patient overlap, the primary analysis used 5 of the 6 studies and found an odds ratio of 2.3 (95% CI: 0.63-8.66; P=0.2) for major arrhythmic events (sustained VAs, sudden cardiac death, or appropriate ICD therapy) in asymptomatic patients with Brugada syndrome and inducible VA on electrophysiological study versus those without inducible VA. Ten studies were reviewed that evaluated ICD use in older patients and 4 studies that evaluated unique patient populations were identified. In our analysis, ICD implantation was associated with improved survival (overall hazard ratio: 0.75; 95% confidence interval: 0.67-0.83; P<0.001). Ten studies were identified that evaluated ICD use in patients with various comorbidities including renal disease, chronic obstructive pulmonary disease, atrial fibrillation, heart disease, and others. A random effects model demonstrated that ICD use was associated with reduced all-cause mortality (overall hazard ratio: 0.72; 95% confidence interval: 0.65-0.79; P<0.0001), and a second "minimal overlap" analysis also found that ICD use was associated with reduced all-cause mortality (overall hazard ratio: 0.71; 95% confidence interval: 0.61-0.82; P<0.0001). In 5 studies that included data on renal dysfunction, ICD implantation was associated with reduced all-cause mortality (overall hazard ratio: 0.71; 95% confidence interval: 0.60-0.85; P<0.001).

Frequent premature ventricular beats in healthy children: when to ignore and when to treat?

PURPOSE OF REVIEW: Premature ventricular beats (PVCs) are frequently identified in healthy children with structurally normal hearts and generally have a benign clinical course often disappearing spontaneously. However, a small percentage of children may develop a cardiomyopathy. The purpose of this review is to understand which children may be at risk of development of left ventricular (LV) dysfunction with idiopathic PVCs. RECENT FINDINGS: There is increasing evidence that a ventricular ectopic burden more than 24% in adults may lead to LV dysfunction. Most of the pediatric studies to date are retrospective, small case series from single institutions and have conflicting results regarding a direct correlation of the PVC burden to LV dysfunction. Development of a cardiomyopathy from frequent PVCs in children is likely multifactorial relating to the burden itself, presence of higher levels of ectopy (couplets and runs of ventricular tachycardia) as well as the duration of ventricular ectopy. Understanding the duration of ectopy is often unknown as patients are asymptomatic and the irregular heart beat was identified at a well-child examination. SUMMARY: Asymptomatic children with normal ventricular function and a low ectopy burden can be followed without any intervention and generally reassured. Children with an ectopy burden more than 30% are at some risk of developing LV dysfunction and should be more closely followed with noninvasive imaging. Development of symptoms attributed to the ectopy or signs of increasing LV dimensions or LV dysfunction should be treated with medication or catheter ablation.

Termination of desynchronization rhythm and restoration of cardiac resynchronization by left-sided ventricular premature complexes.

Cardiac resynchronization devices that sense left ventricular (LV) activity and can detect interruptions of resynchronization therapy are able to record all forms of desynchronization rhythms, which are triggered by misalignment of LV timing cycles. We report five cases of this desynchronization rhythm that were terminated by isolated left-sided ventricular premature complexes (LVPC) undetected by the right ventricular (RV) channel and unaccompanied by changes in the duration of the RV pacing cycles. In three cases, the devices did not even sense the LVPCs responsible for desynchronization termination. The restoration of resynchronization in our cases is in contrast to the traditional termination mode that is invariably associated with changes in the duration of the RV cycles.

Management and outcomes in mitral valve prolapse with ventricular arrhythmias undergoing ablation and/or implantation of ICDs.

BACKGROUND: While there is an association between isolated mitral valve prolapse (MVP) and sudden cardiac arrest (SCA), the baseline characteristics and outcomes of patients with isolated MVP who experience ventricular arrhythmias (VAs) and then subsequently undergo catheter ablation and/or implantable cardioverter defibrillator (ICD) implantation are unknown. METHODS: We performed a retrospective review of all patients at the Cleveland Clinic with isolated MVP between 1997 and 2016 who underwent VA catheter ablation or secondary prevention ICD implantation. RESULTS: Of 617 screened patients, we identified 43 patients with isolated MVP and significant VA who underwent ICD placement (n = 13, 30%) or catheter ablation (n = 30, 70%). Both leaflets were most commonly involved (n = 22, 52%) with posterior MVP being next most common (n = 15, 36%). The most common foci of VA origin was the left ventricular papillary muscle (n = 9, 27%). Ablation was successful in the majority of cases (n = 20, 65%). At a mean follow-up of 2.5 years, 11 patients (26%) had recurrent VT. CONCLUSIONS: Patients with isolated MVP and VA were more likely to have bileaflet prolapse and at least moderate mitral regurgitation. VA originated more commonly from left-sided foci. While ablation was acutely successful in the majority of cases, there was still a moderate rate of VA recurrence. There is still more study needed on factors that will predict malignant VAs and management of these VAs in the MVP population.

Combining noninvasive risk stratification parameters improves the prediction of mortality and appropriate ICD shocks.

BACKGROUND: Sudden cardiac death (SCD) results from a complex interplay of abnormalities in autonomic function, myocardial substrate and vulnerability. We studied whether a combination of noninvasive risk stratification tests reflecting these key players could improve risk stratification. METHODS: Patients implanted with an ICD in whom 24-hr holter recordings were available prior to implant were included. QRS fragmentation (fQRS) was selected as measure of myocardial substrate and a high ventricular premature beat count (VPB >10/hr) for arrhythmic vulnerability. From receiver operating characteristics analysis, detrended fluctuation analysis (DFA), turbulence slope, and deceleration capacity were selected for autonomic function. Adjusted Cox regression analysis with comparison of C-statistics was performed to predict first appropriate shock (AS) and total mortality. RESULTS: A total of 220 patients were included in the analysis with an overall follow-up of 4.3 ± 3.1 years. A model including VPB >10/hr, inferior fQRS, and abnormal nonedited DFA was the best for prediction of AS after 1 year of follow-up with a trends toward improvement of the C-statistics compared to baseline (p = 0.055). The risk increased significantly with every abnormal test (HR 1.793, 95%CI 1.255-2.564). A model including fQRS in any region and abnormal edited DFA was the best for prediction of mortality after 3 years of follow-up with significant improvement of the C-statistics (p = 0.023). Each abnormal test was associated with a significant increase in mortality (HR 5.069, 95%CI 1.978-12.994). CONCLUSION: Combining noninvasive risk stratification tests according to their physiological background can improve the risk prediction of SCD and mortality.

A Steam Pop Detected by Intracardiac Echocardiography During Catheter Ablation of the Left Ventricular Papillary Muscle.

A 60-year-old female with premature ventricular contractions (PVCs) originating from the bottom of the posteromedial papillary muscle of the left ventricle underwent radiofrequency catheter ablation (RFCA) using an irrigated-tip catheter. During ablation of the PVCs, a loud steam pop was observed. Intracardiac echocardiography (ICE) revealed a growing, hyperechogenic intramyocardial microbubble formation around the catheter tip. The formation disappeared slowly and completely, leaving an endocardial laceration without pericardial effusion. ICE imaging is valuable during a difficult RFCA procedure, because ICE reveals the exact anatomical position of the catheter and thus allows rapid evaluation of the occurrence of steam popping and any possible subsequent complication.

Windkessel model of hemodynamic state supported by a pulsatile ventricular assist device in premature ventricle contraction.

BACKGROUND: Counter-pulsation control (CPC) by ventricular assist devices (VADs) is believed to reduce cardiac load and increase coronary perfusion. However, patients with VADs have a higher risk of arrhythmia, which may cause the CPC to fail. Consequently, CPC has not been applied by VADs in clinical practice. The phase-locked loop (PLL) algorithm for CPC is readily implemented in VADs; however, it requires a normal, consistent heartbeat for adequate performance. When an arrhythmia occurs, the algorithm maintains a constant pumping rate despite the unstable heartbeat. Therefore, to apply the PLL algorithm to CPC, the hemodynamic effects of abnormal heartbeats must be analyzed. OBJECTIVES: This study sought to predict the hemodynamic effects in patients undergoing CPC using VADs, based on electrocardiogram (ECG) data, including a wide range of heart rate (HR) changes caused by premature ventricular contraction (PVC) or other reasons. METHODS: A four-element Windkessel hemodynamic model was used to reproduce the patient's aortic blood pressure in this study. ECG data from 15 patients with severe congestive heart failure were used to assess the effect of the CPC on the patients' hemodynamic state. The input and output flow characteristics of the pulsatile VAD (LibraHeart I, Cervika, Korea) were measured using an ultrasound blood flow meter (TS410, Transonic, USA), with the aortic pressure maintained at 80-120 mmHg. All other patient conditions were also reproduced. RESULTS: In patients with PVCs or normal heartbeats, CPC controlled by a VAD reduced the cardiac load by 20 and 40%, respectively. When the HR was greater for other reasons, such as sinus tachycardia, simultaneous ejection from the heart and VAD was observed; however, the cardiac load was not increased by rapid cardiac contractions resulting from decreased left ventricle volume. These data suggest that the PLL algorithm reduces the cardiac load and maintains consistent hemodynamic changes.

Symptomatic arrhythmia in the form of multiple premature ventricular extrasystoles as the first symptom of polymyositis.

Polymyositis (PM) is an autoimmune disease characterized by the involvement of multiple internal organs, including the cardiovascular system. The involvement of heart is observed in up to 75% of patients with PM. Conduction and rhythm disorders are one of the most common cardiological abnormalities in these patients. The presented clinical case is the patient where ventricular arrhythmia (in the form of multiple premature ventricular extrasystoles) was the first symptom of polymyositis.

Inferior lead discordance in ventricular arrhythmias: A specific marker for certain arrhythmia locations.

BACKGROUND: Most idiopathic ventricular arrhythmias (VAs) originate from the outflow tracts and are characterized by an inferior axis on the 12-lead ECG. A group of patients will exhibit inferior lead discordance (ILD), demonstrating a positive QRS in lead II with negative QRS in III or the opposite finding. METHODS AND RESULTS: We identified patients undergoing ablation of idiopathic premature ventricular contractions (PVCs) or ventricular tachycardia (VT) between 2013 and 2015. The site of earliest activation was determined using electroanatomic mapping and intracardiac echocardiography. Out of 281 patients, 25 (8.9%) exhibited ILD. In patients with positive/negative discordance (n = 18), the source was mapped to the parahisian region in 14 cases and to the right ventricular (RV) moderator band (MB) or papillary muscles (PMs) in 4, while all those with negative/positive discordance (n = 7) were mapped to the anterolateral PM (ALPM). In the group with positive/negative discordance, a later precordial transition (>V4), wider QRS duration, and the presence of notch in the inferior leads pointed toward a RV MB/PM origin. Complete PVC/VT suppression was achieved in 72%. In 2 patients with parahisian PVCs, ablation was not attempted due to risk of heart block. CONCLUSIONS: The presence of ILD is associated with particular anatomical locations, namely, the parahisian region, RV MB/PM, and ALPM. The outcomes of ablation are more modest compared to other idiopathic VAs, reflecting the technical difficulties associated with these anatomical locations, such as the proximity to the conduction system in parahisian VAs or stability issues when ablating the PMs or MB.

Premature ventricular complexes in children with structurally normal hearts: clinical review and recommendations for diagnosis and treatment.

Premature ventricular complexes (PVCs) have always been a matter of debate among physicians and a cause for concern for family members of affected patients. The available literature on isolated PVCs in children is limited to case reports and small single-center retrospective series that are consistent in demonstrating the benign course of PVCs and their frequent disappearance during childhood, though many questions remain unanswered. Nevertheless, two key actions should be undertaken in pediatric patients with documented PVCs: 1) to rule out the presence of structural heart disease; 2) to determine whether symptoms are due to PVCs, or whether PVC frequency is responsible for left ventricular dysfunction. This document aims to provide concise and easy to understand recommendations on the diagnostic work-up of healthy children with simple PVCs and the appropriate clinical and therapeutic approach.

[Ventricular arrhythmias : What has been confirmed in therapy?] / Ventrikuläre Herzrhythmusstörungen : Was ist gesichert in der Therapie?

Ventricular arrhythmias include a wide range of potentially benign single ventricular premature contractions to ventricular tachycardia and ventricular fibrillation with a risk for sudden cardiac death. The diagnosis of ventricular arrhythmia is made by 12-lead electrocardiogram, 24 h Holter monitoring, an external or implantable loop recorder, or during in-hospital monitoring. Especially the diagnosis of wide complex tachycardias is challenging in terms of differentiating between ventricular tachycardia and supraventricular tachycardia with aberrant atrioventricular conduction. After documentation of ventricular arrhythmias, diagnostic work-up with respect to structural or electrical cardiomyopathy is mandatory followed by risk stratification for sudden cardiac death. Therapeutic options for treatment of ventricular arrhythmias range from pharmacological therapy and interventional procedures such as catheter ablation and implantable devices. The current article provides an overview of the diagnosis of ventricular tachycardia and underlying cardiomyopathies. Furthermore, medical and interventional therapies are described. In addition, the indications for implantable and wearable defibrillators are presented.

Transient Elimination of Posterior Right Ventricular Outflow Tract Ectopy by Sternal Pressure.

BACKGROUND: Ventricular ectopy (VE) originating in the right ventricular outflow tract (RVOT) is a common arrhythmia. Mechanisms triggering or eliminating VE from RVOT are not entirely understood. METHODS AND RESULTS: A patient with frequent, symptomatic VE underwent an electrophysiologic study: VE origin was mapped by NavX 3D navigation (St. Jude Medical, Inc., St. Paul, MN, USA). Incidental pressure applied manually to the sternum reproducibly eliminated VE for the time of exposure. Radiofrequency-ablation was successfully performed in the posterior RVOT. CONCLUSION: The mechanism resulting in VE suppression remains speculative, since a mechanical alteration of the substrate for VE in the posterior RVOT by sternal pressure seems unlikely. "Mechano-electrical feedback" might have been the mechanism operative in this case.

A Review of the Potential Pathogenicity and Management of Frequent Premature Ventricular Contractions.

Very frequent premature ventricular complexes (PVCs) may be a reversible cause of dilated cardiomyopathy. Literature on this largely unrecognized entity has increased in the last 15 years. This paper reviews the literature on the consequences of frequent PVCs on myocardial function and management of PVC-associated cardiomyopathy. The authors reviewed articles published in English before June 2015 describing pathophysiology, risk factors, symptoms, time course, treatment, and outcome of cardiomyopathy associated with PVCs. The search was conducted using Medline and Embase. Keywords included: cardiomyopathy, catheter ablation, antiarrhythmic drug (AAD), pathophysiology, and ventricular premature contractions or synonyms. PVC-associated cardiomyopathy is associated with a high burden of PVC (over 20% of heartbeats). Other risk factors include electrophysiological characteristics, such as PVC QRS width, presence of ventricular tachycardia, retrograde P waves, interpolation, polymorphic PVCs, and longer coupling intervals. Symptoms include palpitations, light-headedness, dyspnea, cough, and dysphagia. The systolic dysfunction and chamber dilatation progress over a few years. Once the PVCs are suppressed by radiofrequency ablation or AADs, the cardiomyopathy usually resolves within 6 months. The pathophysiology remains unknown, but hypotheses mainly include ventricular dyssynchrony resulting in hemodynamic disturbances and abnormalities in calcium handling and oxygen consumption. PVC-associated cardiomyopathy remains a largely unrecognized entity. It is a reversible cause of dilated cardiomyopathy that results from abnormal calcium and oxygen handling within the myocyte, dyssynchrony, and hemodynamic compromise from inefficient heartbeats. Suppression of the PVCs improves myocardial function, cardiac chamber sizes, and patient's symptoms.