scholarly journals Are premature ventricular contractions in patients without apparent structural heart disease really safe?

2015 ◽  
Vol 2 (1) ◽  
Author(s):  
Charles Jazra ◽  
Oussma Wazni ◽  
Wael Jaroudi
Keyword(s):  
Heart Disease ◽  
Catheter Ablation ◽  
Beta Blockers ◽  
Structural Heart Disease ◽  
Arrhythmogenic Right Ventricular Dysplasia ◽  
Ventricular Outflow Tract ◽  
Left Ventricular ◽  
Channel Blockers ◽  
Premature Ventricular Contractions ◽  
Lv Dysfunction

<p>Premature ventricular complexes (PVC) are considered benign when they occur in patients without apparent structural heart disease. They usually originate from the right, or less commonly, left ventricular outflow tract. Their suppression was not beneficial in patients with heart disease like myocardial infarction and cardiomyopathies. Recently it has been shown that their suppression medically or by ablation, improved the left ventricular (LV) dysfunction. This led to the hypothesis that they may contribute to this LV dysfunction especially when they are particularly frequent (&gt; 20000 per day). Because of some overlap with arrhythmogenic right ventricular dysplasia, the evaluation in patients without apparent heart disease should consider an magnetic resonance imaging if the echocardiography was not able to help in diagnosis especially when there is a suspicion.</p><p>Patients without structural heart disease and low-to modest PVC burdens do not always require treatment.</p><p>When necessary, treatment for PVCs involves beta-blockers, calcium channel blockers, or other antiarrhythmic</p><p>drugs and catheter ablation in selected cases. Catheter ablation can be curative, but it is typically reserved</p><p>for drug-intolerant or medically refractory patients with a high PVC burden.</p>

Abstract P024: Pharmacological Treatment of Hypertension and Lv Dysfunction Predictors in ESRD Patients With AV Fistula

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Sayed Tariq ◽  
James Anderson ◽  
Rohit Dhingra ◽  
Mikhail Torosoff
Keyword(s):  
Systolic Function ◽  
Beta Blockers ◽  
Systolic Dysfunction ◽  
Left Ventricular ◽  
Channel Blockers ◽  
Ca Channel ◽  
Av Fistula ◽  
Fistula Surgery ◽  
Lv Dysfunction ◽  
Ca Channel Blockers

Background: Effects of anti-hypertensive medications on left ventricular dimensions and systolic function in patients with arterio-venous (AV) fistulas have not been well investigated. Material and Methods: Medical charts and echocardiograms of 346 patients with AV fistula were reviewed. Of 346, 149 patients had TTE prior to the AV fistula surgery, 197 had TTE after the AV fistula surgery, and 76 patients had TTE before and after the AV fistula surgery. Data on medication use was available in 314 patients. ANOVA, chi-square, and logistic regression tests were employed. Results: In patients scheduled for AV fistula placement, 20% (31/149) patients had systolic dysfunction and 15% (22/142) had increased LV end-diastolic dimensions (LVEDD). Moderate systolic LV dysfunction was observed in 6% (9/149) and additional 8% (12/149) had severe LV dysfunction. Increased LVEDD with some LV dysfunction was noted in 27% (38/142).Following the AV fistula placement, 18% (36/197) of patients had systolic dysfunction and 12% (22/187) had increased LV end-diastolic dimensions (LVEDD). Moderate or severe systolic LV dysfunction was observed in 6% (5/197). LV systolic dysfunction or dilatation was noted in 23% (43/187). Of 314 patients, 63% were on beta-blockers (BB), 25% were on ACE inhibitor or an ARB , 43% on calcium-channel blocker , and 15% on alpha-antagonist . BB, ACEi-ARB, or AA were not associated with increased LVEDD or systolic dysfunction before or after the AV fistula placement. Prior to AV fistula, CCB treatment was not related to LV dilatation (36% in each group, p=0.981) Post AV fistula, CCB treatment was associated with increased LV dimensions (71% vs. 46%, p=0.029) but not LV systolic dysfunction (49% in LV dysfunction vs. 38% in the rest, p=0.446) . This association persisted after adjustment for co-morbidities and demographic parameters. Conclusions: LV systolic dysfunction and/or dilatation are common in patients undergoing AV fistula surgery. Despite decreased use of Ca-channel blockers in patients with LV dysfunction prior to AV fistula, Ca-channel blockers are associated with increased LV dimensions post AV fistula, and probably should be avoided in this vulnerable patient population.

scholarly journals Additive beneficial effects of beta blockers in the prevention of symptomatic heart failure

2016 ◽  
Vol 72 (1) ◽  
Author(s):  
Alberto Genovesi Ebert ◽  
Furio Colivicchi ◽  
Marco Malvezzi Caracciolo ◽  
Carmine Riccio
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Heart Disease ◽  
Beta Blockers ◽  
Structural Heart Disease ◽  
Symptomatic Heart Failure ◽  
Post Hoc Analysis ◽  
Lv Dysfunction ◽  
History Of ◽  
Post Hoc

The prevention of symptomatic heart failure represents the treatment of patients in the A and B stages of AHA/ACC heart failure classification. Stage A refers to patients without structural heart disease but at risk to develop chronic heart failure. The major risk factors in stage A are hypertension, diabetes, atherosclerosis, family history of coronary artery disease and history of cardiotoxic drug use. In this stage, blockers hypertension is the primary area in which beta blockers may be useful. Beta blockers seem not to be superior to other medication in reducing the development of heart failure due to hypertension. Stage B heart failure refers to structural heart disease but without symptoms of heart failure. This includes patients with asymptomatic valvular disease, asymptomatic left ventricular (LV) dysfunction, previous myocardial infarction with or without LV dysfunction. In asymptomatic valvular disease no data are available on the efficacy of beta blockers to prevent heart failure. In asymptomatic LV dysfunction only few asymptomatic patients have been enrolled in the trials which tested beta blockers. NYHA I patients were barely 228 in the MDC, MERIT and ANZ trials altogether. The REVERT trial was the only trial focusing on NYHA I patients with LV ejection fraction less than 40%. Metoprolol extended release on top of ACE inhibitors ameliorated LV systolic volume and ejection fraction. A post hoc analysis of the SOLVD Prevention trial demonstrated that beta blockers reduced death and development of heart failure. Similar results were reported in post MI patients in a post hoc analysis of the SAVE trial (Asymptomatic LV failure post myocardial infarction). In the CAPRICORN trial about 65% of the patients were not taking diuretics and then could be considered asymptomatic. The study revealed a reduction in mortality and a non-significant trend toward reduction of death and hospital admission for heart failure. Conclusions: beta blockers are not specifically indicated in stage A heart failure. On the contrary, in most of the stage B patients, and particularly after MI, beta blockers are indicated to reduce mortality and, probably, also the progression toward symptomatic heart failure.

Sustained and non-sustained ventricular tachycardia and no associated heart disease (idiopathic ventricular tachycardia)

ESC CardioMed ◽  
2018 ◽  
pp. 2288-2293
Author(s):  
Victor Bazan ◽  
Enrique Rodriguez-Font ◽  
Francis E. Marchlinski
Keyword(s):  
Heart Disease ◽  
Ventricular Tachycardia ◽  
Drug Therapy ◽  
Catheter Ablation ◽  
Beta Blockers ◽  
Young Patients ◽  
Structural Heart Disease ◽  
Holter Monitoring ◽  
Severe Arrhythmia ◽  
The Right

Around 10% of ventricular arrhythmias (VA) occur in the absence of underlying structural heart disease. These so-called ‘idiopathic’ VAs usually have a benign clinical course. Only rarely do these “benign” arrhythmias trigger polymorphic ventricular tachycardia (PVT) and idiopathic ventricular fibrillation (VF). Due to their focal origin and to the absence of underlying myocardial scar, the 12-lead ECG very precisely establishes the right (RV) or left (LV) ventricular site of origin of the arrhythmia and can help regionalizing the origin of VT for ablation. A 12-lead ECG obtained during the baseline rhythm and 24-hour ECG Holter monitoring are indicated in order to identify structural or electrical disorders leading to PVT/VF and to determine the VA burden. The most frequent origin of idiopathic VAs is the RV outflow tract (OT). Other origins include the LVOT, the LV fascicles (fascicular VTs), the LV and RV papillary muscles, the crux cordis, the mitral and tricuspid annuli and the RV moderator band. Recognizing the typical anatomic sites of origin combined with a 12 lead ECG assessment facilitates localization.  Antiarrhythmic drug therapy (including use of beta-blockers) or catheter ablation may be indicated to suppress or eliminate idiopathic VAs, particularly upon severe arrhythmia-related symptoms or if the arrhythmia burden is high and ‘tachycardia’-induced cardiomyopathy is suspected. Catheter ablation is frequently preferred to prevent lifelong drug therapy in young patients.

Sustained monomorphic ventricular tachycardia: the role of catheter ablation

ESC CardioMed ◽  
2018 ◽  
pp. 2279-2288
Author(s):  
Tilman Maurer ◽  
William G. Stevenson ◽  
Karl-Heinz Kuck
Keyword(s):  
Heart Disease ◽  
Ventricular Tachycardia ◽  
Catheter Ablation ◽  
Sudden Cardiac Death ◽  
Cardiac Death ◽  
Therapeutic Option ◽  
Structural Heart Disease ◽  
Premature Ventricular Contractions ◽  
Monomorphic Ventricular Tachycardia ◽  
Premature Beats

Monomorphic ventricular tachycardia (VT) may occur in the presence or absence of structural heart disease. The standard therapy for patients with structural heart disease at high risk of sudden cardiac death due to VT is the implantable cardioverter defibrillator (ICD). While ICDs effectively terminate VT and prevent sudden cardiac death, they do not prevent recurrent episodes of VT, since the underlying arrhythmogenic substrate remains unchanged. However, shocks from an ICD increase mortality and impair quality of life. These limitations as well as continuous advancements in technology have made catheter ablation an important treatment strategy for patients with structural heart disease presenting with VT. Idiopathic ventricular arrhythmias include premature ventricular contractions and VT occurring in the absence of overt structural heart disease. In this setting, catheter ablation has evolved as the primary therapeutic option for symptomatic ventricular premature beats and sustained VTs and is curative in most cases. This chapter presents an overview of the principles of invasive diagnosis and treatment of monomorphic VTs in patients with and without structural heart disease and delineates the clinical outcome of catheter ablation. Finally, the chapter provides an outlook to the future, discussing potential directions and upcoming developments in the field of catheter ablation of monomorphic VT.

scholarly journals Catheter ablation of ventricular arrhythmias and in-hospital mortality: insights from the German-wide Helios hospital network of 5052 cases

EP Europace ◽  
2019 ◽  
Author(s):  
Sebastian König ◽  
Laura Ueberham ◽  
René Müller-Röthing ◽  
Michael Wiedemann ◽  
Michael Ulbrich ◽  
...  
Keyword(s):  
Heart Disease ◽  
Catheter Ablation ◽  
Hospital Mortality ◽  
Ventricular Arrhythmias ◽  
Emergency Admission ◽  
Structural Heart Disease ◽  
Mortality Rates ◽  
Hospital Death ◽  
Premature Ventricular Contractions ◽  
Hospital Transfer

Abstract Aims Catheter ablation (CA) of ventricular arrhythmias is one of the most challenging electrophysiological interventions with an increasing use over the last years. Several benefits must be weighed against the risk of potentially life-threatening complications which necessitates a steady reevaluation of safety endpoints. Therefore, the aims of this study were (i) to investigate overall in-hospital mortality in patients undergoing such procedures and (ii) to identify variables associated with in-hospital mortality in a German-wide hospital network. Methods and results Between January 2010 and September 2018, administrative data provided by 85 Helios hospitals were screened for patients with main or secondary discharge diagnosis of ventricular tachycardia (VT) or premature ventricular contractions (PVCs) in combination with an arrhythmia-related CA using ICD- and OPS codes. In 5052 cases (mean age 60.9 ± 14.3 years, 30.1% female) of 30 different hospitals, in-hospital mortality was 1.27% with a higher mortality in patients ablated for VT (1.99%, n = 2, 955) compared to PVC (0.24%, n = 2, 097, P < 0.01). Mortality rates were 2.06% in patients with ischaemic heart disease (IHD, n = 2, 137), 1.47% in patients with non-ischaemic structural heart disease (NIHD, n = 1, 224), and 0.12% in patients without structural heart disease (NSHD, n = 1, 691). Considering different types of hospital admission, mortality rates were 0.35% after elective (n = 2, 825), 1.60% after emergency admission/hospital transfer <24 h (n = 1, 314) and 3.72% following delayed hospital transfer >24 h after initial admission (n = 861, P < 0.01 vs. elective admission and emergency admission/hospital transfer <24 h). In multivariable analysis, a delayed hospital transfer >24 h [odds ratio (OR) 2.28, 95% confidence interval (CI) 1.59–3.28, P < 0.01], the occurrence of procedure-related major adverse events (OR 6.81, 95% CI 2.90–16.0, P < 0.01), Charlson Comorbidity Index (CCI, OR 2.39, 95% CI 1.56–3.66, P < 0.01) and its components congestive heart failure (OR 8.04, 95% CI 1.71–37.8, P < 0.01), and diabetes mellitus (OR 1.59, 95% CI 1.13–2.22, P < 0.01) were significantly associated with in-hospital death. Conclusions We reported in-hospital mortality rates after CA of ventricular arrhythmias in the largest multicentre, administrative dataset in Germany which can be implemented in quality management programs. Aside from comorbidities, a delayed hospital transfer to a CA performing centre is associated with an increased in-hospital mortality. This deserves further studies to determine the optimal management strategy.

scholarly journals Electrocardiographic Criteria for Differentiating Left from Right Idiopathic Outflow Tract Ventricular Arrhythmias

2021 ◽  
Vol 10 (1) ◽  
pp. 10-16
Author(s):  
Marco V Mariani ◽  
Agostino Piro ◽  
Domenico G Della Rocca ◽  
Giovanni B Forleo ◽  
Naga Venkata Pothineni ◽  
...  
Keyword(s):  
Ventricular Arrhythmias ◽  
Right Ventricular Outflow Tract ◽  
Structural Heart Disease ◽  
Ventricular Outflow Tract ◽  
Left Ventricular ◽  
Outflow Tract ◽  
Premature Ventricular Contractions ◽  
Left Ventricular Outflow ◽  
The Right ◽  
Ecg Criteria

Idiopathic ventricular arrhythmias are ventricular tachycardias or premature ventricular contractions presumably not related to myocardial scar or disorders of ion channels. Of the ventricular arrhythmias (VAs) without underlying structural heart disease, those arising from the ventricular outflow tracts (OTs) are the most common. The right ventricular outflow tract (RVOT) is the most common site of origin for OT-VAs, but these arrhythmias can, less frequently, originate from the left ventricular outflow tract (LVOT). OT-VAs are focal and have characteristic ECG features based on their anatomical origin. Radiofrequency catheter ablation (RFCA) is an effective and safe treatment strategy for OT-VAs. Prediction of the OT-VA origin according to ECG features is an essential part of the preprocedural planning for RFCA procedures. Several ECG criteria have been proposed for differentiating OT site of origin. Unfortunately, the ECG features of RVOT-VAs and LVOT-VAs are similar and could possibly lead to misdiagnosis. The authors review the ECG criteria used in clinical practice to differentiate RVOT-VAs from LVOT-VAs.

Sustained and non-sustained ventricular tachycardia and no associated heart disease (idiopathic ventricular tachycardia)

ESC CardioMed ◽  
2018 ◽  
pp. 2288-2293
Author(s):  
Victor Bazan ◽  
Enrique Rodriguez-Font ◽  
Francis E. Marchlinski
Keyword(s):  
Heart Disease ◽  
Ventricular Tachycardia ◽  
Drug Therapy ◽  
Catheter Ablation ◽  
Ventricular Fibrillation ◽  
Right Ventricular ◽  
Ventricular Outflow Tract ◽  
Left Ventricular ◽  
Polymorphic Ventricular Tachycardia ◽  
The Right

Patients with ventricular arrhythmias (VAs) and without underlying structural heart disease or baseline electrical disorders (‘idiopathic’ VAs) usually have a benign clinical course. Only rarely do these benign arrhythmias trigger polymorphic ventricular tachycardia and idiopathic ventricular fibrillation. Due to their focal origin and to the absence of underlying myocardial scar, the 12-lead electrocardiogram (ECG) very precisely establishes the right or left ventricular site of origin of the arrhythmia and can help regionalize the origin of ventricular tachycardia for ablation. A 12-lead ECG obtained during the baseline rhythm and 24 h ECG Holter monitoring are indicated in order to identify structural or electrical disorders leading to polymorphic ventricular tachycardia/ventricular fibrillation and to determine the VA burden. The most frequent origin of idiopathic VAs is the right ventricular outflow tract. Other origins include the left ventricular outflow tract, the left ventricular fascicles (fascicular ventricular tachycardias), the left and right ventricular papillary muscles, the crux cordis, the mitral and tricuspid annuli, and the right ventricular moderator band. Recognizing the typical anatomic sites of origin combined with a 12-lead ECG assessment facilitates localization. Antiarrhythmic drug therapy (including use of beta blockers) or catheter ablation may be indicated to suppress or eliminate idiopathic VAs, particularly if there are severe arrhythmia-related symptoms or if the arrhythmia burden is high and ‘tachycardia’-induced cardiomyopathy is suspected. Catheter ablation is frequently preferred to prevent lifelong drug therapy in young patients.

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