"Torsade de Pointes" in Patients with Structural Heart Disease and Atrial Fibrillation Treated with Amiodarone, beta-Blockers, and Digitalis

2006 ◽  
Vol 29 (4) ◽  
pp. 363-366 ◽  
Author(s):  
JAN W. SCHRICKEL ◽  
JOERG O. SCHWAB ◽  
ALEXANDER YANG ◽  
ALEXANDER BITZEN ◽  
BERNDT LUDERITZ ◽  
...  
Heart Rhythm ◽  
2005 ◽  
Vol 2 (5) ◽  
pp. S329
Author(s):  
Jan W. Schrickel ◽  
Jörg O. Schwab ◽  
Alexander Yang ◽  
Rainer Schimpf ◽  
Helga Bielik ◽  
...  

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
M Martinez-Selles ◽  
R Elosua ◽  
M Ibarrola ◽  
M De Andres ◽  
P Diez-Villanueva ◽  
...  

Abstract Background Advanced interatrial block (IAB), prolonged and bimodal P waves in surface ECG inferior leads, is an unrecognized surrogate of atrial dysfunction and a trigger of atrial dysrhythmias, mainly atrial fibrillation (AF). Our aim was to prospectively assess whether advanced IAB in sinus rhythm precedes AF and stroke in elderly outpatients with structural heart disease, a group not previously studied. Methods Prospective observational registry that included outpatients aged ≥70 years with structural heart disease and no previous diagnosis of AF. Patients were divided into three groups according to P-wave characteristics. Results Among 556 individuals, 223 had normal P-wave (40.1%), 196 partial IAB (35.3%), and 137 advanced IAB (24.6%). After a median follow-up of 694 days; 93 patients (16.7%) developed AF, 30 stroke (5.4%), and 34 died (6.1%). Advanced IAB was independently associated with AF (hazard ratio [HR] 2.9, 95% confidence interval [CI] 1.7–5.1, p<0.001), stroke (HR 3.8, 95% CI 1.4–10.7, p=0.010), and AF/stroke (HR 2.6, 95% CI 1.5–4.4, p=0.001). P-wave duration (ms) was independently associated with AF (HR 1.05, 95% CI 1.03–1.07, p<0.001), AF/stroke (HR 1.04, 95% CI 1.02–1.06, p<0.001), and mortality (HR 1.04, 95% CI 1.00–1.08, p=0.021). Conclusions The presence of advanced IAB in sinus rhythm is a risk factor for AF and stroke in an elderly population with structural heart disease and no previous diagnosis of AF. P-wave duration was also associated with all-cause mortality. Figure. Age- and sex-adjusted linear and non-linear association between P-wave duration (msec) and atrial fibrillation (A), stroke (B), and atrial fibrillation or stroke (C) risk. Results of a generalized additive model with spline smoothing functions and 4 degrees of freedom. Figure 1. Kaplan-Meyer curves of survival free of atrial fibrillation (A), stroke (B) and atrial fibrillation or stroke (C) in patients with normal P-wave, partial interatrial block (IAB) and advanced IAB. Funding Acknowledgement Type of funding source: None


2010 ◽  
Vol 3 (6) ◽  
pp. 606-615 ◽  
Author(s):  
Maurits A. Allessie ◽  
Natasja M.S. de Groot ◽  
Richard P.M. Houben ◽  
Ulrich Schotten ◽  
Eric Boersma ◽  
...  

2016 ◽  
Vol 72 (1) ◽  
Author(s):  
Alberto Genovesi Ebert ◽  
Furio Colivicchi ◽  
Marco Malvezzi Caracciolo ◽  
Carmine Riccio

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.


2005 ◽  
Vol 105 (3) ◽  
pp. 337-339 ◽  
Author(s):  
Antonio D'Aloia ◽  
Pompilio Faggiano ◽  
Loretta Brentana ◽  
Alessandra Boldini ◽  
Claudio Pedrinazzi ◽  
...  

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Tom Marwick ◽  
Wojciech Kosmala ◽  
Christine Jellis

Introduction: Stage B heart failure (BHF, asymptomatic structural heart disease) is diagnosed in the presence of myocardial scar or impaired LVEF. However, the insensitivity of LVEF may lead to under-recognition of BHF in non-ischemic heart disease. This may be important, as BHF may precede the onset of HF symptoms, and necessitates the initiation of treatment. We sought the implications of using additional LV assessment to identify BHF in pts at risk of HF (stage A HF, AHF). Methods: We studied 510 asymptomatic pts (age 58±12yrs) with AHF (diabetes, hypertension or obesity), but no history of ischemic heart disease and a normal stress echo. All pts underwent echocardiography (including assessment of strain and diastolic dysfunction) and cardiopulmonary exercise testing. Results: BHF was defined as the presence of at least one of; reduced LV longitudinal strain (<18%), increased LV filling pressure (E/e’>13) or moderate-to-severe LV hypertrophy (LV mass index ≥109 g/m 2 in women and 132 g/m 2 in men) in 243 patients (47%). Reduced exercise capacity (peakVO 2 and METS) was identified in BHF compared with other AHF (Table). Using this definition, BHF was associated with lower peak VO 2 (β=-0.20, p<0.00001) and METS (β=-0.21, p<0.0001), independent of higher BMI, insulin resistance, older patient age, male sex and treatment with beta-blockers. Conclusions: LV hypertrophy, elevated LV filling pressure elevation and abnormal myocardial deformation independently contribute to lower exercise capacity in pts at risk of HF. Given the association of exercise capacity with outcome, these factors should be considered grounds for the diagnosis of BHF.


Circulation ◽  
2012 ◽  
Vol 125 (suppl_10) ◽  
Author(s):  
Evan L Thacker ◽  
Paul N Jensen ◽  
Bruce M Psaty ◽  
Barbara McKnight ◽  
W. T Longstreth ◽  
...  

Objective. We sought to determine among people whose initial atrial fibrillation (AF) terminated whether use of statins, beta-blockers, and ACE inhibitors or ARBs was associated with lower risk of recurrent AF or progression to permanent AF. Methods. In Group Health, an integrated health care system, we identified an inception cohort of people aged 30-84 with newly diagnosed AF in 2001-2004 whose initial AF terminated within six months. Follow-up was through 2009. Medication use throughout follow-up was determined from the pharmacy database. Recurrent AF and permanent AF were determined from medical records and ECG and procedure code databases. Permanent AF was defined as AF present on two dates at least six months apart with no evidence of sinus rhythm in between. Cox proportional hazards models were used to estimate hazard ratios. We compared current statin use with nonuse. To reduce healthy user bias, we compared statin use one year prior with nonuse one year prior. To reduce confounding by indication, we compared beta-blocker use with nondihydropyridine calcium channel blocker use. We compared current ACE inhibitor or ARB use with nonuse. Results. Analyses included 1,511 people. Mean age was 70 years and 51% were men. Statins were used for 36% of person-time, beta-blockers for 48%, and ACE inhibitors or ARBs for 42%. Five-year cumulative incidence of recurrent AF was 74% and of permanent AF was 24%. Current statin use vs. nonuse was associated with lower permanent AF risk. However, statin use vs. nonuse one year prior was not associated with permanent AF ( Table ). Use of beta-blockers and ACE inhibitors or ARBs was not associated with recurrent AF or permanent AF. Adjusted hazard ratios of recurrent AF and permanent AF according to medication use. Medication use Recurrent AF Adjusted HR * (95% CI) Permanent AF Adjusted HR * (95% CI) Statins -- current use analysis Nonuse 1.00 (reference) 1.00 (reference) Current use 0.96 (0.82, 1.12) 0.76 (0.58, 0.99) Statins -- lagged analysis Nonuse one year prior 1.00 (reference) 1.00 (reference) Use one year prior 0.94 (0.79, 1.13) 0.98 (0.74, 1.30) Beta-blockers Current nondihydropyridine CCB use 1.00 (reference) 1.00 (reference) Current beta-blocker use 0.91 (0.74, 1.12) 1.04 (0.69, 1.56) ACE inhibitors or ARBs Nonuse 1.00 (reference) 1.00 (reference) Current use 0.99 (0.86, 1.14) 0.98 (0.77, 1.25) * Adjusted for age, sex, BMI, diabetes, hypertension, coronary heart disease, valvular heart disease, heart failure, prior stroke, and chronic kidney disease. Conclusion. The lagged statin analysis suggests that the association of current statin use with lower permanent AF risk may have been due to an acute effect of statins that did not persist after discontinuation of use, or to a healthy user bias. We found little evidence that use of statins, beta-blockers, or ACE inhibitors or ARBs reduces risk of recurrent AF or permanent AF.


ESC CardioMed ◽  
2018 ◽  
pp. 2288-2293
Author(s):  
Victor Bazan ◽  
Enrique Rodriguez-Font ◽  
Francis E. Marchlinski

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.


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