Mauro Biffi

Presence and duration of atrial fibrillation detected by continuous monitoring: Crucial implications for the risk of thromboembolic events

AF and the Risk of Thromboembolic Events. Introduction: Asymptomatic atrial fibrillation (AF) can expose patients to the risk of stroke. The primary objective of this study was to assess the incidence of thromboembolic events in relationship with CHADS2 (congestive heart failure, hypertension, age ≥75 years, diabetes mellitus, and prior stroke, or transient ischemic attack) score and AF presence/duration. The secondary objective was to compare intermittent versus continuous monitoring strategies.

Dynamic Electrophysiological Behavior of Human Atria During Paroxysmal Atrial Fibrillation

BACKGROUND The aims of our study were to investigate the meaning of local atrial activation and its behavior during paroxysmal atrial fibrillation and to study the effect of overdrive pacing on local atrial activity. METHODS AND RESULTS Twenty-five patients with lone paroxysmal atrial fibrillation underwent electrophysiological study. Functional and effective atrial refractoriness was determined. Mean and fifth percentile values of 100 consecutive atrial fibrillation intervals (FF) were evaluated at three atrial sites either at arrhythmia onset or at self-termination (or at minute 5). A high-voltage burst pacing was performed after 6 minutes of stable atrial fibrillation in 10 patients. Mean FF intervals were evaluated 5 seconds before and after atrial pacing. Forty-nine atrial fibrillation episodes were induced: 39 self-terminating within 5 minutes and 10 long-lasting. A significant correlation was found between mean FF and atrial functional refractory period (r = .73, P < .001) and between fifth percentile FF and atrial effective refractory period (r = .57, P < .005). Atrial fibrillation self-termination was associated with significant mean FF prolongation, whereas long-lasting fibrillation behaved the opposite. In 10 patients, burst pacing resulted in significant shortening of the mean FF at the stimulation site; no changes were observed in the two distant recording sites. CONCLUSIONS The analysis of the FF intervals demonstrates a strict correlation with atrial functional refractoriness. The self-termination of atrial fibrillation is related to a prolongation of the functional refractoriness (mean FF), whereas a shortening of both functional and effective refractoriness (fifth percentile) is associated with atrial fibrillation persistence. The provoked shortening of the mean FF at the stimulation site is consistent with the presence of a gap of excitability during atrial fibrillation in the human atria.

Improving Stroke Risk Stratification Using the CHADS2 and CHA2DS2-VASc Risk Scores in Patients With Paroxysmal Atrial Fibrillation by Continuous Arrhythmia Burden Monitoring

Background and Purpose— In patients with atrial fibrillation (AF), stroke risk stratification schema do not consider AF parameters. The aim of the study is to assess the impact of combining risk factors with continuous AF burden monitoring. Methods— In this retrospective study 568 patients implanted with a DDDR-P pacemaker (AT-500; Medtronic) and a history of AF were continuously monitored for 1 year. Results— During follow-up, 14 patients (2.5%) had a thromboembolic event. Patients were divided into 3 groups: AF burden ⩽5 minutes per day (AF-free; n=223 [39%]), AF burden >5 minutes but <24 hours per day (AF-5 minutes; n=179 [32%]), and AF burden ≥24 hours (AF-24 hours; n=166 [29%]). Patients were also classified according to CHADS2 and CHA2DS2-VASc risk scores. The discrimination ability of each risk score was evaluated performing a logistic regression analysis and calculating the corresponding C-statistic. The addition of AF burden improved C-statistics: for CHADS2 from 0.653 (P=0.051) to 0.713 (P=0.007); for CHA2DS2-VASc, from 0.898 (P<0.0001) to 0.910 (P<0.0001). Conclusions— The CHA2DS2-VASc score had a high sensitivity to predict thromboembolism. Implementation of device data on AF presence/duration/burden has the potential to contribute to improved clinical risk stratification and should be tested prospectively.

Oral Propafenone To Convert Recent-Onset Atrial Fibrillation in Patients with and without Underlying Heart Disease: A Randomized, Controlled Trial

The optimal way to convert recent-onset atrial fibrillation to sinus rhythm is a subject of much debate. The effectiveness of intravenous propafenone has been shown [1-3], but the full antiarrhythmic effect of this regimen depends not only on the parent compound but on its 5-hydroxylated metabolite [4, 5]. This dependence provides a strong rationale for the use of oral loading regimens [3]. Results of previous controlled studies have shown that oral loading of propafenone is highly effective in converting recent-onset atrial fibrillation to sinus rhythm [6, 7]. Safety is a major concern with antiarrhythmic therapy. One of the primary proarrhythmic risks of propafenone and flecainide is the transformation of atrial fibrillation to flutter with 1:1 atrioventricular conduction and hemodynamic impairment [8-10]. We sought to determine whether the effectiveness and safety of propafenone differ in patients who have structural heart disease and patients who do not. Methods From June 1990 to June 1994, consecutive patients with recent-onset atrial fibrillation ( 7 days) who presented to one of three centers were considered for enrollment. Onset of arrhythmia was documented by electrocardiography or by an abrupt onset of palpitations with subsequent evidence of atrial fibrillation on electrocardiography. Patients were excluded for any of the following reasons: age greater than 80 years, heart failure greater than NYHA (New York Heart Association) class II, mean ventricular rate during atrial fibrillation less than 70 beats/min, recent myocardial infarction (within <6 months), unstable angina pectoris, previous or current electrocardiographic evidence ventricular preexcitation or complete bundle-branch block, previous electrocardiographic evidence of second- or third-degree atrioventricular block or bifascicular block, the sick sinus syndrome, hypokalemia (potassium level <3.5 mEq/L), renal or hepatic failure with severe hypoxia (Pao 2 < 55 mm Hg), severe metabolic disturbances, or known thyroid dysfunction. Patients who were receiving long-term digoxin therapy or antiarrhythmic drugs or had received such treatments within 8 hours before study entry were also excluded. Patients who had atrial fibrillation that lasted 72 hours or longer were enrolled only if they were receiving long-term warfarin therapy for anticoagulation. Patients provided informed consent. Eligible patients had a 24-hour Holter monitor applied; after 1 to 2 hours of observation to assess the stability of atrial fibrillation, they were randomly assigned by center in a single-blind manner to receive propafenone (300 mg in two tablets as a single oral dose) or placebo. All patients received intravenous saline throughout the study period. The electrocardiogram was monitored by telemetry, blood pressure was measured every 2 hours, and 12-lead electrocardiography was done every hour for the first 4 hours and then every 2 hours for the next 4 hours. When patients converted to sinus rhythm, 12-lead electrocardiography was done immediately. Conversion was defined as a stable sinus rhythm that lasted for at least 1 hour. Eight hours after the study drug was administered, physicians could continue treatment with the study drug or switch to a different therapeutic option. Holter monitor tapes were analyzed by two blinded observers using computer scanning systems (Marquette 8000, Milwaukee, Wisconsin, and Del Mar Avionics, Irvine, California) to determine the time of conversion to sinus rhythm and whether an abnormal rhythm was present. Within 24 hours after enrollment, echocardiography was done for each patient and left atrial diameter was measured in the left parasternal long-axis view. On the basis of clinical history and the results of physical examination, echocardiography, and chest radiography, patients were classified as having structural heart disease (defined as the presence of cardiac abnormalities other than atrial fibrillation), hypertension without structural heart disease (defined as previously recognized systemic hypertension according to the criteria of the World Health Organization), or neither. Continuous outcomes and baseline characteristics of the patients were compared by using the chi-square statistic and t-test as appropriate. The rates of conversion to sinus rhythm were assessed at 3 and 8 hours. Odds ratios and corresponding CIs were calculated according to the methods of Gardner and Altman [11]. We did logistic regression analysis to describe how the interaction of treatment with the presence or absence of heart disease and hypertension affected the probability of conversion to sinus rhythm. Analyses were done using SPS software, version 6.1.3 (SPS, Inc., Chicago, Illinois). Results Patients During the study period, 407 patients presented to the three centers and were screened for eligibility. Two hundred forty-three patients were eligible, and 240 gave consent. A total of 164 patients were excluded for one or more of the following reasons: age greater than 80 years (n = 10), heart failure greater than NYHA class II (n = 33), recent myocardial infarction (n = 20), bundle-branch block (n = 24), the sick sinus syndrome (n = 6), severe hypoxia (n = 13), thyroid dysfunction (n = 12), and previous antiarrhythmic treatment (n = 63). Two hundred forty patients were randomly assigned to receive propafenone (n = 119) or placebo (n = 121). The two groups were similar with regard to age, sex, cause of atrial fibrillation, NYHA class, left atrial dimension (measured by echocardiography), structural heart disease, and hypertension (Table 1). The duration of atrial fibrillation before randomization ranged from 2.5 to 120 hours and did not differ significantly between the treatment groups. Table 1. Patient Characteristics Conversion to Sinus Rhythm and Presence of Heart Disease The probability of conversion to sinus rhythm was greater after propafenone than after placebo at 3 and 8 hours (P < 0.001) (Figure 1). Corresponding odds ratios were 3.8 (95% CI, 2.1 to 6.8) at 3 hours and 5.4 (CI, 3.0 to 9.4) at 8 hours. Figure 1. Conversion to sinus rhythm within 8 hours in patients receiving propafenone or placebo. At 8 hours, the probability of conversion to sinus rhythm was significantly higher in the propafenone group than in the placebo group for patients who had heart disease (odds ratio, 21.7 [CI, 5.9 to 80.1]; P < 0.001), patients who had hypertension (odds ratio, 6.4 [CI, 2.3 to 17.6]; P < 0.001), and patients who did not have structural heart disease (odds ratio, 2.8 [CI, 1.2 to 6.7]; P = 0.02). Conversion rates at 8 hours for patients receiving propafenone were similar among the three heart disease subgroups, but conversion rates for patients receiving placebo differed significantly (56% for patients without structural heart disease, 27% for patients with hypertension, and 17% patients with structural heart disease [P = 0.009 by logistic regression model]). At 3 hours, the probability of conversion to sinus rhythm was higher in the propafenone group than in the placebo group for patients who did not have heart disease (48% for propafenone compared with 26% for placebo; odds ratio, 2.6 [CI, 1.2 to 6.0]; P = 0.02), patients who had hypertension (41% for propafenone compared with 16% for placebo; odds ratio, 3.5 [CI, 1.2 to 10.5]; P = 0.02), and patients who had structural heart disease (47% for propafenone compared with 7% for placebo; odds ratio, 12.3 [CI, 2.5 to 60.5]; P < 0.001). By logistic regression analysis, no significant correlation between heart disease and treatment was seen at 3 hours (P = 0.2). Mean time SD for conversion to sinus rhythm within 8 hours was 181 118 minutes for propafenone and 181 112 minutes for placebo (P > 0.2). Adverse Effects Sustained atrial flutter or tachycardia (lasting 1 min) occurred in eight patients (7%) receiving propafenone and seven patients (6%) receiving placebo (P > 0.2), regardless of heart disease status. Among these patients, atrioventricular conduction was 2:1 in two patients receiving propafenone (heart rate, 115 to 140 beats/min) and three patients receiving placebo (heart rate, 120 to 150 beats/min), 3:1 in six patients receiving propafenone (heart rate, 60 to 95 beats/min) and three patients receiving placebo (heart rate, 60 to 100 beats/min), and 1:1 in one patient receiving placebo (heart rate, 240 beats/min). This patient developed atrial flutter and collapsed. Pauses in ventricular rate lasting longer than 2 seconds were seen in one patient (1%) receiving propafenone and three patients (2%) receiving placebo (P > 0.2). Among patients receiving propafenone, nine (8%) had the following adverse effects: QRS complexes of the electrocardiogram greater than 120 ms (n = 3), hypotension (n = 2), slight hypotension and bradycardia at conversion (n = 3), and phases of junctional rhythm after conversion (n = 1). No ventricular proarrhythmic effects occurred. Discussion Oral loading of propafenone was effective for conversion to sinus rhythm in our study, as it has been in smaller studies [3, 6, 7, 12, 13]. The recent findings of Wijffels and colleagues [14] in a model of chronic atrial fibrillation in animals indicate that electrophysiologic remodeling occurs within a few hours of persistent atrial fibrillation and results primarily from changes in atrial refractoriness that enhance the persistence of atrial fibrillation. This observation provides a strong rationale for prompt conversion to sinus rhythm. Therefore, oral loading of propafenone (which has an effectiveness similar to that of intravenous propafenone [3]) offers many advantages over such regimens as oral quinidine and intravenous amiodarone, which require titration of dose or a longer period of time to achieve an effect [6, 13, 15]. In controlled trials, propafenone was shown to be more effective and to take effect more quickly than amiodarone [13] or digoxin plus quinidine [6]. Intravenous amiodarone was no more effective than placebo and

A simplified biventricular defibrillator with fixed long detection intervals reduces implantable cardioverter defibrillator (ICD) interventions and heart failure hospitalizations in patients with non-ischaemic cardiomyopathy implanted for primary prevention: the RELEVANT [Role of long dEtection window programming in patients with LEft VentriculAr dysfunction, Non-ischemic eTiology in primary prevention treated with a biventricular ICD] study

Aims To investigate the efficacy and safety of a cardiac resynchronization therapy with cardioverter–defibrillator (CRT-D) device with simplified ventricular tachycardia management in patients with non-ischaemic heart failure (HF) and primary prevention implantable cardioverter defibrillator (ICD) indication. Methods and results Prospective, controlled, parallel, multicentre, non-randomized study enrolling 324 primary prevention non-ischaemic HF patients implanted with CRT-D devices from 2004 to 2007: Protect group, 164 patients implanted with a Medtronic Insync III Protect device and Control group, 160 patients utilizing other Medtronic CRT-D devices. Efficacy was assessed by computing appropriate and inappropriate detections and therapies during follow-up; safety compared hospitalizations and syncopal events between groups. Ninety per cent of both ventricular and supraventricular tachyarrhythmias terminated within the 13–29 beat detection interval with the Protect algorithm. The Protect group showed a significantly better event-free survival to first delivered therapy for total (P = 0.0001), appropriately treated (P = 0.002), and inappropriately treated episodes (P = 0.017). The total number of delivered shocks was significantly lower in the Protect group (22 vs. 59, P < 0.0001). In the Protect group, a significantly reduced HF hospitalization (hazard ratio 0.38, 95% CI 0.15–0.98, P = 0.044) was observed without any increase of syncope or death. Conclusion A simplified CRT-D device with fixed long detection reduced overall ICD therapy burden and HF hospitalizations without entailing any additional adverse events in primary prevention non-ischaemic HF patients.

Clinical Relevance of Atrial Fibrillation/Flutter, Stroke, Pacemaker Implant, and Heart Failure in Emery-Dreifuss Muscular Dystrophy A Long-Term Longitudinal Study

Background and Purpose— Emery-Dreifuss muscular dystrophy (EDMD) is a rare inherited disorder associated with cardiac involvement. We investigated the spectrum and relevance of the cardiac manifestations of EDMD, focusing on bradyarrhythmias and tachyarrhythmias (including atrial fibrillation/flutter), embolic stroke, and heart failure. Methods and Results— Eighteen patients (age 42.8±19.6 years) with genetically confirmed X-linked (n=10, including 3 carriers) or autosomal dominant (n=8) EDMD were followed for a period ranging from 1 to 30 years in a research center for neuromuscular diseases and in a university cardiological department. Pacemakers were required by 10 of 18 (56%) patients for bradyarrhythmia, and related complications occurred in 3 of 10 (30%) cases. Atrial fibrillation/flutter developed in 11 of 18 (61%) patients, with atrial standstill subsequently occurring in 5 of 11 (45%) cases and embolic stroke (most often disabling) in 4 of 11 (36%). Heart failure requiring transplantation occurred in 1 of 18 (6%) patients, and asymptomatic left ventricular dysfunction in a further 3 (17%). No relationship was evident between neuromuscular impairment and cardiac involvement. Conclusions— Both X-linked and autosomal dominant EDMD patients risk not only bradyarrhythmia (requiring pacemaker implant) but also atrial fibrillation/flutter, which often anticipates atrial standstill and can cause disabling embolic stroke at a relatively young age. Antithromboembolic prophylaxis has to be recommended in EDMD patients with atrial fibrillation/flutter or atrial standstill. With careful monitoring, survival after pacemaker implant may be long. Heart failure, which seems to occur only in a minority of patients, may be severe.

Phrenic stimulation: a challenge for cardiac resynchronization therapy.

Background—Phrenic stimulation (PS) may hinder left ventricular (LV) pacing. We prospectively observed its prevalence in consecutive patients with cardiac resynchronization therapy (CRT) devices. Methods and Results—In the years 2003 to 2006, 197 patients received a CRT device. PS and LV threshold measurements were carried out at implantation and at 6-month follow-up. LV reverse remodeling was assessed by echocardiography before implantation and at follow-up. LV lead placement was lateral/posterolateral in 86% of patients. Both PS and LV reverse remodeling occurred most frequently at the lateral/posterolateral LV pacing sites (P<0.001). PS was detected in 73 (37%) of patients and was clinically relevant in 41 (22%). The detection of PS at implantation had a poor sensitivity, as it occurred only in left lateral or sitting position in 27 patients. Ten patients (5%) underwent repeated surgery and 4 (2%) had their CRT turned off because of PS. At follow-up, we could manage PS noninvasively in 32 patients with a small PS-LV threshold difference: in 20 by cathode programmability (3 also thanks to automatic management of LV output) and in 12 (without cathode programmability) by programming the LV output as threshold +1 V. Conclusions—PS may seriously hinder CRT. A bipolar LV lead and cathode programmability are mandatory to avoid PS by changing the LV pacing vector at target sites for CRT. LV stability at target sites despite PS should also be pursued by these means. The automatic adjustment of LV pacing output is complementary in patients with a small PS-LV threshold difference.Background— Phrenic stimulation (PS) may hinder left ventricular (LV) pacing. We prospectively observed its prevalence in consecutive patients with cardiac resynchronization therapy (CRT) devices. Methods and Results— In the years 2003 to 2006, 197 patients received a CRT device. PS and LV threshold measurements were carried out at implantation and at 6-month follow-up. LV reverse remodeling was assessed by echocardiography before implantation and at follow-up. LV lead placement was lateral/posterolateral in 86% of patients. Both PS and LV reverse remodeling occurred most frequently at the lateral/posterolateral LV pacing sites ( P <0.001). PS was detected in 73 (37%) of patients and was clinically relevant in 41 (22%). The detection of PS at implantation had a poor sensitivity, as it occurred only in left lateral or sitting position in 27 patients. Ten patients (5%) underwent repeated surgery and 4 (2%) had their CRT turned off because of PS. At follow-up, we could manage PS noninvasively in 32 patients with a small PS-LV threshold difference: in 20 by cathode programmability (3 also thanks to automatic management of LV output) and in 12 (without cathode programmability) by programming the LV output as threshold +1 V. Conclusions— PS may seriously hinder CRT. A bipolar LV lead and cathode programmability are mandatory to avoid PS by changing the LV pacing vector at target sites for CRT. LV stability at target sites despite PS should also be pursued by these means. The automatic adjustment of LV pacing output is complementary in patients with a small PS-LV threshold difference. Received December 14, 2008; accepted June 10, 2009. # CLINICAL PERSPECTIVE {#article-title-2}

Pharmacological cardioversion of atrial fibrillation: current management and treatment options.

Atrial fibrillation (AF) is the most common form of arrhythmia, carrying high social costs. It is usually first seen by general practitioners or in emergency departments. Despite the availability of consensus guidelines, considerable variations exist in treatment practice, especially outside specialised cardiological settings. Cardioversion to sinus rhythm aims to: (i) restore the atrial contribution to ventricular filling/output; (ii) regularise ventricular rate; and (iii) interrupt atrial remodelling. Cardioversion always requires careful assessment of potential proarrhythmic and thromboembolic risks, and this translates into the need to personalise treatment decisions. Among the many clinical variables that affect strategy selection, time from onset is crucial.In selected patients, pharmacological cardioversion of recent-onset AF can be a safely used, feasible and effective approach, even in internal medicine and emergency departments. In most cases of recent-onset AF, pharmacological cardioversion provides an important- and probably more cost effective-alternative to electrical cardioversion, which can then be employed as a second-line therapy for nonresponders.Class IC agents (flecainide or propafenone), which can be safely used in hospitalised patients with recent-onset AF without left ventricular dysfunction, can provide rapid conversion to sinus rhythm after either intravenous administration or oral loading. Although intravenous amiodarone requires longer conversion times, it is still the standard treatment for patients with heart failure. Ibutilide also provides good conversion rates and could be used for AF patients with left ventricular dysfunction (were it not for high costs).For long-lasting AF most pharmacological treatments have only limited efficacy and electrical cardioversion remains the gold standard in this setting. However, a widely used strategy involves pretreatment with amiodarone in the weeks before planned electrical cardioversion: this provides optimal prophylaxis and can sometimes even restore sinus rhythm. Dofetilide may also be capable of restoring sinus rhythm in up to 25–30% of patients and can be used in patients with heart failure.The potential risk of proarrhythmia increases the need for careful therapeutic decision making and management of pharmacological cardioversion. The results of recent trials (AFFIRM [Atrial Fibrillation Follow-up Investigation of Rhythm Management] and RACE [Rate Control versus Electrical Cardioversion for Persistent Atrial Fibrillation]) on rate versus rhythm control strategies in the long term have led to a generalised shift in interest towards rate control. Although carefully designed studies are required to better define the role of pharmacological rhythm control in specific AF settings, this alternative option remains a recommendable strategy for many patients, especially those in acute care.

A randomized double-blind comparison of biventricular versus left ventricular stimulation for cardiac resynchronization therapy: The Biventricular versus Left Univentricular Pacing with ICD Back-up in Heart Failure Patients (B-LEFT HF) trial

BACKGROUND Biventricular (BiV) stimulation is the preferred means of delivering cardiac resynchronization therapy (CRT), although left ventricular (LV)-only stimulation might be as safe and effective. B-LEFT HF is a prospective, multicenter, randomized, double-blind study aimed to examine whether LV-only is noninferior to BiV pacing regarding clinical and echocardiographic responses. METHODS B-LEFT HF randomly assigned 176 CRT-D recipients, in New York Heart Association class III or IV, with an LV ejection fraction < or =35% and QRS > or =130 milliseconds, to a BiV (n = 90) versus LV (n = 86) stimulation group. Clinical status and echocardiograms were analyzed at baseline and 6 months after CRT-D implant to test the noninferiority of LV-only compared with BiV stimulation. RESULTS The proportion of responders was in line with current literature on CRT, with improvement in heart failure composite score in 76.2% and 74.7% of patients in BiV and LV groups, respectively. Comparing LV versus BiV pacing, the small differences in response rates and corresponding 95% CI indicated that LV pacing was noninferior to BiV pacing for a series of response criteria (combination of improvement in New York Heart Association and reverse remodeling, improvement in heart failure composite score, reduction in LV end-systolic volume of at least 10%), both at intention-to-treat and at per-protocol analysis. CONCLUSIONS Left ventricular-only pacing is noninferior to BiV pacing in a 6-month follow-up with regard to clinical and echocardiographic responses. Left ventricular pacing may be considered as a clinical alternative option to BiV pacing.

Effects of Cardiac Resynchronization Therapy on Left Ventricular Twist

OBJECTIVES This study explored the effects of cardiac resynchronization therapy (CRT) on left ventricular (LV) twist, particularly in relation to LV lead position. BACKGROUND LV twist is emerging as a comprehensive index of LV function. METHODS Eighty heart failure patients were included. Two-dimensional echocardiography was performed at baseline, immediately after CRT, and at 6-month follow-up. Speckle-tracking analysis was applied to assess LV twist. The LV lead was placed preferably in a (postero)lateral vein, and at fluoroscopy, the position was classified as basal, midventricular, or apical. Response to CRT was defined as reduction of LV end-systolic volume>or=15% at 6-month follow-up. A control group comprised 30 normal subjects. RESULTS Peak LV twist in heart failure patients was 4.8+/-2.6 degrees compared with 15.0+/-3.6 degrees in the control subjects (p<0.001). At 6-month follow-up, peak LV twist significantly improved only in responders (56%), from 4.3+/-2.4 degrees to 8.5+/-3.2 degrees (p<0.001). The strongest predictor of response to CRT was the improvement of peak LV twist immediately after CRT (odds ratio: 1.899, 95% confidence interval: 1.334 to 2.703, p<0.001). Furthermore, LV twist significantly improved in patients with an apical (from 4.3+/-3.1 degrees to 8.6+/-3.0 degrees, p=0.001) and midventricular (from 4.8+/-2.2 degrees to 6.4+/-3.9 degrees, p=0.038) but not with a basal (5.0+/-3.3 degrees vs. 4.1+/-3.2 degrees, p=0.28) LV lead position. Similarly, LV ejection fraction significantly increased in patients with an apical (from 26+/-7% to 37+/-7%, p<0.001) and midventricular (from 26+/-6% to 33+/-8%, p<0.001) but not with a basal (26+/-5% vs. 28+/-8%, p=0.30) LV lead position. CONCLUSIONS An immediate improvement of LV twist after CRT predicts LV reverse remodeling at 6-month follow-up.