Heart Failure Reviews

, Volume 16, Issue 5, pp 467–476

Assessing patients for catheter ablation during hospitalization for acute heart failure

Authors

    • Department of Internal Medicine, Division of CardiologyNorthwestern University
  • Jason T. Jacobson
    • Department of Internal Medicine, Division of CardiologyNorthwestern University
Article

DOI: 10.1007/s10741-011-9240-8

Cite this article as:
Knight, B.P. & Jacobson, J.T. Heart Fail Rev (2011) 16: 467. doi:10.1007/s10741-011-9240-8

Abstract

Heart rhythm problems are common among patients who are hospitalized with acute heart failure (HF). Although it is often difficult to determine whether a tachyarrhythmia is the major contributor to an acute HF decompensation or merely a consequence of the decompensation, both issues usually need to be addressed. There is also a subset of patients with HF who have a tachycardia-induced cardiomyopathy (TIC), where the sole cause of the ventricular dysfunction is the heart rhythm problem. In most cases, the management of a tachyarrhythmia in a patient with acute HF is not significantly different than the management of a heart rhythm problem in any patient, but there are several special clinical scenarios and important considerations. These considerations include the time urgency for an intervention, the usual need to be more aggressive and definitive, the need to stabilize a patient to allow for a heart rhythm intervention, such as catheter ablation to be performed safely, and the limitations of antiarrhythmic drugs in patients with ventricular dysfunction. Catheter ablation is a highly effective treatment option for many patients with supraventricular or ventricular tachycardias who are hospitalized with HF. This review will discuss the different types of tachyarrhythmias that can be associated with acute HF and are amenable to catheter ablation, and the assessment that needs to take place in potentially eligible patients to determine when catheter ablation is appropriate.

Keywords

Heart failureCatheter ablationAtrial fibrillationVentricular tachycardia

Introduction

Heart rhythm problems are common among patients who are hospitalized with acute heart failure (HF). Although it is often difficult to determine whether a tachyarrhythmia is the major contributor to an acute HF decompensation or merely a consequence of the decompensation, both issues usually need to be addressed. There is also a subset of patients with HF who have a tachycardia-induced cardiomyopathy (TIC), where the sole cause of the ventricular dysfunction is the heart rhythm problem [1].

In most cases, the management of a tachyarrhythmia in a patient with acute HF is not significantly different than the management of a heart rhythm problem in any patient, but there are several special clinical scenarios and important considerations. These considerations include the time urgency for an intervention, the usual need to be more aggressive and definitive, the need to stabilize a patient to allow for a heart rhythm intervention, such as catheter ablation to be performed safely, and the limitations of antiarrhythmic drugs in patients with ventricular dysfunction. Catheter ablation is a highly effective treatment option for many patients with supraventricular or ventricular tachycardias who are hospitalized with HF. This review will discuss the different types of tachyarrhythmias that can be associated with acute HF and are amenable to catheter ablation, and the assessment that needs to take place in potentially eligible patients to determine when catheter ablation is appropriate.

Patients with supraventricular tachycardias

Any type of sustained supraventricular tachycardia (SVT) can occur in a patient with acute HF, but atrial fibrillation (AF) is by far the most common. Sometimes, it can be difficult to distinguish AF from other forms of tachycardia. This is especially true in patients with HF and AF, because during decompensation the ventricular response can be very rapid. When the rate is rapid, the rhythm can have regular enough ventricular intervals that it can be confused with atrioventricular nodal reentry (AVNRT) or other type of regular paroxysmal supraventricular tachycardia (PSVT). In fact, adenosine is commonly given mistakenly to patients with AF and a rapid ventricular rate [2]. It is important to make a correct diagnosis of the type of tachycardia because the treatment options, and success rates of catheter ablation, differ greatly.

The permanent form of junctional reciprocating tachycardia (PJRT)

The differential diagnosis of a regular PSVT includes AVNRT, atrioventricular reentry (AVRT), atrial tachycardia (AT), atrial flutter (AFL), and junctional ectopic tachycardia (JET) [3]. Catheter ablation is a highly effective treatment for each of these different types of PSVT and should be offered as first-line therapy in a patient with acute HF. A special scenario in a patient with acute HF and SVT is when the SVT is incessant. When a patient has an incessant SVT, it is often referred to as the permanent form of junctional reciprocating tachycardia (PJRT). Patients with PJRT can present with a TIC and acute HF as the first manifestations of the heart rhythm problem, especially children. The term PJRT is occasionally used to refer to an incessant long RP tachycardia that is caused by reentry involving a slowly conducting accessory pathway as the retrograde limb of the circuit. However, an incessant type of long RP tachycardia can also be atypical AVNRT using a slowly conducting AV nodal pathway as the retrograde limb, or an incessant focal atrial tachycardia. The most common location for slowly conducting accessory pathways that result in incessant tachycardia is the posteroseptal space. These pathways are usually concealed and are not associated with manifest preexcitation during sinus beats. During tachycardia, the P-waves are inverted in the inferior leads, making it difficult to differentiate a pathway-mediated tachycardia from atypical AVNRT or a low atrial AT. Catheter ablation should be strongly considered in these patients, regardless of the mechanism, because the success rate is over 95% and there is strong evidence that the ventricular dysfunction resolves after restoration of sinus rhythm [4].

Figure 1 shows an example of a nearly incessant long RP supraventricular rhythm that is associated with inverted P-waves in the inferior leads. The rate is slow, and the rhythm is competing with sinus rhythm. In this patient, the mechanism of the arrhythmia was a focal atrial tachycardia arising from an area near the coronary sinus ostium within the right atrial cavotricuspid isthmus. The tachycardia was successfully ablated.
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Fig. 1

A 12-lead electrocardiogram of a patient with a nearly incessant long RP supraventricular tachycardia with inverted P-waves in the inferior leads. See text for details

Patients with ventricular preexcitation who are asymptomatic and have never had an episode of tachycardia are not usually advised to undergo catheter ablation unless the accessory pathway demonstrates high risk features that could lead to a cardiac arrest. However, ventricular preexcitation caused by anterograde conduction over an accessory pathway during sinus rhythm can induce ventricular mechanical dyssynchrony analogous to that caused by a bundle branch block or right ventricular pacing. Therefore, catheter ablation should be considered in the rare patient with ventricular preexcitation and HF specifically to eliminate the mechanical dyssynchrony [5].

Differentiating sinus tachycardia from an atrial tachycardia

At times, a patient can present with acute HF and an incessant AT associated with P-waves that resemble the P-waves present during sinus tachycardia. In this situation, it is difficult to differentiate sinus tachycardia, caused by the elevated sympathetic tone associated with HF, from an AT that is causing a TIC. Properly identifying the patient with an AT that can be cured with catheter ablation is critical and can be life saving. There are a few clues that point toward an AT rather than sinus tachycardia [6]. The first clue is the rate. When the atrial rate is greater than 150% of the expected heart rate for the age of the patient, the rhythm is probably an AT. Another clue is the presence of AV nodal block during tachycardia. An AT is much more likely to be associated with second-degree AV block during tachycardia than sinus tachycardia caused elevated sympathetic tone associated with heart failure, which increases AV conduction. A third clue is the P-wave morphology. Sometimes there are features of the P-wave that make it very unlikely to be arising from the sinus node region, even in a patient with atrial enlargement. During an electrophysiology procedure, pacing maneuvers can also be used to distinguish an AT arising from near the crista terminalis, superior vena cava, or right superior vein from sinus tachycardia [7].

Figures 2, 3, 4 show tracings recorded from a 46-year-old patient who presented with cardiogenic shock, severe left ventricular dysfunction, and an SVT at a rate of 180 beats per minute that was interpreted initially as sinus tachycardia. After resuscitation and initiation of beta adrenergic blockade, her heart rate slowed to just over 100 beats per minute at rest. It was difficult to determine, based on her electrocardiogram, whether or not the rhythm was sinus rhythm (Fig. 2). However, tracings that were obtained from her initial hospitalization showed AV nodal Wenckebach block (Fig. 3). This observation strongly suggested an AT rather than sinus tachycardia. In addition, the morphology of the P-wave, which was unmasked during AV block, was notched and dagger-shaped in the modified chest lead making it unlikely to represent a rhythm arising from the sinus node. During an electrophysiology procedure, the rhythm was confirmed to be a focal AT. Activation mapping was used to localize the focus to the upper crista terminalis in the right atrium, and successful ablation was achieved using a standard ablation electrode and radiofrequency current. Two months after the ablation, the patient was in sinus rhythm and ventricular function had normalized.
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Fig. 2

An electrocardiogram of a patient with an atrial tachycardia who initially presented with cardiogenic shock. The electrocardiogram was recorded after the patient was stabilized and treated with a beta-blocker. Note that the P-wave morphology is similar to a sinus mechanism

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Fig. 3

A rhythm strip is shown of the same patient as shown in Fig. 2. Note that there is intermittent 2:1 AV Wenckebach block during the tachycardia. This finding makes an atrial tachycardia much more likely than sinus tachycardia

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Fig. 4

The tracing was recorded during successful catheter ablation of a right atrial tachycardia in the patient shown in Figs. 2 and 3. Shown are the surface and intracardiac electrocardiograms. Note that the tachycardia terminates and converts to sinus rhythm shortly after radiofrequency current is delivered. Abbreviations: RA right atrium, CS coronary sinus, ABL ablation

Atrial flutter

Typical, common AFL is caused by macroreentry in the counterclockwise direction around the tricuspid annulus using the crista terminalis as a barrier of conduction. The zone of slow conduction is within the cavotricuspid isthmus (CTI). The flutter wave morphology is inverted in the inferior surface leads, and the atrial rate is around 300 beats per minute. At times, AF is misdiagnosed as AFL when there are prominent fibrillatory waves in lead V1 [8]. In order to make a diagnosis of AFL though, there must be flutter waves with a constant morphology and cycle length. When there is organized atrial activity, atrial flutter is generally distinguished from a focal AT by the atrial rate, with AFL having atrial rates over 250 beats per minute. However, patients with HF enlarged and diseased atria can have an atrial rate during typical flutter that is very slow, because it can take a long time for the wavefront to conduct around the tricuspid annulus. Therefore, a patient with heart failure and atrial flutter with 2:1 AV conduction might have a ventricular rate of only 110 beats per minute and might not be immediately recognized as having AFL.

Catheter ablation of typical AFL is achieved by ablating the critical isthmus between the tricuspid valve and the inferior vena cava. This is usually accomplished by delivering contiguous sequential ablation lesions using radiofrequency current. Cryoenergy can also be used. When ablation is performed during AFL, the tachycardia will terminate. After termination of the AFL and when patients who present to the electrophysiology laboratory in sinus rhythm, the endpoint for ablation is complete bidirectional conduction block through the CTI. Therefore, patients who have had an episode of atrial flutter that has an appearance that is typical can undergo ablation even after conversion to sinus rhythm.

Ablation should be considered as first-line therapy for typical AFL, because the recurrence rate after simply performing an electrical cardioversion is high. The success rate for ablation of typical atrial flutter is over 95%, and the risk of a major complication is low. Catheter ablation is considered a Class I indication for patients with poorly tolerated AFL, according to the 2003 ACC/AHA/ESC Practice Guidelines [9]. Ablation should be offered even after only a single episode of typical AFL when a patient experiences HF as a consequence.

Other mechanisms of AFL include clockwise CTI-dependent AFL, incisional AFL, and AFL as a consequence of left atrial ablation or a surgical maze procedure. The success rates for these less common types of flutter are slightly lower than for typical flutter. However, when the tachycardia results in acute HF, ablation should still be considered. For patients who have been in AFL for more than 48 h without anticoagulation, a transesophogeal echo (TEE) should be performed before ablation to exclude a left atrial appendage thrombus.

Atrial fibrillation

Atrial fibrillation is the most common sustained arrhythmia and is very prevalent in patients with congestive HF [10]. Atrial fibrillation can aggravate ventricular function and cause acute HF by causing loss of atrial synchrony, tachycardia, and a chaotic inefficient ventricular rhythm [11]. Unfortunately, pharmacological options in patients with AF and HF are limited, because of concerns related to ventricular proarrhythmia and myocardial depression in patients with ventricular dysfunction, and there is much debate related to which patients with HF and AF would benefit from a rhythm control strategy or are best treated with only rate control [12]. The recent AF-CHF trial suggests that many patients can be treated with rate control alone [13]. However, it is important to individualize AF therapy and to recognize that acceptance of permanent AF at the time of initial diagnosis in a patient with HF might be a missed opportunity.

Several nonpharmacological therapies are available for the management of AF in patients with acute HF. For patients in whom sinus rhythm cannot be maintained and the ventricular rate cannot be controlled, catheter ablation of the AV junction and implantation of pacemaker has been shown to improve symptoms and often improves ventricular function. Biventricular pacing is usually used after AV junction ablation to minimize the mechanical dyssynchrony induced by right ventricular pacing alone [14].

Nonpharmacological options for rhythm control include catheter ablation of the atrium and the surgical maze type procedures. Catheter ablation of AF is now considered an acceptable treatment option for patients with recurrent, drug refractory symptomatic AF. The procedure is based on the recent appreciation that the pulmonary veins are a frequent source of ectopy that triggers AF [15] and are a common location for local reentry during AF. The ablation technique involves transseptal catheterization, usually with placement of both an ablation and a mapping catheter in the left atrium, and point-by-point delivery of radiofrequency current in a contiguous fashion around the ipsilateral pairs of pulmonary veins to achieve complete electrical isolation of the veins [16] (Fig. 5). In patients with persistent AF, additional ablation is also commonly performed. Additional ablation can include linear lesions [17] and focal targeting of complex fractionated atrial electrograms that are thought to represent critical drivers of the AF [18]. The success rate ranges from 50 to 90% depending on the type of AF and underlying substrate. The likelihood of a major complication is 3–6%. Complications include perforation and tamponade, thromboembolism, vascular access complications, pulmonary vein stenosis, phrenic nerve injury, iatrogenic left atrial flutter, left atrial–esophageal fistula, and death. The likelihood of death is approximately 1 per 1,000.
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Fig. 5

This tracing was recorded during a catheter ablation procedure in a patient with atrial fibrillation. Shown is sinus rhythm on the surface electrograms I, II, III, and V5. There are three multipolar electrode catheters in the heart. The intracardiac electrograms from these catheters are shown from the ablation catheter (ABL distal and proximal), the circular pulmonary vein (PV) mapping catheter positioned at the ostium of the right inferior PV (Duo 1–20), and the coronary sinus catheter (CS 1–10). Note that the electrograms from the PV catheter show a small left atrial signal (LA) followed by a sharp PV potential (PVP). When radiofrequency (RF) current is delivered at the inferior antrum of the right inferior PV, there is electrical disconnection of the RIPV with the next sinus beat. There is a spontaneous escape rhythm from the RIPV that persisted during the procedure. This is an example of electrical entrance and exit block into the PV

Much of the experience with catheter ablation of AF has been with patients who have minimal structural heart disease in whom the pulmonary veins (PVs) are the most likely source of atrial fibrillation [19]. However, there is data that ablation of AF in patients with HF, even when the AF has been persistent for many years, is feasible [20]. Hsu and colleagues published in 2004 a series of 58 consecutive patients with HF and an EF less than 45% who underwent catheter ablation for AF. The AF was permanent in 75% of patients. After an average follow-up of 1 year, an impressive 78% of patients were in sinus rhythm and there was a significant improvement in ventricular function over time. However, about half of the patients required at least two ablation procedures, about half continued to require antiarrhythmic drugs, and the follow-up was limited.

The procedure time for catheter ablation for AF is 3–6 h depending on the approach and operator experience. Preprocedural imaging of the LA and PVs is also commonly performed to guide the procedure, transesophageal echocardiography is needed in many cases to exclude a left atrial thrombus, and oral anticoagulation is typically discontinued before the procedure. For these reasons, it is rare that catheter ablation is performed during a hospitalization for acute HF. These patients can usually be stabilized, diuresed, cardioverted, or rate controlled, and return for an elective ablation procedure.

Patients with ventricular arrhythmias

Patients with acute HF can experience ventricular arrhythmias that range from occasional premature ventricular beats to sustained ventricular tachycardia (VT). As with SVTs, the treatment of VT in a patient with acute HF is usually not markedly different than the treatment of a patient with VT who does not have heart failure. In fact, a majority of patients with sustained ventricular arrhythmias have HF or at least ventricular dysfunction. However, there are important considerations when considering catheter ablation of a ventricular arrhythmia in a patient with acute HF.

Arrhythmia substrate

Most patients with VT and HF have some form of cardiomyopathy leading to myocardial scarring as the substrate for the arrhythmia. In patients with prior myocardial infarction, scar occurs in a vascular distribution and is most commonly subendocardial [21]. Patients with a nonischemic cardiomyopathy (NICM) can have various etiologies that contribute to scar formation and can include hypertensive disease, myocarditis, valvular disease, infiltrative diseases, arrhythmogenic right ventricular cardiomyopathy (ARVC), and idiopathic cardiomyopathies. The location of myocardial scar in these patients can vary between both the right and the left ventricles and across the myocardial wall from endocardium to epicardium. In fact, patients with a NICM are more likely to have mid-wall and epicardial substrate [21]. The recent development of a percutaneous subxyphoid approach for accessing the pericardial space [22] has increased the number of patients who are candidates for VT ablation.

Sustained monomorphic ventricular tachycardia

The mechanism for sustained monomorphic VT in most patients with VT and HF is scar-mediated reentry. This is the dominant mechanism in patients with both an ischemic [23] and a nonischemic cardiomyopathy [24]. Recurrent VT can lead to acute heart failure, and the ventricular stretch and increased sympathetic tone associated with heart failure can precipitate VT when the proper substrate is present. Initial therapies for sustained VT include electrical cardioversion, antiarrhythmic drugs to control frequent episodes, and implantable defibrillator therapy to prevent sudden cardiac arrest. Patients in acute HF should have their volume status aggressively managed as an integral part of treatment of VT.

Catheter ablation should be considered in patients with acute HF when the patient is having incessant VT or receiving frequent defibrillator shocks for VT. Similar to AF ablation, these procedures can be quite prolonged in duration depending on the operator, the technique, and the number of distinct VTs that require ablation. Catheter ablation has been shown to decrease defibrillator therapies [25, 26]. Catheter ablation can be used to ablate the critical portion of the reentrant circuit, which is usually located in the subendocardial scar border zone, but can be deep within a large infarct scar or within the epicardium as discussed above. The optimal candidate is a patient with recurrent episodes of relatively slow, hemodynamically stable monomorphic VT. This allows for mapping the tachycardia circuit while the patient is in VT and demonstration of termination of tachycardia during ablation. Patients with hemodynamically unstable VT are less optimal candidates for ablation. However, there are techniques using three-dimensional computer-based electroanatomical and pace mapping that involve localization of the infarct scar and determination of the exit site of the VT, which can lead to successful ablation [27]. The least optimal candidates are patients with recurrent VT of multiple morphologies, but even these patients can achieve at least a significant reduction in VT episodes with more extensive ablation strategies (Fig. 6) that modify the substrate for their arrhythmias [27, 28]. It is important to note that if ablation is only performed in areas of myocardial scar, detrimental effects on ventricular function can be avoided [29]. Additionally, modern catheter technology in the form of open-irrigated tips catheters is often utilized for ablation of scar. These catheters introduce significant amounts of fluid intravascularly, which can worsen HF. In patients that cannot tolerate an ablation due to hemodynamic instability during VT or due to recalcitrant HF, percutaneous ventricular assist devices can be utilized to help support the patient during the procedure [30].
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Fig. 6

A three-dimensional computer-based electroanatomical map of left ventricular scar and substrate ablation. A patient with a prior anteroapical myocardial infarction underwent ablation for recurrent ventricular tachycardia. A three-dimensional shell of the endocardium was created by moving an electrode catheter throughout the ventricle at multiple endocardial sites and collecting voltage recordings. Low voltages (scar) are represented in red, normal voltages in purple, and border zone in the other colors. The maroon octagonal markers indicated areas where radiofrequency ablation lesions were placed. Note the extensive linear nature of the lesion sets in this patient with multiple induced VT, some of which were not tolerated hemodynamically

Electrical storm

Electrical Storm occurs when a patient has multiple episodes of VT or ventricular fibrillation (VF) within a short period of time and is defined in patients with an implantable defibrillator as at least three episodes of VT/VF within a 24-h period. This typically leads to hospitalization and can be associated with acute heart failure. The mortality is high. These patients can be managed with catheter ablation, but it is important to stabilize the patient as much as possible with intravenous antiarrhythmic therapy, inotropic support, and pharmacological sympathetic blockade [31]. General and/or thoracic epidural anesthesia and stellate ganglion blockade can be used to stabilize the patient in preparation for catheter ablation [32]. Ablation can be an effective management approach for both short- and long-term control of electrical storm [33].

There is a subgroup of patients with structural heart disease and recurrent VF or polymorphic VT that have their arrhythmia triggered repeatedly by a consistent morphology of premature ventricular contraction (PVC). These PVCs seem to be associated with spontaneous depolarization of the left ventricular His-Purkinje network. Ablation targeting the initiating beat can successfully eliminate recurrent VF in these patients [34, 35].

High-density ventricular ectopy

In some patients with ventricular ectopy, the sequence of disease progression is reversed. Instead of cardiomyopathy leading to substrate for arrhythmia, the arrhythmia is the substrate for the cardiomyopathy. Patients with idiopathic PVC/VT, if frequent enough, can develop TIC [36]. It is important to recognize a patient who has acute HF and cardiomyopathy due to high-density ventricular ectopy. Unlike sustained tachycardias, frequent ventricular ectopy is an often underappreciated cause of reversible ventricular dysfunction. It is not clear whether there is a critical density of ventricular ectopy that leads to a cardiomyopathy or whether there is a genetic predisposition in some patients with frequent PVCs, but elimination of the PVCs with catheter ablation can result in complete recovery of ventricular dysfunction in many patients [37]. Because patients with HF often have frequent PVCs and nonsustained VT, it can be difficult to identify the patient who should be considered for catheter ablation. When assessing a patient with HF and ventricular ectopy, clues that catheter ablation should be considered include ectopy that is unifocal with a morphology consistent with an idiopathic source, such as the right ventricular outflow tract (RVOT), or ectopy that has a pattern of repetitive monomorphic VT.

The etiology of unifocal PVCs is often idiopathic, and the most common source is the RVOT, just below the pulmonic valve [38]. Therefore, a patient with a nonischemic dilated cardiomyopathy and acute heart failure, who has frequent ventricular ectopy or runs of nonsustained VT with a left bundle branch block, inferior axis pattern, should be evaluated for possible ablation of RVOT PVCs. Figure 7 shows an electrocardiogram of a patient with frequent ventricular ectopy and couplets who presented with acute heart failure. He underwent successful catheter ablation of RVOT PVCs. Other sites [38] of origin for idiopathic PVC/VT include valve annular regions (aortic valve, mitral valve, and tricuspid valve) and the fascicles of the left bundle branch. Occasionally, an epicardial focus originating in or near the coronary venous system can give rise to idiopathic PVC/VT. These sources of ectopy can also be highly amenable to catheter ablation [38].
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Fig. 7

A 12-lead electrocardiogram is shown of a patient with frequent ventricular ectopy and couplets who presented with heart failure. The morphology of the ectopy is left bundle-inferior axis, consistent with a right ventricular outflow tract morphology. This ectopy was successfully ablated from a site just beneath the pulmonic valve

Summary

Many patients with acute HF have arrhythmias of multiple types, both supraventricular and ventricular. It is important to recognize when a heart rhythm disorder is the cause of, or a major contributor to, the HF episode. Rapid treatment of the arrhythmia is necessary to stabilize the patient and optimize HF symptoms. Many of these arrhythmias are amenable to catheter ablation, and these patients should be evaluated for appropriateness of this therapeutic option. In patients with acute HF and volume overload, it is important to be sure that the patient is adequately diuresed and able to lie flat for a few hours before bringing the patient to the electrophysiology laboratory. Patients who have not been adequately stabilized can develop acute pulmonary edema during ablation procedures. Additional studies are needed to determine the outcomes of catheter ablation in patients hospitalized with acute HF.

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© Springer Science+Business Media, LLC 2011