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Ann Thorac Surg 2009;88:1982-1988. doi:10.1016/j.athoracsur.2009.08.048
© 2009 The Society of Thoracic Surgeons
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Right arrow Mechanical Circulatory Assistance

Original Articles: Pediatric Cardiac

Ventricular Actuation Improves Systolic and Diastolic Myocardial Function in the Small Failing Heart

Mark P. Anstadt, MDa,*, Subbaraju Budharaju, MDb, Rebecca J. Darner, ASa, Benjamin A. Schmittb, Lawrence J. Prochaska, PhDb, Anthony J. Pothoulakis, MDa, Peer M. Portner, PhDc

a Department of Surgery, Wright State University School of Medicine, Dayton, Ohio
b Department of Biomedical Sciences, Wright State University School of Medicine, Dayton, Ohio
c Department of Cardiothoracic Surgery, Stanford University School of Medicine, Stanford, California

Accepted for publication August 17, 2009.

* Address correspondence to Dr Anstadt, Department of Surgery, Wright State University, 30 E Apple St, Suite 6252, Dayton, OH 45409 (Email: mpanstadt{at}aol.com).

Presented at the Forty-fifth Annual Meeting of The Society of Thoracic Surgeons, San Francisco, CA, Jan 26–28, 2009.


Dr Anstadt discloses that he has a financial relationship with LifeBridge Technologies, LLC.

 

   Abstract
Top
 Abstract
Introduction
 Material and Methods
 Results
 Comment
 Discussion
 Acknowledgments
 References
 
Background: Direct mechanical ventricular actuation (DMVA) provides non–blood contacting augmentation of ventricular function. The device has promise for supporting the pediatric heart. The purpose of this study was to assess DMVA's effect in a small animal model of heart failure.

Methods: Anesthetized rabbits (n = 6) underwent sternotomy and were instrumented for hemodynamic monitoring. A 10-MHz ultrasound probe was used for transesophageal echocardiography imaging. Heart failure (cardiac output <50% baseline) was induced with esmolol. Phenylephrine was titrated to maintain baseline mean arterial pressure. Transesophageal echocardiography imaging was acquired at baseline, heart failure, and subsequent DMVA support for 2 hours. Image analysis was used to derive ejection fraction, cardiac output, and stroke work as measures of left ventricular function. Speckle tracking software was used to derive myocardial strain rates as load-independent measures of left ventricular myocardial function.

Results: Mean ejection fraction was significantly increased during DMVA support (0.585 ± 0.035) versus failure (0.215 ± 0.014; p < 0.001). Peak global left ventricular systolic and diastolic strain rates (1/second) were significantly increased during DMVA (–2.85 ± 0.33 and 2.92 ± 0.37) versus failure (–1.69 ± 0.11 and 1.99 ± 0.14; p < 0.001 and 0.004, respectively). Peak strain rates during DMVA in the failing heart were similar to baseline.

Conclusions: Direct mechanical ventricular actuation augments both systolic and diastolic left ventricular pump function. Diastolic augmentation distinguishes the device from other direct cardiac compression methods. This study demonstrated that DMVA in the small-sized, failing heart improves both systolic and diastolic myocardial function, which has favorable implications for left ventricular recovery. Direct mechanical ventricular actuation's salutary effects can be provided to the failing pediatric heart without complications of blood contact.

Mechanical circulatory support has seen increased utility in the treatment of pediatric patients [1]. Recent reports indicate that mechanical circulatory support favorably impacts survival of selected pediatric cohorts when compared with adults [2–4]. Results are promising, but unique challenges remain for supporting small pediatric patients. Cannulation, device fit, and hemodilution become increasingly problematic in a small pediatric patient, compounding the already high risk for morbidity and mortality. Bleeding, thromboembolic events, and infection are frequent complications that can relate to blood contact [1–6].

The morbidity and mortality associated with mechanical circulatory support may substantially be reduced by circumventing blood contact. Devices that compress or girdle the ventricles to prevent distention have this advantage, but compromise ventricular filling and may potentiate the diastolic dysfunction of heart failure [7–10]. Direct mechanical ventricular actuation (DMVA) augments both systolic and diastolic ventricular function (Fig 1). The device attaches atraumatically and has proven hemodynamic effectiveness in the adult heart [11–23]. A small animal model of acute heart failure has been developed recently for investigating DMVA. The purpose of this study was to evaluate DMVA's effect on myocardial function in the acutely failing small, pediatric-sized failing heart.


Figure 1
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  		Fig 1. Schematic of direct mechanical ventricular actuation pneumatic drive system and assister cup.

 

   Material and Methods
Top
 Abstract
 Introduction
 Material and Methods
Results
 Comment
 Discussion
 Acknowledgments
 References
 
The Wright State University Lab Animal Care and Use Committee approved the experimental protocol, and all animals were treated in compliance with the Guide for the Care and Use of Laboratory Animals of the National Academy of Sciences, published by the National Institutes of Health, revised 1996.

Surgical Protocol
New Zealand white rabbits (n = 6, 5.3 ± 1 kg) received ketamine (50 mg/kg) and xylazine (5 mg/kg) followed by tracheal intubation and mechanical ventilation. Anesthesia was maintained with 1% to 2% isoflurane and 1 L/min oxygen. Vascular access was gained through bilateral femoral cutdowns. Lactated Ringer's solution was infused at a maintenance rate. A transesophageal echocardiography (TEE) probe was positioned in the esophagus for cardiac imaging. Aortic pressure was measured with a Millar catheter (Millar Instruments, Houston, TX) inserted into the aortic arch from the right internal carotid artery. A median sternotomy was performed and an ultrasonic flow probe (Transonic Systems, Ithaca, NY) was positioned on the ascending aorta for measuring cardiac output). Surface electrocardiogram, hemodynamics, pulse oximetry, end-tidal carbon dioxide, and rectal temperature were recorded every minute using a computer acquisition system (LifeWindow 6000 system; Digicare, Boynton Beach, FL). The digital data were entered into a spreadsheet for statistical analysis.

Heart Failure Protocol
After acquisition of baseline hemodynamics, heart failure was induced by a bolus of esmolol hydrochloride (1,500 µg · kg–1 · min–1) followed by continuous infusion titrated to achieve a cardiac output of less than 50% baseline. Mean arterial pressure was maintained between 40 and 60 mm Hg using an infusion of phenylephrine (initial dose, 5 µg · kg–1 · min–1) and also was followed by continuous infusion titrated to achieve mean arterial pressure throughout the experiment. After 15 minutes of heart failure, an appropriate sized DMVA cup (Specialty Manufacturing Inc, Saginaw, MI) was placed on the heart and DMVA support was initiated. From prior rabbit studies, three cups with long-axis dimensions of 34, 36, and 38 mm were used [19–23]. Best fit was determined with the cup housing encompassing the greatest surface area of the ventricle without impinging the atria.

Direct Mechanical Ventricular Actuation Application and Drive Settings
After selecting the best size device, the DMVA drive variables were adjusted. A computer interface provided control of pneumatic drive variables including volume delivery, systolic duration, and actuation rate. Initial asynchronous support started at 200 cycles/min and was adjusted to between 170 and 210 cycles/min to optimize the hemodynamics. Systolic durations were adjusted between 55% and 60%, and drive actuation rates were altered to achieve optimal aortic flow. Real-time TEE provided additional feedback for optimizing left ventricular (LV) actuation. Native cardiac function showed improvement after 10 to 15 minutes of support. Direct mechanical ventricular actuation was removed every 15 minutes, and the underlying cardiac function was reassessed. The esmolol infusion was injected as a bolus or was titrated to again achieve the target cardiac output of less than 50% baseline. The DMVA cup was reapplied for another 15 minutes. Each DMVA experiment followed this protocol for 2 hours with esmolol-induced heart failure. The animal was then euthanized.

Assessment of Left Ventricular Pump Function
A 10-MHz ACUSON AcuNav 10F ultrasound catheter (Siemens Medical Solutions, Mountain View, CA) was positioned in the esophagus for TEE imaging [24]. Modified basal two-chamber LV views were obtained during the study conditions using a Siemens ACUSON c512 echocardiography system (Siemens Medical Solutions). Left ventricular TEE views were selected for best image quality before analysis. Selection criteria were based on clear delineation of the LV endocardium, standardized two-chamber long-axis image, LV resolution throughout the cardiac cycle, and an electrocardiogram signal. Images were then analyzed for LV pump function variables using biplane Simpson's method of discs [25]. End-systolic volume, end-diastolic volume, ejection fraction, and stroke volume were all calculated from TEE images. Stroke work was derived using arterial pressure measurements recorded during the selected TEE image acquisitions. These were used as estimates of LV pump function.

Assessment of Myocardial Function
Digitalized TEE data used for LV pump function measures were subsequently interrogated to assess myocardial function. Transesophageal echocardiography images were then analyzed by speckle tracking computer software (velocity vector imaging software; Siemens Medical Solutions) to calculate longitudinal myocardial strain rates [26, 27]. The endocardial border was repeatedly traced in end-diastole. Transesophageal echocardiography images were then reviewed to verify that wall-tracking followed the endocardium throughout the cardiac cycle. The TEE images were exported into a digital data file for final statistical analysis. Velocity vector imaging analysis derived velocity, strain, and strain rates from the data files. The LV long-axis images were divided into six standardized myocardial regions (basal septum, midseptum, apical septum, apical free wall, mid free wall, and basal free wall) for strain rate analysis (Fig 2). Means from these six myocardial regions were used to estimate global LV peak strain rates.


Figure 2
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  		Fig 2. Long-axis left ventricular echocardiographic image delineating the six myocardial regions assessed using velocity vector imaging to derive longitudinal myocardial strain.

 
Statistical Analysis
Echocardiographic data were expressed as mean ± standard deviation and compared between baseline versus failure, failure versus DMVA, and baseline versus DMVA. Measures of pump function (ejection fraction, cardiac output, and stroke work) and myocardial function (peak myocardial strain rates) were compared between the three experimental states using two-way repeated measures analysis of variance. Differences were considered statistically significant with an alpha level of 0.05.


   Results
Top
 Abstract
 Introduction
 Material and Methods
 Results
Comment
 Discussion
 Acknowledgments
 References
 
A total of 90 TEE images met criteria for analysis (27 baseline, 33 failure, and 30 DMVA). Representative images are shown in Figure 3. All TEE-derived LV pump function measurements declined during heart failure compared with baseline by approximately 50%. Mean arterial pressure did not differ significantly between the baseline, failure, and DMVA states. Experiment results were compared between baseline, failure, and DMVA support periods.


Figure 3
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  		Fig 3. Long-axis left ventricular echocardiographic images demonstrating velocity vector imaging of systolic and diastolic strain vectors during baseline (A), failure (B), and direct mechanical ventricular actuation (C).

 
Pump function measures (ejection fraction, cardiac output, and stroke work) calculated from TEE images are shown in Table 1. Mean heart rates were significantly decreased during failure compared with baseline, whereas DMVA actuation rates were similar to baseline. Direct mechanical ventricular actuation significantly augmented LV pump function compared with both failure and baseline. Changes in LV myocardial function (Table 2) generally paralleled LV pump function (Table 1). Compared with baseline, LV peak global strain rates were significantly decreased during failure. Direct mechanical ventricular actuation returned these global systolic and diastolic strain rates to values that were not significantly different from baseline.


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  		Table 1 Left Ventricular Pump Function Variables
 

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  		Table 2 Left Ventricular Myocardial Peak Strain Rates
 
Regional alterations in LV myocardial function were generally similar to global measures. All six regions assessed (Table 2) demonstrated decreased peak systolic strain rates during failure versus baseline that were statistically significant except in the basal septum and basal free wall. Direct mechanical ventricular actuation significantly augmented systolic strain rates in all six regions compared with failure. The resulting systolic myocardial function was similar to baseline in all regions. Diastolic peak strain rates were also decreased in all regions during failure versus baseline. As with systolic strain rates, the decrease in diastolic strain rates reached statistical significance again in all but the basal septal and basal free wall regions. Direct mechanical ventricular actuation increased diastolic strain rates in all regions. However, this only became statistically significant in the basal septal, apical septal, and basal free wall regions. The resulting diastolic strain rates during DMVA were similar to baseline in all six regions except in the apical septum, where they remained significantly decreased.


   Comment
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
Discussion
 Acknowledgments
 References
 
This study provides compelling evidence that DMVA can effectively augment cardiac function of the small failing heart. Rabbit hearts approximate the size of the human neonate, and reliably respond to β-adrenergic blockade for achieving ventricular dysfunction [19, 20, 22, 23]. Intravascular ultrasound probes enable noninvasive TEE imaging to assess both ventricular and myocardial function. Derivations of LV myocardial peak strain rates are load-independent measures of myocardial function. Results using this experimental approach can be translated into clinical scenarios pertaining to the small failing heart. Both the methods used in this study and implications of the results deserve further discussion.

The animal model was selected for several reasons. Previous work established β-adrenergic blockade in the rabbit as a reliable model to reproduce global ventricular dysfunction [19–23]. These investigations have revealed early cellular responses similar to maladaptive characteristics of chronic heart failure. β-Adrenergic blockade has been used successfully in a variety of other investigations assessing compression devices [9, 10, 15, 28–30]. Heart failure induced by unopposed β-adrenergic blockade eventually results in decreased peripheral vascular resistance, which is most likely secondary to an exhausted endogenous {alpha}-adrenergic response. Therefore, an {alpha}-adrenergic agent needs to be administered to maintain vascular tone. Utilization of β-adrenergic blockade to model heart failure has several important advantages. Heart failure can be predictably titrated to a desired level and has a homogeneous effect on the ventricular myocardium. The injury that occurs in ischemic models of heart failure may confound DMVA's impact on the myocardium. Although DMVA has already demonstrated favorable effects in the ischemically injured heart [16–18], the β-adrenergic blockade model was determined to be most ideal for this study's objectives. The tendency for myocardial function to recover during DMVA support required the assister cup be temporarily removed to reestablish the failure state. The LV was assessed by echocardiography using transesophageal views that were unobstructed by the DMVA support device.

Two-dimensional strain rate imaging provides a unique opportunity to assess myocardial function in a noninvasive fashion. Speckle tracking is the basis for assessing myocardial function. Speckles represent backscatter of the reflected ultrasound beam moving within the myocardial tissue [31]. An algorithm that identifies and tracks these acoustic speckles enables quantification of myocardial velocity, strain, and strain rate [32]. Echocardiography using speckle tracking has been validated for assessing myocardial function [33–35]. Strain is a measure of tissue deformation or change in length and can be considered a correlate of regional ejection fraction [36]. Strain rate is the rate of deformation and is currently considered the best in vivo measure of myocardial contractility [37]. Numerous studies have validated the use of two-dimensional imaging with speckle tracking for strain analysis [38]. Angle independence makes speckle tracking particularly ideal for assessing strain rate, which represents a relatively load-independent measure of myocardial function.

Strain rate data were acquired by TEE in the longitudinal plane. Longitudinal strain rates have been validated for assessing cardiac resynchronization therapy [39]. Clinical studies have demonstrated that improved longitudinal strain rates during resynchronization are predictive of subsequent reverse remodeling [39, 40]. Radial and circumferential planes provide more detail for dyssynchrony analysis, but require short-axis imaging, which was not possible in this study. Direct mechanical ventricular actuation would be expected to have favorable effects on LV dyssynchrony. Further analysis is required to definitively address this issue. Importantly, the systolic and diastolic strain rates analyzed were load-independent measures of myocardial function [32, 37]. Therefore, the results indicate that mechanical forces delivered to the epicardium of the failing ventricle can be translated into an improved myocardial contractile function. This assertion is analogous to the augmented cardiac contraction sometimes appreciated when providing hand massage to the failing heart.

Notably, DMVA not only improved systolic but also diastolic myocardial function. This is in clear distinction to direct cardiac compression, which only provides systolic augmentation [7]. Most direct cardiac compression devices that have demonstrated efficacy enhance LV pump function without significantly altering myocardial oxygen consumption [9]. However, direct cardiac compression can impose substantial diastolic impairment. This represents a significant limitation given diastolic dysfunction is a contributing factor to most clinically relevant forms of heart failure.

Diastolic augmentation during DMVA support is enabled by the atraumatic vacuum attachment. Attachment of the assister cup's actuating membrane to the epicardium is maintained throughout support, which results in active expansion of the ventricles during the diastolic phase of mechanical actuation. This explains the well-established hemodynamic effectiveness of DMVA when supporting the fibrillating or asystolic heart [11–18]. The importance of diastolic support may be even more critical to pump the small pediatric heart. Importantly, one must avoid the potential of compressive gases from the drive to accumulate at the high cycle rates required for pediatric support. These heart rates are also too rapid for synchronization with support, and optimal drive dynamics need to be defined.

In conclusion, this study demonstrated that DMVA can effectively augment ventricular function of the small-sized failing heart. Augmented pump function is paralleled by enhanced myocardial strain rates. The findings provide compelling evidence that appropriate application of epicardial mechanical forces (ie, DMVA) to the failing heart's surface can be translated into improved contractile function. Additional studies will determine whether DMVA support of the failing heart favorably impacts myocardial dyssynchrony. Direct mechanical ventricular actuation's ease of installation and the lack of blood contact are particularly attractive for supporting the small pediatric heart. Future studies will be required to assess DMVA in congenital models that simulate relevant pathologic conditions, such as the univentricular heart.


   Discussion
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Discussion
Acknowledgments
 References
 
DR CHRISTOPHER CALDARONE (Toronto, Ontario, Canada): In a patient with dilated cardiomyopathy, wall stress in the endocardium is an issue in terms of myocardial blood flow. Presumably with external pressure applied to the myocardium, this would decrease wall stress in the endocardium. Is there a difference in coronary perfusion with the institution of this support?

DR ANSTADT: Previous investigations have demonstrated coronary flow to be equal to control in hearts supported by direct mechanical ventricular actuation (DMVA). In terms of cardiac dilatation, we have utilized rapid ventricular pacing to induce a dilated cardiomyopathy in the laboratory, and supported these hearts with DMVA. Clearly, the girdling effect created by passive constraint devices or direct cardiac compression devices results in improved systolic function in these conditions. The primary benefit of reduced wall stress with these other devices, as you mentioned, is termed the girdling effect. The differentiating feature of DMVA is clearly its effect on diastolic function, which augments overall pump function much more effectively. Importantly, myocardial function, not just pump function, was found to be improved by DMVA in this study.

But to answer your question specifically, myocardial flow has always been similar to control in DMVA-supported hearts and seems to be subject to normal autoregulation mechanisms, that is, based on the myocardial oxygen demands. These attributes appear to be applicable to the pediatric-sized heart based on our recent investigations.


   Acknowledgments
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Discussion
 Acknowledgments
References
 
The authors would like to thank Curtis J. Wozniak, MD (Department of Surgery, Wright State University, Dayton, OH) for his contributions in echocardiographic analysis, and Scott A. Kerns (Department of Pharmacology and Toxicology, Wright State University, Dayton, OH) for his assistance with data collection. Funding provided, in part, by Myotech, LLC, Pittsford, NY.


   References
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Discussion
 Acknowledgments
 References
 

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