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Ann Thorac Surg 2000;70:1275-1280
© 2000 The Society of Thoracic Surgeons

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Original articles: cardiovascular

Passive epicardial containment prevents ventricular remodeling in heart failure

^a Departments of Medicine, Henry Ford Heart and Vascular Institute, Henry Ford Health System, Detroit, Michigan, USA
^b Surgery, Henry Ford Heart and Vascular Institute, Henry Ford Health System, Detroit, Michigan, USA

Address reprint requests to Dr Sabbah, Cardiovascular Research, Henry Ford Hospital, 2799 West Grand Blvd, Detroit, MI 48202
e-mail: hsabbah1{at}hfhs.org

	Abstract

Top Footnotes Abstract Introduction Material and methods Results Comment Acknowledgments References

 
Background. We examined the effects of passive containment of the cardiac ventricles with a surgically placed epicardial prosthetic wrap on indexes of left ventricular (LV) remodeling in dogs with heart failure.

Methods. Heart failure (LV ejection fraction 30% to 40%) was produced in 12 dogs by intracoronary microembolization. Six dogs underwent mid-sternotomy and pericardiotomy with placement of a preformed-knitted polyester device (Acorn Cardiac Support Device [CSD], Acorn Cardiovascular, Inc, St. Paul, MN) snugly around the ventricles and anchored to the atrioventricular groove. Six dogs did not undergo surgery and served as controls. Dogs were followed for 3 months prior to sacrifice.

Results. In controls, LV end-diastolic volume increased after 3 months (67 ± 12 versus 83 ± 8 ml; p = 0.04), while in CSD-treated dogs, it decreased (68 ± 10 versus 61 ± 10 ml; p = 0.002). CSD-containment of LV size was associated with increased LV systolic fractional area of shortening, while in controls, fractional area of shortening decreased. CSD-treated dogs also showed amelioration of myocyte hypertrophy and attenuation of interstitial fibrosis compared to controls.

Conclusions. In dogs with heart failure, passive epicardial containment of the ventricles with the Acorn CSD ameliorates LV remodeling and improves LV systolic function.

	Introduction

Top Footnotes Abstract Introduction Material and methods Results Comment Acknowledgments References

 
Heart failure (HF) is a progressive disorder whereby the hemodynamic status of the affected patient worsens over time despite the absence of clinically apparent adverse intercurrent events [1]. This deterioration is accompanied by progressive left ventricular (LV) chamber remodeling [2, 3], a process characterized by loss of functional cardiac units, myocyte hypertrophy and interstitial fibrosis at the cellular level, and by changes in LV size and shape at the global level [4]. Increased LV size and chamber sphericity are determinants of functional mitral regurgitation (MR); an undesirable sequelae of HF [5]. Among clinical indicators of progressive LV remodeling, LV dilation, and increased LV sphericity are sensitive predictors of poor long-term outcome and harbingers of death [6, 7]. Treatment with angiotensin converting enzyme inhibitors and ß-blockers improve survival in HF [3, 8, 9], in part, by attenuating LV remodeling. In recent years, several surgical approaches have been implemented with the objective of improving cardiac function and ameliorating LV remodeling in patients with HF [10–12]. These include surgical reduction of LV size advocated by Batista and associates [10], dynamic cardiomyoplasty [11], and mitral valve reconstruction to reduce functional MR [12]. The long-term benefits from these procedures, however, remain uncertain. In this study, we examined whether passive epicardial containment of the cardiac ventricles using a preformed-knitted polyester device (Acorn Cardiac Support Device [CSD], Acorn Cardiovascular, Inc, St. Paul, MN) can prevent progressive LV remodeling in dogs with moderate HF.

	Material and methods

Top Footnotes Abstract Introduction Material and methods Results Comment Acknowledgments References

 
Animal model
The canine model of chronic HF used in the present study was previously described in detail [13]. In this preparation, chronic LV dysfunction is produced by multiple sequential intracoronary embolization with polystyrene Latex microspheres (70 to 102 µm in diameter) which results in loss of viable myocardium. The model manifests many of the sequelae of HF seen in humans, including marked depression of LV systolic and diastolic function, reduced cardiac output, and increased LV filling pressures [13]. In the present study, 12 healthy mongrel dogs, weighing between 21 and 31 kg, underwent coronary microembolizations to produce HF. On average, 6.4 microembolizations were performed in each dog 1 to 3 weeks apart and were discontinued when LV ejection fraction was between 30% and 40%. In this model, this target ejection fraction is associated with a 20% to 30% increase in LV end-systolic and end-diastolic volumes from normal values [3, 13, 14]. Microembolizations were performed during cardiac catheterization under general anesthesia and sterile conditions. The anesthesia regimen consisted of a combination of intravenous injection of oxymorphone (0.22 mg/kg), diazepam (0.17 mg/kg), and sodium pentobarbital (150 to 250 mg to effect) and was previously shown to have no effect on global LV function [3].

Study protocol
Two weeks after the last coronary microembolization, all dogs underwent a cardiac catheterization (pretreatment). The CSD was surgically implanted in 6 dogs and the remaining 6 dogs did not undergo surgery and served as concurrent controls. In dogs undergoing a CSD implant, anesthesia was induced with intravenous diazepam (0.2 mg/kg) followed by oxymorphone (0.1 mg/kg) and maintained with 0.5% to 1% isoflurane. A median sternotomy was performed, the pericardium opened, and the CSD placed around the ventricles and anchored with approximately eight stay sutures, 2 cm apart, at the atrioventricular groove (Fig 1). The CSD was tailored anteriorly to fit the ventricles snugly. The chest cavity was drained bilaterally with 16F chest tubes and the sternum closed with wires. Prophylactic antibiotics (cefazolin 22 mg/kg) were administered intravenously preoperatively and 4 hours postoperatively. The postoperative course was uneventful in all 6 dogs. All dogs were followed for 3 months during which time no cardioactive drugs were used. At the end of the follow-up period, a cardiac catheterization was performed (posttreatment), the chest was then opened and the heart removed for histologic examination. The study was approved by the Henry Ford Hospital Care of Experimental Animals Committee and conformed to the National Institutes of Health "Guide and Care for Use of Laboratory Animals."

View larger version (95K): [in this window] [in a new window]   Fig 1. Artist’s depiction of surgical placement of the Acorn Cardiac Support Device.

Echocardiographic and Doppler measurements
Echocardiograms were performed using a model 77030A ultrasound system (Hewlett-Packard, Sonos 1000; Andover, MA) with a 3.5-MHz transducer. Measurements were made with the dog placed in the right lateral decubitus position. In CSD dogs, a parasternal long-axis view was used to measure RV and LV end-diastolic dimensions using M-mode. Measurements were made prior to surgical implantation of the CSD, and 1 week after implantation, to ensure that little or no acute reduction of ventricular dimensions took place during implantation. An LV short axis view at the mid-papillary muscle level was recorded at pre- and posttreatment and used to calculate LV fractional area of shortening (FAS), a measure of LV systolic function. FAS was defined as the difference between the end-diastolic and end-systolic areas divided by the end-diastolic area times 100. To ascertain the presence or absence of constrictive or restrictive physiology in CSD-treated dogs, mitral inflow velocity was measured with pulsed wave Doppler. The following characteristics of mitral flow velocity were measured: (1) peak mitral flow velocity in early diastole (PE); (2) peak mitral flow velocity during atrial contraction (PA); (3) the ratio PE/PA, and the deceleration time of mitral inflow velocity during rapid early filling (DT).

Histologic and morphometric assessments
Once removed, the heart was placed in ice-cold cardioplegia solution. From each heart, LV transverse slices, approximately 3-mm thick, were obtained from the basal, middle, and apical thirds of the LV. The LV free wall from each transverse slice was divided into five transmural blocks, mounted on cork using Tissue-Tek embedding medium (Miles Inc, Mishawaka, IN), rapidly frozen in isopentane precooled in liquid nitrogen. Cryostat sections, approximately 8-µm thick, were prepared from each block and stained with fluorescein-labeled peanut agglutinin to delineate the myocyte border and the interstitial space including capillaries as previously described [16]. Sections were double-stained with rhodamine-labeled Griffonia simplicifolia lectin I (GSL I) to identify capillaries. Ten radially oriented microscopic fields, magnification x100 (objective 40 and ocular 2.5), were selected at random from each section and photographed using 35-mm color film. Images were projected with a photo magnifier and the cross-sectional area of each myocyte, a measure of myocyte hypertrophy, was calculated using computer-based planimetry. The total surface area occupied by interstitial space and the total surface area occupied by capillaries were measured from each randomly selected field using computer-based video densitometry (JAVA, Jandel Scientific, Corte Madera, CA). The volume fraction of interstitial collagen (interstitial fibrosis) was calculated as the percent total surface area occupied by interstitial space minus the percent total area occupied by capillaries [16]. Capillary density was measured using the index capillary per fiber ratio, and the oxygen diffusion distance was calculated as half the distance between two adjoining capillaries. For comparison, measurements of myocyte cross-sectional area, volume fraction of interstitial fibrosis, and capillary density and oxygen diffusion distance were made employing identical techniques in LV tissue sections obtained from 7 normal dogs. For all of the above measurements, microscopic fields containing scar tissue (infarcts) were excluded. A second set of transverse LV tissue slices was obtained, fixed in formalin, and photographed to grossly visualize the epicardial surface. Each slice was then cut into eight transmural blocks and embedded in paraffin-blocks. Sections were stained with Masson trichrome to delineate fibrous tissue. An average volume fraction of replacement fibrosis, a measure of tissue loss, was calculated for each dog using data obtained from all sections. In CSD-treated dogs, trichrome-stained sections were also used to qualitatively evaluate the extent of epicardial fibrosis resulting from the CSD implantation, as well as to evaluate the interface between the CSD and the epicardial surface of the heart.

Data analysis
Intragroup comparisons
Comparisons of hemodynamic, angiographic and echocardiographic variables within each of the 2 study groups were made between pretreatment and posttreatment measures. For these comparisons, a Student’s paired t test was used, and a probability value less than or equal to 0.05 was considered significant.

Intergroup comparisons
To determine whether significant differences in histomorphometric measures were present between the 2 study groups, a t statistic for two means was used with a probability less than or equal to 0.05 considered significant. p Values are reported along with 95% confidence intervals for difference. Data are reported as mean ± standard deviation.

	Results

Top Footnotes Abstract Introduction Material and methods Results Comment Acknowledgments References

 
Autopsy, performed 3 months after implantation, showed a thin, translucent encapsulation of the CSD with connective tissue (Fig 2a). There was no evidence of active inflammation on histologic examination using hematoxylin and eosin staining. Trichrome staining showed encapsulation of the CSD fibers by collagen (Fig 2b, c). The average thickness of the fibrotic layer, including the CSD, was 0.59 ± 0.15. There was a clear demarcation between the CSD and the epicardial surface of the heart with no evidence of invasion of the myocardium by connective tissue (Fig 2c).

View larger version (83K): [in this window] [in a new window]   Fig 2. (a) Transverse slice of left ventricle of a dog treated with the Acorn Cardiac Support Device (CSD) for 3 months. The CSD encapsulated by fibrous tissue appears as a white lining along the epicardial surface. (S = interventricular septum; FW = left ventricular free wall.) (b) Trichrome stained section from the left ventricular free wall of same dog as in panel (a) showing a segment of the CSD fibers encapsulated in collagen (blue) and overlying the myocardium (red). (c) Trichrome stained section showing a magnified view of a single CSD fiber encapsulated in collagen (blue). Note the clear demarcation between the CSD and myocardium (red).

At baseline, prior to any microembolizations, none of the 12 study dogs manifested MR measured using Doppler. Ventriculograms showed that 4 of 6 control dogs developed mild to moderate (1+ to 2+) MR (average severity, 0.83 ± 0.31) before initiating therapy that persisted or worsened (1 of 4 dogs) after 3 months of follow-up (average severity, 1.00 ± 0.37) (p = 0.73). Four of 6 CSD-treated dogs also developed mild to moderate (1+ to 2+) MR (average severity, 1.00 ± 0.37) prior to CSD implantation. In contrast to controls, the MR was completely abolished in CSD-treated dogs after 3 months of follow-up (p = 0.021). The elimination of functional MR in CSD-treated dogs was associated with an increase in the LV end-systolic sphericity index. In contrast, the sphericity index was unchanged in controls (Table 1).

In addition to improving LV systolic function and limiting functional MR, prevention of progressive LV enlargement in CSD-treated dogs had a beneficial effect on cellular components of LV remodeling (Table 2). In CSD-treated dogs, myocyte cross-sectional area was smaller than in controls as was the volume fraction of interstitial fibrosis. Treatment with the CSD was also associated with a higher capillary density and a lower oxygen diffusion distance (Table 2). Overall LV replacement fibrosis tended to be lower in CSD-treated dogs compared to controls, but the difference did not reach statistical significance (Table 2).

	Comment

Top Footnotes Abstract Introduction Material and methods Results Comment Acknowledgments References

Another potential benefit of the CSD is the elimination of functional MR, albeit at mild-to-moderate severity. When present, MR can play a role in reducing LV stroke output and can contribute to worsening of the HF state. The clinical importance assigned to this functional abnormality is exemplified by the recent interest in surgical mitral valve reconstruction in patients with HF and severe functional MR [12]. Functional MR in the setting of HF is frequently attributed to LV enlargement, mitral annular dilation and, more importantly, to changes in LV shape manifested by increased chamber sphericity [5]. Use of the CSD decreased chamber sphericity with a subsequent elimination of functional MR.

It is fair to speculate that dynamic cardiomyoplasty gave rise to the concept of passive ventricular containment as a potential therapeutic modality for preventing progressive LV dilation in HF. Studies in patients by Kass and colleagues [11] suggested that the benefits derived from cardiomyoplasty, in terms of reverse LV remodeling, may be primarily due to passive girdling of the heart rather than to an active squeezing assist effect. Studies in patients with HF [18], and in sheep with myocardial infarction [19], that underwent dynamic cardiomyoplasty also showed that the efficacy of the procedure may be due to a passive "girdling effect" which limits the progression of ventricular enlargement; augmentation of systolic function through active contraction of the latissimus dorsi may be only a secondary phenomenon. In dogs with HF secondary to rapid ventricular pacing, wrapping the ventricles snugly with a Marlex mesh (C.R. Bard, Inc, Murray Hill, NJ) was effective in preventing cardiac enlargement but not as effective as adynamic cardiomyoplasty, possibly due to adaptive capabilities of the skeletal muscle [20]. In dogs with doxorubicin-induced HF, cardiac binding with polytetrafluoroethylene prevented ventricular dilation but without eliciting improvement of LV systolic function [21]. Both studies are limited by having performed cardiac binding prior to inducing HF and, therefore, are difficult to interpret in light of the findings of the present study.

There are some limitations to the study that warrant consideration. The canine model of HF used in this study manifests diffuse infarcts which lead to global LV dysfunction and HF. As such, it differs from clinical situations where HF results from a large regional transmural myocardial infarction. Additional studies are needed to determine the efficacy of the CSD in these circumstances. Another limitation is the lack of a sham-operated group in which the pericardium was opened and left open. The study was conducted for only 3 months and in dogs with moderate HF (LV ejection fraction 30% to 40%). Additional studies are needed to assess the efficacy of the CSD over longer periods of time and in animals with advanced HF. In the present study, only monotherapy with the CSD was examined. Whether or not the CSD can elicit improvements, above and beyond those seen with prototypical drugs used for the treatment of HF, remains uncertain and requires further evaluation.

In conclusion, passive epicardial containment of the cardiac ventricles with the Acorn CSD prevents progressive LV remodeling in dogs with moderate HF. Preventing LV dilation appears to attenuate the adverse effects of LV remodeling and prevent functional MR. Additional studies are needed to further elucidate the mechanisms through which ventricular constraint with the Acorn CSD elicits its benefits in HF. Nevertheless, the findings of this study warrant consideration of this surgical approach as adjunct in the management of chronic HF.

	Acknowledgments

Top Footnotes Abstract Introduction Material and methods Results Comment Acknowledgments References

 
This study was supported, in part, by a grant from Acorn Cardiovascular, Inc, and by a grant from the National Heart, Lung and Blood Institute, HL49090-06.

	Footnotes

Top Footnotes Abstract Introduction Material and methods Results Comment Acknowledgments References

 
Clif Alferness is an employee of Acorn Cardiovascular, Inc, and Hani N. Sabbah, PhD, has a research grant from Acorn Cardiovascular, Inc. This article has been selected for the open discussion forum on the STS Web site: http://www.sts.org/section/atsdiscussion/

	References

Top Footnotes Abstract Introduction Material and methods Results Comment Acknowledgments References

 

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