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J Thorac Cardiovasc Surg 2003;126:983-991
© 2003 The American Association for Thoracic Surgery
Surgery for acquired cardiovascular disease |
a Cardiovascular Institute, Columbia-Presbyterian Medical Center, New York, NY, USA
b Universität Berlin Klinik für Kardiovasculare Chirurgie Charité Universitätsklinikum, Berlin, Germany
c Klinik für Innere Medizin, Unfallkrankenhaus Berlin, Berlin, Germany
d Klinik für Herzchirurgie, Herzzentrum Leipzig GmbH, Leipzig, Germany
e Herzchirurgische Abteilung, Allgemeines Krankenhaus St Georg, Hamburg, Germany
f Austin Repatriation Medical Centre, Heidelberg, Australia
g Hospital of the University of Pennsylvania, Philadelphia, Pa, USA
h The Cleveland Clinic Foundation, Cleveland, Ohio, USA
Received for publication May 13, 2002; revisions received October 21, 2002; accepted for publication October 23, 2002.
* Address for reprints: Mehmet C. Oz, MD, Columbia-Presbyterian Medical Center, 117 Ft Washington Ave, New York, NY 10032, USA
mco2{at}columbia.edu
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Abstract |
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METHODS: The Acorn CorCap cardiac support device (Acorn Cardiovascular, Inc, St Paul, Minn) has been implanted worldwide in more than 130 patients with dilated cardiomyopathy with or without concomitant cardiac surgery. The device is positioned around the ventricles and given a custom fit. A series of 48 patients were implanted with the device in initial safety and feasibility studies, of whom 33 also received concomitant cardiac surgery.
RESULTS: At implantation, 11 patients were in New York Heart Association class II, 33 were in class III, and 4 were in class IV. The average CorCap implantation time was 27 minutes. The mean intraoperative reduction in left ventricular end-diastolic dimension was 4.6% ± 1%. There were no device-related intraoperative complications. Eight early and 9 late deaths occurred during follow-up extending to 24 months. Actuarial survival was 73% at 12 months and 68% at 24 months. There were no device-related adverse events or evidence of constrictive disease, and coronary artery flow reserve was maintained. Ventricular chamber dimensions decreased, whereas ejection fraction and New York Heart Association class were improved in patients overall and in those patients implanted with the CorCap device without concomitant operations.
CONCLUSIONS: The CorCap device appears safe for patients with dilated cardiomyopathy. Randomized clinical trials are underway in Europe, Australia, and North America.
Medical therapy, such as that represented by angiotensin-converting enzyme inhibitors and ß-blockers, is the standard of care for management of heart failure. However, numerous signaling pathways implicated in the promotion and progression of heart failure suggest that drugs might not provide all-encompassing protection against deterioration in cardiac structure and function. Even multidrug regimens might not prevent disease progression, suggesting the need for alternative approaches. Surgical therapies intended to unload the heart have received considerable recent attention. One such means is represented by the Acorn CorCap cardiac support device (CSD; Acorn Cardiovascular, Inc, St Paul, Minn), a mesh-like implantable device that is surgically positioned around the heart and adjusted to provide circumferential diastolic support. The CSD is intended to reduce wall stress and myocyte overstretching during end diastole and periodic hemodynamic overload conditions. By reducing or limiting the stress and stretching on the myocardium, a key component of the remodeling process might be halted or reversed.
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Methods |
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The upper inclusion limit for ejection fraction in this study was 35%, except for patients receiving concomitant mitral valve surgery, in whom a limit of 45% was applied. Patients with primary diastolic dysfunction or restrictive disease were excluded. Previous cardiac surgery was not a contraindication, unless patent coronary artery grafts might be compromised by the presence of the CSD or adhesions might prevent proper CSD placement. Patients in end-stage NYHA class IV receiving continuous intravenous inotropic agents or mechanical support were excluded.
If the device is used as sole therapy, the CSD can be implanted off pump. The device can also be implanted in conjunction with additional reparative operations on the heart that are done during cardiopulmonary bypass. In these cases device implantation should be started during pump support to facilitate placement of the posterior atrioventricular groove sutures. The final fitting of the device is accomplished with the patient off pump with a full and beating heart to ensure appropriate fitting. Additional techniques involving minimally invasive approaches are in development.
After sternotomy, the pericardium is opened, and the diameter of the left ventricle at the midpapillary muscle level is measured by using transesophageal echocardiography. The appropriate CSD size is selected by measuring the heart’s circumference and base-to-apex dimension. A measuring tape or cord is placed around the heart at the base to approximate the circumference, and the length of the heart is measured from the base to the apex anteriorly. These 2 measurements are then used to select the appropriate size device according to a sizing chart provided on the device package.
Once chosen, the CSD is positioned around the ventricles, with particular care to ensure that the hemline lies above or just below the atrioventricular groove. A series of 4-0 polypropylene sutures is used to secure the device in place around the base of the heart, starting in the posterior region and working laterally. Excess fabric is accumulated anteriorly by using a specially designed clamp. The excess material is then removed, and a new anterior seam is formed (Figure 2). We seek to obtain a snug fit, which might result in a slight reduction in the diameter of the heart, as measured by means of transesophageal echocardiography, but avoids any reduction greater than 10% to minimize the potential for any adverse events related to device fit. This snug fit ensures that the CSD relieves a portion of mechanical stress and stretching in the ventricular wall.
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Initial safety studies included a series of 29 patients enrolled at Charité Universitätsklinikum, Humboldt-Universität zu, Berlin, Germany, between April 1999 and July 2000. Of the 29 patients, 12 required no additional cardiac surgery other than the CSD implantation, and the remainder had some type of concomitant cardiac surgery. The majority of these procedures were mitral valve repairs or replacements. The initial safety studies also included a group of 5 patients with ischemic heart disease who were enrolled at the Austin and Repatriation Medical Centre, Melbourne, Australia. Coronary artery bypass grafting was performed on all of the patients concomitant with CSD implantation. None of these patients required valve repair or replacement. Coronary artery angiography was performed at 6 months’ follow-up to evaluate graft patency.
A final group of 14 nonrandomized patients was also included. Three patients required no concomitant surgery; 7 underwent valve repair or replacement, 2 had coronary artery bypass operations, and 2 had both bypass grafting and valve repair or replacement. All of these groups combine for a total of 48 initial safety study patients. Results are reported as means ± SD (range) unless otherwise stated.
Inclusion and exclusion criteria for patients in these safety studies are summarized in Table 1. During the initial experience, it became important to exclude patients with very advanced or late-stage heart failure because of a very high operative risk. A series of 10 criteria were determined, representing late-stage heart failure (Table 2). Patients with 4 or more of these criteria were excluded from the study.
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Results |
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The complete surgical procedure required an average of 2.3 ± 0.6 hours (range, 1.6-3.7 hours) for CSD-only operations compared with 3.5 ± 1.2 hours (range, 2.0-6.7 hours) for procedures involving concomitant cardiac operations. The average implantation time was 23.1 ± 6.1 minutes (range, 15-40 minutes) for patients receiving only the CSD, whereas implantation time in conjunction with concomitant cardiac procedures was slightly greater (29 ± 11 minutes [range, 14-67 minutes]). Crossclamp time was not required for CSD-only implantation, and 49.7 ± 30.3 minutes (range, 21-125 minutes) of crossclamp time was used in conjunction with concomitant procedures. Total cardiopulmonary bypass time was 24.7 ± 9 minutes (range, 20-32 minutes) for CSD-only procedures and 94.8 ± 36 minutes (range, 55-188 minutes) for concomitant procedures. Mean intraoperative LVEDD reduction was 3.2 mm (4.6%). There were no device-related intraoperative complications in this study.
There were 8 deaths attributed to operative mortality (Table 3), having taken place during the first 30 days after the operation or during the initial hospitalization. This included 1 (7%) of 15 patients in the CSD-only group and 7 (21%) of 33 patients in the concomitant surgery group. There were 9 late deaths in total, including several not related to heart failure (cancer in 2 patients and suboptimal anticoagulant level in a patient with a prosthetic mechanical heart valve). Other late deaths were attributed to pneumonia, ventricular arrhythmia, progressive recurrent mitral regurgitation, and cerebral hemorrhage. The 2 remaining long-term deaths were considered cardiac failure, with 1 occurring approximately 1 month after weaning from a left ventricular assist device. Of the 17 total deaths in the series, 5 (38%) occurred in patients with an ischemic cause, and 12 (34%) occurred in patients with an idiopathic cause. No deaths or adverse events were CSD related.
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Various factors were likely active in influencing patient outcome. Among these were patient selection criteria. In light of the operative mortality experienced in this series, alterations were made in selection criteria (see late-stage heart failure criteria) to screen out patients at unacceptably high surgical risk. With the revised selection criteria, patients representing 7 of the 8 early deaths and 1 of the 9 late deaths would have been screened out of the study. Kaplan-Meier survival curves in Figure 3 demonstrate that analysis, in which the lower curve represents all 48 patients, and the upper curve excludes deaths of patients who would have been screened out by the revised selection criteria. In addition, implantation techniques were refined, including fitting the device with no greater than a 10% reduction in LVEDD. The modified criteria are also the basis for enrollment of patients in randomized trials currently underway with this device.
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A subset of study patients underwent hemodynamic and pressure-volume loop analyses at 3, 6, and 12 months’ follow-up. Values obtained for the differences in ventricular end-diastolic pressure, right atrial mean pressure, and right ventricular pressure ratio revealed no indication of cardiac constriction or diastolic dysfunction (Table 6). Left ventricular pressure-volume analysis supported these findings. Figure 5 depicts pressure-volume loop data for a patient implanted with the device only, with no other concomitant cardiac procedures. These results are representative of the series as a whole17 and illustrate a lack of diastolic impairment or development of constrictive physiology.
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Discussion |
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Chaudhry and colleagues18 have reported reduced left ventricular volumes and improved cardiac function parameters in CSD-treated animals by using a microembolic canine heart failure model. At 3 months’ follow-up, left ventricular end-diastolic volume (LVEDV) was reduced (68 ± 4 mL at baseline vs 61 ± 4 mL at 3 months [mean ± SEM], P < .005) but increased in the untreated control group (67 ± 5 mL at baseline vs 83 ± 8 mL at 3 months). LVEF was increased (34% ± 1% at baseline vs 41% ± 1% at 3 months, P < .005) in animals with heart failure treated with the CSD but decreased in the control group (36% ± 1% at baseline vs 28% ± 2% at 3 months). Similar results have been demonstrated at 6 months’ follow-up.
LVEDV and LVEF at follow-up were statistically different between the control and CSD treatment groups. Also, at 3 months’ follow-up, regional wall motion was greater in the CSD-treated group compared with that in the control heart failure group, whereas mitral valve regurgitation was eliminated in the treatment group. A trend toward increased left ventricular end-diastolic pressure in the control group and a decrease in the treatment group at follow-up was also noted.
Power and associates19 used a high-rate pacing ovine model of heart failure and reported similar findings. Heart size (left ventricular diastolic area) was maintained or reduced with CSD treatment in moderate and more advanced heart failure, despite continued high-rate pacing. Cardiac function also improved with CSD treatment, as reflected by improved LVEF, fractional shortening, positive dP/dt, and negative dP/dt. Functional improvement was noted irrespective of whether the CSD was implanted in patients with moderate or more advanced heart failure.
Histomorphologic analysis was performed on cardiac tissue samples from dogs with microemboli-induced heart failure at 3 months’ follow-up. Compared with the control group, the tissue from the CSD-treated study group showed less myocyte hypertrophy, less interstitial fibrosis, and greater capillary density.20 Further testing in this animal model demonstrated enhanced myocyte function (percentage of shortening and peak derivative of shortening and relaxation) in the CSD-treated group compared with that in the control group.20
Biochemical factors implicated in possible mechanisms of actions for CSD therapy have been examined. Sabbah and coworkers21 reported that stretch protein levels (p21ras, c-fos, and p38
/ßMAP kinase) were at lower levels in the CSD-treated group, and Ca2+ cycling was improved (on the basis of an increase in the ratio of Ca2+ ATPase/phospholamban and a downregulation of protein phosphatase activity) in the CSD-treated group.22 In addition, the expression ratio of Bcl-2/Bax was altered after CSD implantation, suggesting an attenuation in proapoptotic signaling in cardiomyocytes.23 These findings suggest that the CSD can prevent or minimize maladaptive gene expression and phenotypic transformation. In summary, these studies indicate that the CSD, by supporting the ventricle and reducing stress-mediated myocardial stretching, can halt progressive remodeling and perhaps allow for reverse remodeling.
Preclinical studies indicate no signs of a constrictive pattern on the basis of analysis of filling pressures and pressure-volume loops.24 In addition, animals with heart failure evaluated at 3 months after CSD implantation demonstrated a normal response to severe volume load by increasing LVEDV, LVEF, and left ventricular stroke volume.25
Clinical study results also indicate that patients receiving the CSD do not exhibit a constrictive physiology. As part of the safety study, 15 patients were entered into a substudy designed to address this question.26 Patients underwent pressure-volume loop analysis and detailed hemodynamic monitoring, including assessment of left and right ventricular end-diastolic pressures, right atrial pressures, right ventricular pressure ratios, and right ventricular indices. Patients were followed up to 12 months after CSD implantation. On the basis of these analyses, there was no evidence of constriction. In addition, coronary flow reserve measurements conducted in these patients showed normal coronary flow without signs of coronary impairment.
Tissue reaction between the CSD and the heart does not appear to contribute to a constrictive physiology and should not interfere with most future cardiac surgeries. Nevertheless, surface fibrosis associated with the CSD might complicate future cardiac surgeries and might interfere with visualization of the cardiac architecture, including epicardial coronary arteries should a redo operation, such as coronary artery bypass, be required. Experience in animal models suggests that the normal fibrotic response to the CSD is self-limiting and thin in cross-section, and limited clinical experience suggests a similar response in human subjects. However, adequate clinical data are not yet available to determine the ease of access to coronary arteries or other cardiac structures if a future redo operation is required.
Coronary artery bypass graft surgery can be safely performed in conjunction with CSD implantation. After positioning the CSD, small openings are created in the device fabric to access anastomotic sites on epicardial coronary arteries. In a limited series of patients undergoing coronary artery bypass grafting, graft patency was evaluated by means of coronary angiography 6 months after the operation, at which time all grafts remained patent.8
Patients with end-stage cardiomyopathy frequently experience severe mitral regurgitation, which contributes to heart failure progression and is predictive of poor outcome.27 Mitral regurgitation in the context of cardiomyopathy is believed to result from dilation of the mitral annular-ventricular apparatus with altered ventricular geometry or from ischemic papillary muscle dysfunction.28-30 In patients with significant mitral valve regurgitation, mitral valve repair or replacement might be performed in conjunction with the CSD implantation. These concomitant procedures have been successfully performed in more than 65 patients to date, with slight modifications to the CSD implantation procedure.
Several limitations are inherent in this study, which represented the initial clinical experience for use of the Acorn CorCap CSD in patients with idiopathic or ischemic dilated cardiomyopathy. As such, patients were not randomized, control patients were not enrolled, and blinding was not used. In addition, a complete record of follow-up was not obtainable for some of the patients. Nevertheless, improvements seen in terms of cardiac structure and function were similar to those observed in several animal models of heart failure.
In conclusion, the CSD provides a promising surgical therapy for dilated cardiomyopathy. On the basis of extensive preclinical studies, the CSD not only halts ventricular dilation but also appears to promote ventricular reverse remodeling without any safety issues. Similar results are reflected in the initial clinical experience, with up to 2 years of patient follow-up. The CSD appears to be a safe product and might improve cardiac function. On the basis of these studies, randomized clinical trials are currently underway in Europe and North America. This surgical approach provides additional evidence supporting aggressive management of ventricular remodeling in the treatment of heart failure.
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