Abstract
Some cardiac surgeons prefer to close the pericardium whenever possible following surgery, others specifically avoid this practice, and still others believe that neither alternative has any meaningful influence on clinical outcomes. Unfortunately, scientific evidence supporting either approach is scarce, making a consensus regarding best practice impossible. In this article, the known functions of the native intact pericardium are summarized, and the arguments for and against pericardial closure after surgery are examined. In addition, the techniques and materials that have been utilized for pericardial closure previously, as well as those that are currently being developed, are assessed.
The optimal method for closing the pericardium following cardiac surgery and whether or not pericardial closure has any discernable impact on clinical outcomes has not been established Citation[1,2]. An accurate evaluation of this issue is problematic because of imprecise terminology and the lack of feasible pericardial substitutes as well as the paucity of scientifically sound prospective studies. Thus, despite performing approximately 238,000 coronary artery bypass grafting, valve and other cardiac surgical procedures requiring a pericardiotomy each year in the USA Citation[2], surgeons close the pericardium or leave it open without clear evidence to support either approach. Our objective is to review the current clinical dilemma and to introduce a new biological material capable of actually regenerating the patient’s own native pericardium, an option that could make the previous question of whether or not to close the pericardium moot.
Pericardial anatomy, mechanical function & physiology
The pericardium is a deceptively complex, specialized membrane that serves as a wide range of normal physiological functions (Box 1). It consists of an inner visceral layer lined with mesothelial cells and an outer parietal layer comprised mainly of collagen and elastin Citation[3,4].
The intact pericardium modulates ventricular filling, heart deformation during ventricular diastole, the structural behavior of the ventricular septum, the left ventricular (LV) and right ventricular (RV) free walls and the heart’s structural response to physical stresses during the cardiac cycle Citation[5,6]. It enhances RV function and is a strong modulator of LV–RV interdependence Citation[7,8]. Evidence also suggests that the intact pericardium prevents abrupt changes in intracavitary volumes and such consequent, stretch-related electrical phenomena such as postoperative atrial fibrillation (AF) Citation[5,9].
Following a thoracotomy and pericardiotomy, normal intracardiac pressures may be associated with larger atrial and RV volumes than are normally associated with those pressures. Moreover, the volume of any cardiac chamber largely depends on its transmural pressure (i.e., intracardiac pressure minus pericardial pressure) rather than on intracardiac pressure alone. Transmural pressure Citation[10] determines the production of atrial natriuretic peptide Citation[11] and the activity of LV mechanoreceptors Citation[12]. Moreover, increased LV volume subsequent to pericardiotomy might effect cascading changes in myocardial blood flow distribution, leading to reduced coronary artery perfusion and decreased myocardial blood flow, especially in the subendocardium. Indeed, two canine studies have shown that thoracotomy and pericardiotomy cause severe disturbances in the distribution of myocardial blood flow Citation[13] and that the constraining effects of the pericardium may prevent the increased oxygen and myocardial blood flow requirements produced by ventricular dilatation Citation[14].
In addition to its effects on these intracavitary pressure/volume relationships and on myocardial blood flow, the pericardium also plays an important role as an intact envelope around the heart that bathes the heart in pericardial fluid which is distinct in chemical and biological composition from that in the mediastinum.
Arguments in favor of pericardial closure
Minimization of postoperative adhesions
Closing the pericardium after cardiac surgery, either primarily or using a substitute, has been shown to protect against the formation of postoperative retrosternal adhesions connecting directly to the heart’s surface Citation[1,2,7,15–27]. Such retrosternal adhesions, when they attach directly to the epicardial surfaces of the heart, may negatively affect patient safety during repeat sternotomy Citation[2,24,28–30]. In addition, it has been demonstrated both clinically Citation[31,32] and experimentally Citation[33] that adhesion of the right ventricle to the posterior sternum can adversely affect cardiac hemodynamics by interfering with normal RV rotational and longitudinal movement.
Of primary importance, however, is the issue of patient safety during cardiac reoperations. In a recent analysis of data from the STS Adult Cardiac Surgery Database, Morales et al. found that reoperations comprise approximately 8–10% of adult cardiac surgical procedures performed annually in the USA and that the incidence of adult reoperations recorded in the STS Congenital Cardiac Surgery Database has risen to 31% Citation[2]. Morales et al. estimated that the total number of resternotomies performed in the USA each year is at least 50,000 Citation[2].
The rate of catastrophic injury during resternotomy has fallen dramatically from around 5% in the 1980s and 1990s Citation[24] to approximately 1% today Citation[34,35]. This decrease is probably due to the adoption of new preventive strategies including video-assisted visualization, alternative dissection instruments and techniques, and the use of other measures aimed at reducing adhesions. While these improvements are encouraging, physician surveys suggest that injury during resternotomy may be chronically underreported Citation[2,24,28,29]. On the basis of the available statistics, it is probable that a nontrivial number of catastrophic injuries still occur each year. Given the increased risk of morbidity and mortality associated with cardiac reoperations, many surgeons have advocated for closure of the pericardium or other protection of the epicardial surface whenever possible Citation[1,2,7,15–27].
Maintenance of retrosternal distance
In addition to preventing postoperative mediastinal adhesions to the heart’s epicardial surface, closure of the pericardium following cardiac surgery provides an increased distance between the heart and the retrosternal surface. It has been suggested that maintenance of native cardiac geometry within the mediastinal space is important for preserving LV function after a cardiac operation Citation[7], while inadequate retrosternal distance is a potential risk factor for injury during resternotomy Citation[7,15,36]. Primary pericardial closure provides a significant and important increase in the distance between the posterior sternum and the heart at both 1 week and 3 months following surgery Citation[7]. Pericardial closure using pericardial substitutes such as polytetrafluoroethylene (PTFE) and polyglycolic acid (PGA) has also been shown to increase the distance between the heart and the posterior sternum Citation[36].
Recompartmentalization of the intrapericardial microenvironment
Complete closure of the pericardium may help to recompartmentalize the mediastinal cavity. The heart can thus be sequestered from shed blood with its component cytokines and other proinflammatory mediators as well as from infections that may develop as the sternotomy heals. Postoperative exposure of the heart to pericardial and extrapericardial shed blood has been implicated in the development of cardiac adhesions Citation[15] and postpericardiotomy syndrome (PPS) Citation[27]. Inflammation has also been implicated in the genesis of postoperative AF Citation[37–39]. Clinical studies have demonstrated that closing the pericardium may improve postoperative outcomes and facilitate patient management by enabling accurate differentiation between postsurgical bleeding of cardiac versus mediastinal origin Citation[18,27].
Improved hemodynamics
The intact pericardium is capable of modulating LV–RV coupling Citation[40]. In anesthetized dogs, Kroeker et al. demonstrated that ventricular coupling is optimal when the intrapericardial pressure is 5 mmHg or greater Citation[40]. Under those conditions, a sudden decrease in RV filling (analogous to the momentary decrease in venous return that sometimes leads to orthostatic hypotension) is accompanied by an immediate, compensatory increase in LV end-diastolic volume and stroke volume. The authors speculated that an endurance-trained athlete might be particularly susceptible to orthostatic hypotension because at rest the heart might be ‘too small’ for the pericardium, a phenomenon that has since been confirmed in humans Citation[41].
Potential route for intrapericardial therapy
Disease diagnosis and intervention within the intact intrapericardial space offer potential advantages over the systemic delivery of cardiac therapies. Several recent clinical studies have documented that intrapericardial therapy (IPT) provides for the localized treatment of diseases of the coronary arteries and veins, autonomic nerves, specialized conducting tissues and myocardium Citation[42], while limiting the potential systemic side effects Citation[43–49]. Although the hemodynamic effects of the pericardium depend primarily on simple surgical reapproximation Citation[50], successful IPT is likely to depend on the pericardium being sealed ‘water-tight’ to prevent loss of the intrapericardial therapeutic agent.
Arguments against pericardial closure
Perceived increase in risk of iatrogenic tamponade
Despite persuasive arguments supporting the practice of closing the pericardium following cardiac surgery, a number of potential drawbacks have also been documented. Some of these negative arguments apply to primary closure, and others are more specific to the materials used as pericardial substitutes. Historically, the pericardium was left open because of the perception that its closure could trap blood and other fluids around the heart resulting in cardiac tamponade Citation[51]. It was assumed that it was safer to allow blood to drain into the mediastinum and/or the pleural space where it could be removed by properly positioned chest tubes Citation[27].
However, this perception is not supported in the literature by any randomized, controlled trials, case–control studies or even case series studies showing an increase in cardiac tamponade following closure of the pericardium. On the contrary, the most recent studies found that primary pericardial closure is protective against cardiac tamponade Citation[25,27], an observation that is attributed to the prevention of clot formation around the heart by shed mediastinal blood Citation[18]. More recent studies evaluating alternative pericardial substitutes for pericardial closure have shown no significant increase in cardiac tamponade when compared with control groups in which the pericardium was left open Citation[7,26,52–56].
Adverse changes in hemodynamic parameters
A transient reduction in cardiac index and stroke-work index following primary pericardial closure has been documented in humans in one prospective, randomized clinical trial Citation[7]. Several clinical case series have also reported mild-to-moderate cardiac constriction, reduction in cardiac output and a fall in arterial pressure resulting from primary pericardial closure Citation[21,27,57–60]. These findings are consistent with the effects of myocardial edema and dilation of both atria and of the right ventricle during operations requiring cardiopulmonary bypass, all of which exaggerate the normal constraining effects of the pericardium Citation[27].
The potential negative effects of primary pericardial closure on overall hemodynamics are usually transient in nature, and there are no known controlled studies showing long-term adverse clinical outcomes due to primary pericardial closure Citation[1]. Thus, the consensus in the literature is that primary closure is preferable when possible Citation[16,57] but that it may not be appropriate for patients with impaired cardiac output or LV function preoperatively Citation[1,7,27,57–60] or in perioperative patients who require high preloads to maintain an adequate cardiac output Citation[7].
Importantly, the adverse hemodynamic effects of closing the pericardium following cardiac surgery have been documented only in the context of primary pericardial closure, not when pericardial substitutes have been used to attain closure. By completely enclosing the postcardiopulmonary bypass-enlarged heart without causing cardiac constriction, pericardial substitutes might confer some clinical benefit in comparison with either primary closure or leaving the pericardium open.
Perceived risks of graft compression
Several reports have suggested that pericardial closure following coronary artery bypass grafting could lead to ‘kinking’ or distortion of the bypass grafts or internal thoracic artery conduits Citation[21,55,61,62]. While alternative ‘tension-free’ closure techniques have been proposed as a solution to this potential problem Citation[21,61,62], these approaches merely provide epicardial cover and do not result in true restoration of the pericardial envelope. As will be discussed below, pericardial substitutes, sewn to the native edges of the pericardium, can be tailored such that they allow full, circumferential closure that approximates normal pericardial constraint around the ventricles, while leaving some space around the great vessels and any bypass grafts.
Epicardial reactions & adhesion formation
An important consideration in the use of various pericardial substitutes is their material-specific propensity to produce epicardial reactions and adhere to the epicardial surface. These reactions are discussed in detail in the section ‘Synthetic & biosynthetic pericardial substitutes’, and point to the critical need for clinical evaluation and extended follow-up to understand the effects of these materials.
Current options for pericardial closure
Primary closure
Over the past three decades the general consensus in the literature among surgeons who advocate closing the pericardium has been that primary closure is the preferred method for protecting the anterior cardiac surfaces Citation[7,21,25,27,63]. Unfortunately, primary closure is frequently not feasible because of physiological pericardial contraction, cardiac enlargement or harvest of sections of the pericardium for use in cardiac repair Citation[21]. In the case of multiple resternotomies, there may not be enough remaining pericardial tissue to even consider primary closure Citation[55,64]. Moreover, there are continuing concerns about the potentially adverse hemodynamic effects of primary pericardial closure in susceptible patient groups Citation[1,7,27,57–60] and with its specific interference with bypass conduits Citation[21,55,61,62].
Autogenous alternatives to primary closure
A number of surgical ‘fixes’ have been proposed to overcome cardiac constriction with primary pericardial closure. While these techniques provide protection to the anterior epicardial surface, they cannot strictly be considered pericardial closure, since they do not restore the integrity of the intrapericardial microenvironment.
‘Tension-free’ closure techniques, the first of which was described by Merav et al. in 1979 Citation[65], involve the creation of lateral pericardial-relaxing incisions to relieve excess membrane tension. Though there are no randomized, controlled studies evaluating this technique, a small case series report by Izzat et al. found that Merav’s approach caused no adverse effects on hemodynamic parameters, such as cardiac output, stroke volume or mean systolic blood pressure Citation[19]. Furthermore, LV dimensions, ejection fraction and wall thickness were not affected by this technique. Other larger clinical studies have documented initial success with similar relaxing incisions Citation[62], rotational flaps Citation[53] and pericardial meshing Citation[66].
Some surgeons have used other fresh autologous tissues for anterior epicardial protection for situations in which native pericardial tissue is in short supply. Approximation of the pericardium to the incised pericardial fat pad to form an epicardial cover has been reported Citation[54,56].
Case reports as well as larger patient series using fascia lata Citation[67,68], a thymus flap Citation[61] or a pedicle flap of diaphragmatic central tendon Citation[69] have also reported initial success, although long-term follow-up and controlled studies using these materials are lacking. Unfortunately, none of the techniques represent a true pericardial ‘closure’ in the sense of recreating a closed envelope with an isolated microenvironment.
Posterior pericardiotomy has been suggested as an alternative intraoperative surgical strategy for decreasing postoperative AF Citation[70]. Although this strategy has been shown to be effective in reducing the incidence of postoperative pericardial effusion, AF and PPS, this technique has also been associated with cardiac herniation and herniation of bypass grafts that have resulted in adverse outcomes Citation[70,71]. The authors believe that this technique should not be used either as a standalone procedure or as an adjunct to circumferential pericardial closure.
Synthetic & biosynthetic pericardial substitutes
Several different types of pericardial substitutes have been used in the past to close the pericardium completely without causing immediate cardiac constriction. In 1990, Bunton and colleagues proposed a list of the necessary properties of a clinically effective pericardial substitute Citation[72]. According to their criteria, pericardial substitutes should: prevent chest wall/lung-to-pericardium adhesions, thus increasing the safety of reoperation by decreasing the likelihood of injury to the anterior cardiac structures on resternotomy; should cause minimal pericardium-to-epicardium adhesions; should not provoke significant epicardial reaction; should be relatively inert to avoid reaction in surrounding tissues; and should not predispose the patient to infection. A number of materials have been tried for this purpose, with varying success.
PTFE (GORE-TEX®)
PTFE is perhaps the most extensively evaluated synthetic surgical membrane that has been used for pericardial closure. Several studies Citation[36,73–78] have suggested that PTFE has nonadhesive qualities and is effective in facilitating resternotomy in adults and children. One randomized trial found that PTFE closure of the pericardium produces no increase in tamponade or infection Citation[55]. PTFE has also proven beneficial in protecting the surfaces of ventricular-assist devices when used in bridge-to-transplant procedures Citation[78–80].
Despite these favorable reports, PTFE’s overall efficacy for routine closure of the pericardium postcardiotomy is questionable, as a number of potentially serious disadvantages have been identified. Both human Citation[81] and animal Citation[72] studies have demonstrated that PTFE may aggravate the normal epicardial reaction resulting in the deposition of a thick, fibrous and often hemorrhagic layer that obscures the epicardial anatomy. PTFE used as a pericardial substitute causes a significant foreign body reaction as shown by microhistological analysis Citation[81,82] and may actually increase the incidence of tamponade when compared with other substitutes Citation[75]. Moreover, there may also be a higher incidence of injury at resternotomy in pediatric cardiac surgery patients with previously implanted PTFE Citation[34].
Glutaraldehyde-treated xenografts
Bovine pericardium, crosslinked with glutaraldehyde for durability, enjoyed early popularity as a pericardial substitute Citation[24,83,84] but unfortunately, later studies have shown that both bovine and equine pericardial substitutes produce intense epicardial reactions and are also subject to calcific, degenerative foreign-body responses Citation[22,23,66,72,85–89]. As a result, most surgeons discontinued the use of glutaraldehyde-preserved xenograft pericardium.
Bioresorbable polymer films
Numerous bioresorbable polymer films have been tried for anterior epicardial protection, based on the notion that they might protect against the formation of epicardial adhesions during the initial, inflammatory phases of healing without leaving a permanent residual foreign body.
PGA mesh was evaluated for pericardial closure in limited preclinical and clinical studies. In a prospective randomized trial, Lahtinen et al. found that patients whose pericardium was closed by anchoring the edges to PGA mesh with interrupted sutures experienced a lower incidence of postoperative tamponade, compared with those similarly treated with PTFE Citation[75]. However, in a follow-up report from the same group, it was found that PGA was more adhesive to the posterior sternum than PTFE as determined by computed tomography measurement of retrosternal distance Citation[36]. Results from other preclinical studies were similarly mixed Citation[72,87].
A number of other resorbable polymer substances have been studied in small human trials Citation[64,90–92], but most have been limited to preclinical evaluation only Citation[82,93–98]. One such material, a barrier film comprised of polylactic acid and polyethylene glycol (REPEL-CV®, Synthemed Inc., NJ, USA) Citation[91], received US FDA approval for cardiac applications but its use is limited to pediatric patients.
Decellularized extracellular matrix
A novel bioresorbable surgical membrane recently used for pericardial closure is a specially processed, acellular, noncrosslinked extracellular matrix (ECM) material derived from porcine small intestinal submucosa Citation[99]. This material has been approved as an implant for pericardial closure in both the USA and Europe, under the trade name of CorMatrix ECM® for Pericardial Closure (CorMatrix, GA, USA). It also has approval for cardiac tissue repair and carotid artery repair. The ECM material is strong enough to provide structural support for the pericardium during healing but lacks the proinflammatory cellular components present in other chemically fixed xenografts. It has been shown to downregulate the inflammatory response and to resist calcification Citation[99,100]. The ECM material also recruits and facilitates the incorporation of the host’s own stem cells into its matrix with eventual bioresorption of the ECM and complete conversion into native host tissue Citation[101–104]. Preclinical studies in cardiac and other tissue types have also shown this material to promote the reconstruction of native tissue by progenitor cell recruitment Citation[99,103,105].
Since its regulatory clearance in 2006, it is estimated that the ECM material has been implanted in approximately 50,000 patients. A retrospective pilot study of the effect of complete, circumferential pericardial closure on the incidence of postoperative AF showed a significant reduction in postoperative AF with a relative risk reduction of 54% (p < 0.001) and an absolute risk reduction of 21% Citation[52]. The use of the ECM material for pericardial closure was associated with no increase in the risk of adverse events such as tamponade, postoperative bleeding, postoperative myocardial infarction or PPS Citation[52].
Although the mechanism of this phenomenon has not yet been studied directly, an intact pericardium may protect against the development of AF by helping to limit atrial stretch Citation[5,9]. There is also increasing evidence in the literature that inflammation plays a role in the pathophysiology of postoperative AF Citation[38,39,106]. A prospective multicenter randomized trial is currently under way to test the hypothesis that reconstruction of the pericardium with the ECM material isolates the heart from shed mediastinal blood, proinflammatory cytokines and other factors that may act as a triggering event for postoperative AF Citation[201]. Other clinical studies have been initiated to evaluate host response to the ECM material and the dynamics of implant remodeling and myocardial tissue regeneration.
Conclusion
Despite decades of experience, the question of whether or not to close the pericardium at the end of a cardiac surgical procedure has not been answered definitively. The proposed advantages of closing the pericardium after surgery include: protection from adhesions and injury during resternotomy; recompartmentalization of the intrapericardial microenvironment and the mediastinum, which protects the heart from extrapericardial blood and other substances and facilitates localization of sources of blood loss after surgery; improvement of cardiac hemodynamics including the modulation of orthostatic hypertension and preservation of a potential route for IPT. Potential disadvantages include cardiac constriction with adverse changes in cardiac output, the development of inflammatory epicardial reactions from pericardial substitutes and the risk of graft compression.
Resolution of this dilemma has been hampered by the absence of a pericardial substitute that fulfils all of the requirements set forth by Bunton and colleagues Citation[72] (section ‘Synthetic & biosynthetic pericardial substitutes’). Recently introduced bioregenerative materials offer the promise of realizing the advantages of pericardial closure without the potential disadvantages.
Expert commentary
With this review, the authors have argued that the question of whether or not to close the pericardium deserves a fresh look. The persistent belief that pericardial closure is detrimental or neutral to postoperative outcomes does not appear to be based on rigorous evidence. What the authors believe will be important in settling this question are better quality, controlled clinical studies and the establishment of a more precise terminology for procedures related to postsurgical closure of the pericardium. For example, studies must clearly distinguish between primary reapproximation and the use of pericardial substitutes. Study methods should include clear explanations about whether the reconstruction is performed in such a way as to restore tension/constraint on the ventricles. They should also state whether the reconstruction created an intact, water-tight envelope (we propose the term ‘circumferential pericardial closure’); a bag that restores constraining tension on the heart but is left in open communication with the mediastinum (‘constraining reapproximation’) or a simple loose cover solely intended to protect the exposed epicardium from other mediastinal surfaces (‘anterior epicardial protection’).
Five-year view
Many questions remain to be answered about the long-term clinical benefits of pericardial closure. However, the clinical studies we know to be currently under way or in planning stages will provide new evidence for this discussion Citation[201]. The authors anticipate that, within 5 years, the results of these studies will greatly raise awareness among the surgical community and even have the potential to settle the matter definitively.
Immediate areas of investigation by the authors and others are as follows:
• Will the observed positive effects of pericardial closure on postoperative AF seen in retrospective studies, and reported by numerous physicians after individual practice quality review, be borne out in a prospective randomized, controlled clinical trial?
• Is the risk of tamponade and/or hemopericardium increased, decreased or unaffected by pericardial closure with bioresorbable pericardial substitutes?
• What are the hemodynamic effects of pericardial closure when bioresorbable pericardial substitutes are used?
• Does pericardial closure affect LV–RV coupling and a patient’s propensity for orthostatic hypertension?
• Does pericardial closure affect paradoxical septal motion, and in turn, hemodynamics?
• What effects, if any, are there if shed blood is washed out immediately prior to closure?
Other important questions that will require longer-term study are as follows:
• Does pericardial closure with a bioresorbable pericardial substitute reduce retrosternal and/or epicardial adhesions, facilitate redo operations and reduce risk of reoperation?
• Does pericardial closure with a pericardial substitute improve long-term clinical outcomes compared with leaving the pericardium open?
• Does pericardial closure with a pericardial substitute protect against PPS?
• What is the relative cost–effectiveness of pericardial closure with pericardial substitutes versus primary closure or open pericardium?
Box 1. Functions of the normal pericardium.
Mechanical functions: promotion of cardiac efficiency, especially during hemodynamic overloads
• Relatively inelastic cardiac envelope
– Maintenance of normal ventricular compliance (volume–elasticity relationship)
– Defense of the integrity of any Starling curve: Starling mechanism operates uniformly at all intraventricular pressures because presence of pericardium
– Maintains ventricular function curves
– Limits effect of increased LV end-diastolic pressure
– Supports output responses to:
– Venous inflow loads and atrioventricular valve regurgitation (particularly when acute)
– Rate fluctuations
– Hydrostatic system (pericardium plus pericardial fluid) distributes hydrostatic forces over epicardial surfaces
– Favors equality of transmural end-diastolic pressure throughout ventricle, therefore uniform stretch of muscle fibers (preload)
– Constantly compensates for changes in gravitational and inertial forces, distributing them evenly around the heart
– Limitation of excessive acute dilation
– Protection against excessive ventriculo–atrial regurgitation (atrial support)
– Ventricular interaction: relative pericardial stiffness:
– – Provides a mutually restrictive chamber favoring balanced output from right and LVs integrated over several cardiac cycles
– – Permits either ventricle to generate greater isovolumic pressure from any volume
– – Reduces ventricular compliance with increased pressure in the opposite ventricle (e.g., limits right ventricular stroke work during increased impedance to LV outflow)
– Maintenance of functionally optimal cardiac shape
• Provision of closed chamber with slightly subatmospheric pressure in which:
– The level of transmural cardiac pressures will be low, relative to even large increases in ‘filling pressures’ referred to atmospheric pressure
– Pressure changes aid atrial filling via more negative pericardial pressure during ventricular ejection
• ‘Feedback’ cardiocirculatory regulation via pericardial servomechanisms:
– Neuroreceptors detect lung inflation and (via vagus): alter heart rate and blood pressure
– Mechanoreceptors: lower blood pressure and contract spleen
• Limitations of hypertrophy associate with chronic exercise
Membranous functions
• Reduction of external friction due to heart movements
– Production of pericardial fluid
– Generation of phospholipid surfactants
• Buttressing of thinner portions of the myocardium (reciprocal variations in parietal pericardial thickness)
– Atria
– Right ventricle
• Defensive immunologic constituents in pericardial fluid
• Fibrinolytic activity in mesothelial lining
• Prostacyclin (PGE2, PGI2 and eicosanoids) released into pericardial sac in response to stretch, hypoxia and increased myocardial loading/work
• Synthesis and release of endothelin, increased by angiotensin III stimulation
• Barrier to inflammation from contiguous structures
Ligamentous function
• Limitation of undue cardiac displacement
• Modify pericardial stress/strain by limiting directions of traction of its fibers
Key issues
• The pericardium is an underappreciated organ that serves a wide range of functions in normal cardiovascular physiology.
• Surgeons’ attitudes toward pericardial closure after heart surgery vary widely, but a review of the literature reveals a lack of quality evidence supporting the principal arguments for or against the practice.
• Imprecise use of surgical terminology further complicates the discussion. For example, many reports fail to distinguish between techniques that restore the pericardial compartment and those designed to provide simple anterior epicardial protection.
• While primary closure is the approach most frequently advocated in the literature, it is frequently not technically feasible. However, dissatisfaction with the safety and performance of synthetic and biosynthetic materials has discouraged surgeons from using them as pericardial substitutes.
• New, bioregenerative materials have been introduced for pericardial closure and show the potential to realize clinical benefits.
Acknowledgements
The authors thank Jeanne McAdara-Berkowitz for expert assistance with manuscript preparation.
Financial & competing interests disclosure
WD Boyd and JL Cox both serve as consultants to CorMatrix Cardiovascular, Inc. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
Professional writing assistance was used in the preparation of this manuscript. Funds for this assistance were provided by CorMatrix Cardiovascular. The authors maintained full and direct control over all aspects of manuscript development.
Notes
LV: Left ventricle.
Adapted with permission from Citation[107].
Related Research Data
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Website
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