Mitral valve repair for ischemic mitral regurgitation: review of current techniques.

INTRODUCTION: Ischemic mitral regurgitation can be defined as moderate to severe mitral leak precipitated by acute myocardial infarction. Valve repair is now the procedure of choice, but some cases can pose difficult anatomy. This review will illustrate current techniques for repairing complex ischemic mitral regurgitation. METHODS: Most patients with ischemic mitral regurgitation have predominant annular dilatation at the posterior commissure and require only ring annuloplasty. Full rigid rings are used preferentially. With leaflet tethering, adjunctive autologous pericardial patches are effective in restoring leaflet coaptation. If papillary muscle elongation or rupture occurs, Gore-Tex artificial chordal replacement performs well. With ischemic mitral regurgitation accompanying posterior ventricular aneurysms, standard trans-atrial mitral repair provides the best results, with associated aneurysms being repaired concurrently. RESULTS: Surgical approaches and technical outcomes of mitral repair in ischemic mitral regurgitation are illustrated in 5 patients using operative images and echocardiograms. Each method is illustrated, including ring annuloplasty, pericardial leaflet augmentation, artificial chordal replacement, and ventricular aneurysm repair. Using these techniques, virtually all ischemic mitral regurgitation can be repaired, with consequential patient benefits, even in the most complex anatomy. CONCLUSIONS: Ischemic mitral regurgitation has been shown to have better outcomes when managed with valve repair. Using combinations of annular, leaflet, and chordal procedures, even complex ischemic mitral regurgitation can undergo autologous reconstruction with excellent long-term results.

Right ventricular gene therapy with a beta-adrenergic receptor kinase inhibitor improves survival after pulmonary artery banding.

BACKGROUND: Increased right ventricular (RV) afterload results in RV hypertrophy and dysfunction, as well as increased levels of intracellular beta-adrenergic receptor kinase (betaARK1). We hypothesize that gene transfer of a betaARK1 inhibitor (betaARKct) may improve RV performance, morbidity, and mortality early after pulmonary artery (PA) banding. METHODS: Rabbits underwent PA banding 3 days after right coronary artery injection of an adenovirus containing the gene encoding the betaARKct peptide (n = 14), beta-galactosidase (n = 10), or an empty adenovirus (n = 19). After banding, hemodynamic instability and maximal rate of increase in right ventricular pressure (RV dP/dt(max)) were documented. For 7 days after banding, animals were monitored for mortality, activity, and appetite. RESULTS: When compared with controls, animals receiving the betaARKct transgene showed improvement in survival at 7 days (92.8% +/- 7% vs 48.3% +/- 9%, p = 0.01), less lethargy, a trend toward greater RV dP/dt(max) (NS), and increased hemodynamic stability at the time of banding (78% vs 41%, p = 0.03). CONCLUSIONS: Selective RV expression of betaARKct improves survival and morbidity after PA banding. This represents a novel therapeutic modality for clinical situations involving increased RV afterload.

Comparison of survival after mitral valve replacement with biologic and mechanical valves in 1139 patients.

OBJECTIVE: We sought to compare 10-year survival in patients after mitral valve replacement with biologic or mechanical valve prostheses. METHODS: Retrospective survival analysis was performed on data from 1139 consecutive patients older than 18 years of age undergoing mitral valve replacement with Carpentier-Edwards (n = 495; Baxter Healthcare Corp, Irvine, Calif) or St Jude Medical (n = 644; St Jude Medical, Inc, St Paul, Minn) prostheses. RESULTS: The 10-year survival was not statistically different between the patients receiving Carpentier-Edwards valves and those receiving St Jude Medical valves (P =.16). Adjusted survival estimates at 2, 5, and 10 years were 82% +/- 2% (95% confidence intervals, 79%-85%), 69% +/- 2% (95% confidence intervals, 64%-73%), and 42% +/- 3% (95% confidence intervals, 37%-48%), respectively, for the Carpentier-Edwards group and 83% +/- 2% (95% confidence intervals, 80%-86%), 72% +/- 2% (95% confidence intervals, 69%-76%), and 51% +/- 3% (95% confidence intervals, 45%-58%), respectively, for the St Jude Medical group. Predictors of worse survival after mitral valve replacement are older age, lower ejection fraction, presence of class IV congestive heart failure, coronary artery disease, renal disease, smoking history, hypertension, concurrent other valve surgery, and redo heart surgery. CONCLUSION: Choice of biologic or mechanical prosthesis does not significantly affect long-term patient survival after mitral valve replacement.

Predictors of operative time in multicenter port-access valve registry: institutional differences in learning.

BACKGROUND: The predictors of operative time and the effects of learning in isolated valve operations using port-access techniques have not been defined. METHODS: Analysis of covariance was used to examine the determinants of procedure time, pump time, and aortic clamp time. In the largest prospective, registry of patients undergoing isolated aortic valve replacement (AVR, N=199), mitral repair (MVP, N=307), or mitral replacement (MVR, N=232) using port-access techniques 1997-1999 at 27 institutions. RESULTS: Institutional case volume ranged from one to 214 (median 6). Operative time was longer in redo procedures (5.3 +/- 1.6 vs. 4.4 +/- 1.3 hr, p = 0.0001), longer with MVP or MVR vs. AVR (4.8 +/- 1.2 vs. 5.0 +/- 1.5 vs. 3.8 +/- 1.2 hr, p = 0.0001), and decreased with case number (mean decrease 1.00 +/- 0.19 min/case, p = 0.04). Operative time also varied between institutions (p = 0.001). Rate of learning (decrease in time per case) varied significantly between institutions only for MVP (p = 0.03). Similar analysis showed that pump time and clamp times did not significantly change over time (p > 0.17) but varied significantly between institutions. Institutional volume did not affect operative, pump, or clamp times or rate of learning (decrease in operative time/case). CONCLUSIONS: These prospective registry data demonstrate that, for port-access valve procedures, procedure times continue to improve (learning) even after 100 cases. Procedure time and learning are affected by institutional differences and by the type of procedure, but are little affected by institutional volume. This data provides a model to understand learning of new surgical procedures, and this data suggests that port-access valve procedures can be mastered by a variety of institutions.

In vivo ventricular gene delivery of a beta-adrenergic receptor kinase inhibitor to the failing heart reverses cardiac dysfunction.

BACKGROUND: Genetic manipulation to reverse molecular abnormalities associated with dysfunctional myocardium may provide novel treatment. This study aimed to determine the feasibility and functional consequences of in vivo beta-adrenergic receptor kinase (betaARK1) inhibition in a model of chronic left ventricular (LV) dysfunction after myocardial infarction (MI). METHODS AND RESULTS: Rabbits underwent ligation of the left circumflex (LCx) marginal artery and implantation of sonomicrometric crystals. Baseline cardiac physiology was studied 3 weeks after MI; 5x10(11) viral particles of adenovirus was percutaneously delivered through the LCx. Animals received transgenes encoding a peptide inhibitor of betaARK1 (Adeno-betaARKct) or an empty virus (EV) as control. One week after gene delivery, global LV and regional systolic function were measured again to assess gene treatment. Adeno-betaARKct delivery to the failing heart through the LCx resulted in chamber-specific expression of the betaARKct. Baseline in vivo LV systolic performance was improved in Adeno-betaARKct-treated animals compared with their individual pre-gene delivery values and compared with EV-treated rabbits. Total beta-AR density and betaARK1 levels were unchanged between treatment groups; however, beta-AR-stimulated adenylyl cyclase activity in the LV was significantly higher in Adeno-betaARKct-treated rabbits compared with EV-treated animals. CONCLUSIONS: In vivo delivery of Adeno-betaARKct is feasible in the infarcted/failing heart by coronary catheterization; expression of betaARKct results in marked reversal of ventricular dysfunction. Thus, inhibition of betaARK1 provides a novel treatment strategy for improving the cardiac performance of the post-MI heart.

Predictors of outcome in a multicenter port-access valve registry.

BACKGROUND: The aim of this study was to examine the predictors of outcome in patients undergoing isolated valve operation using port-access techniques. METHODS: Logistic regression analysis was performed in a prospective, multi-institutional registry of patients undergoing isolated aortic valve replacement (AVR, n = 252), mitral repair (MVP, n = 491), or mitral replacement (MVR, n = 568) using port-access techniques from 1997 to 1999. RESULTS: Endoaortic balloon occlusion was used in 2% (AVR), 93% (MVP), and 90% (MVR) of cases. Conversion to full sternotomy occurred in 3.8% of all cases. For all patients, early mortality was 50 of 1,311 (3.8%) and onset of new atrial fibrillation occurred in 140 of 1,311 (11%) patients. The determinants of 30-day mortality were redo, age, and MVR or AVR. The determinants of reoperation for bleeding were age, reoperation, and MVR. Age was a predictor for stroke, and age and low or medium volume center were predictors of new atrial fibrillation. CONCLUSIONS: Excellent short-term results can be obtained using port-access techniques in isolated mitral or aortic valve operations. Patient outcome is not related to institutional case volume, and the primary determinants of outcome after port-access valve procedures are generally patient-related factors.

Evaluation of early postoperative results after bicaval versus standard cardiac transplantation and review of the literature.

OBJECTIVE: Previous studies have been inconsistent in defining a clinical benefit to the bicaval cardiac transplantation technique relative to the standard technique, and many major centers have not adopted this newer approach. The purpose of this study was to determine whether clinically significant benefits support utilization of the bicaval technique. METHODS: Sixty-eight consecutive adult patients undergoing a standard cardiac transplant were compared with 75 consecutive patients who underwent the bicaval technique during the period from 1991 to 1999. Etiology, recipient sex, recipient age, donor age, and pulmonary vascular resistance were similar between the two groups. RESULTS: Cardiac index at 24 hours after operation was increased for the bicaval group relative to the standard group (3.15 +/- 0.7 vs 2.7 +/- 0.5 L/min/m(2), P <. 05). Inotropic requirements were significantly less, and there was significantly less tricuspid regurgitation in the bicaval group relative to the standard group. In addition, the bicaval group more frequently had a nonpaced normal sinus rhythm at 24 hours after operation (73.9% vs 50.7% [standard group], P =.025) and had fewer postoperative arrhythmias (29.3% vs 47.7% [standard group], P <.01). Finally, although mortality was similar for the two groups, length of postoperative hospitalization was longer for the standard group relative to the bicaval group (12.1 +/- 11 vs 20.4 +/- 12 days, P <. 001). Review of the literature identified reduced tricuspid regurgitation and improved rhythm as consistent benefits of the bicaval technique. CONCLUSION: This review demonstrates a clinical benefit during the early postoperative period with bicaval cardiac transplantation (relative to standard) and encourages further utilization of this technique.

Comparison of benefits on myocardial performance of cellular cardiomyoplasty with skeletal myoblasts and fibroblasts.

Cellular cardiomyoplasty (CCM), or introduction of immature cells into terminally injured heart, can mediate repair of chronically injured myocardium. Several different cell types, ranging from embryonic stem cells to autologous skeletal myoblasts, have been successfully propagated within damaged heart and shown to improve myocardial performance. However, it is unclear if the functional advantages associated with CCM depend upon the use of myogenic cells or if similar results can be seen with other cell types. Thus, we compared indices of regional contractile (systolic) and diastolic myocardial performance following transplantation of either autologous skeletal myoblasts (Mb) or dermal fibroblasts (Fb) into chronically injured rabbit heart. In vivo left ventricular (LV) pressure (P) and regional segment length (SL) were determined in 15 rabbits by micromanometry and sonomicrometry 1 week following LV cryoinjury (CRYO) and again 3 weeks after autologous skeletal Mb or dermal Fb transplantation. Quantification of systolic performance was based on the linear regression of regional stroke work and end-diastolic (ED) SL. Regional diastolic properties were assessed using the curvilinear relationships between LVEDP and strain (epsilon) as well as LVEDP and EDSL. At study termination, cellular engraftment was characterized histologically in a blinded fashion. Indices of diastolic performance were improved following CCM with either Mb or Fb. However, only Mb transplantation improved systolic performance; Fb transfer actually resulted in a significant decline in systolic performance. These data suggest that both contractile and noncontractile cells can improve regional material properties or structural integrity of terminally injured heart, as reflected by improvements in diastolic performance. However, only Mb improved systolic performance in the damaged region, supporting the role of myogenic cells in augmenting contraction. Further studies are needed to define the mechanism by which these effects occur and to evaluate the long-term safety and efficacy of CCM with any cell type.

Adenovirus-mediated genetic manipulation of the myocardial beta-adrenergic signaling system in transplanted hearts.

OBJECTIVES: Ex vivo perfusion of the cardiac allograft during organ procurement is an ideal environment for adenoviral vectors with transgenes that target improving graft contractility. One such target is the beta-adrenergic receptor-signaling system, in which alterations in transgenic mice have elucidated novel means to improve the function of the heart in vivo. The purpose of the current study was to determine the functional consequences of beta-adrenergic receptor manipulation in a rabbit model of cardiac allograft transplantation. METHODS: New Zealand White rabbits weighing 3 kg served as recipients to 1-kg outbred donors. Donor hearts were arrested and harvested, and 1 of 3 adenoviral constructs was administered into the aortic root perfusing the graft. Transgenes delivered encoded either the human beta(2)-adrenergic receptor, a peptide inhibitor of beta-adrenergic receptor densensitization, or the marker transgene beta-galactosidase. RESULTS: Five days after cervical heterotopic transplantation, left ventricular performance was measured on a Langendorff apparatus. A moderate pattern of rejection was seen in all grafts. Biventricular myocyte expression of beta-galactosidase was observed, and beta(2)-adrenergic receptor density was elevated 10-fold in grafts that received adeno-beta(2)-adrenergic receptor. Left ventricular systolic and diastolic performance was significantly increased in grafts transfected with either adeno-beta(2)-adrenergic receptor or adeno-beta-adrenergic receptor densensitization compared with control grafts that received adeno-beta-galactosidase. CONCLUSIONS: Ex vivo adenovirus-mediated gene transfer is feasible in a rabbit allograft model and, more important, genetic manipulation of beta-adrenergic receptor signaling either by increasing beta(2)-adrenergic receptor density or blocking endogenous receptor desensitization improves graft function acutely in this allograft model.

Early effects of right ventricular volume overload on ventricular performance and beta-adrenergic signaling.

OBJECTIVE: Right ventricular dysfunction is a poorly understood but persistent clinical problem. This study was undertaken to evaluate ventricular performance and beta-adrenergic receptor signaling in a tricuspid regurgitation model of right ventricular overload. METHODS: Seventeen dogs were chronically instrumented with epicardial dimension transducers. By means of the shell-subtraction model, right ventricular pressure-volume relationships were evaluated in normal and right ventricular overload states. Right ventricular chamber performance was quantified by the stroke work at an end-diastolic volume relationship. RESULTS: Right ventricular volume overload caused a 28% +/- 11% and 31% +/- 9% decline in chamber performance acutely and at 1 week, respectively, whereas end-diastolic volume increased from 45 +/- 21 to 60 +/- 30 mL (P =. 019). beta-Adrenergic receptor signaling in myocardial samples was assessed, examining adenylyl cyclase and G-protein-coupled receptor kinase activity. Stimulated adenylyl cyclase activity significantly decreased, and G-protein-coupled receptor kinase activity significantly increased in both left and right ventricular samples caused by increased levels of beta-adrenergic receptor kinase 1. No change in beta-adrenergic receptor density was seen at 1 week. CONCLUSIONS: Early right ventricular overload is associated with impaired right ventricular chamber contractility, dilation, and, importantly, a biventricular alteration of beta-adrenergic receptor signaling.

Calcitonin gene-related peptide enhances the recovery of contractile function in stunned myocardium.

INTRODUCTION: Calcitonin gene-related peptide, a potent vasodilating inotropic agent, increases coronary artery perfusion when administered exogenously and reduces ischemic injury in nonmyocardial tissue. However, it is unclear whether this agent improves recovery of myocardial performance after reversible myocardial ischemia. METHODS: Nine dogs underwent complete occlusion of the left anterior descending coronary artery for 15 minutes and were monitored during 24 hours of reperfusion. Calcitonin gene-related peptide (0.07 microgram. kg(-1). min(-1)), nitroglycerin (65 microgram. kg(-1). min(-1)), or saline solution placebo was infused intravenously during initial reperfusion. Ischemia/reperfusion was repeated in concurrent 24-hour periods until all animals received infusions in random order. Micromanometry and sonomicrometry determined left ventricular pressure and myocardial segment length. Myocardial performance, based on the linear relationship between stroke work and end-diastolic segment length, was estimated with the preload recruitable work area. Results were analyzed as percent control and compared statistically with the use of repeated measures analysis of variance. RESULTS: Recovery of myocardial performance was augmented during reperfusion with calcitonin gene-related peptide infusion relative to placebo

Preservation of myocardial beta-adrenergic receptor signaling delays the development of heart failure after myocardial infarction.

When the heart fails, there is often a constellation of biochemical alterations of the beta-adrenergic receptor (betaAR) signaling system, leading to the loss of cardiac inotropic reserve. betaAR down-regulation and functional uncoupling are mediated through enhanced activity of the betaAR kinase (betaARK1), the expression of which is increased in ischemic and failing myocardium. These changes are widely viewed as representing an adaptive mechanism, which protects the heart against chronic activation. In this study, we demonstrate, using in vivo intracoronary adenoviral-mediated gene delivery of a peptide inhibitor of betaARK1 (betaARKct), that the desensitization and down-regulation of betaARs seen in the failing heart may actually be maladaptive. In a rabbit model of heart failure induced by myocardial infarction, which recapitulates the biochemical betaAR abnormalities seen in human heart failure, delivery of the betaARKct transgene at the time of myocardial infarction prevents the rise in betaARK1 activity and expression and thereby maintains betaAR density and signaling at normal levels. Rather than leading to deleterious effects, cardiac function is improved, and the development of heart failure is delayed. These results appear to challenge the notion that dampening of betaAR signaling in the failing heart is protective, and they may lead to novel therapeutic strategies to treat heart disease via inhibition of betaARK1 and preservation of myocardial betaAR function.

Efficacy of the internal mammary artery in combined aortic valve replacement-coronary artery bypass grafting.

BACKGROUND: While internal mammary artery (IMA) use predicts improved survival after coronary bypass grafting (CABG), it remains unknown whether patients undergoing concomitant aortic valve replacement (AVR) realize a similar benefit. METHODS: All patients at a single teaching institution, undergoing combined AVR-CABG, which included a graft to the left anterior descending coronary artery (LAD) from 1984 to 1994 (n = 227) were examined retrospectively. RESULTS: Patients receiving an IMA graft (yesIMA, n = 135) and patients receiving only saphenous vein grafts (nonIMA, n = 92) were not different in their presenting symptoms, or in their incidence of preoperative risk factors. The patients with IMA were more likely to be male, have a later year of operation, be younger, and have a greater body surface. Morbidity was not different between groups. IMA use did not affect 30-day mortality. Long-term actuarial survival was greater in the group with IMA (63% +/- 7% vs 42% +/- 6% at 5 years, p < 0.01). A multivariate Cox proportional hazards model demonstrated that use of an IMA graft improved survival, while recent myocardial infarction, diabetes, earlier year of operation, and lower ejection fraction diminished long-term survival. The relative risk of IMA grafting was 0.570. CONCLUSIONS: Within the limits of a retrospective analysis, patients in a modern era of cardiac operation, who undergo combined AVR-CABG, do not suffer increased morbidity from IMA use, and may realize a survival benefit from use of the IMA as a conduit for bypass of the LAD coronary artery.

Early postoperative changes in regional systolic and diastolic left ventricular function after transmyocardial laser revascularization: a comparison of holmium:YAG and CO2 lasers.

OBJECTIVES: The purpose of this study was to determine the short-term effects of transmyocardial laser revascularization (TMR) on regional left ventricular systolic and diastolic function, myocardial blood flow (MBF) and myocardial water content (MWC). BACKGROUND: Clinical studies of TMR have noted a significant incidence of cardiac complications in the early postoperative period. However, the early post-treatment effects of laser therapy on the myocardium and their potential contribution to postoperative cardiac morbidity are unknown. METHODS: Swine underwent holmium:yttrium-aluminum-garnet (holmium:YAG) (n = 12) or carbon dioxide (CO2) (n = 12) laser TMR. Regional systolic function for the lased and nonlased regions was quantitated using preload recruitable work area (PRWA) and regional diastolic function with the ventricular stiffness constant alpha. RESULTS: Preload recruitable work area was significantly decreased in the lased regions both 1 (59.8+/-13.0% of baseline, p = 0.02) and 6 h (64.2+/-9.4% of baseline, p = 0.02) after holmium:YAG TMR. This decreased PRWA was associated with a significant reduction in MBF to the lased regions (13.2% reduction at 1 h, p = 0.02; 18.4% decrease at 6 h post-TMR, p = 0.01). These changes were not seen after CO2 laser TMR. A significant increase in MWC (1.4+/-0.3% increase with holmium:YAG, p = 0.004; 1+/-0.2% increase with CO2, p = 0.002) and alpha (217.4+/-44.2% of baseline 6 h post-holmium:YAG TMR, p = 0.05; 206+/-36.7% of baseline 6 h post-CO2 TMR, p = 0.03) was seen after TMR with both lasers. CONCLUSIONS: In the early postoperative setting, impaired regional systolic function in association with regional ischemia is seen after TMR with a holmium:YAG laser. Both holmium:YAG and CO2 lasers are associated with increased MWC and impaired diastolic relaxation in the lased regions. These changes may explain the significant incidence of early postoperative cardiac morbidity. The impact of these findings on anginal relief and long-term outcome are not known.

Intracoronary adenovirus-mediated delivery and overexpression of the beta(2)-adrenergic receptor in the heart : prospects for molecular ventricular assistance.

BACKGROUND: Genetic modulation of ventricular function may offer a novel therapeutic strategy for patients with congestive heart failure. Myocardial overexpression of beta(2)-adrenergic receptors (beta(2)ARs) has been shown to enhance contractility in transgenic mice and reverse signaling abnormalities found in failing cardiomyocytes in culture. In this study, we sought to determine the feasibility and in vivo consequences of delivering an adenovirus containing the human beta(2)AR cDNA to ventricular myocardium via catheter-mediated subselective intracoronary delivery. METHODS AND RESULTS: Rabbits underwent percutaneous subselective catheterization of either the left or right coronary artery and infusion of adenoviral vectors containing either a marker transgene (Adeno-betaGal) or the beta(2)AR (Adeno-beta(2)AR). Ventricular function was assessed before catheterization and 3 to 6 days after gene delivery. Both left circumflex- and right coronary artery-mediated delivery of Adeno-beta(2)AR resulted in approximately 10-fold overexpression in a chamber-specific manner. Delivery of Adeno-betaGal did not alter in vivo left ventricular (LV) systolic function, whereas overexpression of beta(2)ARs in the LV improved global LV contractility, as measured by dP/dt(max), at baseline and in response to isoproterenol at both 3 and 6 days after gene delivery. CONCLUSIONS: Percutaneous adenovirus-mediated intracoronary delivery of a potentially therapeutic transgene is feasible, and acute global LV function can be enhanced by LV-specific overexpression of the beta(2)AR. Thus, genetic modulation to enhance the function of the heart may represent a novel therapeutic strategy for congestive heart failure and can be viewed as molecular ventricular assistance.

Direct aortic cannulation for port-access mitral or coronary artery bypass grafting.

A technique is described for direct aortic arterial cannulation during Port-Access mitral valve or coronary artery bypass grafting. Femoral arterial cannulation is avoided, and endoaortic balloon occlusion is used for cardioplegic arrest. To date, excellent results have been obtained in 45 patients.

Means for load variation during echocardiographic assessment of the Frank-Starling relationship.

Because minimally invasive methods of preload variation are not validated for load-insensitive indexes of cardiac performance, intravenous nitroglycerin (NTG), phenylephrine, and saline solution (VOL) boluses were used in blocked and intact autonomic states to alter load and were compared with vena caval occlusion in the assessment of preload recruitable stroke work relationships between stroke work and left ventricular end-diastolic volume in dogs. In both autonomic states NTG and VOL produced comparable linear relationships. NTG and saline solution were combined with noninvasive measurements of left ventricular pressure and volume to construct echocardiographic relationships between stroke work and left ventricular end-diastolic cross-sectional area; NTG produced linear relationships similar to vena caval occlusion. Therefore NTG and VOL reliably alter load in constructing preload recruitable stroke work relationships, and NTG may be used with noninvasive measurements to provide load-insensitive estimates of cardiac function in a minimally invasive manner.

Comparison of direct aortic and femoral cannulation for port-access cardiac operations.

BACKGROUND: Differences in outcome after direct aortic cannulation (AORT) in the chest versus standard femoral arterial cannulation (FEM) have not been defined for minimally invasive cardiac operations utilizing the port-access approach. METHODS: A retrospective study was performed of 165 patients undergoing port-access cardiac mitral valve operation (n = 126) or coronary artery bypass grafting (n = 39). In 113 patients, FEM was used, while in 52 patients, AORT was accomplished through a port in the first intercostal space. RESULTS: AORT eliminated endoaortic balloon clamp migration (0/36 [0%] vs. 17/95 [18%]), and groin wound or femoral arterial complications (0/52 [0%] vs. 11/113 [10%]) without changing procedure times (363+/-55 vs. 355+/-70 minutes). Complications attributable to AORT were injury to the right internal mammary artery and aortic cannulation site bleeding in 1 patient each. CONCLUSIONS: Direct aortic cannulation is technically easy, allows use of an endoaortic clamp, and avoids aorto-iliac arterial disease, the groin incision, and possible femoral arterial injury associated with femoral arterial cannulation. Direct arterial cannulation should expand the pool of patients eligible for port-access operation, and may become the standard for port-access procedures.

Mortality and need for reoperation in patients with mild-to-moderate asymptomatic aortic valve disease undergoing coronary artery bypass graft alone.

BACKGROUND: Patients presenting for coronary artery bypass graft (CABG) surgery may have concurrent asymptomatic aortic stenosis (AS) or aortic insufficiency (AI). This retrospective study was performed to evaluate outcomes in patients with aortic valve disease undergoing CABG with or without aortic valve replacement (AVR). METHODS: Study groups included 414 patients undergoing combined AVR and CABG (AVR-CABG group) and 62 patients with asymptomatic mild-to-moderate AS, AI, or both undergoing CABG but not AVR (CABG group). End points included 30-day mortality rate, time to cardiac mortality, time to all-cause mortality, and time to aortic valve reoperation. Reoperation refers to surgery for replacement of the native aortic valve in the CABG group or replacement of the prosthetic aortic valve in the AVR-CABG group. Important patient characteristics affecting outcomes were determined by using Cox proportional-hazard analysis. These variables were then included in multivariable analyses by using logistic regression analysis and Cox proportional-hazard modeling to compare outcomes between each patient group. RESULTS: No difference was seen in any of the mortality end points between the CABG group and the AVR-CABG group after controlling for significant differences between the groups. However, the need for reoperation for AVR was significantly higher for the CABG group than the AVR-CABG group. For patients followed for up to 6 years, the estimated need for aortic valve reoperation was 24.3% in the CABG group versus 3% in the AVR-CABG group. CONCLUSION: On the basis of these results, patients with asymptomatic AS or AI should be considered for AVR at the time of CABG.