Improved outcomes in CABG patients with atrial fibrillation associated with surgical left atrial appendage exclusion.

BACKGROUND: We sought to determine the impact of left atrial appendage clip exclusion (LAACE) on coronary artery bypass grafting (CABG) outcomes among patients with pre-existing atrial fibrillation (AF). METHODS: From October 1, 2015 to October 1, 2017, 4210 Medicare beneficiaries with pre-existing AF underwent isolated CABG (i.e., without ablation) with (n = 931) or without (n = 3279) LAACE. Inverse probability of treatment weighting was used to evaluate the effect of concomitant LAACE on short- and long-term outcomes after CABG. Long term risks of thromboembolism and mortality were assessed using competing-risk regression and Cox proportional hazard models. RESULTS: Operative mortality, length of stay, and 30-day readmission did not differ between groups. Thromboembolism risk was 26% lower for the CABG + LAACE group compared with isolated CABG over a 2-year time-to-event analysis (sub hazard ratio [sHR] 0.74, 95% confidence interval [CI] 0.54-1.00, p = .049). There were no differences in ischemic stroke rates. All-cause mortality risk was 45% lower for CABG + LAACE during the late follow-up period (91-730 days; HR 0.55, 95% CI 0.32-0.95, p = .031). The late period annual absolute all-cause mortality rate was 3.7% for CABG + LAACE and 6.9% for isolated CABG. There were lower readmission rates (31% vs. 43%, p < .001) and total inpatient days (4.0 days vs. 7.2 days, p < .01.) for the CABG + LAACE during follow-up. Total hospital in and out-patient treatment costs were similar between groups through one year. CONCLUSIONS: Concomitant LAA exclusion via an epicardial closure device is associated with reduced CABG mortality, thromboembolic events, and readmissions in patients with pre-existing atrial fibrillation.

Surgical ablation of atrial fibrillation in hypertrophic obstructive cardiomyopathy: Outcomes of a tailored surgical approach.

OBJECTIVE: To assess outcomes of concomitant ablation for atrial fibrillation (AF) in patients with preoperative AF undergoing septal myectomy for hypertrophic obstructive cardiomyopathy. METHODS: From 2005 to 2016, 67 patients underwent concomitant ablation for AF and septal myectomy and had a follow-up beyond a 3-month blanking period. Ablation strategy (pulmonary vein isolation [PVI], modified Cox-maze III [CM-III], or Cox-maze IV [CM-IV]) was tailored to preoperative AF burden, with high AF burden defined as persistent AF or need for cardioversion. AF recurrence was analyzed as a time-related event and predictors of recurrence identified using a random forest methodology. RESULTS: A total of 38 patients (57%) had low AF burden and 29 (43%) high burden. Patients with low AF burden most frequently underwent PVI (68%). Patients with high AF burden more frequently underwent CM-III (62%) or CM-IV (35%). Besides the preoperative AF burden, baseline characteristics were similar between patients receiving CM-III, CM-IV, and PVI. After surgery, the maximum provoked left ventricular outflow tract (LVOT) gradient decreased from 99 ± 34 to 18 ± 11mm Hg (P < .001). Eight patients (12%) required a permanent pacemaker. Cumulative AF recurrence at 1, 2, and 5 years was 11%, 22%, and 48%, respectively. Age, low preoperative resting LVOT gradient, and large left atrial diameter were predictors of AF recurrence. CONCLUSIONS: Surgical outcomes of concomitant ablation for AF and septal myectomy are good, although recurrence of AF by 5 years is frequent.

Strategies to reduce pulmonary complications after transhiatal esophagectomy.

BACKGROUND: By eliminating a thoracotomy, transhiatal esophagectomy (THE) is purported to reduce postoperative pulmonary complications. However, data from many early series do not support this contention, documenting pulmonary complications in up to 50% of patients and pneumonia in 5%-20%. Since 1990, we have implemented a management strategy designed to maximize airway protection in the postoperative period. The purpose of this study was to determine the current incidence of pulmonary complications after transhiatal esophagectomy without thoracotomy. PATIENTS AND METHODS: From 1990 to 1995, 101 consecutive patients underwent THE. Surgical indications were esophageal carcinoma (90 patients) and Barrett mucosa with high-grade epithelial dysplasia (11 patients). Mean age was 60.2 ± 1.2 years; 89 patients were male. Eighty-two patients were smokers and 26 had chronic obstructive pulmonary disease (COPD). Sixty-five patients were American Society of Anesthesiologists risk score 3 or 4. Postoperatively, all patients were managed according to a standardized clinical pathway that included overnight mechanical ventilation, chest physiotherapy, video pharyngo-esophagram postoperative day 6 or 7, and graduated post-esophagectomy therapeutic diet after acceptable esophagram. RESULTS: Pulmonary complications were classified as major or minor depending upon whether or not a change in therapy was required. Ten patients (10%) had 11 major pulmonary complications. These included pneumonia (3), pleural effusion requiring drainage (4), exacerbation of COPD (2), and mucus plug requiring bronchoscopy or intubation (2). Minor pulmonary complications identified by chest film were atelectasis (97), pleural effusion (85), and pneumothorax (3). Patients with major pulmonary complications were older (69.3 ± 9.8 vs. 59.2 ± 12.1 years, p < .02) and more likely to have COPD (70% vs. 21%, p < .005) than those with only minor complications. There were 3 operative deaths; 2 caused by pneumonia and 1 by fungal sepsis in a patient who had exacerbation of COPD. Mean hospital length of stay was 13.1 ± 1.4 days. CONCLUSIONS: Minor pulmonary complications identified by chest film occur in nearly all patients undergoing THE. Strict adherence to a management protocol designed to maximize airway protection in the postoperative period results in a 10% incidence of major pulmonary complications. Older patient age and COPD are risk factors for major pulmonary complications after THE. Although pneumonia is uncommon, it remains the most frequent cause of death after THE.

Neutrophil adhesion and complement inhibition prolongs survival of cardiac xenografts in discordant species.

Hyperacute rejection results in rapid destruction of a discordant cardiac xenograft and is characterized by antibody deposition, complement activation, and platelet aggregation. The importance of neutrophils is unclear. Complement inhibition prolongs discordant cardiac xenograft survival. The purpose of this experiment was to determine the relative roles of complement and neutrophils. Selective inhibition of complement and neutrophil adhesion was used in a guinea pig-to-Lewis rat cardiac heterotopic xenotransplant model. NPC 15669 (N-[9H-(2,7-dimethylfluorenyl-9-methoxy)carbonyl]-L-leucine), a member of a new class of antiinflammatory agents termed leumedins, specifically prevents recruitment of neutrophils at inflammatory foci by inhibiting upregulation of the CD11b/CD18 adhesion molecule. Soluble complement receptor type 1 (sCR1, BRL 55730) is a potent inhibitor of the alternative and classical complement pathways. Group I (n = 13) received saline vehicle i.v. Group II (n = 15) was treated with NPC 15669 (10 mg/kg i.v. bolus) prior to reperfusion. Group III (n = 13) was treated with sCR1 (20 mg/kg i.v. bolus) prior to reperfusion. Group IV (n = 13) received both NPC 15669 and sCR1. Two xenografts were harvested at each interval time point (Groups I and II, 1, 2, 4, and 6 min; and Groups III and IV, 6, 15, 30, and 60 min). The remainder were followed to cessation of graft function. Graft survival was significantly increased in group IV and group III-375 +/- 13.4 min (mean +/- SD) and 112 +/- 29.4, respectively (P < .05), compared with 9.9 +/- 6.3 in group II and 8.7 +/- 4.9 in group I. Extreme interstitial hemorrhage and edema and contraction band injury were present in group I-III animals at end-stage, and neutrophil infiltration in group III. In group IV grafts, there was a decrease in these parameters despite the longer survival time, and at end-stage rejection the cellular infiltrate was primarily mononuclear. This study demonstrates that complement is an important mediator in early xenograft HYP injury. Combined treatment with NPC 15669 and sCR1 results in reduced histologic injury at all time points and longer graft survival than with sCR1 alone. These results suggest that neutrophil and complement activation play synergistic roles in the pathogenesis of xenograft hyperacute rejection. Neutrophil inhibition may prove to be an important component of multimodality therapy for hyperacute rejection, particularly in less-discordant transplants.

Echocardiographic assessment of the mechanisms of correction of bileaflet prolapse causing mitral regurgitation with only posterior leaflet repair surgery.

Recent data suggest that posterior leaflet repair alone corrects mitral regurgitation in patients with bileaflet prolapse and normal anterior chordae. The purpose of this study was to use echocardiography to define the anatomic differences between posterior and bileaflet prolapse and to determine if posterior leaflet repair alone leads to correction of bileaflet prolapse. We studied patients who underwent quadrangular resection of the posterior mitral valve leaflet to treat bileaflet prolapse (group I, n = 20) or isolated posterior leaflet prolapse (group II, n = 20). Echocardiographic characteristics were compared before and after the procedure. There were no differences in the left ventricular end-diastolic or end-systolic dimensions or function between the 2 groups. However, anterior leaflet length was greater in patients with bileaflet prolapse (3.3 +/- 0.6 cm vs 2.6 +/- 0.4 cm, p = 0.003). In group I, posterior leaflet repair changed anterior leaflet displacement from -0.8 +/- 0.2 to 0.5 +/- 0.4 cm (p <0.001) and posterior leaflet displacement from -0.8 +/- 0.3 cm below to 0.5 +/- 0.4 cm (p <0.001) in front of the mitral annular plane. In group II, anterior leaflet displacement was unchanged from 0.2 +/- 0.1 to 0.3 +/- 0.2 cm (p = 0.22), whereas posterior leaflet displacement changed from -0.7 +/- 0.2 to 0.4 +/- 0.2 cm (p <0.001). Thus, patients with bileaflet prolapse and no ruptured chords have excessive anterior leaflet length. In such patients, posterior leaflet repair alone corrects anterior and posterior leaflet prolapse.

Cardiopulmonary bypass as an adjunct to pulmonary surgery.

Although performance of concomitant open heart and pulmonary operations has been described, there is general reluctance to perform pulmonary procedures in patients receiving cardiopulmonary bypass (CPB). Reasons for this include fear of excess bleeding caused by systemic heparinization, limited exposure afforded by median sternolomy, and alterations in the immune system caused by CPB that might lead to dissemination of lung cancer or infection. We have used CPB to facilitate operations on the lung in four patients who did not require concomitant cardiac surgery. In each case, lesions involving central pulmonary vessels precluded safe operation by conventional techniques. There were no complications related to the use of CPB. We believe that CPB can be a valuable adjunct in the surgical treatment of selected tumors and vascular malformations that involve large or central pulmonary vessels.

Temporary leukocyte depletion reduces ventricular dysfunction during prolonged postischemic reperfusion.

Leukocyte depletion improves early postischemic ventricular performance in neonatal models of global myocardial ischemia. However, the rate of leukocyte reaccumulation after cardiopulmonary bypass and its subsequent impact on myocardial function is not known. This laboratory study examined the effect of leukocyte depletion on myocardial performance during the initial 6-hour period after bypass in an in situ, in vivo porcine model of neonatal cardiac surgery. Fifteen 3- to 5-day-old piglets (eight control and seven leukocyte depleted animals) were instrumented by placement of left ventricular short-axis sonomicrometry crystals and an intraventricular micromanometer catheter. Mechanical leukocyte depletion was achieved with Pall RC100 filters (Pall Biomedical, Inc., Fajardo, Puerto Rico) in the cardiopulmonary bypass circuit. Neonatal hearts were subjected to 90 minutes of hypothermic ischemia after a single dose of cold crystalloid cardioplegia. Two control animals died after the operation and were excluded from data analysis. Leukocyte filtration reduced the granulocyte count during initial myocardial reperfusion to 0.8% of control values. However, circulating granulocyte counts increased in leukocyte depleted animals throughout the postoperative period, reaching 68% of control values by 6 hours. Despite this rapid return of circulating granulocytes, animals subjected to leukocyte depletion had significantly better preservation of left ventricular performance (measured by preload recruitable stroke work, p < or = 0.02), left ventricular systolic function (measured by end-systolic pressure-volume relationship, p < or = 0.05), and ventricular compliance (p < or = 0.04) during the experiment. These changes in ventricular function were associated with a significant increase in left ventricular water content (p < or = 0.02) and tissue myeloperoxidase activity (p < or = 0.005) in control animals compared with leukocyte depleted animals. This study demonstrates that leukocyte depletion during initial reperfusion results in sustained improvement in postischemic left ventricular function despite the rapid return of granulocytes to the circulation.

Cardiopulmonary bypass and the blood-brain barrier. An experimental study.

The diffuse inflammation produced by cardiopulmonary bypass might disrupt the blood-brain barrier and lead to the transient neurologic dysfunction occasionally seen after cardiac operations. To evaluate this possibility, blood-brain barrier integrity was measured by carbon 14-aminoisobutyric acid tracer technique after 2 hours of cardiopulmonary bypass in piglets. Six animals were cooled to 28 degrees C on cardiopulmonary bypass and then rewarmed to 38 degrees C before carbon 14-aminosisobutyric acid was injected intraarterially. A control group of six animals underwent median sternotomy and heparinization but were not placed on cardiopulmonary bypass. Blood-to-brain transfer coefficients for carbon 14-aminosisobutyric acid were calculated for multiple brain regions; higher coefficients reflect greater flux of carbon 14-aminosisobutyric acid and suggest loss of blood-brain barrier integrity. The brain regions examined and their transfer coefficients (cardiopulmonary bypass versus control mean +/- standard error of the mean ml/gm/min) were middle cerebral artery territory cortex (0.0032 +/- 0.0002 versus 0.0030 +/- 0.0002; p = 0.42), diencephalon (0.0031 +/- 0.0003 versus 0.0029 +/- 0.0002; p = 0.50), midbrain (0.0028 +/- 0.0002 versus 0.0027 +/- 0.0002; p = 0.86), cerebellum (0.0036 +/- 0.0003 versus 0.0029 +/- 0.0002; p = 0.22), and spinal cord (0.0035 +/- 0.0003 versus 0.0041 +/- 0.0008; p = 0.48). There were no significant differences in transfer coefficients between animals placed on cardiopulmonary bypass and control animals in any brain region examined. The pituitary gland lacks a blood-brain barrier and had a correspondingly high coefficient in control animals and those undergoing cardiopulmonary bypass (0.077 +/- 0.012 versus 0.048 +/- 0.008; p = 0.07). Two hours of moderately hypothermic cardiopulmonary bypass does not disrupt the blood-brain barrier.

Is repair preferable to replacement for ischemic mitral regurgitation?

OBJECTIVE: This study was undertaken to compare mitral valve repair and replacement as treatments for ischemic mitral regurgitation. METHODS: From 1985 through 1997, a total of 482 patients with ischemic mitral regurgitation underwent either valve repair (n = 397) or valve replacement (n = 85). Patients more likely (P < or =.01) to undergo repair had functional mitral regurgitation or coronary revascularization with an internal thoracic artery graft; those more likely to receive valve replacement were in higher New York Heart Association functional classes or underwent emergency operations. These factors were used for multivariable propensity matching. Risk factors for early and late death were identified by multivariable, multiphase hazard function analysis. RESULTS: Within the propensity-matched better-risk group, survivals after valve replacement were 81%, 56%, and 36% at 30 days, 1 year, and 5 years, but survivals after repair were 94%, 82%, and 58% at these intervals (P =.08). In contrast, within the poor-risk group, survivals after repair and replacement were similar (P =.4). Risk factors (P < or =.01) included older age, higher functional class, greater wall motion abnormality, and renal dysfunction. Approximately 70% of patients were predicted to benefit from repair; the benefit lessened or was negated if an internal thoracic artery graft was not used, if a lateral wall motion abnormality was present, or if the mitral regurgitation jet pattern was complex. Freedom from repair failure at 5 years was 91%. CONCLUSION: Late survival is poor after surgery for ischemic mitral regurgitation. Most patients with ischemic mitral regurgitation benefit from mitral valve repair. In the most complex, high-risk settings, survivals after repair and replacement are similar.

Mitral valve operation in patients with the Marfan syndrome.

Optimal surgical treatment of mitral regurgitation in the Marfan syndrome (valve repair versus replacement) is controversial because the underlying connective tissue defect theoretically might compromise repair durability. To examine the results of mitral valve repair in these patients, we did a retrospective review of 160 patients with the Marfan syndrome who had cardiac surgical procedures between January 1983 and January 1993. Thirty-six patients had mitral procedures, 29 of which were repairs. Mitral valve replacement was necessary in seven patients because of extensive annular calcification and/or severe anterior leaflet abnormalities. The 18 men and 11 women undergoing mitral valve repair had a mean age of 26.5 +/- 2.6 years (range 9 months to 54 years); seven patients were less than 18 years of age. Twenty-four of the 29 patients had concomitant aortic root replacement because of aortic dilation or valvular insufficiency. All 29 repairs included annuloplasty, and 11 patients also required leaflet resection. There were no operative deaths. At mean follow-up of 26.6 +/- 4.8 months, there have been three late deaths, two caused by arrhythmia and one by complications of type III aortic dissection. All survivors are in New York Heart Association class I or II. In three patients recurrent mitral regurgitation developed (grade III or IV); 5-year actuarial freedom from significant mitral regurgitation was 88.3%. One patient required repeat mitral annuloplasty after endocarditis of the composite aortic graft spread to the mitral valve. No patient required late mitral valve replacement. These results demonstrate that (1) 22% of patients with the Marfan syndrome who undergo cardiac operation require a mitral valve procedure, (2) most can be treated by mitral repair rather than replacement, and (3) at early follow-up, results of mitral repair in this population are satisfactory.

Dissection of the ascending aorta after previous cardiac surgery: differences in presentation and management.

OBJECTIVE: This study was undertaken to determine the impact of previous cardiac surgery on the presentation, management, and outcome of late dissection of the ascending aorta. PATIENTS AND METHODS: From 1976 to 1998, type A dissection developed in 56 patients with a history of previous cardiac surgery. Interval from first operation to type A dissection was 49 +/- 47 months (0.3-180 months). Previous operations were coronary artery bypass grafting (n = 40), aortic valve replacement (n = 8), and other (n = 8). RESULTS: Type A dissection was acute in 34 patients and chronic in 22. In acute dissection, aortic insufficiency occurred in 50%, malperfusion in 12%, and rupture in 18%; 2 patients (6%) were in hemodynamically unstable condition because of rupture. Of patients with previous coronary bypass grafting, 98% had preoperative coronary angiography. Type A dissection was treated by supracoronary tube graft (84%), Bentall procedure (14%), or local repair (2%). Strategies for managing previous coronary bypass grafting included reimplantation of proximal anastomoses with a button of native aorta (29 patients), interposition graft to pre-existing saphenous vein grafts (9 patients), and new saphenous vein grafts (20 patients). Eight hospital deaths occurred (14%). CONCLUSIONS: We conclude that (1) patients having type A dissection late after cardiac surgery infrequently have cardiac tamponade and hemodynamic collapse; (2) patients with previous coronary bypass grafting require coronary angiography, because operative management must account for pre-existing coronary artery disease; and (3) operative mortality is low, and this may be attributable to preoperative hemodynamic stability, delineation of coronary anatomy in those with previous coronary bypass grafting, and operative treatment of coronary artery disease.

The atherosclerotic aorta at aortic valve replacement: surgical strategies and results.

BACKGROUND: Aortic valve replacement in patients with severe atherosclerosis of the ascending aorta poses technical challenges. The purpose of this study was to examine operative strategies and results of aortic valve replacement in patients with a severely atherosclerotic ascending aorta that could not be safely crossclamped. PATIENTS AND METHODS: From January 1990 to December 1998, 4983 patients had aortic valve surgery; of these, 62 (1.2%) patients had a severely atherosclerotic ascending aorta and required hypothermic circulatory arrest to facilitate aortic valve replacement. They form the study group. RESULTS: All patients had hypothermic circulatory arrest, but several different strategies were used to manage the ascending aorta. These techniques included aortic valve replacement with the use of hypothermic circulatory arrest (39%), ascending aortic endarterectomy (26%), ascending aortic replacement (19%), aortic inspection and crossclamping during hypothermic circulatory arrest (10%), and balloon occlusion of the ascending aorta (6%). Duration of hypothermic circulatory arrest was substantially longer for patients having aortic valve replacement with hypothermic circulatory arrest than for all other strategies. Hospital mortality was 14%, and 10% of patients had strokes. Increasing New York Heart Association functional class and impaired left ventricular function were risk factors for hospital mortality. Choice of operative technique did not influence patient outcome; however, no patient who underwent replacement of the ascending aorta had a stroke. CONCLUSIONS: Aortic valve replacement in patients with severe atherosclerosis of the ascending aorta is associated with increased operative morbidity and mortality. Complete aortic valve replacement during hypothermic circulatory arrest, the "no-touch" technique, requires a prolonged period of circulatory arrest. Ascending aortic replacement is a preferred technique, as it requires a short period of hypothermic circulatory arrest and results in comparable mortality with a low risk of stroke.

Reoperation for failure of mitral valve repair.

BACKGROUND AND OBJECTIVE: Mitral valve repair is the procedure of choice to correct mitral regurgitation of all types. Up to 10% of patients who undergo mitral valvuloplasty require late reoperation for recurrent mitral valve dysfunction. To determine the causes of failed mitral valve repair, we examined the surgical pathology of patients who underwent reoperation for failed mitral valve repair. PATIENTS AND RESULTS: From 1986 to 1994, 81 patients had 86 reoperations for recurrent mitral regurgitation after mitral valve repair. Mean age was 59.2 +/- 1.4 years; 55 were men. Primary valve disease was degenerative in 48 patients (59%), rheumatic in 16 (20%), ischemic in 13 (16%), endocarditic in 3 (4%), and congenital in 1 (1%). Mean time interval between initial mitral valve repair and reoperation was 15.6 +/- 2.5 months. Causes of repair failure were procedure-related (50 cases, 58%), valve-related (33 cases, 38%), or unknown (3 cases, 3%). Procedure-related valve failure was caused by suture dehiscence (21 cases), rupture of previously shortened chordae (19 cases), or incomplete initial correction (10 cases). Valve-related repair failure was caused by progressive primary valve disease (27 cases), endocarditis (5 cases), or extensive leaflet retraction (1 case). Repair failure was procedure-related in 70% of patients with degenerative valvular disease versus only 13% of patients with rheumatic valvular disease (p = 0.0001). At reoperation, mitral valve replacement was performed in 64 patients (79%) and repeat mitral valve repair in 17 (21%). CONCLUSION: We conclude that (1) most mitral valve repair failures are procedure-related in degenerative disease and valve-related in rheumatic disease; (2) rupture of previously shortened chordae is a common cause of late failure in patients with degenerative mitral valve disease; and (3) repeat mitral valve repair results in successful treatment for a minority of patients.

Glutamate excitotoxicity: a mechanism of neurologic injury associated with hypothermic circulatory arrest.

Glutamate, the major central nervous system neurotransmitter, may have potent neurotoxic activity under conditions of metabolic stress. By receptor autoradiography, we have demonstrated that brain regions most vulnerable to injury during prolonged hypothermic circulatory arrest have the highest density of glutamate receptors. To test the hypothesis that such injury could be mediated by glutamate excitotoxicity, we used dizocilpine (MK-801), a selective N-methyl-D-aspartate-glutamate receptor antagonist in a canine survival model of hypothermic circulatory arrest. Eighteen male dogs (20 to 25 kg) were supported by closed-chest cardiopulmonary bypass, subjected to 2 hours of hypothermic circulatory arrest at 18 degrees C, and rewarmed on cardiopulmonary bypass. All were mechanically ventilated and monitored for 20 hours before extubation and survived for 3 days. Group A dogs (n = 9) received a prearrest intravenous bolus of dizocilpine (0.75 mg/kg) followed by continuous infusion (75 micrograms/kg per hour), resulting in electroencephalographic silence. Dizocilpine was weaned before extubation. Group B dogs received vehicle only. According to a species-specific behavior scale that yielded a neurologic deficit score ranging from 0 (normal) to 500 (brain dead), all animals were neurologically assessed every 12 hours. After the dogs were killed at 72 hours, brains were examined by receptor autoradiography and histologically for patterns of selective neuronal necrosis; they were scored blindly from 0 (normal) to 100 (severe injury). Group A dogs had better neurologic function than group B (neurologic deficit score 21 +/- 15 versus 192 +/- 40, p < 0.001) and had less neuronal injury (7.3 +/- 3 versus 48.3 +/- 9, p < 0.0001). Densitometric receptor autoradiography revealed preservation of neuronal N-methyl-D-aspartate-glutamate receptor expression in group A only. These results represent the first direct evidence of a role for glutamate excitotoxicity in the development of hypothermic circulatory arrest-induced brain injury and suggest that selective glutamate receptor antagonists may have a neuroprotective capacity in prolonged periods of hypothermic circulatory arrest.

Durability of mitral valve repair for degenerative disease.

BACKGROUND: Degenerative mitral valve disease is the most common cause of mitral regurgitation in the United States. Mitral valve repair is applicable in the majority of these patients and has become the procedure of choice. OBJECTIVE: This study was undertaken to identify factors influencing the durability of mitral valve repair. PATIENTS AND METHODS: Between 1985 and 1997, 1072 patients underwent primary isolated mitral valve repair for valvular regurgitation caused by degenerative disease. Repair durability was assessed by multivariable risk factor analysis of reoperation. It was supplemented by a search for valve-related risk factors for death before reoperation. Three hospital deaths occurred (0.3%); complete follow-up (4152 patient-years) was available in 1062 of 1069 hospital survivors (99.3%). RESULTS: At 10 years, freedom from reoperation was 93%. Among 30 patients who required reoperation for late mitral valve dysfunction, the repair failed in 16 (53%) as a result of progressive degenerative disease. Durability of repair was adversely affected by pathologic conditions other than posterior leaflet prolapse, use of chordal shortening, annuloplasty alone, and posterior leaflet resection without annuloplasty. Durability was greatest after quadrangular resection and annuloplasty for posterior leaflet prolapse and was enhanced by the use of intraoperative echocardiography. Death before reoperation was increased in patients having isolated anterior leaflet prolapse or valvular calcification and by use of chordal shortening or annuloplasty alone. CONCLUSIONS: Repair durability is greatest in patients with isolated posterior leaflet prolapse who have posterior leaflet resection and annuloplasty. Chordal shortening, annuloplasty alone, and leaflet resection without annuloplasty jeopardize late results.

Aortic root replacement. Risk factor analysis of a seventeen-year experience with 270 patients.

Between September 1976 and September 1993, 270 patients underwent aortic root replacement at our institution. Two hundred fifty-two patients underwent a Bentall composite graft repair and 18 patients received a cryopreserved homograft aortic root. One hundred eighty-seven patients had a Marfan aneurysm of the ascending aorta (41 with dissection) and 53 patients had an aneurysm resulting from nonspecific medial degeneration (17 with dissection). These 240 patients were considered to have annuloaortic ectasia. Thirty patients were operated on for miscellaneous lesions of the aortic root. Thirty-day mortality for the overall series of 270 patients was 4.8% (13/270). There was no 30-day mortality among 182 patients undergoing elective root replacement for annuloaortic ectasia without dissection. Thirty-six of the 270 patients having root replacement also had mitral valve operations. There was no hospital mortality for aortic root replacement in these 36 patients, but there were seven late deaths. Twenty-two patients received a cryopreserved homograft aortic root; 18 of these were primary root replacements and four were repeat root replacements for late endocarditis. One early death and two late deaths occurred in this group. Actuarial survival for the overall group of 270 patients was 73% at 10 years. In a multivariate analysis, only poor New Year Heart Association class (III and IV), non-Marfan status, preoperative dissection, and male gender emerged as significant predictors of early or late death. Endocarditis was the most common late complication (14 of 256 hospital survivors) and was optimally treated by root replacement with a cryopreserved aortic homograft. Late problems with the part of the aorta not operated on occur with moderate frequency; careful follow-up of the distal aorta is critical to long-term survival.

Neutrophil adhesion inhibition prolongs survival of cardiac allografts with hyperacute rejection.

Hyperacute rejection results in rapid destruction of a cardiac allograft and is characterized by infiltration of neutrophils into the donor organ. We sought to ameliorate this response by using a potent inhibitor of neutrophil adhesion to vascular endothelium, NPC 15669 (N-[9H-(2,7-dimethylfluorenyl-9-methoxy) carbonyl]-L-leucine) and determine its effect on long-term graft survival and histology. This compound specifically prevents recruitment of neutrophils at inflammatory foci by inhibiting upregulation of the CD11b/CD18 adhesion molecule located on the neutrophil surface. Lewis rats were presensitized by three serial ACI rat skin grafts placed 10 days apart. ACI rat hearts were heterotopically transplanted into Lewis recipients 10 to 14 days after the final skin graft. Group I (n = 15) was treated with a 10 mg/kg intravenous bolus of NPC 15669 before reperfusion, followed by 3 mg/kg over 30 minutes. Group II (n = 13) was given saline vehicle intravenously. Two allografts in each group were harvested at 5, 15, 30, and 60 minutes, and the remainder were followed to cessation of graft function. Early 5- to 60-minute allograft histologic findings revealed focal interstitial hemorrhage, edema, and contraction-band necrosis associated with neutrophil infiltration in group II. Group I had significant reduction of all parameters at the earliest time points. Graft survival was significantly increased in group I, 89.2 +/- 20.3 hours (mean +/- SD) compared to 27 +/- 17 hours in group II (p < 0.0001). End-stage rejection was characterized by extensive neutrophil infiltrate and hemorrhage in group II; group I grafts had a predominantly mononuclear cell infiltrate with rare neutrophils.(ABSTRACT TRUNCATED AT 250 WORDS)

Vitamin K reduces bleeding in left ventricular assist device recipients.

BACKGROUND: Despite advances in left ventricular assist device (LVAD) design that permit support without anticoagulation, LVAD recipients often suffer profound bleeding complications. This bleeding diathesis may be attributable to pre-operative right-ventricular failure with concomitant hepatic dysfunction. The purpose of this study was to characterize coagulation abnormalities in LVAD recipients and determine the impact of pre-operative vitamin K administration on the incidence of postoperative bleeding. METHODS: Hemostatic and liver function profiles were obtained in 66 recipients of the Heartmate LVAD; 39 of these patients received perioperative vitamin K. RESULTS: During LVAD support, hepatic synthetic function improved as evidenced by increases in clotting factors II, V, VII, XI. There was ongoing fibrinolysis with elevation of fibrinopeptide A and D-dimers and diminution of fibrinogen; however, plasminogen levels did not decline suggesting that systemic disseminated intravascular coagulation (DIC) did not occur. Bleeding requiring re-exploration more than 48 hours postimplantation occurred in 9 of 66 patients (13.6%). Prior to implantation, patients that bled had decreased levels of factor II (52.2 +/- 27.1% vs 69.7 +/- 26.6%; p = 0.048) and prolonged prothrombin times (16.5 +/- 2.4 seconds vs 13.8 +/- 3.1 seconds; p = 0.005) compared to patients that did not bleed. Seven of 27 patients (25.9%) not treated with vitamin K bled, while only 2 of 39 (5.1%) patients treated with vitamin K required re-exploration for bleeding (p = 0.026). CONCLUSIONS: We conclude that: (1) Liver synthetic function improves during LVAD support resulting in increased levels of circulating coagulation factors; (2) ongoing fibrinolysis occurs but likely only represents remodeling of fibrin on the LVAD surface; (3) perioperative vitamin K reduces nonsurgical bleeding in LVAD recipients.

Aortic dissection in a cardiac allograft recipient: a case report.

Ascending aortic dissection is rare in cardiac allograft recipients. Only two patients with dissection arising from the native aorta have been reported previously and, unfortunately, the diagnosis was made postmortem in each instance. We report the first case of successful surgical treatment of aortic dissection confined to the donor aorta in a recipient of an orthotopic cardiac allograft.