Double valve endocarditis.

BACKGROUND: There are little data concerning surgical outcomes in patients with native valve endocarditis affecting both the aortic and mitral valves. METHODS: From 1977 to 1998, 54 patients had simultaneous aortic and mitral valve grafting for native valve endocarditis. In 78%, mitral valve involvement was limited to the anterior leaflet, suggesting a jet lesion from the aortic valve. Surgical strategies included 31 valve repairs and valve replacement with mechanical (34), bioprosthetic (34), or allograft (9) prostheses. Three hundred twenty-five patient-years of follow-up were available for analysis (mean 6.0 +/- 4.8 years). RESULTS: There were no hospital deaths. Ten-year survival was 73%. Ten-year freedom from recurrent endocarditis was 84%, with risk peaking at 3 months, followed by a constant risk of 1.3%/yr. Choice of valvar procedure did not influence mortality or reinfection risk. CONCLUSIONS: The most common pattern of double valve infection was a jet lesion on the anterior mitral leaflet. Surgical treatment has late survival and freedom from reinfection similar to those of patients with single heart valve infection.

Off-pump reoperative coronary artery bypass grafting by thoracotomy: patient selection and operative technique.

BACKGROUND: Reoperative coronary artery bypass grafting (CABG) in patients with contraindications to sternotomy or cardiopulmonary bypass (CPB) presents a technical challenge. In this study we reviewed patient selection, operative technique, and early results in patients having redo-CABG to the circumflex artery system by a thoracotomy without CPB. METHODS: From January 1996 through December 1999, 21 patients with contraindications to conventional redo-CABG had target vessel revascularization off-pump by thoracotomy. A posterolateral thoracotomy approach was used. RESULTS: No patient required sternotomy or CPB. There was no hospital mortality. Postoperative cardiac morbidity included non-Q wave myocardial infarction (5%), need for intraaortic balloon pump support postoperatively (5%), and atrial fibrillation (5%). Two grafts were studied early and two were studied late (more than 6 months later). One venous graft was found to be occluded early. Survival at 2 years was 95%. Ninety percent of surviving patients were in New York Heart Association functional class I or II. CONCLUSIONS: This approach was associated with no mortality, low morbidity, and favorable early symptomatic improvement. This is the approach of choice in cases of reoperative CABG to the circumflex system when resternotomy or CPB are undesirable, and the culprit coronary vessels are accessible through a thoracotomy.

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.

Long-term effectiveness of operations for ascending aortic dissections.

OBJECTIVE: To evaluate long-term effectiveness of a strategy for managing the aortic root and distal aorta according to the pathology in ascending aortic dissection. METHODS: From 1978 to 1995, 208 patients underwent operations for acute (n = 135) and chronic (n = 73) ascending aortic dissection. Surgical strategies included valve resuspension with supracoronary aortic root repair and ascending aortic graft for normal sinuses and valve (n = 135), composite valve and ascending aortic graft for abnormal sinuses and valve (n = 47), and valve replacement and supracoronary ascending aortic graft for normal sinuses and abnormal valve (n = 26). Resection extended into the arch only if the intimal tear originated in or extended to the aortic arch (n = 31). RESULTS: Hospital mortality was 14%. Cardiogenic shock (P =.002) and concomitant coronary artery bypass grafting (P =.001) were associated with increased risk; use of circulatory arrest (P =.0003) decreased risk. Survival was 87%, 68%, and 52% at 30 days, 5 years, and 10 years, respectively. Advanced age, earlier date of operation, composite graft, and arch resection were associated with decreased survival; residual distal dissected aorta was not. Reoperation was required for 5 proximal and 8 distal problems. CONCLUSIONS: In both acute and chronic ascending aortic dissections, (1) circulatory arrest is associated with low early mortality; (2) with normal sinuses and valve, supracoronary repair of the dissected aortic root and valve resuspension is effective long term; and (3) residual distal dissected aorta does not decrease late survival and has a low risk of aneurysmal change and reoperation for at least 10 years.

Is anterior leaflet repair always necessary in repair of bileaflet mitral valve prolapse?

BACKGROUND: Traditionally, bileaflet prolapse has been treated by posterior leaflet resection combined with one of a number of procedures designed to support the anterior leaflet. However, most patients with bileaflet prolapse do not have important anterior chordal pathology. This study was undertaken to evaluate the effectiveness of a strategy of posterior leaflet resection and annuloplasty alone for patients with bileaflet prolapse and no anterior chordal rupture or severe anterior chordal elongation. METHODS: From 1993 to 1997, 93 patients with transesophageal echocardiography (TEE) demonstrated bileaflet prolapse and without anterior chordal rupture or important anterior chordal elongation had primary isolated mitral valve repair consisting only of posterior leaflet resection (quadrangular in 28 and sliding in 65) and annuloplasty (Cosgrove-Edwards in 83, pericardial in 9, and Carpentier-Edwards in 1). All patients had severe mitral regurgitation documented by intraoperative TEE. Mean age was 55+/-13 years; 60% were men. RESULTS: Postrepair, mitral regurgitation was 0 to trace in 93% and 1+ in 7%. There were no operative deaths. Late follow-up was available in all patients, with 277 patient-years of follow-up available for analysis. Five-year actuarial survival was 95%. At a mean interval of 2.3+/-1.3 (SD) years, echocardiography demonstrated no or trace mitral regurgitation in 65%, 1+ in 28%, and 2+ in 7%. No correlates of late mitral regurgitation were identified by multivariable analysis. No patient has required reoperation. CONCLUSIONS: In the absence of significant anterior chordal pathology, a strategy of posterior leaflet resection and annuloplasty corrects anterior leaflet prolapse and mitral regurgitation, and provides a durable repair without the necessity of additional procedures on the anterior leaflet.

Intra-arterial thrombolysis for perioperative stroke after open heart surgery.

Recent major surgery is an exclusion criterion for thrombolysis. Six patients with acute ischemic stroke underwent intra-arterial thrombolysis after recent open heart surgery without clinically significant bleeding complications, although one patient developed a small, asymptomatic cerebellar hemorrhage. Intra-arterial thrombolysis may be an option for patients with cerebral embolism in the perioperative period.

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.

Minimally invasive valve operations.

BACKGROUND: To reduce the morbidity from valvular heart operations, a right parasternal approach was introduced. We report our initial experience with the procedure. METHODS: From January 1996 through July 1996, 115 patients underwent primary isolated valve procedures. One hundred (85%) patients underwent the operation through a right parasternal incision. RESULTS: There was one hospital death secondary to a stroke on the fifth postoperative day. Three patients (two with aortic valve operations and one having a mitral valve procedure) required conversion to sternotomy. Mean aortic occlusion time was 71 minutes; mean cardiopulmonary bypass time was 93 minutes. Mean stay in the intensive care unit was 27 hours and mean hospital postoperative stay was 5.7 days. Seventy-seven percent of the patients did not receive blood transfusions. Comparison with median sternotomy demonstrated a reduction in both postoperative length of stay and direct hospital costs. CONCLUSIONS: We conclude that this minimally invasive approach is safe for a variety of valve procedures and is effective in reducing surgical trauma and cost.

Long-term results of the Carpentier-Edwards pericardial aortic valve: a 12-year follow-up.

BACKGROUND: Pericardial valves have excellent hemodynamic function; however, long-term durability is questionable. To determine the function of the Carpentier-Edwards pericardial valve in the aortic position, the results of 310 aortic valve replacements performed between 1982 and 1985 were analyzed. Mean age was 64.2+/-10.8 years (range, 22 to 95 years); 190 (61.3%) were men. Isolated valve replacement was performed in 135 patients (43.5%). There were 18 hospital deaths (5.8%), none of them valve related. METHODS: Follow-up of 292 survivors was 100% complete at a mean of 8.8 years; 2,556 patient-years of follow-up were analyzed. There were 150 late deaths (51.4%). Survival at 5, 10, and 12 years were 83%+/-2%, 47%+/-3%, and 34%+/-3%, respectively. The 12-year actuarial and actual freedom from thromboembolism was 87%+/-2% and 89%+/-2%, respectively. Freedom from hemorrhage was 91%+/-2% and 92%+/-2%; freedom from endocarditis was 93%+/-2% and 95% +/- 1%; and freedom from structural deterioration was 82%+/-4% and 91%+/-2%, respectively. RESULTS: Actuarial freedom from structural deterioration at 12 years was considerably higher for 153 hospital survivors 65 years or older, 93% (5 explants) compared to 76% (19 explants) for patients younger than 65 years, p = 0.03. Of 24 explanted valves for structural deterioration, leaflet calcification resulting in stenosis occurred in 20 (83%) and 4 were wear-related leaflet tears. CONCLUSIONS: We conclude that the Carpentier-Edwards pericardial valve has a low incidence of valve-related complications, that structural deterioration is infrequent and results from leaflet calcification, and that the low incidence of structural deterioration in patients 65 years or older makes this an increasingly appropriate option in this age group.

Superficial esophageal carcinoma.

BACKGROUND: The detection of superficial esophageal carcinomas by surveillance endoscopy and the downstaging of advanced carcinomas to superficial carcinomas by induction therapy have increased the number of patients with these carcinomas undergoing resection. The natural history of these carcinomas is not well defined. METHODS: To evaluate the results of surgical resection and identify predictors of improved survival, a retrospective review of (1) patients with superficial esophageal carcinoma at presentation (SECP) and (2) patients with advanced carcinomas that were downstaged to no residual carcinoma or superficial esophageal carcinoma after induction therapy (SECD) was conducted. RESULTS: There were 54 patients with SECP (19 Tis and 35 T1). Survival was significantly better for patients with Tis carcinomas (85.3% at 5 years) and patients with intramucosal T1 carcinomas (79.4%) than for patients with submucosal T1 carcinomas (16.3%) (p = 0.007 and p = 0.045, respectively). Survival at 5 years for the 49 patients without regional lymph node metastases (N0) was 65.2%, whereas none of the 5 patients with regional lymph node metastases (N1) have survived more than 3 years (p = 0.054), and 3 died of recurrent disease. There were 21 patients with SECD (13 T0, 2 Tis, and 6 T1). Survival at 4 years was 58.2%. In this group, survival was not related to depth of tumor invasion (p = 0.76) or regional lymph node status (p = 0.68). CONCLUSIONS: We conclude that (1) patients with Tis and intramucosal T1 SECP have a significantly better survival than those with submucosal T1 SECP, (2) patients with N0 SECP have a significantly better survival than those with N1 SECP, and (3) survival of patients with SECD is not related to depth of tumor invasion or regional lymph node status.

Axillary artery: an alternative site of arterial cannulation for patients with extensive aortic and peripheral vascular disease.

The increasing number of patients with extensive aortic and peripheral vascular atherosclerosis or aneurysms who are undergoing cardiac operations present difficult decisions as to the optimal site of arterial cannulation for cardiopulmonary bypass. Femoral artery cannulation is the most common alternative to ascending aortic cannulation, but severe iliofemoral disease or the danger of atheroemboli caused by retrograde perfusion through an atherosclerotic or aneurysmal descending aorta may make this approach impossible or undesirable. We have used axillary artery cannulation for cardiac operations in 35 patients for indications including severe aortic atherosclerosis (n = 16), extensive aortic aneurysms (n = 11), and aortic dissection (n = 8). The cardiac operations performed were coronary artery bypass grafting (n = 9) aortic valve replacement (n = 1), aortic valve replacement and coronary artery bypass grafting (n = 5), repair of mitral valve periprosthetic leak (n = 1), and resection of ascending and/or aortic arch (n = 19). Deep hypothermia with circulatory arrest was used in 26 patients and retrograde cerebral perfusion in 18. All patients awoke from the operation and no patient had a cerebrovascular accident. One patient required axillary artery thrombectomy and one patient had a mild ipsilateral brachial plexus paresis after the operation. Four patients died in the hospital. We conclude that axillary artery cannulation is a safe and effective means of providing antegrade arterial flow during cardiopulmonary bypass in patients with severe atherosclerotic or aneurysmal disease. This strategy may lower the prevalence of stroke associated with cardiopulmonary bypass in these patients.

High-dose steroids prevent placental dysfunction after fetal cardiac bypass.

Surgical treatment of certain congenital heart lesions in utero may have a therapeutic advantage over postnatal repair or palliation. For fetal heart surgery to be possible, a method to support the fetal circulation is necessary. Early experimental attempts at fetal cardiac bypass were unsuccessful because of increased placental vascular resistance during and after fetal cardiac bypass, which led to decreased placental flow, fetal asphyxia, and death. Our laboratory has demonstrated that the administration of indomethacin (a cyclooxygenase inhibitor) during fetal cardiac bypass prevents this increase in placental vascular resistance during and after fetal cardiac bypass. The specific mechanism by which indomethacin achieves this effect is likely to be either by inhibiting the production of a placental vasoconstrictive prostaglandin or by diverting substrate from the cyclooxygenase pathway to the lipoxygenase pathway, thereby potentially increasing the production of a placental vasodilating leukotriene. To examine these potential mechanisms in more detail, we inhibited both prostaglandin and leukotriene synthesis at the phospholipase stage with high-dose steroids. Fourteen fetal lambs were used in the study. Six animals received indomethacin (3 mg/kg), four received high-dose steroids (Solu-Medrol 50 mg/kg), and four animals were used as controls. Observations were made during a 1-hour prebypass period, a 30-minute bypass period, and a 2-hour postbypass period. Placental blood flow and placental vascular resistance were calculated at four times during the experiments: before sternotomy; after sternotomy; during bypass at 30 minutes; and 30 minutes after cessation of bypass. Similar to indomethacin, high-dose steroid administration during fetal cardiac bypass prevents the rise in placental vascular resistance and preserves placental blood flow during and after fetal cardiac bypass. This study suggests that the production of a placental vasoconstrictive prostaglandin is responsible for the increase in placental vascular resistance and decrease in placental blood flow observed after fetal cardiac bypass.

Halothane as an anesthetic for fetal surgery.

Halothane has become the preferred anesthetic agent during fetal surgery because it can be administered via maternal inhalation and it improves surgical exposure by relaxing the uterus. However, the effects of halothane anesthesia on fetal cardiovascular homeostasis during fetal surgery have not been documented. In 10 pregnant ewes, inhalation halothane anesthesia was administered and their fetuses were instrumented for cardiovascular evaluation. During a 1-hour period we evaluated the acute effects of halothane anesthesia on fetal hemodynamics, arterial blood gases, cardiac output, placental blood flow, total vascular resistance, systemic vascular resistance, and placental vascular resistance. Fetal cardiac output and placental blood flow were determined by the radiolabelled microsphere technique and resistances were calculated using pressure and flow data. These findings were compared to both the results we obtained in 15 fetal sheep anesthetized with the maternal administration of intravenous ketamine, and to the accepted values found in nonanesthetized, chronically instrumented fetal sheep. Our findings indicate that with halothane anesthesia during fetal surgery fetal cardiac output and placental blood flow significantly decrease, and total vascular resistance increases. Placental vascular resistance increases out of proportion to systemic vascular resistance, resulting in the shunting of blood away from the placenta. The combination of decreased cardiac output and increased shunting of blood away from the placenta causes depressed respiratory gas exchange. These findings are not present with other anesthetic agents. Halothane has significant negative effects on both the fetal heart and the peripheral vasculature which disrupt fetal cardiovascular homeostasis. Halothane is a poor anesthetic during fetal intervention.

Prostaglandin synthesis inhibition prevents placental dysfunction after fetal cardiac bypass.

Surgical therapy of certain congenital heart lesions in utero may have advantages over postnatal repair or palliation. For fetal heart operations to be done, it will be necessary to devise a method of fetal cardiac bypass. Previous studies in which standard cardiopulmonary bypass techniques were used have reported fetal death resulting from increased placental vascular resistance, which causes decreased placental blood flow and depressed respiratory gas exchange. The mechanism responsible for this increase in placental vascular resistance has remained unknown. In a series of 10 fetal cardiac bypass experiments we examined the role of prostaglandins as the mediators of this response. Observations were made during a 1-hour prebypass period, a 30-minute bypass period, and a 2-hour postbypass period. The cardiac bypass circuit consisted of a centrifugal pump, and bypass flows were adjusted to equal a normal fetal cardiac output of 400 ml/min/kg. In six of the experiments indomethacin (3 mg/100 ml) was added to the pump priming to block prostaglandin synthesis. By means of the microsphere technique, fetal cardiac output, placental blood flow, individual organ blood flow, and placental vascular resistance were determined at five times during the experiments: presternotomy, poststernotomy, during cardiac bypass, at 5 minutes after cessation of bypass, and 30 minutes after cessation of bypass. Fetal arterial blood gas measurements were made every 15 to 30 minutes. When indomethacin was used to inhibit prostaglandin synthesis, placental vascular resistance did not increase, placental blood flow did not decrease, and fetal blood gases remained at normal prebypass levels during and after fetal cardiac bypass. We propose that production of vasoactive prostaglandins is responsible for the increased placental vascular resistance and decreased placental blood flow observed after fetal cardiac bypass. An understanding of the mechanism responsible for the increased placental vascular resistance seen after fetal cardiac bypass will be an important first step before clinical application.

cea-kil operon of the ColE1 plasmid.

We isolated a series of Tn5 transposon insertion mutants and chemically induced mutants with mutations in the region of the ColE1 plasmid that includes the cea (colicin) and imm (immunity) genes. Bacterial cells harboring each of the mutant plasmids were tested for their response to the colicin-inducing agent mitomycin C. All insertion mutations within the cea gene failed to bring about cell killing after mitomycin C treatment. A cea- amber mutation exerted a polar effect on killing by mitomycin C. Two insertions beyond the cea gene but within or near the imm gene also prevented the lethal response to mitomycin C. These findings suggest the presence in the ColE1 plasmid of an operon containing the cea and kil genes whose product is needed for mitomycin C-induced lethality. Bacteria carrying ColE1 plasmids with Tn5 inserted within the cea gene produced serologically cross-reacting fragments of the colicin E1 molecule, the lengths of which were proportional to the distance between the insertion and the promoter end of the cea gene.

Alternative forms of lethality in mitomycin C-induced bacteria carrying ColE1 plasmids.

We have studied the physiological effects of mitomycin C induction on cells carrying ColE1 plasmids with differing configurations of three genes: the structural gene coding for colicin (cea), a gene responsible for mitomycin C lethality (kil) that we located as part of an operon with cea, and the immunity (imm) gene, which lies near cea but is not in the same operon. kil is close to or overlaps imm. When cea(+) plasmids are present mitomycin C induction results in 100-fold or greater increases in the level of colicin. Within an hour after induction more than 90% of cells carrying cea(+)kil(+) plasmids are killed and macromolecular synthesis stops, capacity for transport of proline, thiomethyl beta-D-galactoside, and alpha-methyl glucoside is lost, and the membrane becomes abnormally permeable as indicated by an increased accessibility of intracellular beta-galactosidase to the substrate o-nitrophenyl beta-D-galactoside. All of these events occur when a cea(-)kil(+)imm(+) plasmid is present and none does when the plasmid is cea(+)kil(-)imm(+), so the damage can be attributed solely to the Kil function and not to the presence of colicin. However, cells carrying a cea(+)kil(-)imm(-) plasmid are killed upon induction, apparently by action of endogenous colicin on the nonimmune cytoplasmic membrane. The pattern of accompanying physiological damage is distinguished from the kil(+)-associated damage by an enhancement of alpha-methyl glucoside uptake and accumulation and efflux of alpha-methyl glucoside 6-phosphate and by an absence of the alteration in membrane permeability for o-nitrophenyl beta-D-galactoside. These features are typical of colicin E1 action on the membrane. The induced damage is not prevented by trypsin and occurs in cells of a strain specifically tolerant to exogenous colicin E1, indicating that the attack is from inside the cell.