Mitral valve repair for bacterial endocarditis.

Twenty-two patients with mitral insufficiency resulting from native valve endocarditis underwent mitral valve repair. Six patients had acute endocarditis with positive blood cultures and active valve infection. Sixteen patients were cured of active infection, but mitral insufficiency developed as a result of prior infection. Mean age was 48.5 +/- 21.7 years; 13 (59%) were male. Mean New York Heart Association functional class was 2.6 +/- 1.2. Multiple valve lesions were present in 11 (50%) patients. Valve abnormalities included leaflet perforation in 13 patients, chordal rupture or elongation in 14, vegetations in 5; and annular abscess in 1. In patients with acute endocarditis all macroscopically infected tissue was excised. Multiple techniques were required to achieve valve competence. Suture or patch closure of perforation was done in 14 patients, chordal shortening or transfer in 9, leaflet resection and closure in 4, leaflet resection with pericardial patching in 5, and annuloplasty in 15. Mitral valvuloplasty was combined with other procedures in 11 (50%) patients. There were two (9%) hospital deaths, both occurring in patients with healed endocarditis. There was one (9%) death in a patient undergoing an isolated procedure and one (9%) in a patient undergoing a combined procedure. Mean follow-up was 24 +/- 16.8 months and was complete. Seventeen (85%) were in New York Heart Association functional class I, and three (15%) were in class II. There were no late deaths, reoperations, recurrent endocarditis, thromboembolic events, or other valve-related morbidity. We conclude that mitral valve repair for insufficiency resulting from bacterial endocarditis (1) is possible in acute and healed disease, (2) has a low operative mortality, and (3) has resulted in patients free of recurrent infection and valve-related morbidity and mortality. Mitral valve repair is an attractive alternate to valve replacement in bacterial endocarditis.

Mitral valve repair for ischemic mitral insufficiency.

Over a 5-year period, 1,292 patients had operation on their native mitral valves. Ischemia was the cause of mitral insufficiency in 84 patients (6.5%). Sixty-five patients (77.4%) had mitral valve repair. Mean age was 66 +/- 10 years; 35 patients (53.8%) were women. Mean degree of preoperative insufficiency was 3.2 +/- 0.7; mean preoperative New York Heart Association functional class was 3.3 +/- 0.7. Eleven patients (16.9%) had acute and 54 (83.1%) had chronic mitral insufficiency. Valve prolapse was present in 26 patients (40%). Restrictive leaflet motion secondary to regional or global left ventricular dilatation occurred in 39 patients (60%). All patients had associated myocardial revascularization followed by transatrial valvuloplasty. Multiple techniques were employed to achieve valve competence: leaflet resection (3), chordal shortening (15), papillary muscle reimplantation (10), papillary muscle shortening (3), and annuloplasty (63). There were six (9.2%) hospital deaths (acute, 9.1%; chronic, 9.3% [not significant]; prolapse, 11.5%; restrictive, 7.7% [not significant]). The mean degree of postoperative mitral insufficiency was 0.6 +/- 0.8 in 51 patients. At a mean follow-up of 3.1 +/- 1.6 years, patient survival was 96% for patients with valve prolapse and 48% for those with restrictive leaflet motion (p = 0.02). New York Heart Association functional class was improved in all groups. Ischemic mitral insufficiency is an uncommon cause of mitral valve disease that is amenable to repair in the majority of cases of both acute and chronic onset. The operative mortality is low, and operation is associated with superior survival in patients with valve prolapse.

Valvuloplasty for aortic insufficiency.

Twenty-eight consecutive patients underwent aortic valvuloplasty for aortic insufficiency caused by leaflet prolapse. The technique involved triangular resection of the free edge of the prolapsing leaflet, annular plication at the commissure, and resection of a raphe when present in bicuspid valves. Mean age of the patients was 46.8 +/- 14.4 years. Twenty-six (92.7%) were male. Seventy-five percent of the patients had a bicuspid aortic valve; the remaining valves were tricuspid. The extent of aortic insufficiency was 3.6 +/- 0.8 by aortography, 3.1 +/- 0.1 by preoperative Doppler echocardiography, and 3.4 +/- 0.7 by intraoperative Doppler echocardiography. The amount of aortic insufficiency decreased from 3.4 +/- 0.7 to 0.6 +/- 0.5 intraoperatively, immediately after repair (p less than 0.001). Mean transvalvular gradient by echocardiography was 12.9 +/- 6.8 mmHg. There was one death in a patient who had an intraoperative cerebral vascular accident. Mean follow-up was complete at 6.9 months. One patient had a cerebral vascular accident and one patient required reoperation for recurrent aortic insufficiency caused by partial suture line dehiscence. In 15 patients with late echocardiograms, aortic insufficiency did not progress (0.7 +/- 0.6 in the hospital and 0.8 +/- 0.5 late). Aortic valve repair for aortic cusp prolapse effectively eliminates aortic insufficiency without causing aortic stenosis. At early follow-up the repair has been stable.

Massive bleeding in a Zenker's diverticulum.

Massive bleeding from a pharyngoesophageal diverticulum is a rarely reported condition, with only two reported cases in the literature. This report describes a patient who had massive bleeding due to ulceration in the base of a pharyngoesophageal diverticulum, presumed to have been caused by chronic aspirin ingestion. The diagnosis was made on upper gastrointestinal endoscopy, and surgical treatment (cricopharyngeal myotomy and diverticulectomy) was curative.

Extracorporeal bypass for the treatment of verapamil poisoning.

A 25-month-old boy ingested six sustained-release verapamil tablets, each containing 240 mg of drug. Charcoal and cathartic were given but were never passed per rectum. Third-degree heart block, hypotension, and hypocalcemia were only transiently responsive to calcium infusions, inotropic agents, and epicardial pacing. Cardiopulmonary arrest with electromechanical dissociation ensued. Standard cardiopulmonary bypass was used to allow sufficient time for liver detoxication. Serum levels of verapamil fell during the bypass procedure, and the patient's cardiac status improved. However, continued absorption of drug after bypass resulted in a level of 4 mg/L, unresponsive circulatory failure, and death. Early, aggressive gut decontamination and the potential value of cardiopulmonary bypass procedures in poisoning that lead to cardiac depression are emphasized.

The effects of calcium and magnesium in hyperkalemic cardioplegic solutions on myocardial preservation.

Sustained left ventricular pressure development during each infusion of a cold calcium-containing hyperkalemic cardioplegic solution has been observed in rat hearts. The present study was undertaken to relate such contraction (i.e., increase in resting pressure) to myocardial preservation and to the calcium and magnesium contents of a crystalloid hyperkalemic cardioplegic solution. Isolated perfused rat hearts with a left ventricular isovolumic balloon were arrested at 8 degrees C by the fully oxygenated cardioplegic solution infused every 15 minutes for 2 hours. Cardioplegic solutions containing ionized calcium in concentrations of 0, 0.1, or 1.2 mmol/L were each studied with (groups 2, 4, and 6) and without (groups 1, 3, and 5) the addition of magnesium (16 mmol/L). Hearts arrested by the cardioplegic solution with no calcium or magnesium (group 1) developed a pressure (averaged over the second to eighth infusion and expressed as percent prearrest left ventricular pressure) of 6.0% +/- 0.4% during cardioplegic infusions. This solution maintained end-arrest myocardial adenosine triphosphate (13.1 +/- 1.0 nmol/mg dry weight) and phosphocreatine (21.7 +/- 2.8 nmol/mg dry weight) contents near the prearrest contents and preserved left ventricular function at 95% +/- 3% of prearrest developed left ventricular pressure at 15 minutes of reperfusion at 37 degrees C. Calcium (groups 3 and 5) increased pressure development during cardioplegic infusions (10.4% +/- 0.5% and 15.1% +/- 0.9%), depleted adenosine triphosphate (7.2 +/- 1.0 and 7.4 +/- 0.9) and phosphocreatine (13.3 +/- 1.8 and 10.7 +/- 1.5), and depressed left ventricular functional recovery (71% +/- 1% and 73% +/- 3%). Magnesium alone (group 2) decreased pressure development during cardioplegic infusions (3.0% +/- 0.3%), maintained adenosine triphosphate (15.6 +/- 0.9), augmented phosphocreatine (38.3 +/- 1.2), and preserved left ventricular function (99% +/- 4%). Magnesium added to calcium (groups 4 and 6) prevented the calcium-induced increased pressure development during cardioplegic infusions (4.0% +/- 0.5% and 6.7% +/- 0.6%), maintained adenosine triphosphate (13.6 +/- 1.4 and 14.9 +/- 0.7), augmented phosphocreatine (31.3 +/- 1.6 and 32.2 +/- 2.4), and ameliorated the depression of functional recovery (82% +/- 2% and 86% +/- 2%). These data suggest that left ventricular pressure development during arrest contributed to calcium-induced energy depletion and impairment of functional recovery and that these deleterious effects were inhibited by magnesium. The inhibitory effects of magnesium on left ventricular pressure development were rapidly reversed on reperfusion. The data support the addition

Aortic and mitral valve replacement in idiopathic hypereosinophilic syndrome.

Idiopathic hypereosinophilic syndrome is a rare systemic manifestation of eosinophilia that may cause endocardial fibrosis. Endocardial fibrosis and overlying thrombus typically lead to a restrictive cardiomyopathy and heart failure. Occasionally mitral or tricuspid regurgitation (or both) occurs as a result of the fibrosis and thrombus formation. This report describes a patient with hypereosinophilic syndrome who was seen with an unusually localized form of cardiac involvement that resulted in predominantly aortic and mitral stenosis. This was treated with bivalvular replacement.

Isolated, contained esophagobronchial fistula complicating esophagogastrectomy.

Esophagobronchial fistula as a complication of esophagogastrectomy is rare. We report our experience with a patient who sustained an esophagogastric anastomotic leak with fistulization to the right mainstem bronchus without free rupture into the pleural space.

Calcium-induced ventricular contraction during cardioplegic arrest.

Cardiac arrest induced by hyperkalemic perfusion is generally considered to represent a state of complete electromechanical arrest. However, high-energy phosphate concentrations and ventricular function decrease with increasing cardioplegic calcium concentrations, possibly because of elevated resting muscle tone produced by calcium influx. We examined isolated rat hearts containing an isovolumic intraventricular balloon for the presence of contractile activity during the administration at 10 degrees C of a cardioplegic solution containing potassium, 20 mEq/L. Significant left ventricular pressure was developed (35.6% +/- 4.3% of prearrest systolic pressure) during administration of a solution containing a calcium concentration of 1.0 mmol/L and far less (9.7% +/- 1.6% of prearrest systolic pressure) with a calcium-free cardioplegic solution. The muscle contraction diminished with repeated doses, was increased by increasing cardioplegic calcium content, and was inhibited by magnesium. Adenosine triphosphate and creatine phosphate concentrations were 9.0 +/- 1.4 and 7.0 +/- 0.9 nmol/mg dry weight immediately after infusion of 15 ml of a hypoxic cardioplegic solution containing calcium, versus 13.3 +/- 1.3 (p less than 0.02) and 31.9 +/- 3.5 nmol/mg dry weight (p less than 0.0001) after a hypoxic acalcemic solution was given. When repeated doses of a hypoxic cardioplegic solution containing calcium in a concentration of 1.0 mmol/L were given at 15 minute intervals at 10 degrees C, ischemic contracture (a sustained development of ventricular pressure, mean 51% +/- 4% of prearrest systolic pressure) resulted within 1 hour. Coronary vascular resistance was increased during the muscle contractions induced by calcium-containing solutions, markedly so during contracture. Calcium-related mechanical activity was also observed during hypothermic cardioplegic arrest in five of six isolated isovolumic canine hearts. We conclude that hearts remain potentially active mechanically during cold hyperkalemic arrest and undergo energetically wasteful contraction when stimulated with calcium-containing hyperkalemic cardioplegic solutions.

Oxygenation of cardioplegic solutions. Potential for the calcium paradox.

Oxygenation of crystalloid cardioplegic solutions is beneficial, yet bicarbonate-containing solutions equilibrated with 100% oxygen become highly alkaline as carbon dioxide is released. In the isolated perfused rat heart fitted with an intraventricular balloon, we recently observed a sustained contraction related to infusion of cardioplegic solution. In the same model, to record these contractions, we studied myocardial preservation by multidose bicarbonate-containing cardioplegic solutions in which first the calcium content and then the pH was varied. An acalcemic cardioplegic solution (Group 1) and the same solution with calcium provided by adding calcium chloride (Group 2) or blood (Group 3) were equilibrated with 100% oxygen. Ionized calcium concentrations were 0, 0.10 +/- 0.06, and 0.11 +/- 0.07 mmol/L and pH values were 8.74 +/- 0.07, 8.54 +/- 0.08, and 8.40 +/- 0.07, all highly alkaline. Hearts were arrested for 2 hours at 8 degrees +/- 2.5 degrees C and reperfused for 1 hour at 37 degrees C. At end-arrest, myocardial adenosine triphosphate was depleted in all three groups, significantly in Groups 2 and 3. In Group 1 the calcium paradox developed upon reperfusion, with contracture (left ventricular end-diastolic pressure = 60 +/- 7 mm Hg), creatine kinase release up to 620 +/- 134 U/L, a profound further decrease in adenosine triphosphate to 1.9 +/- 1.7 nmol/mg dry weight, and either greatly impaired or no functional recovery (17% +/- 10% of prearrest developed pressure). Three hearts in this group released creatine kinase during arrest and did not resume beating during reperfusion. In Groups 2 and 3, the calcium paradox did not occur; functional recovery was 61% +/- 4% and 71% +/- 9% at 5 minutes of reperfusion. In two additional groups (4 and 5), the pH of the acalcemic cardioplegic solution was decreased by equilibration with 2% and 5% carbon dioxide in oxygen to 7.53 +/- 0.03 and 7.11 +/- 0.02. Contractions during arrest were smaller than in Groups 1, 2, and 3; adenosine triphosphate was maintained during arrest; functional recovery was 101% +/- 3% and 96% +/- 4% at 5 minutes of reperfusion. We conclude that acalcemic solutions with carbon dioxide are superior to highly alkaline calcium-containing solutions. If oxygenation of cardioplegic solutions, of proved value, causes severe alkalinity, then calcium paradox may result even with hypothermia. This hazard is prevented by adding calcium or blood to the solution or carbon dioxide to the oxygen used for equilibration.

Maximal oxygenation of dilute blood cardioplegic solution.

The content of dissolved O2 (the major source of O2 for the myocardium) of dilute blood cardioplegic solution (dBCS) varied widely when oxygenated at 4 degrees C by surface flow of O2 in a Bentley BCR-3500 cardiotomy reservoir. We have modified the system to consistently deliver maximally oxygenated dBCS to the heart. Laboratory studies indicated that bubbling O2 through a 16-gauge intravenous catheter in a central Luer-Lok port of the cardiotomy reservoir provided contents of dissolved O2 that were consistently near maximal. We then studied 17 patients in the operating room. The first 6 patients received dBCS oxygenated with 100% O2 with a high dissolved O2 content of 3.2 +/- 0.2 ml/dl. However, the pH of the dBCS became highly alkaline (7.83 +/- 0.11 at 37 degrees C). Therefore, in the remaining 11 patients, 2% CO2 was added to the O2. The dissolved O2 content remained high (3.3 +/- 0.1 ml/dl), and the pH was in a more physiological range (7.35 +/- 0.09 at 37 degrees C). We conclude that consistently maximal oxygenation of a dBCS at a more physiological pH can be achieved by this method.

Transfusion of predonated autologous blood in elective cardiac surgery.

Despite blood conservation techniques, the average transfusion requirement in patients undergoing elective cardiac surgical procedures remains 1 to 3 units. We studied the efficacy of predonated autologous blood in decreasing homologous transfusion in two matched groups of 58 patients each. Group 1 received homologous blood perioperatively, and Group 2 was transfused with predonated autologous blood. An average of 1.97 units was predonated in Group 2 over 18 days. This resulted in a decline in whole blood hemoglobin concentration of 2.2 gm/dl. No complications resulted from phlebotomy in this ambulatory population consisting predominantly of patients with coronary artery disease. Transfusion of an average of 1.7 units of autologous blood in Group 2 reduced the volume of homologous transfusion by 46% compared with Group 1 (p less than .01). In Group 1, 38% of patients required no homologous transfusion compared with 64% in Group 2 (p less than .02). There were no complications related to autologous blood transfusion. Total transfusion requirement was related to the length of cardiopulmonary bypass. We conclude that autologous predonation is a simple, safe, and cost-effective method of reducing homologous transfusion and thereby decreasing the risk of transfusion-related reactions and infections.

Symptomatic bilateral renal angiomyolipomas in a child.

We report a case of bilateral renal angiomyolipomas in a child with Bourneville's tuberous sclerosis. The case is unusual because of the early age of the patient at which symptoms occurred. The presentation and treatment are discussed, and the literature is reviewed. Renal disease can occur in young patients with tuberous sclerosis and it is of clinical importance to document renal involvement in these children.

Colon interposition for esophagus in children.

In 25 years, from 1959 to 1984, esophageal substitution was performed in 32 patients. In most, the transverse colon was used, brought through the left chest on a vascular pedicle of the left colic artery. Indications for operation included: 21, esophageal atresia; 5, caustic injury; 3, peptic stricture; 2, esophageal varices with previous splenectomy; and 1, cartilagenous hamartoma of the esophagus. Six patients had failed prior reconstructions (1, gastric tube; 2, intrathoracic stomach; 1, presternal jejunum; 1, sloughed colon segment, 1, extensive stricture after primary repair). There was one postoperative death from fluid overload early in the series. Two patients had a localized leak at the upper anastomosis in the neck; neither resulted in stricture. One patient had a side leak in the lower intrathoracic colon, probably from an anchoring suture placed too deeply. Most patients had pyloroplasty with their operation. Four who did not required one later. Four patients required late reoperation for redundancy of the lower colon segment which emptied poorly; one lower colon was revised for stricture from exstrinsic compression at the substernal hiatus and another one for an inflammatory pseudopolyp with bleeding. There was no loss of a colon segment from ischemia. There is follow-up on all but one patient. Nineteen are more than ten years postoperative (mean of 18 years). Growth was assessed in that group. In atresia patients growth correlated with weight preoperatively and the presence or absence of associated anomalies. In the others growth was excellent in all but one patient. In our experience the colon conduit provides an excellent substitute esophagus for pediatric patients. The operation should have relatively low rate of major complications, most of which are avoidable, and most of which can be corrected to give a satisfactory long-term result.