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Objective: Warm blood cardioplegia requires interruption by ischemic intervals to aid visualization. We evaluated the safety of repeated interruption of warm blood cardioplegia by normothermic ischemic periods of varying durations. Methods: In three groups of isolated cross-perfused canine hearts, left ventricular function was measured before and for 2 hours of recovery after arrest, which comprised four 15-minute periods of cardioplegia alternating with three ischemic intervals of 15, 20, or 30 minutes (I 15 , I 20 , and I 30 ). Metabolism was continuously measured by phosphorus 31–magnetic resonance spectroscopy. Results: Adenosine triphosphate levels fell progressively as ischemia was prolonged; after recovery, adenosine triphosphate was 99% ± 6%, 90% ± 1% ( p = 0.0004 vs control), and 68% ± 3% ( p = 0.0002) of control levels in I 15 , I 20 , and I 30 , respectively. Intracellular acidosis with ischemia was most marked in I 30 . After recovery, left ventricular maximal systolic elastance at constant heart rate and coronary perfusion pressure was maintained in I 15 but fell to 85% ± 3% in I 20 , ( p = 0.003) and to 65% ± 6% ( p = 0.003) of control values in I 30 , while relaxation (tau) was prolonged only in I 30 ( p = 0.007). Conclusions: Hearts recover fully after three 15-minute periods of ischemia during warm blood cardioplegia, but deterioration, significant with 20-minute periods, is profound when the ischemic periods are lengthened to 30 minutes. This suggests that in the clinical setting warm cardioplegia can be safely interrupted for short intervals, but longer interruptions require caution. (J Thorac Cardiovasc Surg 1997;114:1070-80)

We tested the effects of glucose and oxygen in cardioplegic solutions on myocardial protection in the isolated perfused working rat heart. Recovery from 2 hours’ hypothermic (8° C) cardioplegic arrest was examined in 93 hearts. Cardioplegic solution, which was delivered every 15 minutes, was supplemented with glucose 28 mmol/L as a substrate or sucrose 28 mmol/L as a nonmetabolizable osmotic control; it was equilibrated with either 98 % oxygen or 98% nitrogen, both with 2% carbon dioxide. Four combinations of hyperkalemic cardioplegic solution were studied: nitrogen-sucrose, nitrogen-glucose, oxygen-sucrose, and oxygen-glucose. During hypothermic arrest, oxygcnation of cardioplegic solution greatly reduced myocardial lactate production and prevented ischemic contracture as indicated by coronary vascular resistance. Glucose increased lactate production modestly but significantly only when the cardioplegic solution was nitrogenated. Although end-arrest myocardial adenosine triphosphate and creatine phosphate were greatly increased by oxygenation of cardioplegic solution (p horac C ardiovasc S urg 1992;103:219—29)

The effect of the calcium and oxygen contents of a hyperkalemic glucose-containing cardioplegic solution on myocardial preservation was examined in the isolated working rat heart. The cardioplegic solution was delivered at 4° C every 15 minutes during 2 hours of arrest, maintaining a myocardial temperature of 8° ± 2° C. Hearts were reperfused in the Langendorff mode for 15 minutes and then resumed the working mode for a further 30 minutes. Groups of hearts were given the oxygenated cardioplegic solution containing an ionized calcium concentration of 0, 0.25, 0.75, or 1.25 mmol/L or the same solution nitrogenated to reduce the oxygen content and containing 0 or 0.75 mmol ionized calcium per liter. The myocardial adenosine triphosphate concentrations at the end of arrest in these six groups of hearts were 15.6 ± 1.2, 9.5 ± 0.5, 8.2 ± 1.1, 4.9 ± 1.8, 10.1 ± 2.0, and 1.6 ± 0.4 nmol/mg dry weight, respectively. At 5 minutes of working reperfusion, the percentages of prearrest aortic flow were 80 ± 2, 62 ± 4, 33 ± 6, 37 ± 5, 48 ± 7 and 46 ± 8, respectively. The differences among the groups in adenosine triphosphate concentrations and in functional recovery diminished during reperfusion. In hearts given the hypoxic calcium-containing solution, there was a marked increase in coronary vascular resistance during the administration of successive doses of cardioplegic solution, which was rapidly reversible upon reperfusion. These data indicate that hearts given the acalcemic oxygenated solution had better adenosine triphosphate preservation during arrest and better functional recovery than hearts in any other group. Addition of calcium to the oxygenated cardioplegic solution decreased adenosine triphosphate preservation and functional recovery. Oxygenation of the acalcemic solution increased adenosine triphosphate preservation and functional recovery. The lowest adenosine triphosphate levels at end arrest were observed in hearts given the hypoxic calcium-containing solution. In the setting of hypothermia and multidose administration, the addition of calcium to a cardioplegic solution resulted in increased energy depletion during arrest and depressed recovery.

To determine if, during elective cardiac arrest, the myocardial protection afforded by a cold (4 degrees C) crystalloid potassium cardioplegic solution could be improved by oxygenation of the solution, we placed 16 dogs on cardiopulmonary bypass and subjected their hearts to 4 hours of cold cardioplegic arrest. Group 1 hearts (n = 8) received aerated crystalloid solution perfused through the aortic root every 20 minutes. Group 2 hearts (n = 8) were treated identically except that the crystalloid cardioplegic solution was fully oxygenated. Left ventricular function curves (ejecting heart) were generated before arrest (control) and after 45 minutes of reperfusion. A cardiac output of 1,000 ml/min could be attained in only two hearts of Group 1 after reperfusion, whereas all but one heart of Group 2 had excellent functional preservation. Mean postreperfusion adenosine triphosphate (ATP) levels in Group 1 and Group 2 hearts were 62% and 89% of control, respectively (p less than 0.01). Myocardial water content had increased significantly (p less than 0.002) after reperfusion in Group 1, but not in Group 2. During cardioplegic solution infusion, myocardial oxygen consumption (MVO2) was 1.42 +/- 0.15 ml O2/min/100 gm LV for Group 1 and 6.91 +/- 1.27 ml O2/min/100 gm LV for Group 2 (p less than 0.001). Oxygen consumed per minute of arrest was 0.027 +/- 0.003 ml O2/min/100 gm LV for Group 1 and 0.128 +/- 0.015 ml O2/min/100 gm LV for Group 2 (p less than 0.001). Postreperfusion ultrastructural evaluation of two of the Group 1 hearts revealed severe ischemic damage in contrast to the normal ultrastructural appearance of two of the Group 2 hearts. With careful attention given to maintenance of myocardial hypothermia and cardioplegic delivery methods, the myocardial protection afforded by an oxygenated crystalloid cardioplegic solution exceeds that provided by the aerated control and compares favorably with other methods of myocardial protection during ischemic 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° 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 inihibited 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

The operative management of aneurysms of the ascending aorta continues to present a technical challenge to the surgeon, and the results obtained provide a useful clinical assessment of the means of myocardial protection. We present a series of 35 consecutive patients who underwent operations for aneurysms of the ascending aorta during which myocardial protection was achieved with hypothermia and potassium cardioplegia. Twenty-three patients underwent aortic valve replacement and resection and grafting of a chronic ascending aortic aneurysm. Aortic valve replacement and aneurysmorrhaphy of a chronic ascending aneurysm were performed in five patients. Four patients underwent resection and grafting of a chronic ascending aortic aneurysm and three patients resection and grafting of acute aortic aneurysms. Aortic cross-clamp times varied from 48 minutes to 2 hours, 32 minutes, with a mean cross-clamp time of 1 hour, 29 minutes. There was one death in the hospital in this series of 35 patients for a mortality rate of 2.8%. Of the 34 survivors, there has been one late death from recurrent sternal wound infection. This clinical series documents the efficacy and safety of hypothermic potassium cardioplegia for protection of the myocardium during extended periods of ischemia attending operative correction of ascending aortic aneurysms.

One hundred six consecutive patients underwent elective or emergency coronary artery bypass grafting (CABG) between January, 1974, and November, 1975. There were 90 men of an average age of 54 years and 16 women an average of 64 years. Unstable angina (preinfarction angina, angina decubitus, and crescendo angina) was present in 54 patients of this group and eight were in congestive heart failure. Sixty-two of the 106 had previously had myocardial infarctions and four had evolving infarctions. There were four operative deaths (3.8%) and one early hospital death (less than 30 days’ hospitalization). Perioperative infarction occurred in five of the survivors. Of the 197 grafts placed in the 101 survivors, 94% were patent by angiography at 1 to 2 weeks (175 of 187 vein grafts and 10 of 10 left internal mammary grafts). At 1 to 2 years after CABG, 62% of the survivors consented to repeat angiography at which time 94% of the grafts were patent (101 of 108 vein grafts and seven of seven left internal mammary grafts). Clinical follow-up of 81 of the 101 survivors at 1 year found 99% of them to be asymptomatic or improved. Repeat clinical follow-up of all survivors (99 of 101) at 3 to 4 years found 93.9% asymptomatic or improved. Overall survival, including operative deaths, was 92.4% at 4 years.

Hyperlipoproteinemia is a known risk factor for the development of coronary artery disease. To assess the perioperative and late results of myocardial revascularization for angina pectoris in patients with hyperlipoproteinemia, we reviewed the records of 200 patients (age range 24 to 75 years). Preoperatively the average New York Heart Association (N.Y.H.A.) angina class was 3.1 ± 0.7. One hundred three patients (51.5%) had type 11 disease, 95 patients (47.5%) type IV, and two (1%) had type III or V disease. The mean age of the patients with type II disease was 3 years less than that of patients with type IV disease (50 versus 53 years, p

Repair of coarctation of the aorta has been performed in 164 patients since July, 1947. Eighteen were younger than 6 months of age, 44 were I to 11 years, 87 were 11 to 40 years, and 15 were older than 40 years of age. Resection and end-to-end anastomosis were performed in 92, interposition grafts in 59, and other procedures in 13. Four operative deaths occurred in infants with multiple anomalies (22 percent infant mortality rate). Ten late deaths were due to associated anomalies (three), myocardial infarction (two), cerebrovascular accident (one), rupture of an aneurysm at the graft site (one), and unrelated causes (three). No hospital deaths occurred in patients with isolated coarctation or in patients older than 1 year, including the 15 patients older than 40 years. Late complications were evaluated in 147 patients followed from 2 months to 28 years. Restenosis occurred in eight (three repaired when younger than 6 months) and false aneurysm at graft sites in two (fatal rupture in one). Residual hypertension occurred in 38 of 147 (25.9 percent) and was related to age at the time of repair: younger than 6 months (three of 13), 1 to 11 years (one of 43), 11 to 40 years (29 of 79), and older than 40 years (five of 13). Residual hemodynamic abnormality due to uncorrected associated anomalies, hypertension, ventricular hypertrophy, coronary artery disease, restenosis, or anastomotic aneurysm occurred in 56.1 percent of 98 patients followed at least 2 years. Of this group, 21.4 percent of those repaired before age 11 years and 70 percent of those repaired after age 11 had residual hemodynamic abnormality. Hypertension and other residual hemodynamic abnormalities occur frequently after coarctation repair, but significantly less often when repair is performed between the ages of 1 and 11 years. The incidence of mild hypertension is increased if repair is performed after 6 years of age.

The pedicled omentum finds use in cardiothoracic surgery for management of complicated problems and prevention of serious complications. Its blood supply is excellent and is capable of inducing neovascularity. Based on the right gastroepiploic artery, it reaches anywhere in the thorax or neck. Its bulk helps to fill infected spaces. Thirty-seven patients have been treated with the pedicled omentum. In 16 patients the goal was preventive, to avoid bleeding, anastomotic leakage, or infection or to provide a source of fibroplasia or neovascularity. In eight patients with cervical exenteration the flap protected against innominate artery erosion and esophageal leakage, generally in an irradiated field. In six patients it permitted primary healing of heavily irradiated trachea--formerly unlikely. It was also used to provide coverage of a chest wall prosthesis in two patients. In 21 patients the omentum was used to obtain healing in the presence of infection. Bronchopleural fistulas were successfully closed in eight of nine patients. Six mediastinal infections that developed after cardiac operations were successfully treated. Four unusual vascular infections necessitated the use of omentum. Two patients had closure of esophageal perforations buttressed with omentum. This series demonstrates the efficacy of the omentum in the management of complex cardiac, vascular, esophageal, tracheal, bronchial, pleural, and chest wall problems.

Isolated dog hearts were perfused for 24 hours at 5° C with one of three solutions: plain Krebs solution, Krebs solution containing 167 mg/L of procaine hydrochloride, or Krebs-procaine solution with washed red cells (hematocrit 2%). Coronary vascular resistance (CVR) of hearts perfused with Krebs solution alone increased sharply between the eighth and the twelfth hours of perfusion and then stabilized. Increase of myocardial firmness paralleled the increase of CVR. The addition of procaine to Krebs perfusate kept the heart flaccid and suppressed the steplike increase in CVR but failed to improve significantly the preservation of the hearts. The addition of washed red cells to Krebs perfusate kept CVR near baseline level, improved coronary perfusion flow, doubled myocardial oxygen consumption, reduced edema formation, and improved left ventricular stroke work (LVSW) of the preserved heart. This improvement seems mostly related to a mechanical effect of red blood cells on capillary flow distribution of the heart.

Although the results of coronary artery bypass grafting plus single aortic or mitral valve replacement have been documented, the risk of myocardial revascularization with combined aortic and mitral valve replacement is not well defined. We present a series of 33 consecutive patients undergoing myocardial revascularization with combined aortic and mitral valve replacement during a period of almost seven years. There were 21 men and 12 women with a mean age of 67 years. All patients had congestive heart failure, and 21 (64%) had angina pectoris. Mean New York Heart Association functional classification was 3.4; eight patients (24%) had ejection fractions less than 0.40, and 13 patients (41%) had cardiac indices less than 2.0 L/min/m2. All operations were performed with hypothermic crystalloid potassium cardioplegia. The number of coronary arteries grafted varied from one to four (mean, 1.7 grafts per patient). Four patients died while in the hospital (12.1%). There were no perioperative myocardial infarctions. At a follow-up of 2 to 80 months (mean 40.7 months), death had occurred in eight (27.6%) of the 29 hospital survivors. Actuarial survival rate at 72 months was 60.7%. Although no preoperative factors predicted late death, early deaths were related significantly to severe mitral regurgitation, low ejection fraction, high New York Heart Association classification and extensive coronary artery disease (p

Rupture of the posterior ventricular septum is a difficult lesion to repair. This report describes an operative approach through a left ventriculotomy, with complete excision of the left ventricular infarct. The defect created by infarctectomy is closed with a prosthetic patch. Of 15 patients so treated, 11 have survived.

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° ± 2.5° C and reperfused for 1 hour at 37° 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.

An improved approach to intraoperative myocardial preservation technique to ensure uniform myocardial cooling past critically stenosed arteries was developed for patients undergoing aorta-coronary bypass grafting. Proximal anastomoses are done and then, after institution of cardiopulmonary bypass, a separate roller pump head is used to administer a specific controlled volume of cardioplegic solution (1 L) through a 4 degrees C coil to provide controlled pressure in the root of the cross-clamped aorta. Midmyocardial wall temperatures in the anterior, posterolateral, inferior, and septal walls of the left ventricle are measured. Distal anastomoses are then performed sequentially, beginning with the warmest region. After each distal anastomosis, 400 ml of cardioplegic solution are again administered into the aortic root. This approach has been used in 100 consecutive patients from July, 1979, through July 1980 (Group I). and these patients were compared to 97 consecutive patients undergoing aorta-coronary bypass grafting in the previous year (July, 1978, through June, 1979) (Group II) who had myocardial preservation with potassium cardioplegia administered by syringe injection and without regional temperature mapping. There were no perioperative myocardial infarctions in Group I: there were five (5.2%) in Group II (p less than 0.05). A significant reduction in cardiac deaths was also achieved, with two (2.0%) such deaths in Group I and eight (8.2%) in Group II (p less than 0.05). The data suggest that delivery of adequate volumes of cardioplegia solutions by a pressure-regulated system, in combination with myocardial temperature mapping to determine the sequence of bypass grafting, can improve myocardial preservation.

Despite the requirement of anticoagulation, mechanical valve prostheses offer the advantage of proven durability. We have compared the long-term results of 467 aortic valve replacements and 342 mitral valve replacements using the Starr-Edwards prosthesis with 110 aortic valve replacements and 105 mitral valve replacements using the Bjork-Shiley prosthesis from 1973 through 1977. Improvement in New York Heart Association (NYHA) class was noted in greater than 80% of patients in all four groups. Long-term survival with mean follow-up over 5 years was not significantly different between respective groups. The probability of thromboembolic complications, however, was significantly higher (p less than 0.05) with the Starr-Edwards prosthesis in both the aortic and mitral positions. The probability of valve failure, although low for all groups, was significantly higher (p less than 0.05) in the Bjork-Shiley mitral group due to late thrombotic occlusion. Use of the Starr-Edwards and Bjork-Shiley prostheses is associated with satisfactory functional improvement and similar long-term survival rate. However, the increased risk of valve failure due to late thrombotic occlusion of the Bjork-Shiley prosthesis should be considered when choosing a mechanical mitral prosthesis.

Increasing longevity makes the consideration of coronary bypass common in elderly patients. Seventy-five patients 70 years of age or older undergoing coronary artery bypass grafting (CABG) for angina pectoris were compared to a control group of 75 patients under 70 years of age. The groups were matched for male : female ratio (46:29), previous infarction (28/75), unstable angina (27/75), and the requirement for preoperative intra-aortic balloon pumping (7/75). Patients under 70 years of age had an average preoperative New York Heart Association (NYHA) class of 3.0 ± 0.6 (SEM) and an average left ventricular end-diastolic pressure of 15.5 ± 0.8 mm Hg, compared to 3.3 ± 0.6 and 12.9 ±1.1 mm Hg, respectively, for the older group. Average grafts per patient were 2.7 ± 0.8 in the younger group and 2.8 ± 0.1 in the older group. Overall operative mortality for patients under 70 was 4% (3/75) versus 12% (9/75) (p = 0.06) for patients 70 and older. The incidence of chronic stable angina was 2% (1/48) versus 6% (3/48) (p = 0.30). Perioperative infarctions occurred in 7% of those under 70 and 5% of those 70 or older (p = 0.54). Those under 70 averaged 13.8 ± 0.6 postoperative hospital days versus 18.4 ± 1.2 hospital days for the older group (p

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° 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° 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 of magnesium to calcium-containing cardioplegic solutions and perhaps to calcium-free solutions.

Summary In dogs subjected to barbiturate intoxication, intracaval electrophrenic stimulation has been demonstrated to be an effective form of artificial respiration. The results further suggest that intracaval electrophrenic stimulation effects more physiologic gas exchange and results in better maintenance of the circulation than can be achieved with positive-negative pressure ventilation. The technique of applying negative pressure ventilatory support herein described is envisioned as a potentially applicable method for the treatment of respiratory failure.

Summary Two case reports of resectional treatment for tuberculosis of the azygos lobe are presented. The finding of a separate epiarterial bronchus, not previously described, is noted. The clinical, radiologic, and anatomic findings, including bronchopulmonary segmental relationships, are described. The embryologic abnormality accounting for the anomaly is discussed. Segmental or subsegmental resection in order to conserve functioning pulmonary tissue is advocated.