J. Judson McNamara

Anatomic types of ventricular septal defect with aortic insufficiency: Diagnostic and surgical considerations

Abstract A series of 11 postmortem cases of ventricular septal defect (VSD) with aortic insufficiency (AI) was presented, and an anatomic classification of VSD with AI was proposed. There are two principal anatomic types: VSD beneath the crista supraventricularis (Type I), and VSD beneath the pulmonary valve (Type II). With a subcristal VSD (Type I), there are two subtypes: without pulmonary infundibular stenosis (Type Ia), and with pulmonary infundibular stenosis (Type Ib). Subcristal VSD with AI (Type I) occurred in seven cases. In six of these, the development of AI appeared basically to be related to the underdevelopment of one aortic commissure, usually the right coronary-noncoronary (4:6 cases). A functionally bicuspid aortic valve resulted in five cases. No pulmonary infundibular stenosis (Type Ia) was found in three cases, while four displayed mild to moderate pulmonary infundibular stenosis (Type Ib). The clinical and laboratory picture without pulmonary stenosis was that of AI with a maladie de Roger type of VSD, while the picture with stenosis was that of AI with acyanotic (atypical) tetralogy of Fallot. Subpulmonary VSD with AI (Type II) occurred in four cases. The subpulmonary VSD is a conal septal defect, the conal septal portion of the crista supraventricularis being absent or defective. All four cases had normal aortic commissures. AI resulted from herniation of the right coronary aortic leaflet through the large subpulmonary VSD into the right ventricular outflow tract, resulting in a mild to moderate pulmonary outflow tract gradient in all. Subcristal VSD with AI, with or without pulmonary stenosis, usually was an aortic commissural deficiency problem (in 6:7 cases). Subpulmonary VSD with AI always was a hernia of a basically normal aortic valve into the right ventricular outflow tract (in 4:4 cases). Since the surgical management of the two principal types of VSD with AI is different, their differential diagnosis is of practical clinical importance.

Natural History of Arteriosclerotic Thoracic Aortic Aneurysms

Out of 28 patients with arteriosclerotic aortic aneurysm seen between 1965 and 1975, 22 were not surgically repaired. Of these 22 patients, 9 subsequently died of rupture and 7 of unrelated cardiovascular disease, and 6 are living at the time of this study. Mean survival for the group is less than 3 years. All but 1 rupture occurred in aneurysms larger than 10 cm, and recent increase in size preceded rupture in all patients for whom serial roentgenograms were available. This study documents the high risk of rupture of arteriosclerotic aortic aneurysms of the descending thoracic aorta and suggests a more uniform use of surgical management depending on the patients age and underlying state of health.

Localization and Surgical Treatment of Pancreatic Insulinomas Guided by Intraoperative Ultrasound

BACKGROUND Approximately 20% to 60% of insulinomas cannot be localized preoperatively, and 10% to 20% cannot be found even during surgery. The operative complications associated with the blind surgical explorations are relatively high. METHODS Between January 1987 and December 1995, intraoperative ultrasound was used to localize insulinomas and guide surgical procedures in 28 patients. RESULTS Insulinomas were found by intraoperative systematic palpation in 24 patients (85.7%), while intraoperative ultrasound localized the tumors in 27 patients (96.4%). By the combination of these two techniques, all tumors were discovered. The surgical procedures were guided by intraoperative ultrasound. The operative complication rate was 14.3%. CONCLUSION Intraoperative ultrasound can accurately localize insulinoma, and delineate the spatial relationship between tumor and vital structures, such as pancreatic duct, common bile duct, and critical blood vessels. It can thereby help to increase the successful rate of surgery and avoid unnecessary blind pancreatectomy.

Frequency of mortality and myocardial infarction during maximizing oxygen delivery: a prospective, randomized trial.

OBJECTIVES To determine the frequency of myocardial infarction and mortality during treatment that increased oxygen delivery (DO2) to > or = 600 mL/min/m2. To define the characteristics of patients achieving a high DO2 without inotropes in order to guide future studies. DESIGN A prospective, randomized, controlled trial. SETTING Two surgical intensive care units at The Queens Medical Center in the University of Hawaii Surgical Residency Program. PATIENTS Eighty-nine surgical patients (> or = 18 yrs of age), who were admitted to a surgical intensive care unit and who required pulmonary artery catheter monitoring, were selected for the study. Diagnoses included sepsis, septic shock, adult respiratory distress syndrome, or hypovolemic shock. Patients facing imminent death were excluded from the study. INTERVENTIONS The treatment group received fluid boluses, blood products, and inotropes, as needed, to achieve a DO2 of > or = 600 mL/min/m2 in the first 24 hrs. Using the same interventions, we treated the control group to reach a DO2 of 450 to 550 mL/min/m2. MEASUREMENTS AND MAIN RESULTS Hemodynamic measurements were obtained every 4 hrs until the pulmonary artery catheter was removed. DO2 and oxygen consumption were calculated by standard formulas. Serial creatine kinase myocardial fraction and electrocardiograms were documented for the first 48 hrs after study entry and for any new onset of arrhythmia or increasing hemodynamic instability. The patients who generated a high DO2 (> or = 600 mL/min/m2) with only preload treatment were reflective of patients with better cardiac reserve and low mortality rates. These patients, from both treatment and control groups, were excluded in the final analysis. The treatment group who received inotropes to achieve the high DO2 had a 14% mortality rate. Those patients who failed to achieve the high DO2 had a 67% mortality rate, and the control group who achieved a normal DO2 had a 62% mortality rate (p = .005). The frequency of myocardial infarction after study entry was 5.6% (five of 89 patients). This rate was not higher among the groups who received inotropes. Logistic regression analysis showed that age of > or = 50 yrs could be used to classify patients as not self-generating, with an 83% chance of being correct. CONCLUSIONS The group that required catecholamines to achieve a DO2 of > or = 600 mL/min/m2 had a lower mortality rate, with no increase in the frequency of myocardial infarction. Future prospective, controlled trials examining select groups of patients (age > or = 50 yrs) may demonstrate a difference between control and treatment groups by eliminating the majority of patients who generate the high DO2 with only preload augmentation.

Intestinal blood flow at various intraluminal pressures in the piglet with closed abdomen.

The influence of intraluminal pressure on intestinal blood flow was studied in two segments of the small intestine and two of large intestine ligated after insertion of intraluminal catheters in ten piglets. Intestinal segments were inflated in stepwise increments in intraluminal pressures of 15, 30, 45 and 60 mmHg and blood flow was measured with radioactive micro-spheres using four isotopes (Ce, Cr, Sr, Sc). Other segments were inflated to a pressure of 60 mmHg and then pressure decreased in a stepwise fashion to 30, then 0 mmHg for the last two injections. Small and large intestinal blood flow fell progressively with increasing intraluminal pressure. At 60 mmHg a forward flow of 25% of normal was still present. Furthermore, not only was there an absolute decrease in blood flow with increasing intraluminal pressure but this decrease was disproportionately large in the intestinal mucosa. A hyperemic response lasting approximately 15 minutes was observed after complete decompression. The intestinal blood flow distal to the ligated segments was always moderately increased as compared to intestinal blood flow proximal to the segments. The results reported herein are at some variance from other reported studies performed with the abdomen open and on isolated segment preparations. The reasons for these variations are discussed.

Defining the anatomic perfusion bed of an occluded coronary artery and the region at risk to infarction. A comparative study in the baboon, pig and dog.

Abstract To assess selectively the effectiveness of therapeutic interventions to reduce infarct size, it is important to assess both ultimate infarct size as well as the size of the region of myocardium at risk to infarction. The anatomically defined perfusion bed of an occluded artery has generally been assumed to be synonymous with the region at risk of infarction. This assumption was tested by delineating the anatomic perfusion bed of an occluded artery with microvascular dyes and by examining the relation of the anatomic perfusion bed to the region of acute ischemic injury. In 8 baboons, 12 pigs and 15 dogs a major branch of the left anterior descending or left circumflex coronary artery was occluded. At 2 and 30 minutes after occlusion the eplcardial area of ischemic injury was determined by epicardial S-T segment mapping. The boundary of epicardial S-T segment elevation was resolved to within 1 mm and marked directly on the ventricular surface. The heart was then excised and the perfusion bed of the occluded artery was delineated by either (1) injecting different colored silicone rubber microvascular dyes into the previously occluded artery as well as the adjacent perfusion beds (direct method), or (2) injecting dye only into the adjacent perfusion beds (defect method). Serial cross-sections of the left ventricle from the direct and defect dye-perfused hearts in all three species showed the perfusion bed of the occluded artery to be readily demarcated. Microscopic examination demonstrated no evidence of capillary anastomoses and minimal inter-digitation of capillaries at the perfusion bed boundaries. In dye-perfused hearts, the baboon and the pig showed no evidence of precapillary anastomoses between perfusion beds; however, the dog demonstrated numerous epicardial collateral channels. The epicardial area of the anatomic perfusion bed correlated closely with the epicardial area of S-T segment elevation at 2 minutes after occlusion in the baboon (r = 0.97), pig (r = 0.99) and dog (r = 0.96). The epicardial area of S-T segment elevation did not change through the 30 minute period of occlusion in the baboon and the pig, but in the dog it showed a progressive and variable reduction reflecting the gradual recruitment of existing collateral channels from adjacent perfusion beds. It is concluded that the techniques of direct and defect dye delineation accurately define the anatomic perfusion bed of an occluded coronary artery. This anatomic perfusion bed corresponds to the region of myocardium undergoing acute ischemic injury and hence the region at risk to infarction immediately after coronary occlusion in the three species studied.

Coronary Reperfusion in Primates SERIAL ELECTROCARDIOGRAPHIC AND HISTOLOGIC ASSESSMENT

After acute coronary occlusion in primates, the time period during which reperfusion results in significant salvage of reversibly injured myocardium was investigated. In 23 monkeys, the left anterior descending coronary artery was occluded from 1 to 6 h; and in 5 others, occlusion was maintained for the 1-wk study. Unipolar epicardial electrocardiograms were monitored from mapping points on the anterior and lateral left venticle. S-T segment elevation (S-T upward arrow) and R + S wave amplitude (RS) were measured before occlusion and at regular intervals during occlusion and reperfusion. Summated S-T upward arrow (SigmaS-T upward arrow) and summated RS (SigmaRS), computed for mapping points demonstrating greater than 2 mV S-T upward arrow, were used as serial measures of electrical injury. SigmaS-T upward arrow peaked within 2-h postocclusion and then gradually declined throughout the period of occlusion suggesting the progress of infarction within the area of injury. After reperfusion SigmaS-T upward arrow rapidly declined to near cnotrol values indicating the extent of reversible injury. During the period of occlusion, the magnitude of voltage loss in SigmaS-T upward arrow as a percent of maximum SigmaS-T upward arrow was proportional to the duration of occlusion, though the rate of loss decreased with increasing time of occlusion. Reperfusion after 6 h of occlusion resulted in reversal of only a small remaining component of the maximum current of injury. The voltage decrease in SigmaRS (from control values) was proportional to the duration of occlusion, though the decrease was accelerated during the first 2-h postocclusion. Whereas reperfusion interrupted the decline in SigmaRS, a consistent increase in SigmaRS postreperfusion was observed only after occlusion of 1 h. With respect to reperfusion groups, significance in SigmaS-T upward arrow voltage loss as a percent of maximum SigmaS-T upward arrow was demonstrated between 2-h and 4-h, 4- and 6-h, and 6-h and chronically ligated animals. Significance in SigmaRS voltage loss as a percent of control SigmaRS was demonstrated between 2- and 4-h, and 4- and 6-h reperfusion groups. Hearts were excised at 7 days for histological assessment of infarct size. Planimetric determination of left ventricular areas and areas of necrosis using slides made from 10 serial cross sections were used in estimating the percent of left ventricle infarcted. A significant reduction in infarct size was demonstrated between reperfused animals at 2 h and the 4- and 6-h reperfusion groups. A trend was noted suggesting increasing infarct size up to 6 h after experimental occlusion.

Platelet trapping in myocardial infarct in baboons: Therapeutic effect of aspirin

Abstract Blood platelet trapping has been demonstrated in the area of evolving myocardial infarction in baboons. Sixteen baboons were subjected to ligation of the diagonal branch of the left anterior descending coronary artery, and the extent of myocardial ischemia was monitored with a 64 to 72 electrode epicardial electrocardiographic grid. Eight animals received no treatment and eight were pretreated twice (at 12 hours and at 2 hours before ligation) with aspirin, 600 mg orally. Measurement of infarct extent included all electrode points with S-T segment elevation of 2 mV or greater. Chromium-51-tagged autologous platelets were injected 15 minutes before ligation. In all animals an area of ischemia developed in which typical changes evolved in S-T segments. In three of the eight aspirin-treated animals, double ligation was carried out. Aspirin was administered after release of the first ligature but before religation, and the area of S-T segment elevation was reduced by as much as 23 percent after aspirin treatment. Platelet trapping outside the area of S-T elevation was seen in 25± 3 percent of the total wall samples in aspirin-treated animals compared with 44 ± 7 percent of those in control animals (p

Lung abscess: A changing pattern of the disease☆

Alcoholic stupor with aspiration has been the most commonly recognized cause of lung abscess. Eighty-nine patients treated for lung abscess in a large community hospital from 1968 through 1982 have been described. Forty-six percent of these patients were 60 to 80 years of age. The most common predisposing factors included pneumonia, immunosuppression steroid therapy, carcinoma at a distant site, alcoholism, and lung cancer. Surgical therapy was employed in 23 patients when there was suspicion of cancer and failure to improve with medical management. Fifty-seven percent of patients were either cured or improved at the time of discharge. Twenty-nine percent died from other causes during hospitalization, and 9 percent died as a direct result of the abscess. Thus, the patients encountered in the community hospital setting tended to be older and had a wide variety of illnesses that precipitated the development of lung abscesses.

Failure of nifedipine therapy to reduce myocardial infarct size in the baboon.

The value of nifedipine in reducing the ultimate size of an infarct associated with a period of coronary occlusion followed by reperfusion was assessed. Eight baboons were administered a bolus dose of nifedipine, 5 micrograms/kg intravenously, and then a maintenance dose of 30 micrograms/kg per hour was begun 1 hour before occlusion. This regimen resulted in an 8.5 +/- 1.2 percent (mean +/- standard error) decrease in mean arterial pressure. The left anterior descending coronary artery was occluded for 2 hours and then perfusion restored. At 2 hours after reperfusion the nifedipine infusion was discontinued. Eight control baboons underwent an identical protocol without nifedipine therapy. At 24 hours after occlusion, microvascular dyes were injected into the left anterior descending coronary artery and adjacent arteries to delineate the perfusion bed of the previously occluded artery. The volume of infarction was determined with planimetry and compared with the volume of the perfusion bed of the occluded artery. The area of infarction was always contained within the perfusion bed of the occluded artery. The mean percent of the perfusion bed with infarction was 50.1 +/- 5.8 in the control group and 41.7 +/- 9.5 in the treated group (difference not significant; p greater than 0.05). In both control and treated groups of baboons hemorrhage occurred only within the region of infarction. In both groups electron microscopy revealed large electron-dense granules within the mitochondria. In conclusion nifedipine therapy during a 2 hour period of coronary occlusion followed by reperfusion did not result in any significant reduction in ultimate infarct size in the baboon.