Ernest M. Barsamian

Pathologic findings after cardiac valve replacement with glutaraldehyde-fixed porcine valves

Abstract Although approximately 20,000 glutaraldehyde-fixed porcine cardiac valve prostheses have been implanted in patients there is a lack of detailed pathologic studies of valves removed surgically or examined at necropsy. In this study, of 363 valves implanted in 311 patients, 26 valves (7 percent) from 23 patients (7 percent) were examined morphologically. Of the 23 patients, 14 died intraoperatively or less than 1 month after valve replacement—3 from coronary artery disease, 4 from hemorrhagic myocardial necrosis, 2 from postoperative hemorrhage, 2 from pulmonary disease and 1 from phycomycosis of the prosthesis; in 2 patients no anatomic cause of death was found. Six patients died 1 to 9 months after valve replacement—one from prosthetic thrombotic stenosis, one from prosthetic endocarditis and four from causes unrelated to their prosthesis. Three patients underwent surgical excision of a malfunctioning valve 12 to 31 months after implantation; incompetence was due to infective endocarditis in two patients and to a torn cusp in one. Fourteen of 15 valves implanted for 1 month or less were normal. Eight of 11 valves implanted for more than 1 month were abnormal: 3 were infected, 2 (from one patient) had focal calcification and thrombosis, 1 had only focal thrombosis, 1 had diffuse thrombosis causing stenosis and 1 had a torn cusp. In our experience, clinical cardiovascular deterioration in the early postoperative period in patients with glutaraldehyde-fixed porcine valves is unlikely to be related to dysfunction due to pathologic processes affecting the implanted valve. Although postoperative valve dysfunction has been unusual to date, clinical cardiovascular deterioration in the late postoperative period may be related to pathologic processes (infection, thrombosis or degeneration) affecting the implanted valve.

Pseudoaneurysm of the left ventricle: an unusual echocardiographic presentation. Review of the literature.

Echocardiography showed a large anterior chamber communicating with the left ventricle cavity through the interventricular septum in a patient with a previous left ventricular aneurysmectomy. At postmortem examination this chamber proved to be an 11-cm diameter pseudoaneurysm that opened into the left ventricle through a 3-cm orifice. A review of the literature showed 67 cases of histologically proven left ventricular pseudoaneurysm, most of which occurred after myocardial infarction and cardiac surgery. Twenty-six of 32 left ventricular pseudoaneurysms were successfully operated upon. Among 35 patients with pseudoaneurysms not operated upon, rupture was a cause of death in 11.

Micturitional Static Urethral Pressure Profile: A Method of Recording Urethral Pressure Profile During Voiding and the Implications

Using a tri-lumen graduated 10F catheter we attempted to record static (lateral) pressures at successive points in the urethra, synchronous with intravesical pressure recorded during voiding. Based on our understanding of the essential physical principles described by many earlier investigators we attempted numerous studies in a predominantly male population, which included normal male and female subjects, and male subjects with bladder outlet obstruction of varied etiology. We also attempted to evaluate the effects of the Valsalva maneuver, augmenting the detrusor contraction and artificial distal obstruction (penile compression) on the micturitional static urethral pressure profiles. Studies also were performed to compare the static urethral pressure profiles obtained with the anterograde (catheter withdrawal) and with the retrograde (catheter insertion during voiding) techniques. All of these studies have helped in understanding the various factors, such as double obstructions, artifactual catheter obstructions and incompetent distal sphincter mechanisms, in the interpretation of the micturitional static urethral pressure profile.

Pulmonary embolism after cardiac surgery

OBJECTIVES We examined the incidence of pulmonary embolism after cardiac surgery. BACKGROUND Because venous thromboembolism is considered to be an uncommon complication after cardiac surgery, its incidence was documented in a consecutive series of 1,033 patients who underwent cardiac surgery over a 5-year period. METHODS Parallel cohorts of patients in a tertiary referral center were evaluated and the incidence of pulmonary embolism was compared in subgroups of patients undergoing coronary bypass surgery, valve surgery and combined procedures. RESULTS Pulmonary embolism developed in 33 (3.2%) of the 1,033 cardiac surgical patients, within 2 weeks of a coronary bypass operation in most; it did not develop in any patient who had isolated valve replacement surgery (p < 0.05). The diagnosis of pulmonary embolism was established by pulmonary angiography in 24 patients, ventilation/perfusion lung scan in 3, postmortem examination in 5 and clinical examination in 1 patient. Important risk factors for pulmonary embolism included prolonged postoperative recovery, obesity and hyperlipidemia. The mortality rate was 18.7% in patients with in contrast to 3.3% in those without pulmonary embolism (p < 0.01). CONCLUSIONS Although pulmonary embolism is rare after isolated valve replacement, it is not an uncommon complication after coronary bypass surgery.

The significance of the late fall in myocardial PCO2 and its relationship to myocardial pH after regional coronary occlusion in the dog.

After acute regional coronary occlusion, myocardial tissue PCO2, as measured by mass spectrometry, rises, reaches a peak, and then gradually falls. This late fall in myocardial tissue Pco2 could be due to (1) a gradual increase in tissue blood flow (and hence improved carbon dioxide washout), (2) a gradual consumption of tissue biocarbonate, (3) a gradual reduction in the production of carbon dioxide due to progressive cellular damage, or (4) an artifact caused by the continued presence of the mass spectrometer probe in the ischemic tissue. To determine which of these four mechanisms is responsible for the late fall in myocardial tissue Pco2, we subjected 27 anesthetized open-chest dogs to 3-hour occlusion of the left anterior descending coronary artery. Both myocardial tissue Pco2 and intramyocardial hydrogen ion concentration were measured in the myocardial segment supplied by the left anterior descending coronary artery. Ten dogs (group 1) were killed after the occlusion (occlusion I), and 11 dogs (group 2) underwent reocclusion (occlusion II) at the same site after a 45-minute period of reflow. Regional myocardial blood flow was measured periodically by the intramural injection of 127Xe. Changes in myocardial tissue Pco2 and hydrogen ion concentration were related to ultrastructural changes in the tissues adjacent to the myocardial tissue Pco2 probe. Regional myocardial blood flow remained unchanged throughout the 3-hour occlusion, ruling out increased carbon dioxide washout as a cause for its late fall. Tissue hydrogen ion concentration, as measured by a new lead glass electrode, correlated well with myocardial tissue Pco2, with the reduction in regional myocardial blood flow, and with ischemic damage assessed histologically. Myocardial hydrogen ion concentration also exhibited a late fall after the occlusion, from a peak of 199.8 ± 27.8 nmol/ liter to 91.9 ± 12.1 nmol/liter (mean ± SEM). This ruled out consumption of tissue bicarbonate as the cause for the late fall in myocardial tissue Pco2. Peak rise in myocardial tissue Pco2 after occlusion II (71.2 ± 7.9 mm Hg) was significantly lower than peak myocardial tissue Pco2 after occlusion I (116.7 ± 13.9 mm Hg, P < 0.001). The difference between these latter two values, as well as the magnitude of fall in myocardial tissue Pco2 during occlusion I, related directly to the degree of histological damage observed. In six additional experiments (group 3), peak myocardial tissue Pco2 in myocardial segments supplied by normal (unoccluded) coronary arteries remained unchanged over 3 hours, and hydrogen ion concentration in segments supplied by an occluded left anterior descending coronary artery exhibited a late fall, even in the absence of a mass spectrometer probe. We conclude that, following regional coronary occlusion, there is a late fall in both myocardial tissue Pco2 and hydrogen ion concentration; this late fall probably is a reflection of progressive cellular damage which does not reverse after a 45-minute period of reflow. Myocardial tissue Pco2 and hydrogen ion concentration curves following coronary occlusion reflect the metabolic viability of the ischemic myocardium.

Assessment of the Efficacy of Interventions to Limit Ischemic Injury by Direct Measurement of Intramural Carbon Dioxide Tension after Coronary Artery Occlusion in the Dog

Although numerous interventions have been shown to exert a salutary effect on the ischemic myocardium, the severity of ischemia generally has been measured by indirect techniques. In the present investigation the effect of ischemia on intramural carbon dioxide tension (PmCO(2)) was measured directly in the open-chest, anesthetized dog with a mass spectrometer during repetitive 10-min coronary artery occlusions separated by 45-min periods of reflow; simultaneously, regional myocardial blood flow in the ischemic area was measured by (127)Xenon washout. In all dogs the increase in PmCO(2) from before to 10 min after the first occlusion (DeltaPmCO(2)) exceeded that during subsequent occlusions. In those dogs not receiving an intervention (controls), DeltaPmCO(2) during the third occlusion was similar to that during the second occlusion. When propranolol, hyaluronidase, and nitroglycerin were administered to different groups of dogs before the third occlusion, each caused significantly smaller elevations in DeltaPmCO(2) than those occurring during the control second occlusion, and the combination of all three interventions induced the smallest increase in DeltaPmCO(2). Regional myocardial blood flow rose with hyaluronidase and was unchanged with propranolol, nitroglycerin, and the three drugs in combination. In contrast to these beneficial interventions, isoproterenol infused with the third occlusion caused a higher DeltaPmCO(2) than during the control second occlusion. It is concluded, first, that interventions that modify the severity of ischemia can be evaluated by measuring intramural carbon dioxide tension; second, that propranolol, hyaluronidase, and nitroglycerin reduce ischemic injury, whereas isoproterenol increases it; and third, that the combination of propranolol, hyaluronidase, and nitroglycerin exerts an additive beneficial effect on ischemia.

Noninvasive detection of intracardiac thrombosis: 131-I fibrinogen cardiac survey.

Cardiac survey following administration of 131-I autologous fibrinogen is a noninvasive technique for the detection of intracardiac thrombosis. Fibrinogen is isolated from plasma by a rapid salting-out method with ammonium sulfate and is iodinated with chloramine T. The purity of 131-I fibrinogen, expressed as clottable radioactivity, is greater than 90%. Cardiac survey consisting of serial gamma camera imaging or rectilinear scanning after intravenous administration of 131-I fibrinogen was conducted in dogs with freshly induced thrombosis of the left atrial appendage. An accumulation of radioactivity was detectable in the area of the left atrium and confirmed in each of nine dogs sacrificed. Similarly, 20 patients with heart disease predisposing to intracardiac thrombosis were surveyed. Eight of nine patients with positive studies and 11 of 11 with negative studies were confirmed subsequently at surgery or autopsy. Cardiac survey with 131-I fibrinogen is a simple and noninvasive method of detecting intracardiac thrombosis.

Regional Changes in Myocardial Acid Production during Ischemic Arrest: A Comparison of Sanguineous and Asanguineous Cardioplegia

Regional differences in myocardial acid production have not been characterized during administration of either asanguineous or sanguineous cardioplegia. To investigate this, miniature glass pH electrodes were placed in the right ventricular (RV) myocardium, the left ventricular subendocardial (LV endo) region, and the subepicardial (LV epi) region in a canine model. Multiple doses of either blood cardioplegia (Group 1; N = 11) or crystalloid cardioplegia (Group 2; N = 11) were administered during 4 hours of aortic cross-clamping. The accumulation of hydrogen ions during the cross-clamp period was greater in Group 2 than Group 1 in the LV endo region (629 +/- 79 nm/L versus 66 +/- 31 nm/L; p less than 0.001), the LV epi region (623 +/- 66 nm/L versus 72 +/- 32 nm/L; p less than 0.001), and the RV myocardium (814 +/- 296 nm/L versus 150 +/- 54 nm/L; p less than 0.05). Within each group, the time course of myocardial pH and the accumulation of hydrogen ions did not differ among the LV endo region, LV epi region, and the RV myocardium (p = not significant). These data indicate that transmural and interventricular differences in myocardial pH and hydrogen ion accumulation are not produced in the vented, arrested canine heart. In addition, when compared with asanguineous cardioplegia, blood cardioplegia globally and transmurally reduces acid accumulation during ischemic arrest.

Improved Oxygenation During Bronchoscopy

Abstract A method for the continuous administration of oxygen during fiberoptic bronchoscopy is described. The procedure has proved effective in elevating marginal intraoperative arterial oxygen tensions to safe levels in most patients. The technique is based on insufflation of oxygen through a fenestrated endotracheal balloon. This in no way further compromises the somewhat cramped conditions common with most forms of endoscopy.

Pulmonary embolism, pulmonary microcirculation, and thrombolytic therapy.

For over 30 years, the mainstay of the acute treatment of venous thromboembolism has been heparin therapy. Because it performed its task so well and has withstood the test of time, many have considered its use definitive. Heparin’s action, however, is only preventive. It stops enlargement and propagation of thrombi and, in doing so, prevents recurrent pulmonary embolism. It does not, however, have any direct action upon thromboemboli in the circulation. The therapeutic need, then, was for the development of an